General organization of the cardiovascular system 1.1 INTRODUCTION TO THE CARDIOVASCULAR SYSTEM
arteries to circulate though all the tissues of the body.
The primary function of the cardiovascular system is to deliver blood to the tissues, over long distances, and to evacuate waste products from the tissues. The cardiovascular system has many jobs: • The cellular distribution of oxygen and nutrients (amino acids, fatty acids, vitamins) • The elimination of cellular waste (carbon dioxide, lactates) • The transport of oxygen, carbon dioxide, and hormones • The regulation of body temperature, blood pH, water volume, mineral salt levels, etc. The system contributes to homeostasis by helping keep certain physiological values either constant or relatively stable. The cardiovascular system delivers oxygen and nutrients to the various tissues, according to a hierarchy of regional distribution: first the brain, then the kidneys, the splanchnic territory (digestive system), and finally the limbs.
1.1.2 Vascular network
1.1.1 Circulatory system The circulatory system refers to the cardiovascular and the lymphatic systems. The cardiovascular system comprises the heart and its vessels: arteries, capillaries, and veins. The heart is a hollow muscle that functions like a pump, propelling the blood through the ©
2011 Elsevier Ltd
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When looked at from an anatomical rather than a functional point of view, the vascular circuit can be divided in two (Fig. 1.1): • The systemic or great circulation carries oxygen and nutrients to the tissues. The systemic circuitry feeds the organs of the body through a series of blood vessels arising from the left ventricle via the aorta. The systemic veins collect blood from these organs and convey it back to the right atrium of the heart. • The pulmonary or small circulation denotes the shuttle between the heart, which generates the flow, and the lungs, which provides the oxygen. Through this short vascular network, blood moves from the right ventricle, by way of the pulmonary artery, and returns to the left atrium, via the pulmonary veins.
1.1.3 The heart The heart is a pair of valved muscular pumps whose different functions work in parallel. The ‘left heart’ distributes the systemic circulation, and the ‘right heart’ provides the pulmonary circulation. The blood flow delivered by the two circulations is more or less the same. However, because the resistance in the pulmonary arterioles is five or six times weaker than the
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General principles Brain
Lungs
Heart
• a ventricle that expels blood: – from the right ventricle, to the pulmonary artery to enter the lungs – from the left ventricle to the aorta, in the direction of the other organs. The main function of the heart is to maintain blood flow.
1.1.4 Vascular sections – resistance and capacitance In terms of hemodynamics, the right and left heart circuits operate in series. These sectors are nevertheless different in: • the pressure of their driving blood force • the compliance of their vessels • the resistance of their vessels to blood flow. The mechanical pressure in the vessels depends on the cardiac pump, the refilling pressure of the vessels, and the deformability or compliance of the vascular wall. The more compliant the blood vessel, the more volume can be added without causing a rise in pressure.
High pressure system
Other organs
Inferior limbs
Fig. 1.1 Systemic and pulmonary circulation.
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resistance in the systemic arterioles, the pressure is not the same in the two networks. Both sides of the heart have: • an atrium (once known as ‘oriellette’) that receives blood
The resistant, or high pressure system, displays high resistance and low compliance (the distension capacity of a vessel). It comprises all of the arteries of the systemic circulation from the left ventricle in systole, to as far as the arterioles. It contains only 10–15% of blood volume. In this system, the progressive ramifications and subdivisions diminish the caliber of the vessels, but increase the total sectional surface. Mean pressure in the aorta is 100 mmHg, six to seven times higher than in the pulmonary artery. Several subcompartments can be distinguished: • The reservoir vessels comprise the aorta and its large branches. Their walls are elastic and they convert, without notable modification in average pressure, the intermittent pressure of the cardiac pulsation into a smooth type of flow.
General organization of the cardiovascular system These are the main vessels of blood distribution to the periphery. • The arterioles are the site of regional resistance and are the regulatory vessels of blood flow. • The precapillary sphincters are smooth muscle bands that lie ‘before’ the capillaries and determine the flow at the entrance to the capillaries in order to control perfusion.
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1.1.5 Blood distribution
Low pressure system The capacitance, or low pressure system, has weak resistance and high compliance. It consists of the veins, right heart, pulmonary circulation, left atrium, and left ventricle, in diastole. The low pressure system retains 75–80% of blood volume. The remainder is found in the peripheral capillaries, which are also included as part of the low pressure system. This system is named for the relatively low pressure prevailing in it: on average 15 mmHg or 2 kPa. Owing to its large capacity and high compliance, it can act as a blood reservoir. This system’s capacity to hold blood regulates blood volume. Capillaries are the vessels of exchange between blood and tissues. Veins collect the blood and return it to the heart. The distribution of blood volumes is depicted in Fig. 1.2.
The cardiovascular system is designed to deliver oxygen and nutrients, according to the prevailing need: brain, then kidneys, splanchnic (digestive) territories, and limbs. Tissue blood flow or irrigation is adjusted precisely to the functional need of each tissue and organ – neither more nor less. In general, the most active tissues receive the greatest perfusion. The selection of one territory at the expense of another occurs by vasoconstriction (reduction in vessel caliber) in the neglected territories. Hyperthermia refers to an increase in blood supply to a tissue. By contrast, ischemia means the opposite: interrupted circulation within a tissue. The term active hyperthermia corresponds to an increased flow rate linked to increased tissue or organ activity. This is what happens in skeletal muscles during strenuous activity.
At rest At rest, cardiac output is around 5–6 L/min. The blood arrives in the tissues with the same average arterial pressure and approximately the same force. The blood flow within each organ depends solely on the extent of the vascularization and local arterial resistance. At rest, the digestive system and the kidneys attract about 50% of the blood distributed, whereas the heart brings in only 3–4% (Table 1.1 & Fig. 1.3).
Lungs 9%
Capillaries 5%
Arterioles 7% Large arteries 8%
Veins 64%
Fig. 1.2 Blood volume distribution (Silbernagl & Despopoulos 1985).
Heart 7%
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General principles
With exertion
1.1.6 Types of circulation
During heavy muscle work, the cardiac output increases to 17–25 L/min. Distribution to various tissues is modified, with the exception of the brain, whose supply remains remarkably constant (Table 1.2 & Fig. 1.3).
Depending on the purpose of the blood running through an organ, three types of circulation occur: • Nourishing circulation: cerebral arteries, muscular arteries, coronary arteries, bronchial arteries, hepatic arteries
Table 1.1 Resting blood flow
Table 1.2 Blood flow on exertion
Organs
Organs
% total
% total
Digestive
25
Heart
4
Kidneys
20
Brain
14
Brain
13
Kidney
20
Skin
9
Skeletal muscle
22
Heart
4
Skin
8
Other organs
750
750 12 500 Brain
750
Heart
250
Skeletal muscles
1200
Skin
500
Kidneys
1100
Abdomen
1400
Others
600
Total blood flow at rest : 5 800 mL/min
1900
600 600 400
Total blood flow during intense exercise : 17 500 mL/min
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Fig. 1.3 Blood output at rest and with exertion. Adapted from Marieb (2005).
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General organization of the cardiovascular system • Functional circulation: pulmonary arteries, portal vein • Mixed circulation: renal arteries, mesenteric arteries, cutaneous arteries. Blood flow distribution calculation does not clearly reflect the true needs of the organ, but accounts for circulatory draw based on extra work or environmental changes. For this reason the oxygen extraction coefficient provides a clearer picture of the intrinsic requirement of an organ than the isolated notion of blood flow.
1.2 THE HEART Formed in the third week in embryo, the heart remains rhythmic throughout life: 100 000 beats per day, 2 billion times in an average lifetime. One is hard pressed to imagine a machine capable of the same work. It has its own rhythm, independent of our will, adjustable according to events taking place outside or inside the body. The heart can race following an emotion, an exertion, or a high temperature. Its weight varies according to a person’s size and sex, averaging 275 g.
1.2.1 Anatomy review Form and orientation On the outside, the heart is a somewhat rounded conical form, lying on its side. • The apex of the heart is directed caudad, anteriorly and to the left. • The base of the heart, opposite the apex, is directed cephalad, and faces mainly posteriorly and to the right. • The main axis of the heart is oblique from posterior to anterior, from right to left. This obliqueness varies with the shape of the thorax; the heart lying more vertically in a narrower thorax.
Chambers The hollow muscle of the heart is divided into right and left parts by the interatrial septum. Each side of the heart has two chambers, an
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atrium (superior chamber) and a ventricle (lower chamber) connected by atrioventricular valves (Fig. 1.4). Atria Functionally, the atria are receiving chambers, into which blood flows from the circulation. As they do not have to contract strongly for the blood to pass into the ventricles just beneath them, the atria are small in size, and their walls are relatively thin. They contribute only modestly to the filling of the ventricles and the pumping action of the heart. Three veins enter the right atrium: • the superior vena cava • the inferior vena cava • the coronary sinus. Four pulmonary veins, two right and two left, enter the left atrium. Ventricles The ventricles, with their thick walls, form the bulk of the heart. From a functional viewpoint, they insure that the heart pumps properly. The right ventricle ejects the blood into the pulmonary trunk, which dispatches it into the lungs where gaseous exchange occurs. The left ventricle pumps blood into the aorta whose successive branches feed all the organs. Valves Valves, which separate the chambers, keep the blood flowing in one direction inside the heart.
Arterioventricular valves Each arterioventricular valve is formed by a fold of endocardium, reinforced by fibrous tissue. The right arterioventricular valve comprises of three valvules or cuspids (tricuspid valve), whereas the left arterioventricular valve has just two (bicuspid or mitral valve). They prevent the blood from flowing back during contraction of the ventricles. Arterial valves The valves of the aorta and the pulmonary trunk are located at the base of the aorta and the pulmonary trunk. Each of these valves, also called sigmoid, have there semilunar
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General principles
Aortic arch
Pulmonary artery Superior vena cava
Pulmonary veins Right atrium Pulmonary valvule
Left atrium Aortic valve Mitral valvule
Tricuspid valvule
Interventricular septum Left ventricle
Right ventricle Myocardium Inferior vena cava
Fig. 1.4 Cardiac chambers
valvules in the form of a crescent or a pocket. They open when the ventricles contract to pump the blood into the arterial trunk. They close and prevent blood from returning to the ventricles, during ventricular relaxation when the ventricles are refilling.
Myocardium The myocardium is made up of: • striated muscle fibers anchored to a fibrous framework • differentiated fibers forming the nodal tissue or conducting system of the heart.
Structure of the heart
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The heart is formed by a thick muscle called the myocardium, and lined internally by a smooth membrane layer called the endocardium. This arrangement is continuous in the pericardium, which is a double-walled sac composed of the serous pericardium layer and the fibrous pericardium layer.
Fibrous skeleton The fibrous framework or fibrous skeleton of the heart denotes the four rings of dense collagen that surround the orifices of the auriculoventricular and arterial valves. The two auriculoventricular rings and the aortic ring are located in the same fibrous body. The
General organization of the cardiovascular system pulmonary ring is situated anterior and superior to the others.
The ventricular fibers fasten solely to the periphery of the auriculoventricular rings.
Muscular fibers The heart is composed of ventricular and auricular fibers (Fig. 1.5). The ventricular fibers consist of: • fibers specific to each ventricle whose oblique moorings attach to the fibrous rings of the skeleton • Common fibers that envelop and join the two sacs formed by the individual fibers. ‘The ventricular heart is composed of two muscular sacs contained in a third muscular sac’ (Winslow, cited by Bouchet & Cuilleret).
Conduction system of the heart
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The heart has an intrinsic system by which it is able to beat without the participation of external nerves. This property is termed autorhythmicity. This autonomous command system is the tissue nodal or impulse conducting system (Fig. 1.6) made up of three parts: • The sinoatrial (SA) node (Keith and Flack) is located in the wall of the right atrium, at the junction of the superior vena cava and the external atrial orifice. This is the pacemaker of the heart.
Fibrous ring of the ostium of the aorta Muscle fibers of the left ventricle (middle layer)
Fibrous ring of the ostium of the pulmonary trunk
Trajectory of superficial muscle fibers of the myocardial layer
Right ventricle (middle layer)
Fig. 1.5 Tendinomuscular structure of the heart.
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General principles
Left atrium Sinoatrial node Internodal tract Right atrium Auriculoventricular node
Auriculoventricular bundle (bundle of His) Cardiac conducting muscle fibers Interventricular septum
Purkinje fibers (branches of AV bundles)
Cardiac conducting myofibers
Fig. 1.6 Conduction system of the heart.
• The atrioventricular (AV) node (Aschoff– Tawara) is a smaller collection of nodal tissue situated in the interauricular septum, near the atrioventricular valves. It functions as a secondary pacemaker. • The atrioventricular (AV) bundle (of His) is a collection of specialized muscle fibers beginning at the AV node and dividing into right and left bundles at the junction of the membranous and muscular parts of the interventricular septum. • The AV bundles proceed on either side of the septum, deep to the endocardium, and then ramify into the subendocardial branches (Purkinje network), which extend into the walls of the respective ventricles.
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Endocardium The endocardium is a thin internal layer lining all cardiac cavities and continuous with the endothelium of the vessels. This fine
smooth glistening membrane permits the blood to circulate easily inside the heart. A fold of endocardium forms the valvules of the orifices anchored on the fibrous skeleton, arising from the periorificial ring. Pericardium The pericardium is a fibroserous sac surrounding the heart and the roots of the great vessels at the base of the heart. Extending 12–14 cm in height with a width of 13– 14 cm, it comprises two layers: • The serosal pericardium: this glistening serous membrane facilitates all manner of movements, glidings, and deformations of the heart, in relation to its neighboring organs. • The fibrous pericardium clothes the serous pericardium. The heart is protected and somewhat tethered in place inside this fibrous sac.
General organization of the cardiovascular system Generally in the body, mobile organs or those capable of significant movement are often surrounded by connective tissue that attenuates mechanical forces at play, thus harmonizing connections with neighboring organs. The lungs are a good example of this: they deploy considerable mechanical forces within the thorax.
Serous pericardium Between the parietal and visceral layers of the serous pericardium is a virtual space called the pericardial cavity. The visceral layer, or epicardium, covers the myocardium, the coronary vessels, and the structural fat layer on the surface of the heart, and is reflected onto the aorta, pulmonary trunk, veins, and vena cavae. The parietal layer covers the visceral layer and lines the internal surface of the fibrous pericardium. The pericardial cavity is contained between the two layers of serous pericardium. It is a space designed for the frictionless gliding of the heart, lubricated by several cubic centimeters of pericardial fluid. • The large pericardial cavity surrounds the heart and expands over the vascular trunks. • The transverse pericardial sinus, or sinus of Theile, is a reflection of the large cavity,
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located behind the arterial and venous trunks.
Fibrous pericardium The fibrous pericardium is the external layer of the fibrous serous sac that encloses the heart. The internal layer of the fibrous pericardium is lined with the parietal serous pericardium. Its exterior surface is reinforced by a layer of sturdy intertwined collagen fibers. Thus, its elasticity is reduced and this unyielding quality is what protects the heart from overexpansion. The fibrous pericardium is attached to the thorax wall and neighboring organs by ligaments (Fig. 1.7, Box 1.1): • Caudally: to the central tendon of the diaphragm, by the phrenicopericardial ligaments • Ventrally: to the sternum by the sternopericardial ligaments • Dorsally: to the vertebral column by the vertebropericardial ligaments. Several more modest fibers connect the pericardium to the bifurcation of the trachea, the thoracic esophagus, and laterally to the pulmonary veins and bronchi. Vestiges of the pleuropericardial membrane unite the mediastinal pleura and the fibrous pericardium.
Box 1.1 Pericardial ligaments Physicians and surgeons are often surprised to hear us use the term ‘ligament’ to describe structures mooring the pericardium. The anatomy is nevertheless very clear on the subject, and we are not inventing this. Several authors, such as Testut, Cruveilher, Paturnet, and a few contemporary anatomists such as Kamina, have given excellent descriptions of these structures and the individual ligament fiber directions identifiable within the intrathoracic connective tissue. Curiously, description of these ligaments is lacking in most English-language anatomy texts. It is true that very often surgeons do not find
them, or in any case do not look for them, in the course of operations. However, the dissections we have performed on unpreserved fresh cadavers clearly show the organization of the pericardial ligaments. We would draw the reader’s attention to the fact that descriptive anatomy is a science of observation, and a somewhat biased procedure. In effect, to view certain discrete structures clearly, it is necessary to ‘clean’ and remove certain ‘parasitic’ structures that obstruct their observation. For example, to render the arterial tree clearly visible, all surrounding tissues must be cleared off: fascia, nerves, veins, muscle, Continued
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General principles
Box 1.1 Pericardial ligaments—cont’d aponeurosis, etc. In the case of muscles, they must be divested of their aponeurotic envelopes … It is generally from what anatomists justifiably call a ‘preparation’ that anatomical schematics and descriptions have been developed to facilitate the teaching of anatomy. The same applies in the observation of visceral ligaments: the connective tissue must be exposed and all the rest discarded. It is not usual to dissect away what are termed ‘noble’ structures with the sole aim of conserving connective tissue, reputed to be uninteresting and generally the first discarded in any dissection. However, it is only under these conditions that these ligaments can be observed. Bear in mind, as well, that visceral ligaments are not exposed to the same mechanical strain to which articular ligaments are subjected. As a consequence, their development and sturdiness are not
comparable to those of the cruciate ligament of the knee or lateral ligaments of the elbow, for example! Visceral ligamentous structures are tenuous arrangements that play a suspensory and stabilizing role for the viscera, within a precise mechanical context and a particular pressure system. The visceral mechanism is a subtle and singular mechanism, a system of mutually adaptive parts working together for optimal cohabitation of the organs. To summarize, it is necessary to carry out dissection research biased towards making these ligaments clearly visible, and, if some anatomists fail to find them, it is simply because they are not looking for them. This holds true for the uterine ligaments, prostatic ligaments, and, in a general way, for all visceral ligaments, whose existence is sometimes contested or called into question.
Esophagus Trachea
Vertebropleural ligament Aorta Vertebropericardial ligaments
Superior sternopericardial ligament
Right bronchus
Inferior vena cava Right phrenicopericardial ligament
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Fig. 1.7 Ligamentous connections of the pericardium.
Inferior sternopericardial ligament Anterior phrenicopericardial ligament Diaphragm
General organization of the cardiovascular system
Cardiac vessels The heart has many vascular connections. They can be described anatomically as vasa publica and vasa privata. Vasa publica These are the great vessels at the base of the heart, such as the aorta and the pulmonary artery which depart the left and right ventricles. Here also we find the vena cavae and the pulmonary veins, connected to the right and left atria respectively. Vasa privata These are the coronary arteries (Fig. 1.8A,B) that feed the heart. The left and right coronary arteries are the first collateral branches of the aorta. They transport nutrients and oxygen to the myocardium. The coronary veins eliminate waste and collect in the coronary sinus. This main drainage vessel of the heart empties into the right atrium. The coronary arteries function almost only during diastole (especially at the left ventricle) because the vessels are compressed by the contractile cardiac muscle during systole. The small anastomoses between them are not quite sufficient to constitute a collateral circulation. These branches are considered functional terminals. In case of obstruction, the part of the myocardium affected is supplied inadequately and a myocardial infarction results. Apart from obstructive causes such as atheroma or atherosclerosis, coronary arteries can spasm due to: • cold • anxiety • physical exercise.
1.2.2 Extrinsic innervation The heart is an autonomous organ endowed with an intrinsic conduction system, whose activity coordinates the cardiac cycle. However, some functions of the heart can be altered by extrinsic influences, principally nervous and hormonal.
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The efferent cardiac nerves, via which the function of the heart can be modified, are sympathetic and parasympathetic fibers (Fig. 1.9).
Sympathetic system The sympathetic cardiac fibers derive from the cervical sympathetic system. They reach the organ by three pairs of cardiac nerves: superior, middle, and inferior (right and left). These nerves issue from the lateral vertebral chain arising from the superior, middle, and inferior cervical ganglia (also called the stellate ganglion) respectively. Note that the middle ganglion is not always present, in which case it is fused to the inferior ganglion. In these postganglionic fibers, the relay occurs in the paravertebral ganglia. The cell bodies of the preganglionic neurons are located in the lateral horn of the cervicothoracic spinal cord, between C4 and T4. After passage in the cardiac plexus, the sympathetic fibers are distributed to all the nodal and myocardial tissues.
Parasympathetic system The major cardiac parasympathetic supply runs from the right and left vagus (X) nerves, where again they descend by three paired branches, arising above the recurrent nerve, from the recurrent nerve itself, and below the recurrent nerve. These are preganglionic fibers that derive essentially from the dorsal vagal nucleus. After passage in the cardiac plexus, they relay in the atrial wall and end in the atrioventricular (AV) and sinoatrial (SA) nodes. This innervation is composed of very short postganglionic neurons that do not invade the ventricle (Buser & Imbert 1994). As such, they differ notably from sympathetic system innervation.
Cardiac plexus Sympathetic and parasympathetic fibers unite to compose two cardiac plexuses.
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General principles
Superior vena cava
Pulmonary veins Left coronary artery
Aortic valve
Pulmonary valvule Circumflex branch
Right coronary artery Coronary sinus
Right marginal branch
Left marginal branch Anterior interventricular branch Posterior interventricular branch
A. Anterior view
Coronary sinus
Right atrioventricular valve
Left atrioventricular valve
Right coronary artery
Left coronary artery
Aortic valve
Pulmonary valve
B. Superior view after removal of the atria
Fig. 1.8 Coronary arteries. (A) Anterior view. (B) Superior view after removal of the atria.
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General organization of the cardiovascular system
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Stellate ganglion
Vagus nerve
Recurrent vagus nerve
Sympathetic Parasympathetic
Fig. 1.9 Autonomic innervation of the heart.
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General principles • The arterial plexus is formed from the superior part of the sympathetic and vagus nerves. The fibers descend in front of and behind the arterial trunk, and constitute the ganglion of Wrisberg, situated beneath the aortic arch and in front of the right pulmonary artery. The cardiac plexus gives rise to the periarterial coronary plexus, from which the subpericardial and subendocardial plexuses originate. • The venous plexus originates below the arterial plexus, descending behind the pulmonary artery to reach the atrial part of the heart. On the posterior surface of the right atrium, it forms the central ganglion of Perman.
Actions Although there is much intermingling of the sympathetic and parasympathetic fibers in the cardiac plexus, it is possible to systematize their actions. Two categories of fiber, centrifugal (visceromotor) and centripetal (viscerosensory), can be isolated. Both types are designed to regulate the heart rhythm and adapt the cardiovascular tone to the changing needs of the body. Adaptation of cardiac activity The following aspects of cardiac activity can be modified: • the frequency of contractions (chronotropism) • the force of contraction (inotropism) • muscle tone (tonotropic effect) • muscular excitability (bathmotropism) • the speed of muscle relaxation following contraction (lusitropic effect).
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Sympathetic action Sympathetic fibers innervate all regions of the heart: the sinoatrial node, atrioventricular node, atrial myocardium, ventricular myocardium (particularly the left) and coronary arteries. Postganglionic sympathetic cardiac fibers mediate by way of their neurotransmitter,
norepinephrine (noradrenaline). Norepinephrine reacts with type β1 adrenoreceptors, which represent about 80% of all heart receptors, the remaining 20% being type β2. Circulating catecholamines, norepinephrine and epinephrine (adrenaline), secreted by the adrenal medulla, have the same effect on the heart as sympathetic innervation. Sympathetic stimulation increases cardiac output by: • increasing the heart rate (tachycardia, from the Greek tachus, meaning rapid) by acting on the sinoatrial node (positive chronotropic effect) • stimulating conduction towards the AV node (positive dromotropic effect) • increasing the power of the ventricular contraction (positive inotropic effect) • increasing cardiac and vascular tonus (positive tonotropic effect) • accelerating the speed at which the heart muscle relaxes following contraction (positive lusitropic effect) • increasing myocardial excitability (positive bathmotropic effect). The sympathetic nervous system comes into play in the course of everyday life, such as during physical exercise, when under stress or hemorrhaging. Parasympathetic action Parasympathetic fibers innervate the sinoatrial node, the atrioventricular node, and the myocardium of the atria. There is virtually no parasympathetic supply to the ventricles. The neurotransmitter of the major postganglionic sympathetic cardiac fibers is acetylcholine. The cardiac receptors for acetylcholine are the muscarinic type. At the sinoatrial node, the muscarinic receptors are seven times more plentiful than sympathetic receptors. The action of the parasympathetic system is opposite to that of the sympathetic, and its effects are more limited. The lowering of cardiac output is achieved by: • lowering the heart rate by vagal fibers that terminate on the sinoatrial node
General organization of the cardiovascular system (negative chronotropic effect, bradycardia (from the Greek bradus, meaning slow) • stimulating impulse conduction towards the atrioventricular node (negative dromotropic effect) • indirectly reducing the force of the heartbeat contraction (negative inotropic effect). NB: The viscerosensory fibers of the vagus nerve transmit information about pressure and parietal stretching. This partly explains how the heart rate can be lowered by applying manual techniques on the heart or on the large vessels. Vagal sympathetic tone In the heart alone, isolated from hormonal or nervous influence, the intrinsic heart rate is around 100 beats per minute (bpm). This corresponds to the spontaneous rhythm of the sinoatrial node. In the living person, the resting heart rate averages about 70 bpm, due to the continuous and dominant tonifying activity of the sympathetic nervous system. There is a variation of this vagosympathetic tone – vagal break – during the evening and night. • The vagal influence on the heart rate increases after the evening meal and during sleep. • The influence of the sympathetic system is strongest during the day (Coumel 1993, Coumel et al 1994). The sympathetic–parasympathetic balance varies in connection with respiration. • With inhalation the vagal influence diminishes and the sympathetic tone rises. Thus the cardiac rate naturally increases during inspiration. • With exhalation the sympathetic tone falls while the vagal parasympathetic tone increases. The heart rate decreases during expiration. These completely normal phenomena, referred to as respiratory sinoatrial arrhythmias, are not at all pathological. On the contrary, they are a feature of a well functioning autonomic nervous system.
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1.3 VESSELS Vessels can be divided in three main categories: arteries, capillaries, and veins. Laid end to end, the blood vessels of a human adult would measure about 100 000 km. The arteries, which transport the blood from the heart, ‘branch out’ or ‘divide’ into smaller and smaller vessels. The veins, which carry the blood towards the heart, merge or converge to form larger and larger trunks.
1.3.1 Histology Vascular walls The overall structural plan of the blood and lymphatic vessel walls is in large part the same. However, depending on function and particular demands, vessel walls display different characteristics. Vessel walls (Fig. 1.10) have three layers (Latin, tunicae): • the tunica intima or internal layer • the tunica media or middle layer • the tunica adventitia or external layer. Tunica intima The tunica intima is a layer of endothelial cells that rest on a basal membrane and a slight thickness of connective tissue. In arteries, an elastic fenestrated membrane is found. The tunica intima serves as an exchange for gas, liquids, and oxygen. It is directly subject to the pressure of circulating blood. The endothelium produces vasodilator agents. Tunica media The middle layer is composed of smooth muscle cells and an elastic network. This layer resists dilation of the vessel wall in relation to changes in blood pressure. It can alter the vascular lumina, as a function of the degree of tension in the smooth muscle cells. • arterial pressure within the vascular system is regulated mainly by the degree of tonus (firmness) of the smooth muscle in the arteriole wall. Arteries are a continuum, and the farther away from the heart, the fewer the elastic
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General principles
Tunica adventitia
Tunica media
Elastic membrane
Valve
Endothelium (tunica intima)
Fig. 1.10 Vascular walls.
fibers and the greater the quantity of smooth muscle fibers.
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Tunica adventitia The outer coat is essentially made up of connective tissue fibers. The cells and the fibrous network of this layer are laid out along the vessel axis. This layer allows the vessel to adapt to its environment, and to resist outside influences, notably vessel strain, such as overstretch. In the large vessels, the vasa privata, called the vasa vasorum, is encountered at this layer. These tiny vessels supply the outermost layers of the vessel wall. Autonomic nerve fibers, called the nervi vasorum, supply the musculature of the blood vessels that penetrate the tunica adventitia.
Arterial smooth muscle fibers The vascular smooth muscle fibers, or vascular myocytes, are composed of short fusiform fibers (maximum 0.4 mm). These cardiac pacemaker cells share the capacity to create an intrinsic cycle of electrical activity called automaticity. The contraction of vascular myocyte responds to two types of mechanism: • The electromechanical coupling that occurs at the membranous receptors, where different substances fasten to cause a contraction, without altering the polarity of the cell membrane • The electromechanical coupling that initiates the neuromuscular synapse and produces a depolarization of the membrane.
General organization of the cardiovascular system The relaxation of vascular myocytes may also involve a chemicomechanical or electromagnetic coupling. Many nervous and hormonal factors are thus susceptible to the rate of contraction of the vascular myocytes. • The sympathetic system, epinephrine, norepinephrine, vasopressin, angiotensin, etc., all have a vasoconstricting effect. • The parasympathetic system, natriuretic atrial peptide and adrenomedullin, etc., all have a relaxing effect.
Endothelium Blood vessels are lined with endothelium, made of very smooth flattened cells designed to reduce blood friction. This barrier between the blood and the rest of the vessel produces these vasoactive factors. • nitrogen monoxide • endothelin • angiogenic stimulants (formation of neovessels) • histamine, a local mediator found in connective tissue (mastocytes) and some blood cells.
1.3.2 Arteries Arterial network According to size and function, the arteries can be divided into three groups: elastic arteries, muscular arteries, and arterioles. Elastic arteries The elastic arteries are the largest type and lie nearest the heart. The aorta and branches of the aorta are in this group. They are thickwalled structures of large caliber able to ‘conduct’ the blood at low resistance, from the heart to the medium size arteries. For this reason they are termed conducting arteries. The elastic arteries contain more elastin than all other vessels. Muscular arteries The muscular arteries carry blood to the various parts of the body. They are called
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distributing arteries. Their interior diameter runs from 1 cm (the size of your little finger) to 0.3 mm (the size of pencil lead). Their middle tunica layer is the thickest of all the vessels. These arteries contain more smooth muscle fibers and less elastic tissue than the elastic arteries. Although they play a more active role in vasoconstriction, they are also less extensible. Arterioles The arterioles are the smallest arteries, with a caliber of between 0.3 mm and 10 microns (µm). The largest arterioles are endowed with three tunica, but the smallest arterioles, which lead into capillary beds, constitutes no more than a single layer of smooth muscle cells, arranged in a spiral around endothelium. In all types of arteriole the adventitia is much reduced. The flow of blood in the capillary beds is determined by variations in arteriole diameter. Selective perfusion occurs in response to the metabolic need of the tissues. Nervous stimulation and local chemical influences signal the smooth muscles of the arteriole wall. When the arterioles contract (vasoconstriction) the blood bypasses the tissues, and when they dilate (vasodilation) the blood flow in the local capillaries increases markedly.
Anastomoses Anastomoses are numerous and varied. This natural communication between arteries permits the constant supply to the body’s countless tissues (Fig. 1.11). The different types of arterial anastomosis are described below. Inosculation Two vessels of the same caliber can bend towards each other to cross-connect. The left and right gastric arteries are good examples. Transversal When two arteries run parallel, they can exchange cross-pieces that run perpendicular to them.
19
General principles
Longitudinal anastomosis
Anastomosis by inosculation
Anastomosis by convergence
Transverse anastomosis
Fig. 1.11 Types of arterial anastomosis.
Convergence Two arteries that are oblique in relation to each other can converge into a single trunk; this happens, for example, with the vertebral arteries and the basilar trunk. Plexus The term plexus signifies interlacing or braiding. Arterial plexuses are rare in the large trunks, but common nearer the capillaries.
Vasculature and innervation Vasa vasorum The vasa vasorum are encountered in the large arteries and veins.
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Nervi nervorum The autonomic nerve fibers innervate the musculature of the vessels penetrating the outermost tunica (adventitia). These vasomotor nerves derive from the sympathetic system. The diameter of the vessels is controlled by the nerve fibers that go to the smooth muscle fibers. The fibers of the amyelinic plexus are motor and sensory. Some myelinated sensory fibers run in the adventitia.
Angiogenesis Angiogenesis is the formation of new blood vessels. During embryological development, it is a primary activity; after birth, it continues in various situations: • the scarring of wounds • regeneration of the uterine lining after ovulation • the make-up of the corpus luteum after ovulation • vessel development around obstructed coronaries • arteriole formation in the adipose tissue during weight gain • the proliferation of arterioles to feed tumor cells. Malignant tumor cells secrete a protein, called tumor angiogenesis factor (TAF), that stimulates the development of blood vessels.
1.3.3 Capillaries Capillaries are very thin-walled structures with no contractile properties. They divide and branch, without their caliber diminishing. They contain no more than 5% of the
General organization of the cardiovascular system total blood volume. The radius of capillaries is 3000 times smaller than that of the aorta, and 100 times finer than a strand of hair. There are 10 to 40 million capillaries, giving them an exchange surface on the order of 600 square miles. The number of capillaries in organs is determined by their metabolic function. Lungs have the largest capillary network, necessary for the transformation of venous blood into arterial blood. In organs such as the liver, spleen and thyroid, capillaries are also plentiful. NB: Our viscoelasticity techniques have a large effect on capillary function.
Capillary bed Capillaries are generally arranged in networks called capillary beds (Fig. 1.12). There are between 10 and 100 true capillaries in a capillary bed, depending on the organ or tissue supplied. In most regions of the body, the capillary beds are made up of two types of vessel: • Vascular diversion vessels which consist of a metarteriole and a thoroughfare channel directly linking the arteriole and the venule, on either side of the bed • The true capillaries, where blood and interstitial fluid are exchanged.
Microcirculation The circulation of blood from an arteriole to a venule across a capillary bed is called microcirculation. Blood flow slackens in the capillaries to permit the exchange of nutrients and other cellular material between the blood and the surrounding tissue. Red blood cells can pass through only singly, by deforming. By altering the degree of tonus in their smooth muscle walls, arterioles can regulate blood pressure and thus the perfusion of a given region. A cuff of smooth muscle called a precapillary sphincter surrounds the root of each true capillary that detaches itself from the metarteriole. Like a tiny valve, it controls the flow of blood through the capillary.
1
If the precapillary sphincters dilate, blood flows in the true capillaries and contributes to the exchange with the tissue cells. If the precapillary sphincter contracts, blood flows into the metarteriole and the thoroughfare channel, bypassing the true capillaries and the cells. Depending on the requirement of the organism or of a given organ, blood can flood the capillary bed, or bypass it entirely.
1.3.4 Veins Veins are blood vessels that return blood from the capillary bed to the heart, under low pressure.
Walls The walls of veins are thinner than those of their companion arteries. Although vein walls are comprised of the same three tunica, there is less muscular and elastic tissue in the middle coat. Veins flatten when empty. Very extensible transversally, their diameter can be multiplied by five, as opposed to just two for the arteries.
Number Veins are about twice as numerous as arteries, giving them a network approaching 200 000 km. There are two veins for every artery, except in regions where vessels are of large caliber: the knee, armpit, thoracic inlet. Veins have many anastomoses. The large veins are rectilinear (straight lines).
Capacity Venous tributaries converge into larger and larger trunks, and the total venous surface diminishes as veins approach the heart. Like a tree, the total volume of peripheral branches is greater than that of the terminal trunk.
Valves Certain veins have valves that permit blood to flow towards the heart but not in a reverse direction. These flap valves are folds of the
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General principles Vascular diversion
Sympathetic innervation Thoroughfare channel Metarteriole Precapillary sphincters
Postcapillary venule
Terminal arteriole
A
Pericyte
True capillaries
Sphincters open Vascular diversion
Sympathetic innervation Thoroughfare channel Metarteriole Precapillary sphincters
Postcapillary venule
Terminal arteriole
Pericyte
B True capillaries
Sphincters closed
Fig. 1.12 Capillary bed.
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General organization of the cardiovascular system tunica intima, reinforced by connective tissue. Semilunar folds present a concavity towards the heart. They function like safety valves, operating in companion and opposing pairs. Valves are abundant in the veins of the limbs, especially the lower extremities, where the blood must oppose the pull of gravity when an individual stands. Skeletal muscle contraction compresses the veins and helps to push the blood superiorly towards the heart. Valves are absent in the small-caliber veins, just as there are no valves in the large thoracic and abdominal veins.
Venous sinus A venous sinus is a vein with a thin wall of endothelium that is devoid of smooth muscle to regulate its diameter. The thick connective tissue surrounding it lends the support normally provided by the tunica media and tunica adventitia. For example, the cranial venous sinuses, reinforced by dura mater, convey the venous blood from the brain to orifices at the base of the skull. The coronary sinus of the heart has the same kind of arrangement.
Properties Veins are called capacitance vessels (low pressure). Thanks to their wide lumina and ability to expand, they have the capacity to contain a large proportion of the body’s blood. At any given time, veins contain as much as twothirds of corporeal blood, and constitute a blood reservoir. The vascular system is able to absorb most changes in blood volume. In case of hemorrhage, for example, the veins contract to avoid a sudden drop in blood pressure.
with their external milieu to take from it nutrients and oxygen, and to discharge into it their wastes, such as carbon dioxide and hydrogen ions.
1.4.1 Functions of blood Blood is a perpetually renewed, complex fluid that supports innumerable vital functions. Propelled by the heart, it circulates constantly, providing regulation, defense, and homeostasis.
Transport In the service of metabolism, blood transports: • oxygen from the lungs to the tissues, and carbon dioxide from the tissues to the lungs • products of digestion absorbed by the intestines and conveyed to the liver and other tissues • metabolic waste from tissues towards the lungs and kidneys. Blood participates in intercellular communication and systemic interactions via its role as an endocrine carrier or in the transport of neurotransmitters.
Regulation
The vascular network is depicted in Fig. 1.13.
The blood intervenes in several regulatory activities: • It participates in the exchange of water and mineral salts between various parts of the organism, thus contributing to the equilibrium of the internal environment in terms of pH and hydroelectrolytic balance. • It maintains vital homeothermia, by distributing heat from the deep organs towards the superficial tissues of the body.
1.4 BLOOD
Defense
Thanks to the constant exchange between blood and interstitial fluids, the cells of various tissues are brought into relationship
The blood contributes to immune defense through the phagocytes and antibodies contained in its plasma.
1.3.5 Vascular network
1
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ch
0.16×109
Crossed
9
5×10
in
in
s
s
an Uncrossed
cm
ve a
C av
rg La
no Ve
e
us
s le nu Ve 9
0.5×10
ve
br
s ri e illa C ap
Ar
te r
io
le
lb
Ar
rg
te r
e
ia
ar 1
La
rta Ao Number
s
ra
te r
ie
nc
s
he
s
es
General principles
2
3.2 2.6 0.8
0.3–0.06 0.002
0.0009
0.0025
0.15–0.7
1.6
Diameter of the single vessel cm
3500
2
2700 500 5.3
20
100
20
30
18
Common cross-sectional area 1550
cm3
900
550 180
250
250
300
Total volume of systemic circulation (without the heart)
Common volume of blood
Fig. 1.13 Vascular network.
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250
125 4.41
General organization of the cardiovascular system
Hemostasis Hemostasis describes several biological phenomena involved in the cessation of bleeding. Platelet clumping occurs at the site of bleeding and then coagulation takes over, whereby circulating fibrinogen is converted to a mesh of insoluble fibrin, called a clot.
1.4.2 Blood volume According to Laborit (1961), the total blood mass in humans comprises on average 7–9% of body weight; about 13 pounds for people and animals of average size. This amounts to 5–6 L, but varies with physiology and physiopathology. It is generally assumed that the volume is about 75 mL/kg in men and about 65 mL/kg in women.
1.4.3 Composition Blood consists of several elements (blood cells), suspended in a clear fluid called plasma.
Plasma Plasma is what remains once the cellular components of blood that has been rendered incoagulable have been centrifuged off. It contains about 70–80 g protein/L. When blood coagulates, the clot is the result of fibrin, a protein that precipitates out and immobilizes blood cells, and blood serum in an insoluble network.
Blood cells Erythrocytes or red blood cells Under the microscope, erythrocytes appear like biconcave discs. The surface area of all erythrocytes is estimated at 3000 m2. The diameter of a single cell is 7.2 µm, slightly larger in venous blood than in arterial blood. In a normal adult, there are approximately 5 million cells per cubic millimeter of blood. Erythrocytes are elastic and deformable. When crossing a capillary, their caliber is sometimes less than their diameter.
1
Red blood cells are one-third water. Their solid part is 90% hemoglobin. Hemoglobin carries oxygen to the cells. This respiratory pigment of the blood transports oxygen and carbonic anhydride, regulates pH balance, gives rise to bilirubin, and gives the blood its red color. An erythrocyte normally lasts for 100–120 days, before being broken down in the spleen. Leukocytes, or white blood cells White blood cells are found in blood and lymph, cerebrospinal fluid, lymphatic ganglions, connective tissue, and inflammatory effusions, as they are mobile and migratory. Their average dimension varies between 9 and 18 µm. Normal blood values are about 8000 leukocytes per cubic millimeter. This increases during digestion and with pathology. Leukocytes are classified in two groups according to the shape of their nuclei; about one-third are mononuclear and two-thirds are polynuclear. White blood cells are able to squeeze through intercellular spaces by way of diapedesis, and migrate by ameboid movements. Cellular movement is initiated by pleudopods. This distinctive motility is controlled by chemotaxis and is especially well developed in the polynuclear neutrophils. Leukocytes are able to glide in the interstitium and migrate to all tissues, especially at sites of inflammation. Phagocytosis is the ability of white blood cells to engulf and destroy microorganisms and cellular debris. Some leukocytes, such as granulocytes, live for only a few hours. Platelets or thrombocytes Platelets are the smallest cells in the blood. Colorless and fusiform, they measure 2–3 µm in diameter. Normally between 200 000 and 300 000 are found per cubic millimeter of blood, and they live for 8–10 days. Platelets are essential for the coagulation of blood and are rich in serotonin. 25
General principles
1.4.4 Hematocrit Hematocrit defines the relative volume occupied by red blood cells in a given volume of whole blood. Normal hematocrit is about 45% and varies depending on the quantity of plasma or red blood cells in circulation.
1.4.5 Physical properties Blood is a viscous liquid whose color is bright red in the arteries (oxygenated blood) and darker in the veins (deoxygenated). It smells bland, a little sickening, and tastes salty. Blood density is about 1060 kg/m3. Blood pH is relatively fixed, approximately 7.35.
1.4.6 Viscosity Blood is a concentrated suspension of red blood cells. Viscosity is what characterizes fluid cohesion. Plasma viscosity can be differentiated experimentally from blood viscosity. The viscosity coefficient determines the
26
cohesion of a liquid. The ability or inability of a fluid to flow easily is determined by several factors, among which is the adhesive effect of adjacent molecules. In a normal state and at 37°C, global blood viscosity relative to water (being 1 unit) is equal to about 5. In fact, in vivo, blood flows more easily than its viscosity and complex composition would indicate.
Clinical notes An increase in red blood cells is called polycythemia; a decrease signifies anemia. In an anemic patient the cellular volume falls and consequently the viscosity of the blood decreases. Conversely, a patient whose blood cell volume is abnormally high will have thicker and slower-moving blood. These pathologies have hemodynamic repercussions (see section on ‘Reynolds’ number’ in Chapter 2).
Circulatory physiology
If the laws of fluid dynamics were applied, the cardiovascular system would form an unusually complicated hydraulic system. Our biological vascular plumbing arrangement is a much more difficult study and is harder to conceptualize than the circulation of water through central heating pipes! This system comprises a far greater number of variables than those governing the function of most systems of pumps, pipes, and fluids to be found in the industrial world.
• the cardiovascular system has some porous tubes (capillaries) • the cardiovascular system is made up of elastic tubular elements and not rigid structures • the volume of its contents is subject to changes depending on digestive absorption, as well as renal and digestive elimination. These characteristics fundamentally complicate any more basic conceptualization.
2.1 CIRCULATORY FUNCTION – GENERALITIES
2.1.2 Pressures
2.1.1 Conceptualization
Blood pressure is the force exerted by the circulating blood on the artery walls. Its pressure by surface unit depends on the volume of blood in the vessels and the compliance of the vessel walls.
One can simplify the workings of the circulatory system by looking at functional parts: • An alternating pump: the heart • A hydraulic circuit: the vascular system, which can be considered, at least in the short and middle term (independent of renal resorption) a constant volume. This hydraulic circuit (Fig. 2.1) comprises: • a distribution network: – the arteries terminating in arterioles, which have variable resistance – the capillaries, a circuit of tiny blood vessels responsible for the bi-directional exchange of fluid • a return circuit towards the heart: the veins. If at first glance the cardiovascular system appears to be a closed hydraulic system of constant volume, and not an open and linear system, it must be emphasized that: ©
2011 Elsevier Ltd
2
Blood pressure
Arterial pressure Arterial pressure results from the pressure exerted by the blood in the large arteries. Blood pressure depends on cardiac output and total peripheral resistance. Arterial pressure fluctuates with each heart beat, according to the pumping of the heart. It: • increases during the emptying phase (ventricular systole) • decreases during the filling phase (ventricular diastole). Systolic pressure Systolic pressure is the blood pressure measured during the period of cardiac contraction.
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General principles This can be expressed by the formula:
Tubing
Pave = Pd + 1/3(PS – Pd ) For example, in a person whose arterial pressure is 140/80 mmHg, the average pressure is: 80 + 1/3 (140 − 80) = 100 mmHg
Double pump Control system
Fluid
Fig. 2.1 Hydraulic principle schematic.
According to the law of Hagen–Poiseuille, it depends on three factors: 1 cardiac output 2 elasticity of the large arteries 3 viscosity of the blood. Diastolic pressure Diastolic pressure corresponds to the arterial pressure during the cardiac relaxation phase. It depends on the speed of blood flow and therefore on the total peripheral resistance. This attests to the resistance provided by vessels to blood flow. It is a good indicator of arterial wall elasticity.
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Average blood pressure Blood pressure values oscillate between a maximum (Ps) and a minimum (Pd) value. The average arterial pressure (Pave) is obtained by integrating the pressure curve in the course of a cardiac cycle. In practice, for the peripheral arteries, take one-third of the difference between maximum and minimum pressures, and add to the minimum pressure.
Values Normal arterial blood pressure in a healthy 40-year-old man is 140 mmHg during systole at the maximum and 80 mmHg during diastole at the minimum. According to the World Health Organization, pressure is considered pathological (arterial hypertension) if systole pressure is greater than 160 mmHg and/or diastolic pressure is higher than 95 mmHg. Arterial pressure varies with: • Sex: up to the age of 40 years males have higher arterial values than women, becoming lower than women after age 50 (D’Alché 2008). • Age: on average blood pressure rises with age. • Measurement circumstances. • Cardiac output: a rise in output tends to increase blood pressure. For example, during physical exertion, arterial pressure increases. By contrast, blood pressure falls during sleep. Systolic pressure comes down as much as 10 to 30 mmHg, and diastolic pressure lowers 5 to 10 mmHg. (D’Alché 2008). • Blood volume: increased blood volume increases blood pressure. An injection of 250 mL water causes blood pressure to rise by 10 mmHg within 60 min. • Blood flow to individual organs depends on the degree of vasoconstriction of the arteries supplying the particular organ. Digestion modifies arterial pressure. Clinical note With arterial hypertension the heart must work harder and consume more energy to supply the same output. Arterial hypertension therefore represents a form of energy squandering for both the heart and the organism.
Circulatory physiology
T Pe
Pi
2
The regular recurring expansion and contraction of an artery (the pulse) is produced by waves of pressure and is not the same as the sensation of fluid pulsation linked to a rhythmic blood flow, passing under the fingers (pulse taking). Moreover, the pulse wave velocity is much higher (from 5 to 15 m/s) than the speed of blood!
2.1.5 Compliance and elasticity
Pe : External pressure Pi : Internal pressure T : Tension of the elastic wall
Fig. 2.2 Pressure tension relationship in an elastic tube.
2.1.3 Arterial tension In France, the term ‘arterial tension’ refers to arterial pressure measurement. Normally, the term fluid pressure denotes fluid pressure on the walls of a deformable tube. Blood vessels are elastic tubes and as such are deformable. Laplace’s law expresses the relationship between the tension, T, exerted on the wall of such a tube and the prevailing pressure at the interior of the tube (Fig. 2.2). This relationship between tension and pressure allows us to understand the role that vessels play in blood pressure.
2.1.4 Arterial pulse The arterial pulse is the wave of rhythmic arterial pressure perceived by palpating an artery. The normal number of pulse beats per minute varies from 60 to 80. The pulse is caused by the sudden increase in blood pressure, ejected by the left ventricle into the aorta and large arteries. It propagates along the entire length of the arterial tree.
In a deformable hollow organ the ratio between changes in volume and pressure is defined as compliance (or capacitance or volume dispensability). The inverse relationship defines elasticity. In cardiovascular physiology, the term compliance can be understood to mean the opposite of rigidity. It describes the ability of a vessel, or of the heart, to return to form. Veins have greater compliance than arteries and arterioles. Inversely, arteries and arterioles possess greater elasticity than veins. These differences are due to the structure of their walls and their shape: circular for the arteries and elliptical for the veins. The large compliance of the venous network allows them to serve as a blood reservoir.
2.2 CARDIAC PHYSIOLOGY As described above, the heart’s valves permit a one-way blood flow from the atria to the ventricles, and from the ventricles to the aorta or pulmonary artery. Each ventricle ejects about 5 L/min, which amounts to 2.5 million liters an hour at rest.
2.2.1 Cardiac mass In mammals whose weight varies somewhere between that of a mouse and a horse, the cardiac mass represents about 0.6 of living weight. Thus a 500-kg horse has a cardiac mass of 3000 g, whereas a 2.5-kg cat’s heart weighs just 15 g. A blue whale’s heart weighs in at 450 kg!
Heart rate The functioning of the cardiac pump is discontinuous. Heart rate is intermittent and
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General principles 0.1 s Auricular systole
General diastole 0.4 s
Ventricular diastole Ventricular systole
Auricular diastole
0.3 s
Fig. 2.3 Cardiac cycle.
pulsatile. The heart beats normally about 70 times per minute (bpm). In mammals, cardiac frequency is much more rapid if the heart is small. For example, the heart rate of a mouse is on average 500 bpm, whereas that of an elephant is only about 25 bpm. In mammals, the relationship between the resting heart rate and life expectancy is indubitable. The lower the heart beat, the longer the lifespan. In humans, many studies show a relationship between a raised resting heart rate and an increased mortality rate in subjects at cardiovascular risk. A low resting heart rate seems to be associated with longevity. Bradycardia is a slower than normal heart rate, whereas tachycardia describes a faster than normal heart rate. Many factors can alter heart rate such as age, sex, physical exertion, and stress.
Cardiac cycle 30
The contraction of the heart, or systole, is followed by a period of rest, called diastole.
Together they constitute the cardiac cycle (Fig. 2.3). When the heart rate changes, diastole is shortened or extended, whereas the duration of the systole remains relatively unchanged, at least on a broad scale frequency. At 75 bpm, the duration of systole is 0.27 s, whereas that of diastole is 0.53 s, giving a systole to diastole relationship of about 1 to 2. The resting time between heart beats is about twice that of a contraction.
Terminology Cardiovascular literature can be daunting in its use of prefixes. Notions such as ‘telediastolic’ or even ‘protosystolic’ are encountered. Although they are brief events in the cardiac cycle, diastole and systole are of a particular duration nonetheless. Sometimes it is necessary to be more specific about a particular moment during these occurrences or, in contrast, it can be helpful to refer to the overall
Circulatory physiology
2
Table 2.1 Meaning of prefixes with regard to the cardiovascular system Diastole
Systole
Beginning
Middle
End
Beginning
Middle
End
Protodiastolic
Mesodiastolic
Telediastolic
Protosystolic
Mesosystolic
Telesystolic
Holodiastolic total
Holosystolic total
picture. Table 2.1 summarizes the meaning of these various prefixes.
Cardiac cycle The heart can be likened to a hollow muscle that propels blood by alternately contracting and relaxing. This sequence affects the size of various cavities, especially the ventricles. During ventricular contraction (systole) the walls thicken and the cavity size diminishes, whereas during ventricular relaxation the walls thin and the cavity enlarges (Fig. 2.4). The cardiac cycle is a repetitive sequence of systole (period of myocardial contraction) and diastole (period of myocardial relaxation). Within this sequence the cardiac valves open and close at key moments, to manage the flow of blood. The adult human heart ‘beats’ about 70 times per minute, which means the four action phases of the heart are accomplished in less than 1 s. The four phases (Fig. 2.5) are: • The ventricular filling phase, during which the atrioventricular valve is open. Blood flows from the atrium towards the ventricle, while the aortic valve (for the left ventricle) and the pulmonary valve (for the right ventricle) remain closed. During this phase, blood flow first flows passively from the atrium to the ventricle, and then more actively during auricular diastole. • In the isovolumetric contraction phase, myocardial ventricular contraction increases the pressure in the ventricle, and all valves are closed.
Diastole
Systole Fig. 2.4 Ventricular cross-section in diastole and systole.
• Systolic ejection begins when pressure in the ventricle (ventricular pressure) overtakes the pressure in the aorta (aortic pressure) or the pulmonary artery, during the course of which the blood is expelled
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General principles
Left atrium
Right atrium
Left ventricle Right ventricle
1. Ventricular filling
2. Isovolumetric contraction
3. Systolic ejection
4. Isovolumetric relaxation
Fig. 2.5 The cardiac cycle.
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from the ventricle. The semilunar valves are opened. • Isovolumetric relaxation begins at the end of the ventricular contraction. Ventricular pressure falls below that of the aorta and the pulmonary artery causing closure of the semilunar valves. The atrioventricular valve remains closed.
2.2.2 Cardiac output Cardiac output is the volume of blood ejected by each ventricle per unit of time. It can be calculated from the heart rate × stroke volume. With a heart rate of 70 bpm and a volume of systolic ejection of 80 mL, this represents
Circulatory physiology a cardiac output of 5.6 L. A man weighing 70 kg possesses about 6 L of blood, which means that his total blood mass is pumped in about 1 min.
Regulation of output The right and left heart can be likened to two pumps arranged in series. This implies that the two ventricles have the same output. Suppose that the right ventricular output is 5.1 L/min and that of the left ventricle only 5 L/min. After 10 min, 1 L of blood will have accumulated in the lungs, causing pulmonary edema. As the two pumps operate at the same rate, output regulation can occur only through a change in the volume ejected from the two ventricles, dependent on the force of contraction of the ventricle itself.
Frank–Starling law Each ventricle must be able to change its force of contraction and therefore stroke volume in response to changes in venous return. The Frank–Starling law describes the mechanism by which changes in pressure alter stroke volume. It states that the force of ventricular contraction is increased when the ventricle is stretched prior to contraction. The myocardial fibers experience an increase in load due to the extra blood entering the heart. And the force of contraction of the cardiac muscle is proportional to its initial length. The capacity of the stretched heart to contract is a quality shared by all striated muscles. The Frank–Starling law allows the heart to be synchronized with the venous return without depending on external regulation to make alterations. It is vital that stroke volume of both ventricles match so exactly that neither stagnation nor total emptying of the pulmonary circulation can occur, either of which would be fatal.
Volume of systolic ejection Systolic ejection volume (Vs) is the quantity of blood ejected from the left ventricle during systole and depends on three factors:
2
1 The pre-charge corresponds to the volume of blood present in the left ventricle just before ejection. Volume depends on the pressure of venous return to the heart, called central venous pressure (CVP). 2 The contractility of the myocardium, regulated by the autonomic nervous system. 3 The post-charge represents those factors that oppose the work of the heart: – Parietal resistance of the ventricle – Impedance of the aorta (aortic resistance, inertia of the blood column, reflection waves aortic compliance) – Peripheral vascular resistance, also controlled by the autonomic nervous system. The activity of the heart is dependent on vascular activity, and vice versa. Pre-charge Pre-charge is the degree of ventricular myocardial stretch just before contraction. It refers to the accumulated blood load imposed on the left ventricle. It equals ventricular filling, represented by the telediastolic volume. When the pre-charge increases, this stretches the heart muscle fibers, and this leads automatically to an increase in the force of contraction in the left ventricle. The stretch of the cardiac muscle depends on the venous return. The quantity of blood returned to the heart by the veins distends the ventricles. Everything that increases the volume or the speed of the venous return raises: • the telediastolic volume • the force of ventricular contraction • the systolic volume. This is what happens during physical exercise. Post-charge The post-charge is the counterpressure exerted by the arterial blood. It is the brake on ejection. It comprises all the forces against which
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General principles the right ventricle must struggle to eject its blood. The post-charge corresponds to the charge displaced by the left ventricle and is directly dependent on aortic resistance expressed by the size of telesystolic volume. In simple terms it refers to aortic resistance. For example, the post-charge is increased by clamping of the aorta when the volume of systolic ejection falls; as a result the residual volume (telestolic volume) rises. In healthy people, the post-charge has no significant influence on the systolic volume because it is relatively constant. However, in the case of arterial hypertension, the postcharge can reduce the capacity of the ventricles to eject blood, and blood remains in the heart following the systole phase (augmentation of telestolic volume). To summarize: • The pre-charge refers to all the forces that work towards ventricular filling. • The post-charge describes all the forces that run counter to ventricular ejection.
Output adaptation
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Cardiac output can also be modified by extrinsic factors, such as the autonomic nervous system. Stimulation of the sympathetic cardiac nerves through the intermediary of norepinephrine (noradrenaline) has the following effects: • increase in the heart rate (positive chronotropic effect) • increase in cardiac and vascular tone (positive tonotropic effect) • increase in the force of contraction (positive inotropic effect) • increase in the speed of cardiac muscle relaxation (positive lusitropic effect) • increase in the speed of conduction of excitation of the cardiac muscle (positive dromotropic effect) • increase in excitability via alteration in the excitation threshold (positive bathmotropic effect). Circulating catecholamines, norepinephrine and epinephrine (adrenaline),
synthesized by the adrenal medulla, have the same effects as the sympathetic nervous system. All of these elements increase cardiac output. By contrast, vagal parasympathetic activity stimulated by acetylcholine, causes: • lowering of the heart rate (negative chronotropic effect) • decreased contractility (negative inotropic effect) • reduced cardiac and vascular tone (negative tonotropic effect) • decreased speed of cardiac muscle relaxation (negative dromotropic effect) • reduced myocardial excitability (negative bathmotropic effect). These factors lower cardiac output.
2.2.3 Endocrine function It is increasingly evident that many tissues produce hormones and have an endocrine function. The heart is no exception. The atria, especially the right atrium, are sensitive to stretch. They contain endocrine myocardial cells that produce a hormone called natriuretic atrial peptide (NAP) or cardiodilatin. NAP controls vascular wall contraction, as well as sodium and water exchange in the kidneys. Atrial dilation is one of the effects of this hormonal secretion (see Chapter 3).
2.3 HEMODYNAMICS It is useful to review several definitions pertaining to the circulation of blood. As a liquid, blood is subject to certain physical and biophysical laws: • Hydrostatic law because of discrepancy in height between the head, the heart and the lower extremities • Hydrodynamic law because of the flow impulse from the heart. However, blood is also one of a kind on account of: • Heterogeneity, by which special macromolecules (proteins) and
Circulatory physiology deformable cells (red and white blood cells) confer various properties to whole blood and isolated plasma • Its vascular container that has walls with their own tension, elasticity, and inertia. Blood has very special circulatory properties in relation to fluids as a whole.
2.3.1 General hemodynamics Speed of blood flux Blood speed or perfusion speed corresponds to the displacement distance of blood cells per unit of time. It is generally expressed in centimeters per second (cm/s). Remember, flow velocity is not the same as pulse wave velocity.
Output The flow of a fluid across a canalization is defined as the volume of fluid that crosses in a unit of time. It is denoted by the sign Q, and it is expressed in cubic meters per second (m3/s). Definitions Blood flow is the volume of blood circulating in a tissue in a given period of time. Total blood flow is the volume of circulating blood at each minute in the pulmonary circulation. It is the cardiac output. Blood flow is generally expressed in liters per minute (L/min) or milliliters per second (mL/s).
The principle of continuity of output when an incompressible static fluid circulates. section × speed, corresponds to output which remains constant along the conduit.
Output–speed relationship With V being the speed of a fluid flowing in a tube of cross-section S, the flow of fluid is calculated to be equal to the product of its speed multiplied by the cross-section (Fig. 2.6). Principle of continuity When an incompressible fluid circulates in a static state through a conduit, the product is cross-section × speed. That is to say, the output remains constant all along the conduit (Fig. 2.7). Cross-section effects From the above it is clear that, assuming output is constant, when the cross-section varies, the speed of the liquid changes proportionally. • If the cross-section increases, speed diminishes. • If the cross-section diminishes, speed increases.
V
S
Q=S×V
Fig. 2.6 Speed–flow relationship.
S1 V1
2
S3
S2 V2
V3
S1 × V1 = S2 × V2 = S3 × V3 = constant = output
Fig. 2.7 Principle of output continuity of a static fluid.
35
General principles
S1 = 1 cm2
S2 = 10 cm2
S3 = 2 cm2
Q’ 10 ml/s
Q 10 ml/s
V1 = 10 cm/s
V3 = 5 cm/s
V2 = 1 cm/s
Fig. 2.8 The effects of tube cross-section on speed.
This principle extends to conditions in which tubes of flowing fluids subdivide into smaller tubes, or the inverse, when several tubes converge into one (Fig. 2.8). Thus, the speed of blood flux is inversely proportional to the area of the transverse cross-section of the blood vessel, or, more precisely, to the vascular sector being considered. • In the aorta, the area of the transverse cross-section is no more than 3–5 cm2 and the average blood flux speed is from 40 cm/s. • In the capillaries, the total transverse cross-sectional area is between 4000 and 6000 cm2 and the blood flux rate is less at 0.1 cm/s (Fig. 2.9).
Effects on pressure
36
When the cross-section changes, the lateral pressure of liquid exerted on the tube walls also modifies. If you have horizontal flow with a constant cross-section and speed, the lateral pressure is constant (Fig. 2.10A). If you consider a horizontal flow in a tube of variable cross-section, when the crosssection diminishes speed increases, and pressure declines beyond the zone of the stricture (Fig. 2.10B).
3500
cm2
2700
500 5.3
20
20
100 30
18
Common cross-sectional area
Fig. 2.9 Cross-sections of a vascular bed.
Circulation time Circulation time approaches that of cardiac output. We have seen that, at rest, the totality of the blood is pumped in about 1 min, which matches the time theoretically required for a drop of blood to complete the circuit from left ventricle to left atrium.
Blood flow Circulatory gradients The term gradient expresses the level with which a physical property increases or
Circulatory physiology
2
S
S constant, V constant, P constant
V
Lateral pressure
P
Lateral pressure
V
V A
B
Fig. 2.10 Effect of the cross-section of the tube under pressure.
diminishes in magnitude as observed in passing from one point to another. There is no life without gradient. • A dead system has homogeneous properties, without gradient or flux. In this state equilibrium is true, stable, and non-excited. • A living system requires, by necessity, ‘heterogeneous’ properties. Life demands incessant disequilibrium and permanent flux of matter or energy. A continuous supply of energy is required to maintain gradients and generate the passive flux indispensable to it. A constant expenditure of energy is needed to sustain excitement and instability in a system, despite apparent equilibrium. • Active blood flux can insure the passive exchanges necessary to the life of every tissue and cell. It is not until death that all flux ceases and the gradients disappear. The notion of vascular charge At any given point along a hydraulic conduit, the energy of an incompressible fluid comprises: • potential energy, linked to the effects of gravity on the liquid • pressure energy, linked to volume and pressure of liquid on walls • kinetic energy, linked to the speed of the fluid: E hydraulic = E potential + E pressure + E kinetic The energy restored to the unit of volume is also called a charge.
V1
V2
V3
Fig. 2.11 Blood viscosity.
In waterworks, it is common usage to express charge in meters of columns of water. This is also referred to as hydraulic charge. When considering fluid in a pipe, hydraulic energy corresponds to the total mechanical energy, and is also called charge or total charge. The energy consumed by friction constitutes loss of charge. A liquid always flows from the most elevated charge towards the weakest charge. To understand blood circulation, it is better to consider differences in charge, rather than differences in pressure. Charge gradients established all along the circulatory circuit are the true ‘motor’ of the overall movement of the blood mass.
Blood viscosity Two moving solids have friction between them when they are in contact, and displace at different speeds. In a viscous liquid, two adjacent flow layers also have friction (Fig. 2.11). These forces oppose movement by tending to slow the faster layer and accelerate the slower layer. In vivo, blood behaves much like plasma. Accordingly it can:
37
General principles • either increase its viscosity by the aggregation of red blood cells • or diminish its viscosity by the deformation and change in direction of its hematies. This is called fluid rheofluidifying. Because of this, blood is sometimes considered to be a perfect (ideal) fluid. Loss of charge Owing to its viscosity, blood does not have the same characteristics as a perfect fluid, in the sense that physics understands it to be. In a perfect fluid there is no molecular friction, and the fluid flows without energy loss. However, there is a loss of usable hydraulic energy during blood flow. This loss of charge is linked to the dissipation of energy in heat due to the viscosity of the liquid. These charge losses result from friction against vascular walls and friction within blood tissue itself. Venturi effect From the above, it is possible to envisage how a stricture affects pressure and flow velocity. This is what happens with arterial stenosis (Fig. 2.12).
Blood flow is conserved on either side of the stenosis, but the velocity must change. Blood flow accelerates as it passes through the restriction (Fig. 2.12A). Globally the charge is conserved, and the total energy does not change. As a result, if the speed increases, kinetic energy augments proportionately. This results in a pressure change through the restriction. What follows is (Fig. 2.12B): • suppression upstream of the stenosis that can cause dilation or fatigue of the vessel wall. • depression downstream of the stenosis that can lower the filling pressure of vessels downstream (as a function of squaring the percentage of stenosis).
Nature of the flow Velocity profile Molecules of a fluid that flow at identical speeds are called a ‘fluid filet.’ Each filet can be represented by a vector proportional to its flow velocity. The arrangement of these different vectors is called the velocity profile (Fig. 2.13).
S
P
v
P
A
Fig. 2.12 Venturi effect and stenosis.
Velocities at a given instant, at a given place and along a given axis
38
Fig. 2.13 Fluid velocity profile.
P
P
B
Circulatory physiology Flow velocities Depending on its velocity profile, a viscous fluid can have various flow speeds (Fig. 2.14).
Laminar flow If the average speed of a viscous fluid is low, the flow is described as laminar (Fig. 2.15). The fluid remains coherent and flows in concentric fluid layers. Adjacent layers of blood move at different speeds. Fluid velocity is maximal at the center of the stream and decreases towards the vessel
Laminar flow
Intermediate flow
Turbulent flow
Fig. 2.14 Types of flow.
V3
V2
V1
V4
Fig. 2.15 Laminar flow of a viscous liquid.
2
wall. An extremely thin layer adheres to the vessel wall and essentially does not move. A parabolic profile develops (Fig. 2.16). In this type of flow, all the energy consumed is used to overcome fluid viscosity. There is a linear relationship between pressure and flow.
Turbulent flow If the average speed of a viscous fluid increases, flow becomes turbulent. Viscosity ceases to be a cohesive factor and the fluid molecules become turbulent, flowing in a disrupted manner, with no systematic distribution of speeds. In this type of flow, energy is wasted in propelling blood in a disorderly manner. Flow is no longer proportional to pressure. This is a very inefficient type of flow. Reynolds’ number The boundary between laminar and turbulent flows depends on four factors: 1 diameter of the blood vessel 2 mean velocity of flow 3 viscosity of the blood 4 density of the blood. Reynolds’ number is a dimensionless number, used to predict whether blood will be laminar or turbulent. Blood flow loses its laminar characteristic and becomes turbulent when Reynolds’ number passes a critical value. Empirically it is known that: • if Reynolds’ number is less than 2400, flow remains laminar • if Reynolds’ number is greater than 10 000, flow is always turbulent.
Parabolic velocity profile is linked to viscosity. Speed is maximal at the center of the stream and an infinitely small layer in contact with the wall moves at zero speed
Fig. 2.16 Velocity profile of laminar flow.
39
General principles Between the two there exists a zone of uncertainty, in terms of critical fluid speed. In this zone, we find intermediate flow. Blood flow is laminar except where the great vessels branch off and turbulence occurs. Blood flow is turbulent in the heart and the arch of the aorta during a great part of systolic ejection. At rest, Reynolds’ number in the aorta is about 1650 and flow is laminar. However, in certain physiological or pathological circumstances, the calculated values can change. This is the case, for example: • on exertion: output, and consequently blood velocity, increases • anemia associated with lowered hemoglobin and decreased velocity. Moreover diminishing levels of blood oxygen cause a compensatory increase in flow • in stenosis: the diameter diminishes and speed increases through the stricture resulting in an unchanged flow. In all these examples, Reynolds’ number rises and blood flow becomes turbulent. Turbulent flow is often accompanied by audible vibrations called vascular murmurs. These murmurs are normal with exertion, but pathological in the case of stenosis or anemia. If Reynolds’ number remains higher than the critical value during the entire cardiac cycle, these murmurs are permanent. If Reynolds’ number is higher during only part of the cardiac cycle, the murmurs are not permanent. If Reynolds’ number is higher than the critical value only at certain moments in the
cycle, the murmurs are intermittent or transitory.
2.3.2 Arterial hemodynamics According to their topographical location, artery walls have different histological characteristics. Their hemodynamic properties vary according to their location and make-up.
Elastic arteries The intermediate layer (tunica) of elastic arteries is rich in elastic fibers, conferring compliance. These are the major arteries of large diameter located near the heart. They are distributing arteries like the pulmonary artery, the aorta and its branches, such as the brachiocephalic trunk, the subclavian and renal arteries. Windkessel effect Thanks to their elastic fibers, the aorta and the large arteries convert the intermittent blood flow to a smooth continuous flow. The dampening effect on pulsatile flow is similar to the action of an air chamber in a bottle. The artery is somewhat like an elastic reservoir. This effect is called the Windkessel effect, from the German Kessel meaning bottle and Wind, meaning air (Fig. 2.17). As the heart contracts and blood pressure increases, the arteries stretch and store potential energy. When the heart relaxes, blood pressure decreases and the stretched arteries rebound (Fig. 2.18). This keeps blood flowing
Air Piston Water
Windkessel – air bottle 40
Fig. 2.17 Windkessel effect.
Circulatory physiology
Open aortic valve
2
Closed aortic valve
Fig. 2.18 Regulation of flow in the elastic arteries.
during diastole even though the aortic valve is closed. Aortic compliance saves the heart work. Thanks to its softening effect on pulsation, blood flow is normalized. Reduced aortic compliance leads to increased systolic pressure. This explains age-related hypertension. Pressure wave It is not possible for the total volume of systolic ejection (about 80 mL blood) to flow across the entire vascular tree during a single ventricular contraction. We will see that a large part of blood is temporarily stored, thanks to aortic compliance. Flow is determined by the interaction of stroke volume and compliance. The Windkessel mechanism produces a sort of arterial wave that propagates the length of the arterial tree at several meters per second. This rate is proportional to the thickness and rigidity of the arterial wall. It increases when the arterial wall becomes thicker (in the lower extremities for example) or abnormally rigid (as in patients suffering from hypertension, arteriosclerosis, atheroma, or diabetes).
The universal tangible manifestation of this wave of arterial pressure is none other than the pulse, palpable at the peripheral arteries.
Muscular arteries The arterial media becomes richer in smooth muscle fibers and poorer in elastic fibers the further the distance from the heart. Arteries of medium and small diameter are considered muscular arteries. These are the coronary, splenic, and mesenteric arteries. These vessels are capable of dilation or constriction. They distribute the blood mass. In addition they are known as resistance arteries. Resistance to blood flow depends essentially on the caliber of these vessels. Peripheral vascular resistance Vascular resistance is the force that opposes blood flow in the vessels. It results from blood friction against the vessel wall. As resistance is weak in the elastic arteries, the blood rubs up very little against the walls. By contrast, it is much higher in the muscular
41
General principles arteries, whose diameter is considerably smaller. Law of Hagen–Poiseuille According to the law of Hagen–Poiseuille, vascular resistance is proportional to: • the viscosity of the blood • the length of the vascular segment. It is inversely proportional to the radius of the vessel lumen. The higher the resistance, the weaker the blood flow. Resistance depends on the viscosity of the fluid and is inversely proportional to the fourth power of the radius. This relationship constitutes the law of Hagen–Pouiseuille. The radius is thus the principal determinant of blood flow resistance. For example, if the radius of a tube is doubled, the flow is multiplied 16-fold! In hemodynamics, vasomotion plays a very important role in peripheral territory irrigation. Put another way, when the diameter of a vessel decreases by half, its resistance to flow becomes 16 times greater. For this reason atheromatous plaques are injurious, not just because of their local consequences, but also because of the general health of the person as they contribute to arterial hypertension. Arterioles and circulatory resistance The arterioles are the main site of circulatory resistance (Fig. 2.19).
Veins 7% Arteries 19%
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Arteriole vasoconstriction causes total peripheral resistance to rise. In the face of unchanged cardiac output, high blood pressure results.
2.3.3 Microcirculation Organization The arteries divide and subdivide to form arterioles via which the blood reaches the tiny capillaries whose walls consist of a single layer of epithelium. The density of capillary vessels varies depending on average tissue metabolic activity.
Exchanges Circulation exchanges across the capillary wall occur though different mechanisms. Pores are orifices whose number and dimension vary according to the organ. They afford passage of lipid-insoluble molecules. Flow is limited by size, number of available pores, and blood flow. Lipid-soluble molecules can diffuse across the same capillary wall, which is itself made up largely of lipids. Water movement across the capillary wall is by osmosis, driven by the sum of hydrostatic and osmotic pressures. Starling’s curve (Fig. 2.20) shows that in the initial part of a capillary hydrostatic pressure overcomes osmotic pressure, resulting in
Capillaries 27%
Small arteries and arterioles 47%
Fig. 2.19 Peripheral resistance distribution (after Silbernagl & Despopoulos 1985).
Circulatory physiology Lymph vessel Arteriole
Venule
~ 10% ~ 90% Resorption Filtration
Interstitial milieu
Pressure
Blood pressure
Colloidal osmotic pressure
Arterial extremity
venous cross-section, the dispensability of the wall coming into play only when pressure is increased. From a functional point of view, it is convenient to distinguish two large venous categories: 1 Postcapillary venules are resistant vessels, whose muscular component influences blood pressure and blood flow. 2 Systemic veins, called collector veins, are rich in elastic fibers. Their increased capacitance makes them potential blood reservoirs.
Venous return Postcapillary sphincter
Precapillary sphincter
2
Capillary length
Venous extremity
Fig. 2.20 Starling’s curve.
filtration, with the result that the fluid moves out of the capillary into the interstitial fluid. In the second part of the capillary, osmotic pressure (derived from blood proteins, particularly albumin) prevails, drawing the water towards the capillary vascular lumen.
2.3.4 Venous hemodynamics Capacitance and elastic veins Although more elastic than the arterial wall, the venous wall is not all that distensible, having a large number of collagen fibers. Large adaptations in venous volume are due mainly to variations in the shape of the
Venous circulation collects blood and returns it to the heart. The difference in charge between the aorta and the vena cava is sufficient to explain the return of blood to the heart. Nevertheless, three categories of force (vis) can be conceived that participate in venous return, depending on whether the force is acting from behind (a tergo) on the sides (a latere) or in front (a fronte) of the blood mass. • Vis a tergo corresponds to the residual force of propulsion in the left ventricle. • Vis a latere involves: – the flattening of the plantar venous sole (plantar veins) – the venous muscular pump of the calf – muscle action of the venous wall tunica, reinforced by the valvules – the abdominodiaphragmatic pump and the pressure gradients of the visceral column. • Vis a fronte refers to the force of thoracic aspiration during inspiration. Also note that gravity favors the veins situated above the heart and is unfavorable to those below.
Abdominothoracic pressure The pressure gradients of the trunk (Fig. 2.21) are fundamental factors in subdiaphragmatic venous return. Whereas the veins of the lower
43
General principles
−10 cmH2O
5 cmH2O
Heart
0 cmH2O Liver Diaphragm +5 cmH2O
+10 cmH2O
+15 cmH2O
+20 cmH2O
+25 cmH2O
Fig. 2.21 Pressure gradients of the trunk.
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Circulatory physiology extremities are endowed with valves, vessels above the inguinal ligament, such as the iliac vessels and the inferior vena cava are no longer equipped with these devices. In the trunk, regularity of blood flow towards the right atrium rests on differences in venous charge, to which thoracoabdominal pressure gradients contribute in a major way. Because of the force of gravity, intraabdominal pressure is not homogeneous in the standing or sitting position. Instead, craniocaudal pressure applies. The greatest pressures are located at the pelvic level, while weaker pressures prevail just below the diaphragm. In the thorax, pressure is even subatmospheric and known as negative pressure. Blood moves from areas of stronger charge to areas of weaker charge. Normal, harmonious, and balanced pressure gradients are a vital component of venous return. In order for these gradients to be well tiered and regular, a balanced and free visceral mechanism is essential. Fixation, ptosis, dysfunction, or irritation can all create areas where the blood slows down in the collector vessels. This causes venous stasis in the territories located upstream of the slowing
2
down, usually the pelvis and lower extremities. Numerous venous problems, such as pelvic weightiness or heaviness in the lower limbs, are the consequence of deregulation of this thoracoabdominal pressure system.
Central venous pressure The value of central venous pressure (CVP) near the right atrium is on the order of 7–10 mmHg. Average arterial pressure is 10 times higher, about 96 mmHg. The notion of pre-charge demonstrates that CVP presides over the filling of the heart. The greater the volume of blood entering the heart (pre-charge) the greater the volume of blood ejected. This provides the heart with an intrinsic factor in the modification of cardiac output, without autonomic intervention. In the case of transitory volume increase, as in the course of too-rapid perfusion, the CVP can initiate the Bainbridge reflex. Stimulation of venoatrial stretch receptors increases the heart rate by invoking the sympathetic system. The physiological significance of this reflex is not entirely clear, but it is generally acknowledged to complete the Frank–Starling mechanism.
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3
Homeostasis of the cardiovascular system
Regulation of the circulatory function ensures that sufficient blood is provided to all parts of the body, whether the individual is resting or working and whatever the ambient conditions. It must: • Ensure a minimal perfusion to each organ • Control cardiac function and arterial pressure • Provide for blood to be distributed to active organs, at the expense of resting ones. Silbernagl & Despopoulos (1985) emphasize that maximal and simultaneous perfusion of all the organs would overtax the heart. To maintain vital circulatory homeostasis for optimal organ function, the cardiovascular system must continually adapt itself to variations in hemodynamic parameters. These adjustments depend upon cardiac output and vascular resistance.
46
• Cardiac output changes constantly and instantaneously, in accordance with demand. Cardiac activities that can be modified include the frequency with which impulses are initiated by the pacemaker, and the volume of systolic ejection. Adaptations in heart rate are described as chronotropic, and alterations in the volume of systolic ejection as inotropic (influencing muscular contractility). • Peripheral resistance plays a major role in cardiovascular flexibility, essentially ©
2011 Elsevier Ltd
through vasomotion, which controls blood vessel diameter. Changes in vascular diameter regulate perfusion to a particular body part or organ. The smooth muscle tone of the vessels depends on local factors, as well as neural and hormonal signals. Circulatory function regulation includes three levels of control: local vascular control mechanisms, the autonomic nervous system, and the endocrine system. Each system has a particular time limit and duration.
3.1 CARDIOVASCULAR ADAPTATION FACTORS 3.1.1 Local circulatory regulation Within each tissue, vasomotion depends first of all on local activities, continuously adapting blood flow to tissue requirements, within the limits imposed by systemic neural and hormonal control. Arterioles are the main site of circulatory adjustment. Arterioles respond to: • metabolic changes • local chemical messages • temperature • myogenic stretch.
Vascular self-regulation If the vascular system were passive, there would be a linear relationship between debit and pressure: an increase in the pressure
Homeostasis of the cardiovascular system gradient would cause a proportional rise in blood flow through an organ. In fact many organs, including the brain and the kidney, are equipped with vessels that respond to a rise in blood pressure through vasoconstriction. Such vasoconstriction opposes the increase in blood flow that would otherwise cause pressure to go up in a totally passive vascular system. Thus, across a gamut of pressures, perfusion in such organs remains stable. Autoregulation is achieved mainly by the arterioles in their significant vasomotor capacity. Their action protects the capillary network from pressure variations that would otherwise be harmful to the equilibrium of its tiny exchange vessels. Vascular self-regulation has two functions: • One is to ensure constant blood flow to an organ in the face of changing arterial pressure. For example, in the kidneys, the arterial resistance of the nephrons adapts automatically to prevailing blood pressure. When systemic arterial pressure rises, renal vasoconstriction occurs in order to maintain constant renal blood flux. • The other adjusts blood flow to the demand and need of organ activity. For example, in the case of cardiac or active skeletal muscles, the rate of perfusion can be several times greater than the value of resting blood flow.
Mechanisms of autoregulation Myogenic effects Myogenic stretch response means that, when a vascular smooth muscle is stretched, it contracts. If arterial pressure rises, the arteriole muscle responds with increased myogenic activity. This passive stretch depends upon the volume of blood reaching the arterioles. The lessening of the stretch prompts the reduction of myogenic tone. Temperature In most tissues, a rise in temperature causes vasoconstriction. This is because cutaneous circulation is rich in α2 receptors, whose
3
affinity for norepinephrine (noradrenaline) increases with a reduction in temperature. However, higher temperature at the skin produces vasorelaxation, via the central nervous system command and vascular characteristics. Calories are conveyed towards the skin and evacuated to the external environment by the process of cutaneous vasodilation occurring when the individual must compensate for heat. Conversely, cutaneous vasoconstriction occurs with exposure to cold, reducing thermal exchange with the environment and limiting caloric loss. Oxygen deficiency Generally, local hypoxia provokes vasodilation, which means that perfusion varies as a function of tissue oxygen consumption. Metabolites Most products of local tissue exchange, whose levels increase as a function of metabolism, have a vasorelaxing effect. In a general way, carbon dioxide (CO2), nitrogen monoxide, acidic ions (H+), adenosine diphosphate (ADP), and adenosine monophosphate (AMP), as well as all the substances with an osmotic effect, such as potassium (K+), increase perfusion, in effect regulating the evacuation of these very products. Autacoids Autacoids are ‘local hormones’ in immediate proximity to their site of production. Numerous substances belong to this group. The main ones are: • Histamine produces either vasoconstriction, with an accompanying increase in the permeability of the vascular wall, or vasodilation. In inflammatory processes, histamines produce arteriole vasorelaxation, venular vasoconstriction, and increased capillary permeability. Allergy symptoms such as hay fever illustrate the resulting effect. • Bradykinin is produced by salivary glands and sweat glands.
47
General principles • 5-Hydroxytryptophan (5-HTP) is produced by blood platelets, the central nervous system, and some cells of the digestive tube wall. • Prostaglandins are made by macrophages, fibroblasts, leukocytes, and vascular endothelium. These compounds have an array of significant effects. Prostaglandin F (PGF) is a vasoconstrictors, whereas, for example, prostaglandin E (PGE) and prostacyclin are vasorelaxants, very much involved in inflammatory phenomena. • Leukotrienes are released by leukocytes during the inflammatory response. They are vasoconstricting and also increase the permeability of the capillary wall. • Platelet activating factor (PAF) is produced by macrophages as part of the inflammatory response. It causes vasodilation and increased capillary permeability.
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Vascular endothelium The endothelium lining the lumina of the vascular wall plays an important role in vasomotion. • It constitutes a mechanical barrier, guaranteeing relative vessel water tightness and controlling permeability, especially at the capillary level. • It is a true interface between the blood and the vascular wall, ensuring the transmission and translation of chemical messages. • It is involved in variation of the vascular diameter. • By way of its surface characteristics and secretions, it is able to limit platelet aggregation. These various endothelial functions are carried out only when the structural integrity of the endothelium is protected. Consequently any factor altering endothelial cell morphology or physiology (e.g. nicotine, cholesterol, or mechanical overload accompanying arterial hypertension) changes the permeability of the endothelium,
diminishing its antithrombogenic capacity as well as its secretion of vasorelaxing factors. This is how endothelial changes are implicated in numerous pathological processes, and even lie at the heart of the physiology of atherothrombosis.
Results • In functional or metabolic hyperemia, blood flow to an organ is proportional to its metabolic activity. Changes in arteriole diameter achieve this result. Every tissue adapts its blood flow to its own metabolic requirements. • By the mechanism of flux-dependent vasodilation, involving nitrous oxide and prostaglandins, there is an adjustment in arterial diameter and in the distribution of the blood flow that they transport. Every vessel adapts its diameter to its flow. Local factors are depicted in Table 3.1.
Table 3.1 Local factors Local vasodilators
Local vasoconstrictors
Produced by blood-deficient tissues
Produced as a reaction to a rise in systemic arterial pressure
Vasodilation of smooth muscles of the precapillary sphincters
Vasoconstriction of pre-capillary sphincters. At high concentration, a narrowing of arterioles and reduced blood flow to the tissue
Hypoxia ↑ CO2 (carbon dioxide) ↑ K+ (potassium) ADP, AMP Histamine Acidity (lactic acid) Nitrous oxide (N2O) Warmth
Endothelin Prostaglandins Thromboxanes Leukotrienes
Homeostasis of the cardiovascular system
3.1.2 The nervous system The autonomic nervous system regulates blood flow on the basis of interactions and reflexes coming from the receptors and passing to autonomic centers where it is integrated and acted upon. The autonomic nervous system plays a role in the short-term control of systemic arterial pressure.
Receptors Arterial pressure is under the constant surveillance of arterial baroreceptors. These receptors stimulate a short-term response in a matter of seconds. Baroreceptors modify heart rate and total systemic resistance via autonomic nervous system activity at the heart and the smooth arteriole muscles. Long-term adaptations are made by adjustments in blood volume, in response to thirst and urine volume. Arterial receptors Baroreceptors and chemoreceptors are essential to homeostasis.
Baroreceptors Baroreceptors are pressure-sensitive free nerve endings found in the adventitia of the carotid sinus and the aortic arch. Carotid baroreceptors are optimally located to monitor the pressure in arteries supplying the brain, whereas the aortic baroreceptors relay information about the major arteries that furnish the rest of the body. Information from the carotid sinus baroreceptors is carried to the brainstem on the carotid sinus nerve, which joins the glossopharyngeal nerve. Fibers issuing from the baroreceptors of the aortic arch form the aortic nerve, which merges with the vagus nerve. These two nerves ascend to the nucleus of the tractus solarius at the brainstem. Baroreceptors are mechanoreceptors that are sensitive to pressure or stretch of the vascular wall. Thus, changes in arterial pressure
3
cause more or less stretch on the baroreceptors. Some receptors respond to increased stretch whereas others are designed to detect decreased stretch.
Chemoreceptors Chemoreceptors are sensitive to chemical changes and are located in the corpuscles of the carotid glomus and the aortic arch. Fibers issuing from the carotid glomus travel the length of the IXth pair of cranial nerves. Fibers from the aortic corpuscle accompany the Xth cranial nerves along their pathway. They join together at the brainstem. Chemoreceptors are sensitive to hypoxia and hypercapnic acidosis. In response to these stimuli, chemoreceptors signal an increase in sympathetic activity, resulting in peripheral arterial vasoconstriction and splanchnic venoconstriction. They signal an increase or decrease in respiration during extreme conditions such as asphyxia or severe hemorrhage. Chemoreceptors help keep arterial pressure constant in cases of grave hypertension, when the limits of baroreceptor reflexes are overcome. Other receptors Beyond aortic and carotid receptors are receptors that contribute to cardiovascular regulation. Venous baroreceptors situated in the wall of the right atrium detect variations in central venous pressure. In addition, stretch receptors are located in the pulmonary vessel walls. These mechanisms relay information to the brainstem, signaling the autonomic nervous system to adapt to variations in intrathoracic venous pressure due to respiration. Venoatrial receptors are involved in the hormonal response of atrial natriuretic peptide, which aids in regulating mean arterial pressure. Striated skeletal muscles have muscular or ergo receptors, sensitive to metabolic perturbation and mechanical actions. They inform
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General principles the central nervous system about muscle activity.
Central control Pathways from the various receptors terminate in the medullopontine region of the brain. Cardiovascular motor centers in the brainstem The cardiovascular centers receive information continuously. The baroreceptors constantly relay information about arterial pressure. In turn, vasomotor centers coordinate responses to pressure variations. Impulses are sent to the sympathetic system, the heart, and vessels to create a relaxed vascular tone (relaxed vasoconstriction). Apart from messages coming from different receptors, the cardiovascular center receives stimuli from the higher cerebral centers: the cortex, hypothalamus, and limbic system. For instance, the limbic system can engender cardiovascular modifications before a physical test or at the time of a particular emotion such as when taking an exam. It will stimulate the cardiovascular center to increase the heart rate. During physical activity, internal body temperature rises. In this case, the hypothalamus, which governs the internal thermostat, sends impulses to the cardiovascular center, whereupon the vessels of the skin dilate to give off heat.
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Responses The cardiovascular center adjusts sympathetic and parasympathetic activity at the heart and the vessels. Groups of neurons scattered through the cardiovascular system direct changes in: • heart rate • ventricular contraction • blood vessel diameter. Arterial pressure must be maintained at a level satisfactory to the metabolic needs of every organ. For example, to lower systemic arterial pressure, the cardiovascular center reduces sympathetic influx from the
vasomotor nerves in peripheral vessel smooth myocytes. Systemic arterial pressure can be lowered by changing cardiac output and altering peripheral resistance. Base adjustment notwithstanding, during physical activity arterial pressure rises. It is as if the baroreceptors increase their sensitivity threshold. Should arterial pressure not rise on exertion, a left ventricular problem is indicated.
Electrical pathway The two efferent branches of the autonomic nervous system have antagonistic effects and operate in different timeframes. • The sympathetic outflow accelerates the heart rate by about ten beats. • The parasympathetic outflow decreases the heart rate in the order of a single heart beat. This is called a ‘vagal brake.’ Increases or decreases in outflow from the sympathetic and parasympathetic nervous systems have three actions: 1 An effect on the heart rate, either by rhythm modification by the pacemaker, or by changing the speed of the transmission of electrical impulses in the heart wall. 2 An effect on cardiac muscle to increase contractility either directly on the speed of contraction, or on the tension and relaxation of these fibers. 3 Action on peripheral vascular resistance: vasoconstriction or vasodilation. Sympathetic system A premier contingent of sympathetic fibers emerges from the spinal cord between C6 and C7, joining the sympathetic ganglions (superior, middle, and inferior cervical ganglions), distributing to the walls of the large vessels and the heart, and innervating the entire myocardium. Another sympathetic contingent arises from the spinal cord between T1 and T3, destined for the arteries, arterioles, and the splanchnic veins.
Homeostasis of the cardiovascular system Stimulation of the sympathetic system causes an increase in cardiac activity. It can modify the: • frequency of the heart rate • contractility of the heart • excitability of the myocardium • the speed of conduction. The sympathetic postganglionic fibers, which innervate most arterioles, release the vasoconstrictor norepinephrine. However, the arterioles of the skeletal muscles have both adrenergic sympathetic fibers and vasodilating cholinergic sympathetic fibers. Sympathetic vasodilation facilitates the adaptation of muscle to exercise (D’Alché 2008). Parasympathetic system Fibers of the vagus nerve distribute over the atria and the nodal tissue, whereas the rest of the myocardium receives no parasympathetic innervation. Cell bodies of the preganglionic fibers are found in the brainstem, whereas the bodies of the postganglionic secondary neurons are situated in the subaortic plexus. The majority of vessels are devoid of parasympathetic innervation. However, there are exceptions: • A parasympathetic contingent is devoted to the arteries of the erectile genital organs.
• Several cranial parasympathetic nerves distribute to the arteries of the salivary glands, the pancreas, the digestive mucosa, and the coronary arteries. The parasympathetic system has an inhibitory action on the array of cardiac functions. An increase in parasympathetic activity lowers the heart rate (by acting on the sinoatrial (SA) node and slowing conduction), reduces the excitability of the nodal tissue, and diminishes contractility. If the stimulation is intense, the slowing could be significant and lead to cardiac arrest. Such a heart stoppage is spontaneously resolved when nodal tissue plays a decisive role by escaping the vagal braking action after a few seconds. The term is ‘nodal escape’ (Fig. 3.1). This is why fainting spells of emotional origin are generally brief and resolve rapidly. The cardiac section of the parasympathetic system accelerates the frequency of the heart beat, which demonstrates the continuous braking action of the parasympathetic system. In the normal state, the heart rate is in the neighborhood of 70 beats per minute. Parasympathetic cardiomoderator tone takes away from the sympathetic tone.
Mediators The mediators and receptors of the autonomic cardiovascular innervation supplement and modulate vessel responses.
Effects on nodal tissue: Chronotropic, Dromotropic Parasympathetic system
Neurotransmitter: acetylcholine
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Heart rate
The heart Salivary glands Vasodilation ′Special′ vessels
Fig. 3.1 Cardiovascular effects of the parasympathetic nervous system.
Pancreas Erectile tissues
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General principles
Neurotransmitter: acetylcholine
Secretion of epinephrine & norepinephrine
hormonal effects
Adrenal medulla Preganglionic neurofibers Effects on nodal tissue: + Chronotropic + Dromotropic
Sympathetic system
Postganglionic neurofibers
Heart receptors β1
Effects on muscle fibers: + Inotropic + Bathmotropic
Heart rate Force of contraction
Neurotransmitter: norepinephrine
Vessels
"Special" vessels β2 receptors (coronary, hepatic, muscular)
vasorelaxation
Systemic vessels: α1 receptors
vasoconstriction
Fig. 3.2 Cardiovascular effects of the sympathetic nervous system.
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Postganglionic neurons of the sympathetic system that innervate the heart and the vessels release a hormonal signal called norepinephrine. Norepinephrine stimulates α receptors on the smooth vascular muscles and β1 receptors on the cardiac cells. Note, however, that certain vessels are equipped with β2 type receptors whose stimulating effects are opposite to the first (Fig. 3.2). • The α1 receptors are most common on the membrane of the vascular smooth muscles; they are vasoconstrictors. • The α2 receptors are located mainly on the walls of the cutaneous vessels. They create a phenomenon of neuromodulation.
• The principal role of β1 receptors is increasing the frequency (positive chronotropic effect) and the myocardiac contractility (positive inotropic effect) of the heart. – The β2 receptors are situated at the arteriole level of striated skeletal muscles, of the liver, and of the coronary arteries. They have a vasorelaxing effect (see Fig. 3.2). Adrenal gland innervation comes from sympathetic fibers sent without relay in the sympathetic ganglions. The second neuron is thus represented by the adrenal medullary cells themselves. These cells secrete epinephrine (adrenaline) into the bloodstream.
Homeostasis of the cardiovascular system The coordinated actions of the different autonomic components are integrated in what is called the baroreflex. This reflex organizes rapid systemic arterial pressure readjustment (Fig. 3.3).
3.1.3 Hormonal system If the nervous system intervenes in the rapid and permanent regulation of cardiovascular function, the hormonal system provides slower but longer-term control. Four main systems converge towards this regulation: 1 Catecholamines from the adrenal medulla (epinephrine and norepinephrine) 2 Vasopressin or antidiuretic hormone 3 The renin–angiotensin–aldosterone system 4 Atrial natriuretic peptide. Other hormones have recently come to light as having direct or indirect cardiovascular effects. However, they are still rather imperfectly understood.
Adrenal medullary hormones Production The central part of the adrenal gland, or the adrenal medulla, comprises endocrine cells that release epinephrine into the bloodstream. The adrenal medulla constitutes a sort of hypertrophic sympathetic ganglion. It is a neuroendocrine transducer that transforms electrical impulses into hormonal signals. Effects Epinephrine and norepinephrine are catecholamines produced by the adrenal medulla that are circulated through the bloodstream to their receptors. Their effects are both metabolic and cardiovascular (Fig. 3.4). • The metabolic effects of catecholamines are mainly the mobilization of hepatic glycogen and lipolysis. • The cardiovascular effects of catecholamines concern: – the heart: their attachment onto the β1 receptors induces an increase in the
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heart rate (chronotropic effect via the nodal tissue) and contractility (inotropic effect via the cardiac muscle cells). – the vessels: their attachment onto the α1 receptors provokes vasoconstriction. In certain vessels equipped with β2 receptors, particularly those located in the myocardium, the striated skeletal muscle, and the liver, catecholamines promote by opposite effect, vasodilation. Conversely to norepinephrine, epinephrine has a greater affinity for β receptors than for α receptors. This explains why the direct and indirect effects of the sympathetic nervous system are different. The direct effect of the sympathetic nervous system, by the release of norepinephrine, is dominated by peripheral vasoconstriction, causing an increase in total peripheral resistance and consequently a rise in arterial pressure. The indirect effect of the sympathetic system is achieved by the adrenal medulla. Circulating epinephrine manifests as an increase in cardiac frequency and contractility, resulting in increased cardiac output, whereas vasorelaxation occurs at the striated skeletal muscles. Application The intervention of the adrenal medulla in cardiovascular regulation comes into play during physical exercise, arterial hypotension, and also when the skin reacts to strong emotions. Catecholamines are circulated in alarm situations when the fight or flight response comes into play. These hormones mobilize reserve chemical energy (lipolysis and glycogenolysis), increase cardiac output, and, through vasodilation, assist the activity of the skeletal musculature.
Vasopressin Production Antidiuretic hormone (ADH), or vasopressin, is a hormone secreted by the hypothalamus,
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General principles Carotid bifurcation Baroreceptors Chemoreceptors Subclavian artery Baroreceptors
Baroreflex
Aortic arch Baroreceptors Chemoreceptors
Right atrium Vena cava Pulmonary arteries Baroreceptors Stretch receptors
CN IX CN X
Sympathetic center cardio accelerator Stimulus: lowers arterial pressure
Parasympathetic center cardio moderator Stimulus: raises arterial pressure
Inhibition Preganglionic Acetylcholine
Adrenal medulla
Postganglionic Norepinephrine
β1 heart receptors
Neurotransmitter: acetylcholine
Vessels Heart
Systemic vessel α1 receptors
Nodal tissue effect: + Chronotropic + Dromotropic
Epinephrine & norepinephrine secretions
Fig. 3.3 The baroreflex.
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Nodal tissue effects: – Chronotropic – Dromotropic
Muscle fiber effects: + Inotropic + Bathmotropic
Heart rate Force of contraction
Vasoconstriction
Lowering of sympathetic tone Vasorelaxation
Heart rate
Homeostasis of the cardiovascular system
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General effects: Lipolysis Glycogenolysis
Sympathetic system
b2: vasodilation Hepatic Striated skeletal muscles Coronary
Adrenal medulla
b2: heart + Inotropic + Chronotropic Epinephrine
a: vasoconstriction Systemic
Norepinephrine
Fig. 3.4 Cardiovascular effects of adrenal catecholamine.
Osmoreceptors Central nervous system
Kidney: Increases tubular water resorption
Hypothalamus
Vasorelaxation: Cerebral arteries Coronary arteries
Posterior pituitary gland
Vasopressin (ADH)
Vasoconstriction: Cutaneous peripheral
Fig. 3.5 Cardiovascular effects of vasopressin.
and sent by axonal transport to the posterior pituitary gland where it is released into the bloodstream. Effects Circulating ADH acts on the kidney and the cardiovascular system. • ADH decreases the volume of urine by increasing the reabsorption of water in the kidneys. • ADH causes contraction of vascular smooth muscles, constriction of arterioles, and peripheral
vasoconstriction. This manifests at the skin as palor and brings about vasodilation of the coronary and cerebral arteries (Fig. 3.5). This action, which explains its name vasopressin, occurs only when ADH is present in high, non-physiological concentrations. Application ADH is concerned with the regulation of body fluid osmolarity. An increase in blood osmolarity is detected by central osmoreceptors, connected with the hypothalamus.
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General principles
Renin–angiotensin– aldosterone system Production Renin is an enzyme produced by the juxtaglomerular apparatus of the kidney in response to a drop in local or systemic blood pressure. Renin catalyzes the conversion of angiotensinogen (a renin substrate from the liver) to angiotensin I. Angiotensin I is then transformed into angiotensin II under the effect of a conversion enzyme produced by vascular endothelium. The principal site of this conversion is the lungs. Effects Angiotensin II has many effects (Fig. 3.6) in its effort to normalize blood pressure: • At the adrenal cortex it stimulates the secretion of aldosterone, which increases water and sodium retention in the kidney. • It acts directly on the arterioles, causing system vasoconstriction.
Reduced arterial pressure
Juxtaglomerular apparatus
• It reinforces contractility of the heart (positive inotropic effect) • At the level of the peripheral nervous system, it favors the release of norepinephrine by the process of neuromodulation. • In the central nervous system it reinforces sympathetic command. Application The production of renin is initiated with any drop in arterial pressure, whether this is a lowering of systemic arterial pressure or a local diminution of intrarenal arterial pressure. This secretion can also be triggered by the renal sympathetic system or by circulating epinephrine, in the framework of a baroreflex, for example. Lowered renal tubule sodium charge increases renin production. Under normal conditions, renin levels determine the activity of the renin– angiotensin–aldosterone system. This mechanism can be upset during chronic hepatic
Vascular endothelium
Conversion enzyme
Renin
Pulmonary circulation
Liver
Inactive angiotensinogen
Inactive angiotensin I
Active angiotensin II
Adrenal cortex: Aldosterone secretion
Vessels: Vasoconstriction
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Heart: + Inotropic
CNS: Sympathetic tone
Fig. 3.6 Actions and production of the renin–angiotensin mechanism.
Kidney: Water and sodium resorption in tubules
Homeostasis of the cardiovascular system
Volume increase
Increased central venous pressure
Atrial receptors
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Kidney: Increased water elimination Natriuretic atrial peptide (NAP) Vessels: Vasorelaxation
Fig. 3.7 Cardiovascular effects of natriuretic atrial peptide.
illness, if antiotensinogenic synthesis is disturbed.
Natriuretic atrial peptide Production Natriuretic atrial peptide (NAP) is produced by specialized muscle cells in the atrial wall. Effects Natriuretic atrial peptide (Fig. 3.7) affects: • the kidneys, by allowing more sodium to be released in the urine • the bladder, by a relatively modest vasorelaxation. Application The secretion of NAP is initiated by an increase in average atrial distension, that is, by an increase in central venous pressure.
3.1.4 Complementary systems Together, the nervous and hormonal systems help to maintain systemic cardiovascular equilibrium. They intervene as soon as arterial pressure, central venous pressure, blood osmolarity, or blood pH changes. • The hormonal system acts in the middle and long term as a response to central and cardiopulmonary osmotic receptors. It acts principally on the total blood volume (volemia). • The nervous system intervenes quickly and momentarily to keep arterial pressure
constant in the short term. While baroreceptors instigate changes in heart rate, cardiopulmonary receptors adjust peripheral vasomotor tone. If the nervous and hormonal systems provide overall equilibrium to the cardiovascular apparatus, local or regional circulatory variations respond first to local mechanisms. However, when local circulatory changes alter general circulatory parameters, systemic arbitration is required. For example, during physical exercise, vasodilation in the striated muscle bellies is essentially the result of local mechanisms, linked to metabolic changes that result from effort. Systemic control intervenes by way of reflexes only when the total muscle mass implicated in the effort is such that the muscular vasorelaxation reduces total peripheral vascular resistance, lowering arteriole pressure and triggering a baroreflex.
3.2 EXAMPLES OF LOCAL CIRCULATORY ADAPTATION 3.2.1 Cerebral circulation Anatomically, cerebral circulation rests on four pedicles: 1 The right and left internal carotid arteries 2 The right and left vertebral arteries. Three levels of anastomosis between the pedicles ensure constant circulation to all the cerebral regions, in all circumstances and postural positions. These three levels are:
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General principles 1 The circle of Willis 2 The extracranial and intracranial anastomoses notably between branches of the external and internal carotid arteries via the ophthalmic artery or internal maxillary artery 3 The anastomosis between adjoining cortical territories unites branches of the anterior, middle, and posterior cerebral arteries, although branches feeding the cerebral parenchyma are terminal.
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The brain does not possess any significant energy reserves and therefore any interruption in blood supply causes a nearly instantaneous loss of consciousness. The brain’s intolerance of hypoxia means that a constant oxygen supply is imperative. Average cerebral blood flow is on the order of 55 mL/min for every 100 g brain tissue, which represents 12–15% of cardiac output. The gray matter requires even more oxygen, up to 100 mL/min per 100 g tissue. Intellectual cerebral activity does not entail any notable change in total cerebral blood flow, but rather prompts a change in its distribution. For example, visual observation of a scene or an image requires an increase in blood in the occipital cortical areas. Listening to a recital draws more blood flow to the temporal lobes. Variations in cortical blood flow distribution depend on metabolic vasodilation. Local blood flow adapts to the needs of local tissues by way of metabolic hyperemia. The brain is dense with capillaries. As cerebral arteries are short, circulatory resistance is located more at the level of the arteries than the arterioles. Likewise, sympathetic innervation predominates at the extracerebral arteries rather than the arterioles. The brain has some measure of control over the constancy of its blood supply, independent of systemic vasomotor commands, which it is capable of escaping. In this way it can resist systemic vasomotor control, which is beholden to the needs of the central nervous system. Cerebral circulation is thus endowed with very effective autoregulation, permitting it to
maintain a stable blood flow as long as the systemic arterial pressure remains between 60 and 180 mmHg: the cerebral arteries react with constriction to a rise in systemic arterial pressure and, conversely, by relaxation to a drop in pressure. When the pressure falls below 60 mmHg or rises above 180 mmHg, cerebral blood flow varies. Cerebral autoregulation also occurs in response to chemical changes, notably to carbon dioxide. This is why voluntary hyperventilation is triggered by alkalosis hypocapnia, and causes immediate cerebral vasoconstriction. By contrast, apnea occurs with hypercapnic acidosis and results in vasodilation. Cerebral circulation is distinguished by the watertightness of its epithelial lining. The blood–brain barrier is watertight, as there are no pores on its endothelial surface. Because the adult brain is located in a rigid box, increased intracranial pressure can alter cerebral perfusion. Cerebral edema is an example. When intracranial pressure approaches systolic arterial pressure, it opposes blood flow causing ischemia. Ischemia itself promotes acidosis, which results in more edema, leading to an accumulation of fluid in the interstitial spaces.
3.2.2 Coronary circulation Coronary circulation is distinctive in its anatomy. The coronary arteries originate at the aortic valves. The blood circuit is short and drains into the right atrium by way of the coronary sinus. The coronary vessels have a great density of capillaries and a high rate of oxygen extraction. The coronary circulation must provide oxygen and energy, delivering substrates to an organ in constant activity. This provision must be able to increase substantially when the work of the heart intensifies: when cardiac output and/or arterial pressure rise. Coronary blood flow is subject to a wide variation, depending on the heart’s activity: from 70 to 80 mL/min for 100 g tissue at rest,
Homeostasis of the cardiovascular system to as much as 300–400 mL/min per 100 g tissue on exertion. Coronary blood flow declines during systole, at which time the vessels are compressed by the contracting cardiac muscle and blood flow is impeded. The majority of cardiac blood flow takes place during diastole, when blood flow is 80% of the total coronary blood supply. Thus, cardiac perfusion is precarious when the heart rate rises, especially in a subject presenting with coronary artery pathology. Anatomically, the coronary arteries are of the terminal type, which means that functionally they lack anastomoses, leaving them no ability to substitute supply channels in case of obstruction. Metabolic vasodilation is the predominant regulatory factor in the provision of coronary blood flow. Epinephrine has a vasodilatory effect on coronary circulation by its action on β2 receptors. The cardiac muscle has a great deal of flexibility, as it can use several energy sources – not only glucose, but fatty acids and ketone bodies such as lactic acid. Moreover, it has reserve oxygen in the form of myoglobin.
3.2.3 Splanchnic circulation Gastrointestinal circulation has particular anatomical features. The three principal arterial trunks (celiac artery, superior mesenteric artery, inferior mesenteric artery) constitute, along with their branches, a large network of anastomoses. This natural communication system provides effective alternate routes, in cases where one or more trunks are obstructed. The splenic vein and mesenteric veins converge to form the portal vein, which enters the liver. En route, the blood traverses two capillary networks, the mesenteric or splenic network, and finally the hepatic network. The portal system is a true vascular serial montage. Total blood flow to the liver is approximately 1–1.5 L/min, accomplished by a double blood supply: • Arterial flow from the oxygenated hepatic artery (approximately one-third)
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• Venous flow from the portal vein (about two-thirds). Functional adaptation occurs through the arterial portal mechanism (hepatic arterial buffer response), whereby flow from the hepatic artery increases while portal vein flow decreases, and vice versa. The ingestion of food, but not water, causes mesenteric hyperemia, with an increase in the mesenteric venous return and consequently augmented flow through the portal vein. Hepatic artery output diminishes in response to this rise in portal circulation. On an empty stomach, in contrast, the portal blood flow is weak and this causes hepatic arterial relaxation, which increases its flow. Basic hepatic circulation represents 20% of total cardiac output and is thus much greater than the liver’s intrinsic metabolic needs. This is explained by the organ’s significant excretory role, linked to its exocrine and manifold endocrine functions. The splanchnic circulation plays a big part in regulating arterial pressure. Prolonged intense splanchnic vasoconstriction is sometimes recruited to support arterial pressure. This is what happens, for example, during major sporting activity. • On the arterial side, vasoconstriction compensates for a decrease in peripheral resistance, following muscular vasorelaxation. • On the venous side, venous constriction plays an essential accommodating role, by supporting central venous pressure. After a meal, mesenteric vasodilation increases portal venous flux, accompanied by hepatic arterial vasoconstriction, as a consequence of the balancing mechanisms described above.
3.2.4 Pulmonary circulation Pulmonary circulation provides the gaseous exchanges between the pulmonary alveoli and capillaries. This circuit extends from the heart to the lungs and back to the heart; 100% of cardiac output goes through it. The blood moves from the heart to the lungs by way of the pulmonary arteries, the
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General principles only arteries in the body that carry deoxygenated blood. In the pulmonary capillary beds, carbon dioxide is removed from the circulation and added to alveolar gas, while oxygen is added to the blood from lung alveolar gas. The oxygen-rich blood is then returned to the left side of the heart through the four pulmonary veins. Pulmonary circulation has weak resistance, thereby facilitating higher blood flow. Blood pressure is relatively low and the arterial walls are quite thin. The pressure in the right ventricle and the pulmonary trunk is six to eight times lower than in the left ventricle and the aorta. Although their pressures are different, the two ventricles eject the same quantity of blood. When cardiac output rises, resistance in the pulmonary vessels falls. The great dispensability of the pulmonary vessels allows significantly more flow without any marked rise in pressure, thus protecting the fragile alveolar capillary barrier. The volume of the pulmonary circulation represents about 10–12% of the total blood
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volume and is subject to very little variation. In cross-section, the pulmonary arteries appear oval and do not become circular until the pulse wave passes through. Because of their compliance, the large arteries are able to convert the intermittent blood flow coming from the heart to the smoother flow of the pulmonary capillaries (Windkessel effect). Due to their great dispensability, gravity has an effect on the pulmonary circulation. In upright posture, which creates differences in hydrostatic pressure, the vessels at the base of the lungs are wide open, while the vessels at the apex can be collapsed. Perfusion is more evenly distributed when lying down. In contrast to all other circulatory territories, the pulmonary circulation responds by vasoconstriction to hypoxia, histamine, and bradykinin. Finally, recall the big role played by the pulmonary circulation in systemic circulatory regulation, via the production of conversion enzyme.
Cardiovascular risk factors
People are not at equal risk for heart disease. Atherosclerotic lesions can develop early, sometimes even in adolescence. However, they form even earlier in the presence of known cardiovascular risk factors. Risk factors include behaviors, situations, or antecedents that influence the frequency of heart problems. A predisposing factor can be defined as a physiological state (e.g. age), pathological condition (e.g. hypertension), or a habit (smoking, for example) that is associated with a higher rate of occurrence. Cardiovascular risk factors are: • age and sex: over age 50 years in men, and age 60 years in women • smoking: current or having quit for less than 3 years • diabetes: treated or not • arterial hypertension: treated or not • heredity • an excess of ‘bad’ cholesterol, insufficient ‘good’ cholesterol, or both • obesity or overweight • sedentary lifestyle • stress • alcohol.
4.1 AGE AND SEX Arteries lose elasticity and become more rigid with age. Atheromatous plaque forms on the artery walls and these endothelial lesions can be the starting point for cardiovascular problems. ©
2011 Elsevier Ltd
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The probability of cardiac disorders or cerebral vascular accident rises sharply after the age of 50 years in men and 60 years in women. The variation in cardiovascular rates between the sexes is most likely explained by hormonal differences. • Before menopause, women have a reduced risk. • After menopause, when estrogen falls, cardiovascular disease rises sharply in women and reaches that of men of the same age. • Several years after the menopause, women are at higher risk than men.
4.2 SMOKING Smoking is directly or indirectly responsible for many deaths. Aside from the numerous lung pathologies it causes, tobacco is a key factor in cardiovascular disease. Smoking is linked particularly to the sudden death associated with myocardial infarction. Smoking 10 cigarettes a day doubles the risk of a heart attack. Smoking 20 cigarettes daily increases the risk threefold compared with that in a non-smoker. Passive smoke inhalation presents the same health risk. It has been demonstrated than a nonsmoking spouse married to a smoker has a 25% increased risk of infarction. The benefits of quitting are progressive. Two to three years after quitting, the coronary
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General principles risk is still not significantly different from that of a smoker. However, in the case of myocardial infarction, the risk of recurrence or death diminishes significantly after the first year of quitting and eventually falls to the same risk level as that in nonsmokers.
4.3 DIABETES The consequences of diabetes carry numerous health risks. Excess blood glucose over many years is toxic to the arteries and the nervous system. In terms of small arteries, diabetes chiefly affects the eyes and the kidneys: • In the eyes, the disease creates retinopathy, which manifests as visual disturbances and can eventually cause blindness. Diabetes is the principal cause of adult blindness. • In the kidneys, arteriopathy – ‘disease of the artery’ – can evolve into chronic renal insufficiency requiring dialysis, and even renal transplantation. In large arteries, diabetes favors the formation of atheromatous plaque, greatly increasing cardiovascular risk. The three target areas are: 1 The heart: coronary heart disease and angina pectoris 2 The brain: affected carotid arteries can be the source of cerebrovascular accidents 3 The lower extremities: there is a predisposition to the development of arteriosclerosis obliterans of the lower extremity. Nerves can suffer diabetic neuropathy, bringing with it intractable leg pain. Frequency increases with the duration of the diabetes and the age of the person affected. Such neuropathy linked with affliction to the smaller vessels can cause wounds to the foot leading to amputation.
4.4 ARTERIAL HYPERTENSION 62
The link between cardiovascular tension and risk is well established. The incidence of
hypertension is particularly high in industrialized countries. Often it has no identifiable origin and for this reason is called essential hypertension. Nevertheless, in some cases there are known causes (alcohol, drugs such as corticosteroids, oral contraceptives, cocaine, ecstasy, and certain illnesses, notably renal disease), in which case the term secondary hypertension applies. Arterial hypertension is usually silent; it has no symptoms or visible sign and is therefore called the ‘silent killer’. It is detectable only through regular blood pressure testing. Large-scale epidemiological studies show that the relationship between arterial pressure and cerebral risk is greater than the relationship between arterial pressure and coronary risk. Arteriosclerosis (hardening of the arteries) linked specifically to high blood pressure (HBP) and aging is distinguished from the process of atherosclerosis (formation of plaque) in which HBP does not intervene except as a general risk factor. Arteriosclerosis is mainly a pathology of the intima of the large arterial vessel walls, notably in the areas of turbulent flux. In the brain, arteriosclerosis is implicated in at least 50% of cardiovascular accidents. It is responsible for the small cerebral infarcts resulting from the occlusion of perforating arteries. Atherosclerosis is responsible for one-third of cerebral lesions in people with hypertension. It causes large cerebral infarcts. Hemorrhage occurs in only 20% of cases. In the heart HBP: • favors the formation of atheromatous plaque in the large coronary trunks responsible for ‘organic’ cardiac insufficiency • contributes, in collaboration with various neurohormonal factors, to hypertrophy of the left ventricle. This hypertrophy then contributes to structural and functional anomalies of the small coronary arteries, further contributing to coronary insufficiency.
Cardiovascular risk factors
4.5 HEREDITY Heredity is a major risk factor for cardiovascular disease. Illness in the immediate family (father, mother, or sibling) is especially significant. Even one such family member suffering from heart disease increases the chances of it developing. Nevertheless, only cardiovascular accidents occurring early are taken into consideration: • sudden death from myocardial infarcts: – before age 55 in the brother or father – before age 65 in the mother or sister. • Cerebrovascular accidents in a member of the family before age 45.
4.6 BLOOD LIPIDS The link between hypercholesterolemia and atherosclerosis is particularly well established, essentially in regard to coronary pathology. Cholesterol is widely distributed in the tissues and fluids of the body. This sterol, which stabilizes lipids, is necessary for the formation of sex hormones, corticoids, and bile. Part of cholesterol derives directly from food, but it is synthesized mainly in the liver. After reaching the various tissues of the body via the blood, cholesterol attaches to the plasma transporters. These complexes, called lipoproteins, are classed according to density. • Low density lipoprotein (LDL) transports cholesterol from the liver to the cells of the body that require LDL for the function and reconstruction of their cell membranes. Low density lipoproteins have a tendency to form fatty deposits on the lining of the artery wall. Increased LDL in plasma is associated with an increased risk of atherosclerosis, and is thus termed ‘bad cholesterol.’ • High density lipoprotein (HDL) collects and converts cholesterol and carries it to the liver for removal from the body. Thus, HDL serves to protect the artery walls. When HDL levels are low, their protection becomes insufficient. A concentration of HDL lower than 0.35 g
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(French recommendation) or 0.4 g (American recommendation) is thus considered an additional cardiovascular risk factor.
4.7 OVERWEIGHT AND OBESITY Body mass index (BMI) is a measure of body fat based on height and weight: • BMI 20–25 kg/m2: normal weight • BMI 25–30 kg/m2: overweight • BMI ≥30 kg/m2: obese • BMI >40 kg/m2: morbidly obese. Overweight and certainly obesity are clearly associated with a raised coronary risk. This increase is dependent partly on the impact of excess weight on other risk factors. Remember that each kilogram of extra fat adds 650 km to the length of the vascular network! More than 75% of cases of arterial hypertension are due, in part, to excess weight. Today, obesity is on the rise. Indeed practically half of the inhabitants of rich countries are overweight. Besides being overweight, weight distribution has as impact. Excess abdominal fat increases cardiovascular risk. This can be measured by the waist to hip ratio or by the waist circumference alone. A ratio >0.95 in men and >0.80 in women indicates cardiovascular risk. Excess abdominal fat is strongly associated with a number of disturbances, making up what has been designated Syndrome X. This metabolic disease is a combination of medical disorders, among which are found: • insulin resistance, hypoglycemia, or type II diabetes • hyperlipidemia, typically found with raised triglyceride and HDL levels • a tendency towards arterial hypertension.
4.8 SEDENTARY LIFESTYLE Regular physical exercise is associated with both a lower heart rate and decreased blood pressure, thus reducing the oxygen requirement of the myocardium. In addition, physical exercise helps to keep weight in check,
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General principles lowers triglyceride levels, increases HDL concentrations, diminishes plaque aggregation, lowers the sympathetic stress response, and stimulates fibrinolysin (an enzyme that promotes the dissolution of thrombi). For the majority of urban dwellers, energetic expenditure is limited to leisure activities. A meta-analysis (Berlin & Colditz 1990) combining the results of several studies found that a sedentary lifestyle increases the risk of dying from heart trouble 1.9-fold. As therapists, it is important that we recommend that patients practice at least 30 min of moderate physical exercise daily, which amounts to 30 min of brisk walking.
4.9 STRESS It has taken the scientific community a number of years to admit that stress is an integral part of cardiovascular risk. Stress is an interaction between the individual and the constraints of their environment. Cardiovascular risk is linked more to the response of the individual than to the circumstances themselves. Stress can be divided in two categories: 1 Emotional factors such as anxiety, depression, relationship problems, or the inability to express anger. 2 Chronic stress, connected with low socioeconomic status, overwork, or a weak social network. Psychosocial stress develops when there is an imbalance between the stress load (all the
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demands arising from the environment, ourselves, our daily responsibilities, and extraneous events) and our capacity to face these difficulties. This imbalance bring with it signs of stress in our feelings, thoughts, behavior, and body, which can aggravate and maintain the problem. Stress increases sympathetic activity and causes a rise in the blood levels of catecholamines such as epinephrine (adrenaline). Raised catecholamine levels contribute to an increase in cholesterol and blood sugar concentrations, in turn causing blood pressure to rise and reducing the flexibility of fluctuations in cardiac rhythm (Black & Garbutt 2002). The most common alarm signs of stress are difficulty falling asleep and/or early waking, persistent fatigue, muscle tension in the jaw, neck, and shoulders, diminished power of recuperation, reduced ability to concentrate, failing short-term memory, and agoraphobia.
4.10 ALCOHOL In a person suffering from hypertension, excessive alcohol consumption is calculated to be: more than three glasses of wine per day in men and two glasses in women (Haute Autorité de Santé 2005). Taking into account the cumulative effect, three glasses of wine per day adds up to about 120 bottles per year!
Common cardiovascular diseases
5.1 ATHEROMA 5.1.1 Pathological anatomy Atheromatous plaque (atheromas) can develop on the intima of large- and mediumcaliber arteries. Plaque is an accumulation of cholesterol and other lipid compositions that forms on the inner walls of vessels. This deposit is covered by a cap of fibrosity. These fatty deposits extend the length of the arterial wall and protrude on the vessel lumen. Sometimes the entire thickness and very long segments of the vessel wall can be affected. Plaque may break off, stimulating the production of blood clots created when the material beneath the intima comes in contact with the blood. This can cause a thrombus and a vasospasm, impeding blood flow. The most commonly affected arteries are those of the heart, brain, kidneys, small intestine, and lower extremities.
5.1.2 Etiology Arterial obstruction is considered a disease of old age, as it is usually in this age group that clinical signs appear. However, plaques have been found in infancy in the developed world. The origin of atheromatous plaque is uncertain, but it seems that predisposing factors exert their effects over a long period of time. These include: • family history • higher incidence in men than in women until menopause ©
2011 Elsevier Ltd
aging arterial hypertension diabetes smoking excessive stress food rich in refined carbohydrates, cholesterol, and saturated fatty acids • obesity • sedentary lifestyle • excessive alcohol consumption. Most of the time, a combination of factors underlies the formation of plaque. Arterial obstruction by deposits in an arterial wall may be partial or total. These deposits can reduce or abolish blood supply. Their effects depend on the location and caliber of the associated artery, as much as on the available collateral circulation. Incomplete arterial stenosis causes ischemia in the tissues downstream of the stenosis. The tissues can still receive adequate blood to meet their minimum requirements, but not enough to cope with increased metabolic activity. For example, when muscular activity increases, ischemic pain can occur, similar to a muscle cramp. The heart muscle and the skeletal muscles of the lower extremities are those most commonly affected by this phenomenon. Ischemic heart pain is called angina pectoris; ischemia of the lower extremity is called intermittent claudication. In cases of complete occlusion of an artery, the tributary tissues degenerate rapidly and die. The extent of tissue lesions depends on the caliber of the occluded artery, the extent and type of tissue affected, and the degree of collateral circulation.
5
• • • • • •
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General principles If the occlusion impacts: • a coronary artery, myocardial infarction results • a cerebral artery, the resulting cerebral ischemia leads to cerebral infarction.
5.1.3 Complications of atheroma Thrombosis and infarction If the fibrous coating of a plaque breaks off, blood platelets can become activated and a blood clot forms. These more or less plug the artery and can result in ischemia or infarction. Fragments of the clot may detach and be carried in the bloodstream where they cause an embolism in smaller arteries downstream of the clot.
Hemorrhage If calcium salts deposit in plaque, the arterial wall becomes fragile, rigid, and responds poorly to high blood pressure. Plaque can break off and cause a hemorrhage.
Arterial aneurysm A localized dilation of a blood vessel wall can be caused by atherosclerosis and hypertension.
5.1.4 Symptomatology
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In atherosclerosis, the vessel lumen narrows as a result of atheromatous plaque lesions. Certain vessels are especially vulnerable to this arterial disorder and all may be involved by atheroma in the same patient. The most frequent locations are: • the coronary arteries • the carotid bifurcations • the iliac and femoral arteries. The pulse provides important information. An obliterated pulse in the lower extremity can be found in cases of extreme stenosis. Atherosclerosis may be present in the aorta for some time before symptoms are noticed. Symptoms may not appear in the aorta itself owing to its large caliber. However, a blood
clot may form in the aorta and migrate as an embolism to a distant area, or the disease may manifest as an abdominal aneurysm. Usually there are no symptoms until one or several arteries have been obstructed by atheromatous plaque, and blood flow is severely reduced provoking ischemia. Atherosclerosis progresses quietly and remains asymptomatic for a long time. For example, a coronary artery can gradually become 75% occluded and remain asymptomatic or produce episodes of angina sine dolore (painless episode of coronary insufficiency). The first symptom may be myocardial infarction, caused by obstruction of the residual lumen, from either atherosclerosis or a blood clot. Typical symptoms of atherosclerosis are thoracic pain, when the coronary artery is involved, or leg pain, when an artery of the lower extremity is diseased. Arterial hypertension often accompanies atherosclerosis.
5.2 ARTERIOSCLEROSIS Arteriosclerosis is a progressive degeneration of the arterial wall that develops with aging and hypertension.
5.2.1 Large- and medium-caliber arteries The vessel wall is infiltrated by fibrous tissue and calcium. As a result, the vessels lose elasticity. The diameter of the arteries decreases, and they become stiffer and less compliant. The loss of elasticity increases systolic arterial pressure, to the degree that it can no longer dilate during systole. Thus, in arteriosclerosis, the gap between systolic and diastolic pressures widens.
5.2.2 Small arteries and arterioles The thickening of the arterial media narrows the lumen. Arteries, as we have explained, determine peripheral resistance. The narrowing of their lumen increases peripheral
Common cardiovascular diseases resistance and arterial pressure rises accordingly. Tissue ischemia may occur. The lower extremities are vulnerable to gangrene. The risk is especially severe in diabetics. Senile arteriosclerosis is an affliction of the aged whereby progressive hardening of the arteries causes cerebral ischemia and a loss of mental function.
5.3 ARTERIAL ANEURYSM
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Blood clots
Fusiform aneurysm
5.3.1 Pathological anatomy Aneurysm refers to the localized dilation of the wall of a blood vessel. The thinning and weakening of a segment of arterial or venous wall creates a dilated pouch or ballooning. Aneurysms are variable in size.
5.3.2 Etiology Although the pathogenesis of an aneurysm is unclear, there are several predisposing factors: • atherosclerosis • trauma • atheroma • arterial hypertension • congenital anomalies in blood vessel formation • defective collagen formation in the artery wall • syphilis.
Saccular aneurysm
Dissecting aneurysm
5.3.3 Forms Types of aneurysm (Fig. 5.1) include: • Fusiform distensions occur in the entire circumference of the vessel wall, affecting mainly the aorta and sometimes the iliac arteries. These aneurysms present with atheromatous lesions. • Saccular aneurysm is a localized dilation of a vessel wall in which a small area, rather than the entire circumference, is distended, forming a sac-like swelling. These aneurysms can be due to defective collagen, atheromatous lesions, or congenital weakness. • Dissecting aneurysm is a localized dilation, most commonly in the arch of the aorta.
Fig. 5.1 Arterial aneurysms.
It is characterized by an infiltration of blood between the outer and middle layers of the vessel wall. It begins as an endothelial tear and extends little by little to become a longitudinal dissection along the artery. • Microaneurysms occur in small arteries and arterioles of the brain. They are linked to hypertension. Transitory ischemic accidents are often the result of a thrombus or hemorrhage of these aneurysms.
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General principles
5.3.4 Progression and treatment Left untreated, aneurysms tend to enlarge. It is advisable periodically to monitor the thickness and size of the artery wall. Surgical treatment consists of resection and replacement of the excised section of aorta with a synthetic prosthesis.
5.3.5 Complications Hemorrhage The vessel wall may become so thin that it bursts. A ruptured aneurysm causes lifethreatening hemorrhage, often accompanied by shock, severe pain, cerebrovascular accident, death, or incapacitation, depending on the caliber and location of the artery involved.
Compression Even when an aneurysm does not rupture, the swelling of the artery can compress adjacent tissues causing: • an interruption of blood flow due to the compression of other vessels • compression exerted on neighboring organs, nerves, and bones.
Thrombosis and embolism A blood clot may form in the dilated pouch. A fragment, called an embolus, may detach and travel through the bloodstream, becoming lodged in a smaller blood vessel. Such an embolism can cause ischemia and infarction.
5.3.6 Symptomatology
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Generally aneurysms are not painful. Sometimes even large ones are entirely asymptomatic and detected only by accident through imaging tests. Cerebral, thoracic, and abdominal aneurysms are the most likely to produce symptoms if they grow large enough to exert pressure on neighboring structures, or because they stimulate nociceptive nerve endings.
Unfortunately, the onset of symptoms is delayed in relation to the initial weakness. Often the aneurysm is not discovered until it has increased considerably in size. Aneurysms that grow rapidly are most susceptible to rupture. In any event, it is important to be vigilant in the presence of cardiovascular risk factors, together with the following signs and symptoms: • When cerebral aneurysms begin to dilate, the following symptoms can appear: – headache (worsening headache can indicate minor bleeding) – double vision – loss of vision or visual field – trembling or uncontrollable movement of the eye or eyelid – strabismus – facial pain. • In the case of thoracic aneurysm, symptoms are rare but can include: – thoracic pain, pain at the cervicothoracic junction, or both – wheezing – coughing tinged with blood – hoarseness of voice – dysphyagia (difficulty swallowing) – Claude Bernard–Horner syndrome (oculosympathetic palsy). • Ptosis (drooping of the upper eyelid) • Enophthalmos (impression that the eye is sunken in) • Miosis (constricted pupil) • Decreased sweating on one side of the face • Abdominal aneurysms present as: – abdominal pulsation – pain in the upper abdomen – pain at the thoracolumbar junction, the lumbar column, or both. In the event of a rupture, symptoms vary according to location. • A ruptured abdominal aneurysm causes intense pain and sensitivity in the stomach or lower back. • Rupture of a thoracic aneurysm provokes excruciating pain in the upper chest,
Common cardiovascular diseases which spreads to the vertebra and sometimes the trunk. • A ruptured cerebral aneurysm causes hemorrhagic cerebrovascular accident, accompanied by symptoms in relation to the location and magnitude of the hematoma.
5.4 ANGIOMA Angiomas are benign tumors of blood vessels (hemangioma) or of lymph vessels (lymph angioma). The latter are rarer to the extent that the suffix angioma commonly refers to hemangioma. Angiomas are an excessive growth of blood vessels arranged in a nontypical fashion and separated by collagen fibers. They are not true tumors but are classed as such because of their resemblance to tumors.
5.5 CORONARY INSUFFICIENCY OR CORONARY HEART DISEASE In coronary insufficiency the heart muscle receives an insufficient flow of oxygen due to a blockage in the blood supply. According to the severity of the blockage, symptoms range from mild chest pain to a massive heart attack. The underlying causes of coronary insufficiency are numerous and varied. The main ones are atherosclerosis and coronary spasm. NB: Stenosis of the coronary arteries does not present clinical signs except in advanced stages.
5.6 DEEP VEIN THROMBOSIS 5.6.1 Pathophysiology This disorder involves a thrombus in one of the deep veins of the body, often a vein of the lower extremity. The two grave complications are pulmonary embolism and phlebitis. In the first instance, a thrombus detaches and enters the pulmonary circulation. In the case of thrombosis, edema and cutaneous changes either accompany the clot or result from valve destruction.
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Diagnosis is made by ultrasonography. Deep vein thrombosis is considered a medical emergency.
5.6.2 Symptomatology In about 50% of cases, venous thrombosis produces no symptoms, especially at the beginning when the clot is still small and localized. Frequently symptoms appear only once the clot has obliterated the vein. Symptoms are diverse: • Local and distal edema: swelling is more or less pronounced in one leg only, at the ankle, calf, or thigh, sometimes with pain on flexing the foot • Pain: spontaneous calf or thigh pain that worsens with walking • Sensitivity: the leg can become sensitive, with tenderness and warmth of the skin • Cyanosis: bluish discoloration of the skin. Other warning signs: • Arrhythmia: redness or pallor in the limbs • Persistent ankle cramps • Pins and needles • Venous distension: with superficial thrombosis, the vein just under the skin forms a red, hardened cord that is sensitive to pressure • Light fever • Warmth. The symptoms are numerous, but none is really specific to venous thrombosis. In effect, lymphangitis, an infection of the skin or leg, or even a kidney problem, gives the same signs. The loss of flaccidity of the calf and the pain on dorsiflexion at the ankle are the classic diagnostic signs. Unfortunately they are often absent. For this reason, in the presence of symptoms or simply when in doubt, it is vital to send the patient for an immediate medical consultation and a Doppler examination to confirm what you suspect on palpation. Note that smoking, obesity, and estrogen supplementation can predispose a person to deep vein thrombosis.
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General principles
5.7 ARTERIAL HYPERTENSION Hypertension (high blood pressure) is the most common of all heart diseases. • Essential hypertension has no single identifiable cause; 90–95% of cases are of this type. • Secondary hypertension is found in the remaining 10–15% of cases; the causes are identifiable as: – Renal disease, of which hypertension is a classic complication due to the increased secretion of renin. This enzyme affects blood pressure by catalyzing the conversion of angiotensinogen to angiotensin. – Endocrine disease involving: – the adrenal cortex, which can secrete excessive aldosterone and cortisol, stimulating renal retention of sodium and water, and thereby increasing arterial volume and pressure – the adrenal medulla with excessive secretion of epinephrine (adrenaline) and norepinephrine (noradrenaline), increasing arterial pressure, as occurs with pheochromocytoma. • Narrowing of the aorta: hypertension develops in the arteries arising upstream of the stenosis.
5.7.1 Consequences
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Untreated hypertension is an important cause of heart, brain, and kidney damage. • In most cases, the heart is affected by hypertension. When blood pressure is raised, the heart expends more energy to carry out its work of propulsion and overcome the extra demands created by the rise in blood pressure. With sustained hypertension the arteries thicken and the left ventricle becomes hypertrophied in its effort to maintain normal circulation. The heart requires increased oxygen. If this demand is not met, angina pectoris (inadequate blood supply to the left side
of the heart) or myocardial infarction can result. • In the brain, sustained hypertension causes cerebrovascular accidents. Small or large cerebral arteries rupture causing hemorrhage. • The kidneys are also targeted by hypertension. Lesions are found in the renal arterioles. Sustained high blood pressure causes the renal arterioles to thicken with a consequent narrowing of their lumen. Renal blood flow is gradually reduced and in response the kidneys secrete renin, which aggravates hypertension compounding the problem. Reduced blood flow to renal cells can cause cell death and an attendant loss of kidney function, which may progress to renal insufficiency.
5.7.2 Progression and treatment At present there is no remedy for essential hypertension. Secondary hypertension can be treated by eliminating its underlying causes, as long as it is diagnosed early. In certain cases of essential hypertension, blood pressure can be lowered rather spectacularly by observing certain measures: • reducing sodium intake (table salt) • increasing calcium and potassium levels • drinking less alcohol • losing weight • quitting smoking • increasing physical activity • managing stress and emotional disturbances • consulting an osteopath, acupuncturist, etc. Medical treatment may be necessary. Several medications are available, each with different actions. • Diuretics reduce the volume of extracellular fluid by promoting the formation and elimination of urine. Blood volume falls and consequently so does blood pressure. • Conversion enzyme inhibitors reduce the production of angiotensin, blocking the
Common cardiovascular diseases
• •
•
•
formation of angiotensin II, favoring vasodilation, and reducing the secretion of aldosterone. Beta-blockers (antiadrenergic) inhibit the secretion of renin, reducing the force and rate of heart contractions. Vasodilators encourage relaxation of the smooth muscle of the vascular system, reducing blood pressure by lowering systemic vascular resistance. Calcium channel blockers slow the flow of calcium across the membranes of smooth muscle cells of the vascular system, and are an important category of vasodilator. By reducing calcium flow, the smooth muscle tone of the myocardium is relaxed and the risk of muscle spasm diminished. Antihypertensive agents stimulate central inhibitory α-adrenergic receptors which diminish blood pressure. These drugs are prescribed when high blood pressure cannot be controlled by other means.
5.8 RAYNAUD’S DISEASE This chronic circulatory disorder affects mostly females, and is characterized by intermittent ischemia of the fingers and toes. During attacks the skin becomes pale, burning, and painful. It can be triggered by cold or by emotional stimuli. There are two forms of this disease, classified by cause: • Raynaud’s disease, or primary form, is the most frequent kind, representing 90% of cases. The symptoms are mild in the form of unpleasant sensations, but the illness does not damage vessels or tissues. This form occurs most frequently in young women aged 15–25 years, and sometimes disappears spontaneously after a few years. Symptoms sometimes diminish during pregnancy. Women are more often affected than men. • The secondary form is called Raynaud’s phenomenon. This is generally more rare and altogether more serious. It is caused by:
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– vascular diseases, autoimmune diseases such as scleroderma, lupus, or rheumatoid arthritis – certain activities or events that cause damage to vessels: chilblains due to excessive exposure to cold, handling ice or refrigerated items, the use of vibrating implements, or repetitive strain to the hands – some toxins such as vinyl chloride – certain medications and long-term treatments, notably beta-blockers, ergotamine tartrate, and some chemotherapies. Secondary Raynaud’s usually occurs around the age of 40 years. In serious cases, permanently reduced circulation can cause deformity of the fingers or toes, painful ulcers, or even gangrene.
5.9 HORTON’S ARTERITIS Horton’s arteritis is an inflammation of the arteries that strikes after the age of 50 years, peaking in frequency at around 70–80 years of age. It is a progressive inflammatory disorder of the arteries, especially the temporal artery wall, for which reason it is also known as temporal arteritis. The main symptoms are: • Intractable headache at the temple, forehead, or nape of the neck. Often there is hypersensitivity of scalp as well. • Difficulty in chewing, jaw claudication, and painful muscle weakness due to insufficient circulation to the muscles when masticating. • A generally weakened condition with mild fever, weight loss, fatigue, various joint pains, etc, reminiscent of flu. One or both of the temporal arteries are visible, swelled, painful, and sometimes hardened. Their pulse is generally abolished. Horton’s disease can affect any artery. Its manifestations depend on the regions affected, and diagnosis is sometimes difficult. Respiratory problems (dry cough), neurological, psychiatric (depression), rheumatological
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General principles conditions (rhizomelic pseudo-polyarthritis with shoulder and hip pain), etc. One in three patients presents with visual disturbances: diplopia, blurred vision, ptosis, etc. Moreover, the main risk linked to this arteritis is loss of vision should the central retinal artery becomes occluded. This is a medical emergency; treatment involves massive doses of corticosteroids, which are generally effective in preventing otherwise permanent blindness.
5.10 CARDIAC INSUFFICIENCY The heart is deemed weakened or insufficient when cardiac output is incapable of satisfying the body’s requirements in all circumstances. In mild cases, cardiac output is sufficient for the body at rest but becomes inadequate when more is required, for example during exercise. Cardiac insufficiency may predominate on one side of the heart, but as the two sides form a circuit, once half of the pump weakens, the extra burden placed on the other side eventually causes it to pump insufficiently as well. The principal clinical manifestations depend on the side of the heart affected first. In our consultations, we are generally confronted with chronic cardiac insufficiency. This condition advances gradually and may initially present with few symptoms because of the compensatory mechanisms that come into play.
5.10.1 Right chronic cardiac insufficiency
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The right ventricle becomes insufficient when the pressure in its cavity, under the effect of the myocardial contraction, is less than that required to propel the blood effectively into the lung. When the ventricle fails to empty out completely, the right atrium and the vena cava contain the excess blood and become congested. This phenomenon causes back-up repercussions for the venous system. The main organs affected are the liver, spleen, and
kidneys. Edema in the lower extremities and ascites may be part of the picture. This problem can be due to increased vascular resistance in the lungs, myocardial weakness, stenosis, and/or insufficiency of the tricuspid or pulmonary valves.
5.10.2 Left chronic cardiac insufficiency Left cardiac insufficiency occurs when the pumping pressure in the left ventricle is insufficient to eject the blood it receives. This ventricular weakness causes dilation of the left atrium and a retrograde rise in pulmonary circuit pressure. Pressure in the right cardiac cavities also increases, and finally global cardiac insufficiency results. Congestion in the lungs entails pulmonary edema and shortness of breath, often more pronounced at nighttime. This problem can be due to arterial hypertension, mitral and/or aortic inadequacy, or myocardial weakness, generally as a result of coronary disease.
5.11 AGING AND THE CARDIOVASCULAR SYSTEM Physical aging is associated with a loss of elasticity of the different body components. The cardiovascular system is no exception, and among the numerous changes that occur are: • a loss of aortic distensibility • a reduction in the volume of cardiac muscle cells • a progressive loss of the heart’s muscle force • a reduced cardiac output and maximal heart rate • a rise in systolic arterial pressure. With a diminution of stature due to osteoporosis and the loss of tissue elasticity, the arteries of the abdomen curve in and become more tortuous. Low density lipoprotein (LDL) cholesterol levels tend to rise with age, whereas high density lipoprotein (HDL) levels may fall. Coronary insufficiency increases with age and
Common cardiovascular diseases constitutes a major cause of cardiopathy and death. Cardiac insufficiency, which refers to a series of symptoms associated with inadequate heart pumping, may also be manifest. Changes in cerebral blood vessels, notably atherosclerosis, reduce brain irrigation resulting in cell dysfunction or brain cell loss. Compared with a 20-year-old, an 80-year-old
5
person has 20% less cerebral blood flow and 50% reduced renal circulation. With age, the arteries become more winding and dilated as they are less able to resist blood pressure. They have a tendency to lengthen, as the distance between an artery’s point of origin and its termination remains the same. This change is visible at the temporal artery of the elderly.
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6
Cardiovascular semiology simplified
This book is not a medical treatise. It has neither the attributes nor the competence to provide the elements necessary for a complete medical diagnosis. As manual therapists, we must continue to train our hands, and this is no small thing. It demands a long, complex, and never ending apprenticeship. On the other hand, some patients misguidedly attribute their symptoms to purely mechanical causes, when they may in fact be of some other origin. We have had patients consult us for thoracic pain, neglecting to mention their previous myocardial infarctions. Because of this, it is necessary to appreciate the terrain of the patient. The explanation of common pathologies reveals that cardiovascular symptoms can be far from specific, are often absent, or remain quiet for a long time, and that it is sometimes necessary to have a bit of a ‘nose’ to avoid pitfalls in daily practice. Be rigorous in your work by relying on objective findings such as risk factors, a detailed interview, and a thorough clinical examination.
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• The evaluation of risk factors provides an initial and fairly accurate picture of the quality of the vascular terrain of a patient and at the same time, the advisable level of vigilance. • The interview, tailored to cardiovascular symptoms, provides more detail as to the possible existence of underlying pathology. • Finally, the clinical examination can reveal an established illness, or one still in the early stages, prompting referral to a specialist. ©
2011 Elsevier Ltd
6.1 INTERVIEW • Find out whether the patient has had: – an infarction – coronary insufficiency – a pneumothorax – a cardiopulmonary intervention. • Ask whether they have any of the following: – cardiac malformation – arterial malformation – valve anomalies – hiatus hernia. • Ask whether they have: – an artificial valve – an endovascular prosthesis (stent) – a pacemaker (heart stimulator). • Ask whether they have ever had one of the following diseases: – acute articular rheumatism (risk of valve problem) – diabetes or other systemic illness (connective tissue disorder, lymph or reticuloendothelial system disorders, etc.) – congenital or acquired vascular fragility – recurrent tonsillitis. • Inquire about lifestyle: – sedentary lifestyle – eating habits (excess sugar, fat, alcohol) – toxic habits (smoking, addictions, etc.) – escalating psychoemotional tension. • Ask patients: – whether they know what their normal blood pressure is – whether they take antihypertensive medication.
Cardiovascular semiology simplified • Question patients about pain: – Does it arise spontaneously without apparent cause? – Does it arise with activity, exertion? – After eating? (a postprandial full stomach is a common cause of angina pectoris) – Does it occur on exposure to cold or wind? – Do they have pain while lying down? – When sleeping, does the pain oblige the patient to stand or sit up? – Is it accompanied by shortness of breath? – Does it occur when lying down? • Ascertain the location of the pain: – retrosternal – retrocostal – constrictive pain in the chest – radiating to the neck, mandible, arm, little finger. • Inquire about the intensity of the pain: – discomfort, numbness, or burning sensations – constriction – excruciating pain preventing all activity – nausea, palpitations, painful heat beats, lack of coordination. • Ask about the duration of the pain: – Does it stop when activity is over, letting up rapidly at rest? – Is it accompanied by belching as the pain subsides? • Ask about the following signs, which could indicate arterial hypertension: – bedazzlement, seeing sparks and flickers – other visual disturbances – buzzing in the ears – the impression of having a heavy head – morning occipital headache – cervical pain – tension or pain in the mandible without mechanical reason – palpitations on exertion – nonpositional vertigo. • Do not hesitate to refer the patient to a physician in case of: – precordial pain when walking or on exertion (possibly signifying a
6
transitory insufficiency of oxygen supply to the myocardium) – thoracic pain that stops rapidly with the cessation of activity – squeezing sensation, clamping or clawing in the chest, obliging the patient to cease all activity – profound sense of anguish: it is very rare that a patient expresses this fear without a substantial reason; they sometimes have the feeling they are going to die – sudden headache, violent and random (risk of aneurysm or brain tumor) – sleep apnea: an absence of spontaneous respiration, or the inability to breathe on exertion that resolves at rest – pain in the medial aspect of the left arm, reaching the little finger – vagal syncope – dyspnea with exercise (shortness of breath disproportional to the activity) – palpitations with irregular heart rhythm, translating as hyposystolia (contractions of low intensity) – pain accompanied by dysphasia and dysphonia (can indicate mediastinal tumor or thoracic aortic aneurysm). Recall the features of mechanical pain: • It is triggered by activity and effort. It does not subside within minutes, but remains constant. • It is aggravated by movement and activity. • It diminishes considerably by lying down or assuming different positions. In addition, pain that is mechanical in nature is never or almost never accompanied by: • • • • •
cough dysphasia (speech impairment) fever anxiety attacks lipothymia (feeling of malaise, abundant perspiration, nausea, short respiration, and weakness) • hypertension or hypotension • and finally, it does not provoke deep anguish.
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General principles
6.2 VISUAL INSPECTION The visual inspection is a major part of the examination. Osteopaths, even the ‘tactile’ ones, cannot forget to look at their patients. We do not pretend to reduce the inspection to these few lines, but our purpose is to confine our remarks to the most relevant elements. A careful examination of particular parts of the body can reveal a number of small indicators related to cardiovascular pathology.
6.2.1 The face
may be dry or damp, if accompanied by sweating. This is a transitory erythema of the face that can extend to the neck and upper thorax or even the abdomen. Vasodilation of neurogenic origin or vasoactive circulating substances can cause this increased blood flow to the skin. The causes of flashes are numerous: susceptibility to alcohol, some food additives, certain medications, systemic illnesses, and some cancers. – Cyanosis of the face can indicate right ventricular insufficiency or mitral valve constriction.
Complexion
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Diffuse facial pallor can indicate: • Anemia: Examination of the mucous membranes and discolored conjunctiva reinforces this hypothesis. Anemia has multiple causes. In women, abundant periods of long duration are a frequent and benign cause. These can be simply due to an intrauterine device. • Iron deficiency • Toxicity: Facial color can be linked to occupational hazard or to an aesthetic treatment with products containing phenol derivatives. Certain mediations are another possible underlying cause. Hyperpigmentation of the face can have these causes: • Metabolic, e.g. hemochromatosis, where there is a build-up of iron in the skin. • Endocrine, the classic example being Addison’s disease. However, Cushing syndrome can manifest as acromegaly, pheochromocytoma, and hyperthyroidism. Reddened face can be due to: • A diffuse facial erythrosis: – If permanent, this may be associated with cyanosis of the lips, in cases of polycythemia, or an excess of deoxygenated hemoglobin. – If it comes in bouts, it is called vasomotor flashes or flushes which
6.2.2 Eyelids The eyelids should be looked at closely, by having the patient firmly close their eyes. Some systemic diseases can be diagnosed by this simple inspection. • Xanthelasmata are yellow spots appearing at the inner angle of the eye or on the lid close to the bridge of the nose. This finding indicates raised levels of cholesterol. Cholesterol levels should be determined, and evaluated for chronic hepatic cholestasis. • Eyelid edema is notably present in the nephrotic syndrome.
6.2.3 Pupils The most frequent iris anomaly is an opaque ring surrounding the periphery of the cornea (gerontoxon or arcus senilis). It can be limited to one part of the circumference of the iris, or appear as a full circle. This sign indicates high cholesterol but is also observed in patients with atheromatous plaque and no hyperlipidemia. It is advisable to be wary when this sign appears together with hypertension. In view of arcus senilis, it is advisable to look for lipid deposits in other areas (xanthelasma of the eyelids, xanthoma tendinosum).
Cardiovascular semiology simplified
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Lichstein's sign
Fig .6.1 Oblique groove in the earlobe (Lichstein’s or Frank’s sign).
6.2.4 White of the eye
6.2.6 Gums
Look for a change of color: • A yellow eye shows an accumulation of bilirubin in the blood. This can be due to hemolytic anemia, biliary obstruction, or Gilbert’s syndrome. • Red in the eye can indicate conjunctival hemorrhage, which is usually harmless, but is suggestive of hypertension.
Bleeding gums can mean trouble with hemostasis. They are common in patients undergoing anticoagulant treatment.
6.2.5 Lips Cyanosis of the lips should prompt a blood gas test to check for possible hypoxia and verify hemoglobin levels. This bluish discoloration is seen in cases of polycythemia, cardiopathy, or chronic bronchiopathy. In telangiectasia there are small vascular dilations of superficial capillaries and venules. Very red, these can be found on the tongue as well. If telangiectasia is observed in a female suffering from Raynaud’s phenomenon, consider the possibility of scleroderma.
6.2.7 Ears An oblique incisura in the earlobe (Fig. 6.1) indicates the need to ask the patient about vascular risk factors and signs of coronary insufficiency. Also called Lichtstein’s sign or Frank’s sign, this oblique groove – often bilateral – seen on the earlobe indicates premature aging of the connective cutaneous tissue of the heart. Frequently observed in patients over 50 years of age, this sign is a more or less reliable indicator of coronary disease. A study carried out in Sao Paulo on 1500 people demonstrated the correlation between this anomaly and coronary disease (Tranchesi et al 1992). In the event of somewhat atypical thoracic pain, this mark in the earlobe is strongly suggestive of angina.
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General principles
6.2.8 The hand Telangiectasia This condition is caused by dilations of superficial vessels, disappearing with vitropression. It is encountered with scleroderma, pulmonary arterial hypertension, or atrial myxoma (benign primary heart tumor).
Digital clubbing (digital hippocratism) Clubbing is an abnormal enlargement of the distal phalanges. The affected phalange becomes full and fleshy. Nails become arched longitudinally and transversely. Clubbing is sometimes idiopathic (congenital), but when acquired it indicates thoracic problems: • advanced chronic pulmonary disease • tumor • congenital cardiopathy.
Palmar erythema This redness of the palm of the hand is classically linked to jaundice. It is also implicated with the cardiovascular system. It is seen in cases of: • polycythemia • thrombocythemia • infectious endocarditis at the periphery of the palm (Janeway lesion) • tricuspid insufficiency • vasculitis. Remember that palmar erythema is also seen in rheumatoid arthritis, pregnancy, and Basedow’s goiter.
6.2.9 Other signs
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Also investigate: • edema of the lower extremities • distension and fullness of the venous trunks (trouble with venous return) • swelling of the jugular vein or veins of the neck, upper extremities, and thorax (can be attributable to compression from a mediastinal tumor or aneurysm)
• dilation of abdominal veins (compression of the inferior vena cava or right ventricular insufficiency).
6.3 PALPATION 6.3.1 Arterial test As a rule, an artery is supple, and regular on palpation. Feel for the possibility of: • sclerosis or hardening of the arteries • Musset’s sign: head nodding in time with the heart beat (aortic insufficiency or, more rarely, aneurysm) • Cardarelli’s sign: an abnormal pulsation of the trachea when the head is thrown back (aneurysm or dilation of the aortic arch) • an abnormal dilation of a main artery (investigate for aneurysm).
6.3.2 Pulse analysis Take the radial pulse. Some researchers consider a pulse over 80 beats per minute (bpm) to be a cardiovascular risk factor. We emphasize that this book is not a cardiology manual. While we know our place as manual therapists, this does not keep us from expanding our general medical knowledge. Here are some pulse features: • An alternating pulse is characterized by the regular alteration of weak and strong beats (myocardial lesions). • A capillary pulse is an abnormal alternate blanching and reddening of the skin. This rhythmic pulsation of the capillaries and veins is characteristic of aortic insufficiency. • A wiry pulse is very hard but weak in amplitude (arterial hypertension). • A thready pulse is almost imperceptible, weak, and with low pressure. It is found when diastolic pressure is weak (in cases of hypotension). • A hepatic pulse corresponds to systolic expansion of the liver signifying tricuspid insufficiency.
Cardiovascular semiology simplified • An unstable pulse is characteristic of arterial hypertension; it is more evident when changing position. • A jugular pulse is caused by dilation of the jugular veins provoked by changes in right atrial pressure. • A paradoxical pulse (Kussmaul’s) is an abnormal decrease in pulse wave amplitude during inspiration (problem with breathing owing to mechanical obstruction, pericardial tumor, pericarditis, aneurysm, etc.). • A respiratory pulse is the waxing and waning of any pulse produced by respiration. It can be palpated at the jugular vein after physical exertion. • A physiological venous pulse is a normal collapse of the jugular vein during ventricular systole.
compensated. For example, if the systolic pressure is 140 mmHg in the upper extremity and 110 mmHg in the lower limb, the relationship is 0.78 of what is considered normal. An abnormal systolic index is classically a sign of: • arteriopathy • an arterial obliteration • a lumbosacral problem. For our part, we have also found this pulse discrepancy with lumbar stenosis. Obliterative arteriopathy of the lower extremities is a serious illness, often underestimated if it comes up during the patient interview. A simple, low-cost measurement of the systolic index should be undertaken systematically in the presence of cardiovascular risk factors, and sometimes indicates the need for a medical referral.
6.3.3 Arterial pressure
6.3.4 Adson–Wright test
Classical measurement
Highly prized in medical manuals, the Adson–Wright test consists of taking the radial pulse during abduction and external rotation of the homolateral upper extremity. The test is deemed ‘positive’ when the arterial pulse diminishes or is abolished. As a rule, it shows a compression of the subclavian artery in the homolateral thoracic outlet. However, in practice, the problem may be located far from the thoracic outlet, although always on the homolateral side. The cause can be: • osseous (for example, clavicular malobliquity) • osteoarticular or visceral ligaments (for example, pleura or corococlavicular) • nerve plexus (celiac or cardiac) • neural (phrenic nerve). Note that the vein is situated in front of the artery and is the first to become compressed. This can cause pudgy, bluish-tinted hands, which take some time to return to normal. The brachial plexus is also implicated in thoracic inlet problems. In this case the patient feels numbness in the fingers, as
This measurement is an integral part of an osteopathic consultation. We will not describe the classical technique for blood pressure measurement (see Croibier 2005). Apart from the values themselves and the relationship of systolic to diastolic pressure, we are interested in comparing the systolic pressure of both arms. When there is a disparity, it is called anisotension. Most of the time, the side with the weaker systolic pressure is the side of the body with the ‘fixation’. The fixation can be vascular, osteoarticular, fascial, visceral, etc. It is important to retake this arterial tension measure during a treatment session: the ‘white coat’ syndrome is often seen!
Systolic pressure The systolic index is the relationship between the systolic pressure at the ankle to the systolic pressure at the humerus. This ratio is normally equal to 0.9. Any inferior value is evidence of a perfusion deficit, more serious when the arterial lesion is not well
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General principles though they have ‘fallen asleep,’ and shakes the hands and fingers. Thoracic inlet compression usually occurs at night, when the patient is in a restricted position. Depending on how long it took the fingers to ‘fall asleep,’ the sensation will take more or less time to disappear.
6.3.5 Vagosympathetic balance Good health depends, among other things, on the equilibrium of the autonomic nervous system; the ‘harmony’ of two nervous systems is often considered opposites, but which are in reality complementary. Some of what amounts to poor health can be traced to vagosympathetic disequilibrium. Listed below are some of the main features of this lack of balance. Viscerovascular manipulation allows the organism to restore some degree of harmony between the sympathetic and parasympathetic nervous systems.
Sympathicotonia Behavior • nervousness • hypermotility • instability • irritability • aggressiveness • anxiety • pessimism • hyperactivity • insomnia Neurological (general) • hyperreflexia • tremors • weight loss Ocular system • mydriasis • mild exophthalmia
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Circulatory system • tachycardia • precordial pain
• palpitations • slightly raised arterial systolic pressure
Digestive system • • • • • •
dyspepsia inhibited secretions (saliva, gastric juice) solar plexus tension (emotional pain) meteorism (intestinal gas) frequent constipation postprandial pain
Vagotonia Behavior • sadness • depression • discouragement • melancholy Vasomotor symptoms • pallor • abundant sweating • cyanosis of the extremities • overcautiousness • deficient peripheral circulation Digestive system • hypersecretion • hypersialorrhea (excessive production of saliva) • hyperchloridia (excessive secretion of hydrochloric acid) • heartburn • vomiting • sea-sickness, motion sickness • colic • intestinal spasm • hyposthenia Ocular system • miosis Circulatory system • bradycardia • extrasystole • hypotension • lipothymia (profound melancholy: malaise, profuse sweating, nausea,
Cardiovascular semiology simplified
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Box 6.1 Precautions to take before viscerovascular manipulation 1. Take the patient’s blood pressure. 2. Look for anisotension. This can reveal stenosis of large vessels, innate or acquired atherosclerosis, or indicate problems of the following origins: • homolateral visceral • thoracic inlet • cervical • cervicobrachial plexus. 3. Perform the Adson–Wright test. It is positive in cases of: • thoracic inlet syndrome • pleurocervical system • acromioclavicular or sternoclavicular ligamentous system • corococlavicular ligaments (conoid and trapezoid) • Pancoast–Tobias syndrome (pulmonary tumor).
superficial respiration, hypotonia, visual disturbance) Respiratory system • bradypnea
4. Analyze the radial pulse for: • arrhythmia • dysrhythmia • tachycardia • bradycardia. 5. Check the condition of the lower extremities, looking for edema. Take the blood pressure of the lower extremities to check the systolic index. 6. Palpate the main abdominal pulses, especially those of: • abdominal aorta • splenic artery • common hepatic artery • superior mesenteric artery. These pulses serve as evidence and landmarks for manipulation.
• thoracic constriction or obstruction • bronchial spasm Box 6.1 shows the precautions to be taken before viscerovascular manipulation.
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Principles of visceral vascular manipulation
7.1 THE VISCERA: WHAT AN EVOLUTION! • Mobility above all. In the beginning, the techniques were designed to restore mobility and motility to the organs. With a focus on the main axis of an organ’s mobility, they consisted of the manipulation of the visceral attachments: peritoneum, fascia, and omentum. The goal was to harmonize the viscera’s movements and pressures. These techniques are valuable and indispensable for the healthy function of an organ. • The tubes and functional sphincters. Organs of excretion require tubes and sphincters in good working order. If we take the liver as an example, it is imperative to its function that the intrahepatic and extrahepatic biliary ducts be free from all constraints. The cystic duct, hepatic ducts, bile ducts, and sphincter of Oddi must be able to carry out their roles fully. • A free viscoelasticity. Following traumatic events due to digestive, surgical, medical, alimentary, alcoholic or drug intoxication, the solid organs can become fibrotic. Viscoelasticity techniques effectively restore much of the organ’s viscoelastic property, which is vital to the healthy function and energy of an organ. • Fluid circulation. An organ’s circulatory system – arteries, veins, and lymphatic network – is designed for optimal fluid exchange. Visceral vascular manipulations, even when focused on the arteries, act on ©
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the entire circulatory system. Also, bear in mind that hormones must travel through the circulation to stimulate their target organs. • A balanced nervous system. Good health depends in large measure on a balance between the sympathetic and parasympathetic nervous systems. Their complementary actions are responsible for constant adjustments in local, regional, and central functions. These modulations represent the eternal search for balance between ‘more’ and ‘less.’ Visceral vascular manipulations allow us access to this autonomic balance. Anatomically, numerous filaments of the nervous plexus accompany the arterial tree. Thus, in manipulating the arteries, our fingers are in contact with the nervous system and promote central autoregulation. • A harmonious electromagnetic field. Experiments carried out by scanning thermal detectors a short distance from the body demonstrate that visceral manipulation can change the infrared wavelength emitted by an organ. An organ in dysfunction gives off more heat. Infrared wavelengths are a component part of the electromagnetic field. A thermal change almost always accompanies a reaction in one of the other wavelengths, such as ultrasound, short waves, radio waves, and electrical waves. Visceral manipulation has a regulating effect on the harmony of the electromagnetic field.
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The practice of visceral vascular manipulation • Emotional discharge. The brain constantly tries to rid itself of the incalculable number of emotional charges it receives daily. Most of the time, emotion is discharged onto an organ. Depending on the degree and kind of stress received, this can result in a particular organ being under constant emotional strain. A vicious cycle results. For example, when the liver functions poorly, we feel rather drained, worn out, and depressed. Improving the function of the liver can strengthen a person’s ability to adapt to the vicissitudes and difficulties of life. Thus osteopathy is a perpetual endeavor – a search for the hand trained to be able to help a person who is suffering.
7.2 THE GLOBAL CONCEPT OF VISCERAL VASCULAR MANIPULATION To give an organ every chance to regain its full function, it is necessary to extend visceral vascular manipulation to the organs and viscera that are vascularly linked. It is because of their circulatory connection that when we treat the liver our manipulations can affect the duodenum, pancreas, stomach, and spleen. Similarly, in order to improve ovarian circulation, it is helpful to perform visceral vascular manipulation techniques on the uterus and kidneys. For this reason, knowledge of vascular anatomy is important.
7.2.1 Concept of vascular supply and interdependence
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An organ in good health requires an uninterrupted blood supply. In case of failure, it tries to replenish its ‘circulatory deficit’ from the other organs. In the abdomen, for example, the liver, pancreas, duodenum, stomach, and spleen all draw most of their blood from the celiac trunk. However, their arterial supply from this common trunk is not sufficient: they also exchange circulation between one another by means of numerous anastomoses.
Some examples Described below are several examples of vascular interdependence. The stomach • The left gastric artery comes directly off the celiac trunk. • The right gastric artery arises from the proper hepatic artery. • The left gastroepiploic artery is a branch of the splenic artery. • The gastroduodenal artery gives off the right gastroepiploic artery. All of this makes up the vascular circle of the stomach. The pancreas • The superior anterior pancreaticoduodenal artery arises from the gastroduodenal artery. • The superior posterior branch of the superior pancreaticoduodenal artery given off the gastroduodenal artery. • The inferior pancreaticoduodenal artery arises from the superior mesenteric artery. • The splenic artery. • The right gastric artery has anastomoses with the right gastroepiploic artery via the splenic artery. The small intestine • The superior mesenteric artery has branches to the cecum and jejunal loops. • The inferior mesenteric artery. • The inferior pancreaticoduodenal artery arises from the first jejunal branch of the superior mesenteric artery. The duodenum • The anterior superior pancreaticoduodenal artery divides off the gastroduodenal artery. • The posterior superior pancreaticoduodenal artery divides off the gastroduodenal artery.
Principles of visceral vascular manipulation • The inferior pancreaticoduodenal artery arises from the superior mesenteric artery. • The pancreaticoduodenal artery arises from the first jejunal branch of the superior mesenteric artery. These are a few of many examples that emphasize the important role of the duodenum in the abdominal vascular system.
7.2.2 Arteries and pain Migraine For a long time it was thought that migraines were an entirely vascular problem. Initially vasodilation was incriminated as a theory, followed by vasoconstriction. Hyperemia succeeded oligemia as an explanation. However, the vasomotor system of the artery is entirely dependent on its intrinsic or extrinsic nervous system.
Nervous and chemical hormonal systems At the beginning of a migraine attack, neuronal activity is observed in the cerebral trunk and the hypothalamus. What occurs is a massive and transitory depolarization of neurons (according to the findings of Gilles Géraud, Rangueil Hospital, University Hospital Center of Toulouse, France). Hypoperfusion may be the result of the neuronal depression due to the activation of vasoconstrictor neurons.
Trigeminal cervical system This problem is outlined in our book Manual Therapy for the Cranial Nerves (Barral & Croibier 2006). The vessels of the cortex, pia mater, and dura mater receive sensory fibers from the trigeminal ganglion, other cranial nerves, the medulla oblongata, and the upper cervical region. Their stimulation causes a rise in blood levels of serotonin, a powerful vasoconstrictor.
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Migraine attacks demonstrate the complexity of neurovascular relationships. This very intricate system is further illustrated by the pathophysiology of mammary pain.
Pathophysiology of mammary pain The vessels of the mammary connective tissues are very estrogen sensitive. Vasodilation in the breast is closely linked to endogenous, exogenous, and local estrogen supply, all of which increase breast vascularization. Interstitial edema, brought on by a local increase in capillary permeability, can result. Connective tissue edema can cause the distension of connective tissue fibers, compressing sensitive nerve fibers and triggering mammary pain (Seippel & Bäckström 1998). Bertrand Tournant, a gynecologist at Saint-Louis de Paris Hospital, France, has closely analyzed these complex reactions. Gentle local massage techniques can reduce interstitial edema and ease pain. Massage produces a short-term analgesia by activating one of the mechanisms of peripheral pain control, the gate control (closing of the passage of nociceptive influx towards the brain at the level of the spinal cord). The arteries are sensitive to circulating estrogen levels, the stimuli of peri- and intra-arterial mechanoreceptors, to catechol amines, histamine and serotonin, the vagal and sympathetic nervous systems, and central factors (hypothalamus, limbic system, etc.).
7.3 PRINCIPAL VASCULAR TECHNIQUES 7.3.1 Glide induction Certain areas are very sensitive and easily irritated. In these cases glide induction techniques are the best. They consist of superficially and delicately sweeping the artery surface on induction. These maneuvers are addressed to small nerve fibers that surround and cover an artery. It is important to concentrate on the rough areas where there is less gliding, as these
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The practice of visceral vascular manipulation respond best to the techniques. The unevenness on their surface may be due to a lack of elasticity, microcalcifications of the artery wall, or neural indurations.
7.3.2 Stretch induction The stretch induction technique is used to treat the large elastic arteries. Stretching stimulates the mechanoreceptors of the tunica media. This middle layer of the vessel wall is sensitive to axial, lateral, and anterior–posterior stretching.
7.3.3 Compression–decompression induction Over certain precise areas, where it is not possible to palpate the entire course of an artery, one can slowly compress and decompress a portion of the artery with the thumb or finger pad. This technique is applied to the celiac trunk and the aortic bifurcation, for example.
7.3.4 Combined stretches Long, easily palpable arteries such as the brachial artery benefit from local stretching in combination with movement of the associated limb. In flexing a limb, an artery is shortened. In extension, the vessel elongates – even more so if some abduction is included. It is important to maintain a fixed point on the artery while mobilizing the limb.
7.3.5 ‘Accordion’ technique Certain organs, such as the pancreas and uterus, have a very flexible and adaptable arterial system. To have an effect on these sinuous arteries, first try to shorten them and then allow them to return to their initial length. This ‘accordion’ technique has a double effect, acting on both the vascularity and the viscoelasticity of the organ.
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vascular performance. The main hindrances are: • sedentary lifestyle • prolonged sitting • overweight • poor diet • parietal and obstructive artery disease • vertebral fixation • rib fixation • post-traumatic or postsurgical adhesions • scoliosis • osteoporosis. In addition, take into account the reduced height of the spinal column that occurs with aging. The resulting compression of the organs against one another causes reduced mobility as well as arterial, venous, and lymphatic compression.
Irrigation technique principles These techniques can be carried out by either a maintained lift or a maintained stretch, depending on the disposition of the organ in relation to its vascular pedicle. Some arteries are located beneath an organ, and in cases of congestion, inflammation, fibrosis, or adhesion can become compressed or even diverted from their initial course. The lift irrigation consists in maintaining the organ for about 20 s in a cephalad direction, allowing the circulation an opportunity to improve. In this way the brain receives mechanical stimulation from the vasovasorum that it may have been lacking for some time. Other organs, such as the stomach, have an anatomical and vascular arrangement that responds better to stretching techniques. Remember that our results are in large part due to a retroactive central effect.
Arteriovenous axis As the arteriovenous tree is often compressed, 7.3.6 Visceral irrigation technique lifting the organs in the direction of the large For optimal function, an organ requires arteriovenous trunks temporarily augments perfect irrigation. Several factors impede the local circulation.
Principles of visceral vascular manipulation
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Strongly activated, the arteriovenous mechanoreceptors stimulate the locoregional circulatory centers, the medulla and thalamus.
manipulated with the ‘accordion’ technique. In addition, it has numerous small arteries that run perpendicular to its main axis. We manipulate its vascular system according to Maintained lift or stretch its longitudinal axis and also perpendicular Once the organ has been mobilized along to this axis. the axis of the large arteriovenous trunks, maintain this for about 20 s. Irrigation is Preliminary vascular shortening immediately improved, and as a result the Doppler experiments have shown that premechanoreceptors can act more effectively. liminary shortening of a vessel can improve The cerebellum and brain will receive new arterial flux immediately. information about good irrigation that they There are several possible reasons for this: have not had for some time. By a feedback • The ‘surprised’ arterial mechanoreceptors effect, they will reorganize the local circulareact instantly to any stimulation. tory system. • The shortening has an immediate venous and lymphatic effect that reflexively Unpleating arteries and veins provides central stimulation. With time and all the features accompanying Note that the preliminary shortening techpoor irrigation, arteries and veins become nique instantly improves the arterial flux, twisted and pleated. Lifting the visceral vascuwhereas vascular lifting slows it down for lature unpleats them. The stretching of any several seconds. tube increases its function considerably, owing to the direct stimulation of arterial Main organs affected by irrigation muscle fibers. techniques These organs are: Experimentation One of our surgical friends permitted us to • the lungs verify the effect of the visceral vascular lift • the liver technique on a uterus during surgery. At the • the stomach outset, the organ was congested and purplish • the intestines in color. We observed that, on lifting and sup- • the duodenum porting the organ along the arteriovenous • the pancreas axis, the uterus immediately took on a pinkish • the thyroid hue, its venous circulation having been • the uterus restored. This occurred only when the uterus • the ovaries. was lifted on its axis. All retro or lateral movements served to increase the purplish coloration of the organ.
Irrigation technique methodology Respect the direction of the vascular axis The lifting is done first in the direction of the large arteriovenous axis; this is a key preliminary point. Next, perform the maneuver perpendicular to the large axis. For example, the pancreas has arteries that follow its longitudinal direction from right to left, from the sphincter of Oddi to the spleen. These can be
7.4 ARTERIES AND VEINS: AN INDISSOLUBLE SYSTEM When we speak of vascular manipulation, we include the venous system. Every artery is surrounded by one or two veins that follow its course closely. Therefore, it is not necessary to describe the anatomical course of the veins. Veins approach the heart. This is why, before attempting to elongate an artery, we shorten it slightly as a preliminary step, to include the entire arteriovenous system in our effect.
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The practice of visceral vascular manipulation If we speak mainly of arteries, it is because their beats permit us to be more precise in location and palpation. By the same token, we can be objective in our results by way of the Doppler test.
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It is important to remember that each time we perform a maneuver ‘on an artery’ the treatment addresses the vascular pedicle and thus has an effect on the veins contained within it.
SECTION 1 VESSELS OF THE THORAX
The thorax: from container to contents
8.1 THE CONTAINER
8.2.1 Sagittal evaluation
Before approaching the cardiovascular component of the thorax, it is imperative to release, as much as possible, any osteochondral or ligamentofascial tensions of the thorax. Intervertebral and costovertebral articulations can also affect the intrathoracic organs. A free thoracic cage allows us to refine our intrathoracic visceral vascular techniques and to better distribute the pressures they exert.
In decubitus position
8.2 THE RIGID COMPONENTS The sternum is a flat bone that has an excellent intraosseous memory for trauma, or for prenatal or postnatal malposition. It is similar to the sacrum, whose bone and periosteum have the same ability. The sternum serves us both as a means of testing and as a handle for freeing restrictions. The ribs, with their osseous and cartilaginous components, are subject to numerous physical traumas through the course of life. When one suffers a fall or a car accident, the ribs are more affected than is the spinal column – although this is not the case in severe trauma. ©
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The patient lies down, with their hands resting on the abdomen and their elbows on the table to release myofascial tension in the shoulders.
First test The palms are placed one on top of the other, over the angle of the sternum. Begin by compressing the sternum in a posterior and slightly caudal direction (Fig. 8.1). Move your palms towards the left and towards the right to appreciate the chondrosternal and chondrocostal elasticity. Perform the same maneuver below the angle of the sternum. This is a test to find anterior chondrosternal fixations. These restrictions offer a distinctive resistance in the thoracic cage on compression. Second test Slide the flat of your palm under the dorsal spine. Using your fingers, push the costovertebral and costotransverse junctions, and the posterior rib angles (the most prominent part of the posterior ribs) anteriorly while externally rotating the upper extremity with your free hand.
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The practice of visceral vascular manipulation This excellent test allows you to distinguish clearly between posterior osteoarticular fixations and those of neighboring soft tissue.
In procubitus position The patient lies face down with their forehead on the back of their hands. With both palms,
apply pressure on the costovertebral, costotransverse, and posterior rib angles.
8.2.2 Lateral evaluation There is often a tendency to forget the lateral parts of the ribs, which are very important mechanical receptors in cases of trauma. It is possible to find ribs that are free of anterior or posterior fixations, but are fixated laterally. Lateral restrictions have nociceptive effects on the neighboring organs and on the parietal pleura. One can test for them in a side-lying position or in the double pressure test described below.
8.2.3 Double compression evaluation This evaluation (Fig. 8.2) is indispensable as you may find areas of rigidity that might escape you in the tests described above. When you carry out this test, try to think in three dimensions. The thorax is a large container that encompasses other smaller containers. Except for the sternum, none of the parts is flat.
Position The patient is supine with both hands placed on the abdomen. The practitioner is beside the patient. Fig. 8.1 Sagittal evaluation of the thorax.
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Fig. 8.2 Double compression evaluation of the thorax.
The thorax: from container to contents
Test Place a palm against the lateral part of the thorax and exert pressure in the direction of the sternum, first towards its cephalad part, then middle, and finally towards its caudal aspect. Position your elbow against your own chest to be able to apply powerful but not painful pressure, and with no effort to yourself. In our experience, the more we use force, the more we feel our own fingers, and risk not being able to feel the true fixation. All techniques that tire us are to be banished. After all, the road is long and, what’s more, such fatigue makes us feel our own body rather than that of the patient. With the other palm, exert an anterior– posterior pressure at the sternum or the anterior ribs. You must feel the two pressures meet and thereby identify an area of firmness. You will be surprised by this double compression test as it will reveal new zones of rigidity that were not apparent in the initial tests. Thoroughly test the different anterior– posterior planes by applying fairly deeply from both sides.
8.2.4 Double compression treatment This follows the same principle and can be used in different positions. First, directly compress the rigid part identified in the double compression test several times. This will stimulate the locoregional mechanoreceptors. Next follow with induction (exaggerate the movement in the Listening direction)
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without releasing the double compression pressure. Repeat twice.
First time With one palm compress the thorax laterally, and with the other palm exert a sagittal pressure on either the sternum or the anterior ribcage.
Second time The two pressures should meet at the restricted zone. Compress several times to stimulate the mechanoreceptors and then perform the induction technique with both palms. Next, exert a second anterior–posterior pressure on the sternum or the ribs, the other palm compressing the lateral thorax. When the two pressures meet at the most rigid area of the thorax, treat again with induction. At this stage it is sometimes necessary to go slightly past the limit of induction. Finally, you must feel for the melting of the thorax, and that it presents no more distinct areas of resistance. You feel as though there is a hard ball gradually deflating. This technique not only gives good results, but also permits you to feel the treatment in three dimensions.
8.3 THE CONTENTS It is only once the thorax has no more rigid areas that the thoracic contents – the pericardium, mediastinum, heart, and lungs – are addressed. We will look particularly at the heart and the vascular system of the lung.
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The heart
The heart is often described in the form of a clenched fist resting on the diaphragm. The average heart weighs about 275 g. It has a height of 10 cm, a width of 11 cm, and a circumference of 25 cm. It is inclined to the left in relation to midline of the body, its apex is oriented anteriorly and to the left, with its base (its cephalad part) facing posteriorly and to the right. The heart is of great interest to us, because it is the point of arrival and departure of the great vessels and thus the whole vascular system.
9.1 ANATOMY REVIEW 9.1.1 External configuration
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The ventral surface of the heart is formed mainly by the anterior wall of the right ventricle and a small part of the left ventricle. Between the ventricles is the anterior interventricular groove in which runs the anterior interventricular artery, a branch of the left coronary artery. • The right border of the heart corresponds to the right atrium, and extends between the superior vena cava and the inferior vena cava. The right coronary artery runs in the coronary groove separating the atria from the ventricles. The anatomical landmark of the right border is approximately one fingerwidth from the right border of the sternum. • The left border of the heart is formed mainly by the left ventricle and, to a slight extent, superiorly by the auricle of ©
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the left atrium. The anatomical landmark for the left border is a little medial of the left mid-clavicular line. In our techniques, it is mostly the ventral part that we contact through the intermediary of the ribcage.
9.1.2 Excitability of the cardiac fibers The cardiac muscle has a neuromuscular conduction system that ensures the transmission of nerve impulses from fiber to fiber and coordinates the cardiac cycle. The heart is able to beat without the participation of external nerves, thanks to its autonomous nervous system. The excitation comes from the sinoatrial (SA) node, first described in 1907 by Keith and Flack. The contraction signal spreads through the musculature of both atria to the atrioventricular (AV) node (Tawara’s node) from where, via the bundle of His and its two branches, it reaches the Purkinje network, which carries the impulse to the ventricular muscle. The conducting system of the heart cannot initiate a new stimulation until the cardiac muscle is in diastole. Therefore it is important that the heart avoid any form of spasmodic contracture.
Central nervous system The central nervous system has little influence over the autonomic nervous system. It can vary the heart rate, but without having any
The heart effect on autonomous auricular–ventricular sinus interdependence.
Vagal parasympathetic system The parasympathetic system lowers the heart rate and reduces the force of contractions. Note that, as manual therapists, we can obtain the same result when we: • compress the eyeball (oculocardiac reflex) • increase intracranial pressure (bitemporal compression and, to a lesser degree, frontal–occipital compression).
heart contractions, and result in a slowing of the heart rate. As a general rule, compression of the upper part of the heart stimulates the vagal parasympathetic response. We will revisit this concept in later chapters.
9.1.3 The great vessels of the heart
The sympathetic nervous system increases both the heart rate and contractility. This is why emotions and sympathicotonic substances (coffee, alcohol, and tobacco) raise the heart rate. Strong transverse compression of the left little finger has a tendency to stimulate the heart. This is important to know in the event of a vagal attack.
At the ventral heart: • The pulmonary trunk arises from the right ventricle inside the aorta. • The aorta begins at the base of the left ventricle and winds around the pulmonary trunk. It then extends in a caudal direction behind the heart. • The arch of the aorta begins at the level of the sternal angle as a curved continuation of the ascending aorta. From this arch the arteries destined for the neck, head, and arms emerge. • The apex of the heart lies posterior to the left fifth intercostal space near or just medial to the mid-clavicular line. It is at this level that the heart beat can be palpated on the thoracic wall (Fig. 9.1).
Vagosympathetic actions
9.1.4 Landmarks simplified
These systems have a strong action on the vasomotor system and vascular pressure. The sympathetic system is vasoconstrictive and hypertensive. The parasympathetic system is vasodilatory and hypotensive.
Figure 9.2 provides a simplified view of the anterior thoracic relationships of the heart. Variations certainly exist, depending on constitutional differences among people. • Base: a horizontal line passing through the sternal angle (second sternochondral junction) • Apex: a horizontal line passing just inferior and between the left fourth and fifth right ribs • Right border: a vertical line passing slightly outside the margin of the sternum • Left border: a vertical line passing just medial to the left mid-clavicular line.
Sympathetic nervous system
Carotid sinus The carotid sinus is a baroreceptor that responds to changes in blood pressure. When intracarotid blood pressure rises, it triggers bradycardia resulting in a lowered heart rate. A technique for the carotid sinus is described in Chapter 23.
Vagal cervicothoracic depressor nerve The depressor nerves (of Cyon) are located in the endocardia and aortic arch. When stimulated, these vagal afferent fibers inform the brain of changes in the rhythm and force of
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9.1.5 Fibrous skeleton of the heart From a transverse section of the upper heart it is apparent that all the valves are grouped closely together. The fibrous skeleton is a
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The practice of visceral vascular manipulation
Right common carotid artery Left common carotid artery Right subclavian artery
Left subclavian artery
Aortic arch Superior vena cava Ascending aorta
Left pulmonary artery
Pericardium Left superior pulmonary vein Right atrium
Left atrium
Great cardiac vein
Right coronary artery
Left coronary artery, anterior interventricular branch
Right ventricle
Left ventricle
Apex of heart
Fig. 9.1 Heart and great vessels.
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complex framework of dense collagen configuring four fibrous rings which surround the orifices of the valves (Fig. 9.3). The firmest areas on compression are formed by the valves (aortic, tricuspid, and mitral) and the fibrous connective tissue that unites them. The fibrous skeleton functions as a stable but deformable base for attachment of the leaflets and cusps of the valves. NB: The pulmonary valve is not anchored to the fibrous skeleton of the heart, and it is less firm on compression palpation.
Nevertheless we are beginning to be able to palpate its distinctive area of resistance. When compressing different parts of the heart, some areas are clearly more firm and resistant than others. These are located towards the upper heart, which is the base. It is understandable that some are skeptical of the ability to differentiate particular parts of the heart by manual compression. Nevertheless, there is a methodical protocol of approach that allows such subtlety of perception.
The heart
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Aortic arch Pulmonary valve Aortic valve True ribs (1st to 7th)
Tricuspid valve
Mitral valve
Diaphragm
False ribs (8th to 10th)
Fig. 9.2 Anterior thoracic relationships of the heart.
Pulmonary valve Fibrous ring of the ostium of the pulmonary trunk Aortic valve
Fibrous ring of the ostium of the aorta
Left fibrous trigone
Left atrioventricular valve
Fibrous ring of the ostium of the left atrioventricular valve
Fig. 9.3 Fibrous skeleton of the heart.
Fibrous ring of the ostium of the right atrioventricular valve Right atrioventricular valve
Right fibrous trigone
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9.2 CLINICAL EVALUATION OF PRECORDIAL PAIN 9.2.1 Chest pain Who has never felt, at one time or another, pain in the heart region without having a heart problem? Nevertheless, caution must be observed. Even if our patients have excellent medical care, we must be on our guard. We have seen about ten patients with coronary problems where the location of the pain led us to assume a banal mechanical rib restriction. In one instance the patient assured us that it was after excessive exertion that he felt intercostal pain, and that it was of purely mechanical origin. It turned out to be a heart problem that the physical strain had awakened. Conversely, we have had a patient hospitalized under the care of a cardiologist on account of simple costovertebral fixations. Listed below are a few questions to ask in case of suspicious precordial pain. When the patient responds in the affirmative to most questions, a medical examination is imperative. At the end of the questionnaire the essential characteristics of pain of mechanical origin are provided.
Circumstances of onset Did the symptoms appear: • spontaneously and randomly? • during physical activity? • after a meal? • on exposure to cold? • when lying down? • during sleep?
Location of pain
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Is the pain is located: • at the intercostal level? • behind the sternum? • on one side only? Does the pain radiate to: • the inner arm? • the left little finger?
• the neck? • the jaw?
Intensity of the pain • Is it more a discomfort than a pain? • Is the pain dull, oppressive (feeling of suffocation), or a tight or burning sensation? • Is it bearable or intolerable? • Is it accompanied by a sense of anguish? Does the patient have a fear of imminent death? • Does it cause vagotonia, syncope, shortness of breath, palpitations, heart rhythm irregularity.
Duration of the pain • Do the symptoms subside immediately after stopping activity? • Does a chain of belching bring relief? • Does an ache persist after the pain subsides?
Dyspnea With dyspnea, the patient has the impression that: • Even routine activity is accompanied by shortness of breath. • In the night, for no reason, the patient feels an oppression that makes them sit up or remain upright in bed with pillows supporting the back, or impels the patient to sit astride a chair with the chest leaning forward against the back of the chair. • The patient feels their heart beating strongly in the chest to the point of discomfort. • The patient feels as though a peach stone has been swallowed and lodged in the esophagus.
Discussion In general, pain of mechanical, vertebral, or intercostal origin:
The heart • follows a strain or trauma • is relieved by changing position • is intensified by coughing, sneezing, or by leaning on the ribs or sternum • is identified by a mobility test in the case of a costal, sternocostal, chondrocostal, or costovertebral fixation in the area of complaint • is usually unilateral • does not cause dread or a subjective sense of being in danger. It is advisable to pay attention to pains that are: • random • disordered • triggered by cold • occur at night, unrelated to movement • accompanied by a feeling of suffocation or oppression • set off by activity or exertion • postprandial • generate anxiety • independent of osteoarticular fixations.
9.2.2 Precordial pain of noncardiac origin Many symptoms can make one think a patient has a heart problem. The differential diagnosis is not always obvious, especially in the presence of symptoms coming from the esophagus or the stomach, which share the same nerve pathway. The most common chest pains not of cardiac origin are described below.
The stomach Precordial pains are frequently due to gastric dilation caused by air in the stomach. In this instance, on percussion one hears a very clear hollow sound in the left subcostal region. Often, the patient burps to relieve the discomfort, to the point of having a tic: the more the patient belches, the more they need to belch. Note, however, that a heart problem can also trigger belching. We think that, in addition to producing local mechanical discomfort, gastric tension stimulates the vagus nerves abnormally. This
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causes hyperchlorhydria and spasm of the gastric musculature, creating a sort of air pocket. The vagus nerves provide a large part of the heart’s innervation. Sometimes the brain cannot tell the difference between what is digestive and what is cardiac.
The esophagus The vagus nerve provides both sensitivity and the motor control for the esophageal musculature. Although not the only nerve innervating this region, its role is considerable. Because of its anatomical position so near to the heart, a spasm or irritation in the esophagus can alarm the patient into thinking there is a heart problem. In addition, hiatus hernia and gastroesophageal reflux can provoke chest pain.
Costovertebral neuralgia This pain typically occurs after a fall onto the back, rib, or upper extremity. Several months later the patient feels mild left thoracic discomfort accompanied by the impression of small stabs to the chest. These various symptoms lead the patient to believe they have a heart condition. Costovertebral fixations can give respiratory discomfort and the impression of the thorax being in the grip of a vice. Little by little, rather insidiously, the patient senses danger and the smallest additional symptom gives the feeling of an imminent heart attack. It is imperative to refer this patient to their family physician or cardiologist, for his brain is in a state of hypervigilance with regard to the cardiac region. It literally waits for the slightest physical manifestation in the thorax to transform it into a message of danger. We like to give our patients the following illustration of this phenomenon. You might live in an apartment whose neighbors above are so noisy that they disturb your tranquility and cause stress. One day you no longer hear noise. ‘Hold on, how is it that they are not making any noise today?’ Your brain was on
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The practice of visceral vascular manipulation guard for these noises and it waited for them to the point of sometimes amplifying them! The same thing happens with all recurrent nociceptive information: the brain lies in wait and often exaggerates it. NB: Beware of pains that appear for no apparent reason and where the patient cannot attribute any cause and effect to them. Be suspicious, in the absence of osteochondral– articular fixations. One must also be cautious in cases of jaw pain with no evidence of temporomandibular joint (TMJ) dysfunction or malocclusion. Be circumspect in the face of thoracic discomfort, even when located on the right, without previous trauma. Finally, always take a patient’s anguish into consideration.
Other causes Numerous organs can cause patients to believe that they have a cardiopathy. The following list, inevitably incomplete, is founded on our clinical observations: • the bronchi, notably during bronchospasm • the gallbladder, perhaps because of its relationship to the phrenic nerve • the spleen, due to the left-side intercostal neuralgia it can provoke • kidney stones • vertebral and rib fixations.
9.2.3 Psychoemotional factors The heart reacts quickly and readily to stress. It begins to pound, giving the impression that it is tightly bound inside the chest. It may also create a sensation of a thoracic vice grip or stranglehold. We have seen numerous patients perfectly convinced they have a heart problem, in whom all objective tests find nothing. In fact, they were suffering from an emotional reaction.
9.3 MANUAL APPROACH 9.3.1 Precautions 100
Osteoporosis demands precaution in terms of osteocartilaginous pressure.
9.3.2 Indications The following are indications for manual therapy of the heart: • Major thoracic trauma. Recall that it is not the osseous framework itself but rather the intrathoracic organs that provide, by virtue of their viscoelastic resistance, the solidity of the thorax • Following cardiopulmonary surgery • Thoracic hypersensitivity due to anxiety. We have worked in departments of pneumology and cardiac surgery. It is astonishing to see how many patients experience fear when we touch the exact part of the thorax where surgery was necessary • A patient’s subjective sensation of heart disease when all objective examinations are negative. • Cardiophobia • Arterial hypertension • Tachycardia • Dysrhythmia.
9.3.3 Contraindications Manual therapy should not be undertaken following cardiac surgery where a foreign object has been placed. Stents, artificial valves, and pacemakers are all contraindications. It is advisable to be wary of patients who have never consulted their doctor and who present with: • non-positional vertigo • the impression of having weak legs or legs that give way from under the patient • violent and random headaches • a weak femoral pulse. These various signs and symptoms can indicate an aortic aneurysm. Finally, it is important to pay attention to signs of mediastinal compression: • retrosternal pain • cough • dysphonia – due to compression of the recurrent nerve • dysphagia.
The heart
9.3.4 Compression – palpation of the heart A methodical approach is necessary in order to feel the differences in the consistency of the heart.
Protocol The patient is in decubitus, with hands folded on the abdomen. Place yourself beside the patient. Place your palms one over the other on the sternum, in the space between the sternal angle and the sternoxiphoid junction (avoid putting pressure on the xiphoid process). Sagittally compress the sternocostal framework to pass beyond the first osteocartilaginous barrier. Think in three dimensions; as we have said before, the thorax is a solid volume that contains other, more supple, volumes. When you perceive the heart beat, your hands are on a second barrier consisting of the heart and its attachments. Without releasing your pressure, overtake this second barrier slightly, to appreciate the firmer parts of the heart. NB: This approach need not ever be painful or anxiety provoking. Perform the maneuver softly and very gradually, with the impression that each time that you open a barrier, you enter into another space. During the compression, you initially feel the elasticity of certain parts of the heart. It is also possible to appreciate the viscoelasticity of the structure by releasing your compression very gradually and evaluating the gradual return of the structures to their original form.
Naturally hard areas of the heart These zones correspond to the skeletal fibers of the heart. Looking at a transverse section of the base of the heart we can see that the valves are grouped in the same area. Topographically they are located between the left second intercostal space and the right fourth sternochondral joint (Fig. 9.4).
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The fibrous skeleton is strongest at the junction of the aortic, mitral, and tricuspid valves. Anatomically this part is called the central fibrous body of the heart (trigonum fibrosum). Adjoining this area, the orifice of the pulmonary artery and the tricuspid valve can be found. The tricuspid and mitral valves are surrounded by a fibrous demi-ring encircling the insertion of these valves. The pulmonary valve is not anchored to the fibrous skeleton of the heart. Apart from its mechanical role of muscular support, the fibrous skeleton forms an electrical ‘insulator’ by separating the myenterically conducted impulses of the atria and the ventricles, so that they contract independently (Dauzat et al 2002).
What the palm feels It is possible to palpate the constituent parts of the fibrous skeleton of the heart, and also the engagement of the pulmonary trunk and the superior vena cava. With practice, the palm can distinguish naturally hard places. By contrast, a sensation of uneven hardness, less homogeneous, and one that creates a feeling of suffocation is not normal. It is here that we must apply our techniques. When the palm is in good contact with the heart, it is advisable to do a Local Listening to determine with precision the hardened points to release.
9.3.5 Manipulations Technique for the fibrous skeleton Position This is the same position as described for the test. Direct technique Apply the direct technique on the hard areas discovered by the test of viscoelasticity (Fig. 9.5). First compress the hard zone, then release the pressure slightly and carry out
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The practice of visceral vascular manipulation First rib Anterior scalene muscle
Esophagus
Clavicle Subclavian muscle
Left vagus nerve (X)
Left subclavian artery and vein
Sympathetic trunk
Left thoracic artery Left pulmonary artery
Aortic arch Left main bronchus
Left pulmonary vein
Diaphragm Harder parts of the heart Barrier of the heart and its system of attachments
Osteo-cartilaginous barrier
Fig. 9.4 Sagittal section of the thorax to evaluate palpation depth.
induction, all the while allowing the gradual viscoelastic return of the indurated zones. Repeat this maneuver several times until you feel a marked release, first in the quality of a full viscoelastic return and then by confirming through Listening – the Listening no longer attracts your hand.
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Double pressure technique Do not hesitate to apply the double pressure technique (Fig. 9.6) that we employ for both
the thoracic cage and intrathoracic structure. Double pressure allows you to release very deeply situated areas with great precision. The heart beat is an objective indicator of the effectiveness of our techniques. When all mechanical tensions have been resolved, heart beats are more distinct, fuller, and more harmonious. It is important to differentiate cardiac viscoelasticity from other elements surrounding the heart.
The heart
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Fig. 9.5 Manipulation of the fibrous skeleton of the heart.
Fig. 9.6 Double pressure manipulation of the fibrous skeleton.
Aortic arch technique Test The chief reason for manipulating the aortic arch is because of the different nerve fibers that surround the origin of the aorta (Fig. 9.7). As we described in our simplified schematic of the heart, the arch of the aorta, the endocardium, and the upper part of the heart are under parasympathetic vagal control.
The mechanical test of the aorta demands long and fairly difficult practical experience, as it is not easy to perceive. The quality of change detected at the radial pulse is what verifies the effect of visceral vascular manipulation. When the technique succeeds, one feels a progressive slowing and a regulation of the cardiac rhythm. We have demonstrated this numerous times with the aid of an oximeter.
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Esophagus
T2
Trachea T3 Aortic arch T4
Sternum
T5
T6 Aortic valve T7 Heart in the pericardium T8
T9
Diaphragm
T10
T11
T12
Fig. 9.7 Aortic arch.
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The heart
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As stated above, we have had several patients who have been hospitalized following precordial pain where the suspicion of an infarction or coronary insufficiency was strong and all tests proved negative. It turned out that the patients had either chondrocostal fixations, pericardial connective tissue tension, or coronary spasm. With these types of functional problem we obtain excellent results.
Position The patient is in decubitus, with their hands on the abdomen. Place yourself to one side.
Technique Place your two palms, one over the other on the sternal angle (Fig. 9.8). Compress the sternum softly and gradually to pass beyond the osseous barrier, until you feel the heart beat. Still in compression, direct your palms cephalad and slightly left. Beneath and to the left of the sternoclavicular junction, change direction tipping caudally to follow the curvature of the aorta. The goal is to stimulate the mechanoreceptors that constantly discharge central information. These receptors ensure optimal vascular circulation
Fig. 9.8 Manipulation of the aortic arch.
for the body. Finish with the induction technique. Learn to appreciate the quality of the heart beat to refine the direction of your manipulations.
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The thymus
10.1 CAN THE THYMUS BE FELT?
10.2.2 Vascularization
Concealed and protected by the sternum, the thymus is impossible to palpate. It lies against the upper surface of the heart, at the root of the great vessels, in the anterior mediastinum.
The thymus is supplied mainly by the internal thoracic artery, a branch of the subclavian artery (Fig. 10.4). The thymus sometimes receives small branches from the inferior thyroid and pericardial arterioles.
10.2 ANATOMY REVIEW
10.2.3 Innervation
The thymus is situated in front of the brachiocephalic vein and the superior vena cava (Fig. 10.1). It is surrounded on either side by folds of pleura. At the level of the sternal angle (second costosternal junction) it forms the thymic triangle whose apex is directed caudally.
As with all organs of the thorax, the thymus is innervated by the vagus nerves and the sympathetic chain. It exchanges fibers with the phrenic nerve and the cardiac plexus.
10.2.1 Evolution
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In the newborn, the thymus weighs about 10 g. By puberty, at 40 g, it has reached its maximum development (Fig. 10.2). The thymus has two lobes which normally extend superiorly to the lower edge of the thyroid gland and in the adult can migrate inferiorly as far as the fourth intercostal space. During dissections with Professor Arnaud, we have rarely seen the adult thymus present as anything more than small islands, imbedded in connective tissue. Professor Arnaud maintained that the gland evolves into a ligament of the heart, reinforcing the pericardium. As a result it is impossible to gauge its weight in the adult. Because of the numerous possibilities of involution, the thymus displays multiple morphological variations (Fig. 10.3). ©
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10.2.4 Structure The thymus is composed of reticular epithelial cells, enclosed in connective tissue fibers and surrounded by a protective capsule.
10.3 PHYSIOLOGY SIMPLIFIED The thymus provides immune function. Until puberty it is responsible for the provision of T lymphocytes whose lifespan is 5–6 months. These thymus-dependent cells are small lymphocytes that mature and differentiate in the gland where they acquire specific immune capability. They become agents of cellular immunity. Detecting antigens to which they have become sensitive, they destroy them by cytotoxicity (T-lymphocytic cytotoxics) or by triggering macrophage activity. They also play a role in the secretion of humoral antibodies. T lymphocytes represent 60–75% of blood lymphocytes. They are
The thymus
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Thymus
Lungs Heart in the pericardium Diaphragm
Fig. 10.1 Location of the thymus.
Thymus in a newborn.
Thymus in a 2-year-old child.
Fig. 10.2 Evolution of the thymus.
Thymus in an adult
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Thoracic thymus (51.6%)
Cervicothoracic thymus (31.6%)
Cervicothoracic thymus with a cervical predominance (16.6%)
Fig. 10.3 Morphological variations of the thymus.
Right internal thoracic artery
Left internal thoracic artery
Thymus
Pericardial sac
108 Fig. 10.4 Vascularization of the thymus.
The thymus capable of distinguishing between the body’s own components and foreign cells. T lymphocytes pass through the circulation across the capillary endothelium.
viscoelasticity induction technique. Refer to the preceding chapter and to the points concerning the fibrous skeleton of the heart and the arch of the aorta.
10.4 MANUAL APPROACH
10.4.2 Vascular manipulations
It is important to be very clear here: there are no specific manipulations for the thymus, because the gland cannot be manually differentiated.
When we manipulate the various arteries of the region – subclavian arteries, inferior thyroid arteries, and internal thoracic arteries – we imagine that we have an effect on the circulation of the thymus. When there are recurrent ear, nose, and throat (ENT) and bronchiopulmonary infections, we treat with compression– decompression around the sternal angle. We often teach mothers to do this technique 20 times once a day on their babies. They often tell us that these maneuvers have a positive effect – but what is it exactly? Of course, in compressing the sternum, we also contact the lungs, the bronchi, the heart, and the pulmonary circulation.
10.4.1 Retrosternal technique Even in the patients with thymoma whom we have seen, the Listening tests were neither obvious nor conclusive. As the thymus is situated between the sternum and the heart, we think that manipulations affecting the cephalic part of the heart can perhaps stimulate the thymus. Perform the compression–release techniques on the sternum and carry out the retrosternal
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The subclavian arteries
The importance of the subclavian arteries cannot be overstressed, as they are located at strategic crossroads in the human body. The thoracic inlet is one of the weak points of the human body. It was certainly better protected and more functional when our ancestors walked with four points of contact on the ground.
11.1 ANATOMY REVIEW 11.1.1 Origin The two subclavian arteries (Fig. 11.1) have different origins: • The left subclavian artery springs directly from the aortic arch below the left common carotid artery. Because of this, on the left the artery is topographically thoracocervical and has intrathoracic relationships. • The right subclavian artery arises from the bifurcation of the brachiocephalic trunk, behind the upper border of the right sternoclavicular joint at the level of T1. Thus, on the right the artery is exclusively cervical in its topography. Despite these differences, the same maneuvers are used on both sides.
11.1.2 Dimensions
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The subclavian artery has an average caliber of 9–12 mm. It is a bit smaller on the left, and on the right it is slightly narrower at its middle section by the isthmus. The left ©
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subclavian artery is 9 cm long and the right one is 6 cm long.
11.1.3 Pathway The subclavian artery runs laterally, following a concave bend posteriorly. It passes above the first rib, between the scalene muscles. In its cervical segment, the artery is described in three parts: prescalene, interscalene, and postscalene.
11.1.4 Relations Prescalene segment The artery rests on the anterior slope of the pleural dome where it is surrounded by a nerve plexus composed of filaments from the inferior cervical ganglion and the subclavian loop (ansa subclavia). It relates to the medial end of the clavicle and the sternoclavicular joint. The artery is crossed by the phrenic and vagus nerves. On the right, the recurrent laryngeal (branch of the vagus) loops around the subclavian artery. It also relates to the confluence of the subclavian vein and the internal jugular veins. The left subclavian artery has a more extensive relationship with the pleura and lung than does the right subclavian.
Interscalene segment The artery arches between the anterior and middle scalene muscles. The main trunks of the brachial plexus are found posterior
The subclavian arteries
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Left vertebral artery Right vertebral artery
Left common carotid artery
Thyrocervical trunk Right common carotid artery
Left subclavian artery
Right subclavian artery
Internal thoracic artery
Fig. 11.1 Subclavian artery.
and superior to the artery. The subclavian vein runs in front of the anterior scalene muscles.
muscle, by which it is separated from the clavicle.
11.1.5 Collaterals Postscalene segment Here the most superficial part of the subclavian artery lies partly in the supraclavicular region and crosses the anterior lateral surface of the first rib. It is covered by the platysma, and by the superficial and middle cervical aponeuroses. It relates anteriorly to the subclavian vein and the subclavian
All the collateral branches arise from the prescalene parts of the subclavian arteries, except the posterior scapular artery, which arises from the interscalene segment. The collateral vessels are the: • vertebral artery • thyrocervical trunk (formerly the thyrobicervicoscapular trunk)
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The practice of visceral vascular manipulation • costocervical trunk (formerly the cervicointercostal) • internal thoracic artery (formerly the internal mammary) • posterior scapular artery.
11.1.6 Termination The subclavian artery extends to the outer border of the first rib, where it becomes the axillary artery.
11.1.7 Irrigation territories The areas irrigated underline the eminent role of these arteries. Many victims of ‘rabbit punch’ accidents (blows to the back of the head) show us this every day. The subclavian arteries are more or less directly involved in the blood supply to the following structures: • spinal cord • medulla oblongata • pons • cerebellum • posterior brain • inner ear • posterior cranial dura mater • breast.
11.2 MANUAL APPROACH Several mechanical factors can affect the thoracic outlet: • fetal malposition • dystocia • trauma to the shoulder girdle or upper extremity • brain injury • cardiopulmonary surgery • rib fractures, etc. On the emotional plane, chronic emotional withdrawal can, little by little, compress the thoracic inlet by way of muscle spasms. The thoracic cage is the symbol of occupying one’s personal space and opening up to the world.
11.2.1 Contraindications 112
An aneurysm of the subclavian artery is rare. When it does occur, it is more often found on
the right side. It feels like a strong pulsation extending vertically beyond the medial clavicle or the sternum. Beware of strong pulsations in general.
11.2.2 Indications The indications for subclavian artery manipulations are numerous in view of the large territory supplied by these vessels. The main indications are: • vertigo and instability • tinnitus • hypoacousis • numbness of the upper extremity • carpal tunnel syndrome • recurrent capsulitis or tendinitis of the upper extremity.
11.2.3 Palpation Location of the brachial artery We enlist the brachial artery to create a distal traction on the subclavian artery (Fig. 11.2). Contact the brachial artery by placing your thumb between the biceps and triceps muscles, about midway down the arm. The pulse is strong and easy to palpate. With compression of the subclavian artery, a variation in the subclavicular pulse can often be perceived.
Location of the subclavian artery Place your other thumb on the subclavian artery, just outside the clavicular attachment of the sternocleidomastoid muscle (Fig. 11.3). Here the artery is large, almost 1 cm in diameter, with easily perceptible generous pulsations. If you have any difficulty in palpation, bring the homolateral shoulder medial and place the opposite thumb behind the clavicle, about two fingerwidths lateral to the sternoclavicular joint. You can also ask the patient to place their two hands on the anterolateral part of their shoulders in an effort to open the thoracic outlet. This position allows you to compare both arteries simultaneously.
The subclavian arteries
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Axillary artery Deltoid branch Deltoid muscle Coracoid process
Thoracoacromial artery Pectoral branch
Pectoralis major muscle (cut) Humerus
Biceps brachii muscle Medial cutaneous nerve of arm Deep artery of arm Median nerve
Brachial artery Medial cutaneous nerve of forearm
Muscular branch
Ulnar nerve Long head of triceps brachii muscle Superior ulnar collateral artery
Radial recurrent artery
Medial head of triceps brachii muscle Inferior ulnar collateral artery
Medial epicondyle of humerus Pronator teres muscle Bicipital aponeurosis
Radial artery Flexor carpi radialis muscle
Fig. 11.2 Brachial artery in situ.
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11.2.4 Manipulations First method Position The patient is in decubitus with both hands up and back in external rotation. Should the patient have difficulty assuming this position, place a pillow under the upper back to allow
the upper extremities to maintain their internal rotation. You are seated on the side of the subclavian artery to be treated. Maneuver The thumb on the subclavian artery creates lateral traction on the artery by drawing it laterally, distal and very slightly caudal; the thumb does not glide on the artery (Fig. 11.4). This subclavian contact serves as an indicator to find the ideal brachial traction – the place that increases the intensity of the beats. With the fingers on the brachial artery, draw the vessel distally and slightly laterally to create a longitudinal tension that can be felt at the subclavian artery. To coordinate your hands well, close your eyes and imagine a long pipe that you are trying to stretch between your thumb and fingers. Repeat this technique about ten times and, as you proceed, you will have the impression of continuity between your two contacts. This is a marvelous feeling.
Second method
Fig. 11.3 Location of the subclavian arteries.
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Sweeping the subclavian artery Like all large arteries, the subclavian is surrounded by nerve fibers that inform the hypothalamus and the cerebellum about blood pressure and heart rate. The technique described below has two steps:
Fig. 11.4 Combined manipulation of the subclavian and brachial arteries.
The subclavian arteries
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towards the anterior surfaces of the transverse processes of C5, C6, and C7.
Fig. 11.5 Sweeping the subclavian artery.
1 The first is to release the pleurocervical attachments. 2 The second is to sweep the subclavian artery (Fig. 11.5).
Pleurocervical attachments The patient is in lateral decubitus on the side opposite the subclavian artery to be treated. Position yourself behind the patient. Your goal is to penetrate deeply into the thoracic inlet without pain, following two steps. Step one The fingers of one hand are placed just behind the clavicle, near the clavicular attachment of the sternocleidomastoid muscle. Bring the shoulder forward without trying to direct it cephalad. Place the fingers of the other hand
Step two Bring the shoulder towards the patient’s ear. If you feel the patient resist, ask them gently to bring their shoulder towards their cheek. The retroclavicular fingers point towards the pleural dome. To refine your pleural contact, ask the patient to breathe in several times so that you clearly feel the pleural cervical tensions. Allow your fingers to move, following the Listening, towards the fixations, and carry out about ten rounds of induction. Be aware that your fingers must always be flat so as to not aggravate the nerve fibers in the region. There are often numerous pleural cervical microfixations due to respiratory movements and all the trauma that affects the cervical spine, the thorax, and the upper extremities. Frequently the patient is not aware of these problems. They attribute everything to the sacrosanct cervical arthrosis. This technique has the advantage of releasing mechanical restrictions around the subclavian arteries.
Sweeping During the final pleurocervical maneuver to free the subclavian artery from its mechanical constraints, gently move your fingers along the length of the artery to feel the pulsations. Next run your fingers along the surface of the length of the artery, looking for small hardened neural fibers. This palpation requires a long apprenticeship. Nevertheless, even without individually identifying them, one can have an effect on the quality and frequency of the pulse.
Third method Position The patient is prone, shoulders and arms in chandelier position resting on the table; arm
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The practice of visceral vascular manipulation at 90° to the thorax, forearm at 90° to the arm (Fig. 11.6). You are seated at the patient’s head. Technique Position your fingers on the brachial arteries that you have already stretched distally. First compare the respective pulses of both brachial arteries. In this position we can easily feel the difference in resistance between the paired vessels. Elongate the arteries laterally, following the Listening. Close your eyes and think in three dimensions. The maneuver is complete when the resistance of traction is balanced. NB: This technique also affects the median nerve. Always remember that nerves hate compression.
Fig. 11.6 Manipulation of the subclavian artery – third method (aortobrachial induction).
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The pulmonary vessels
12.1 ANATOMY The pulmonary vasculature can be divided into two circulatory pathways: • the vasa publica – part of the circulation serving the interests of the whole body • the vasa privata – arising from the systemic circulation and serving an organ.
12.1.1 Vasa publica The pulmonary trunk splits into two pulmonary arteries sending deoxygenated blood to the pulmonary alveolae for reoxygenation. These vessels are located anterior to the main bronchi.
12.1.2 Vasa privata The pulmonary tissue of the left lung is irrigated by the bronchial branches of the thoracic aorta. The parenchyma of the right lung is irrigated by the third and fourth posterior intercostal arteries, which supply the bronchial arteries. It is for this reason that our pressure is deeper for the right artery.
12.1.3 Pulmonary hilum Located on the medial surface of the lung, the pulmonary hilum is narrow, being no more than 4–5 cm in height and 4 cm wide. It is at equal distance from the base and the apex of the lung, but more posterior in the sagittal plane. ©
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On the right, the pulmonary hilum is larger but not as high as on the left. The hilum projects posteriorly and superiorly to the cephalad edge of the fourth rib, and inferiorly as far as the cephalad border of the sixth rib.
12.1.4 Comments One can note three features when viewing the pulmonary vascular trunks: 1 They are located anterior to the trachea and the bronchi. 2 They are covered in large part by the heart. 3 They are clearly transverse in orientation. For these reasons: • We avoid the cardiac region with our two points of contact. • We stretch the pulmonary hilum laterally.
12.2 PRECAUTIONS One must be cautious of osteoporosis when applying costochondral pressure. In the case of vascular fragility, especially venous, it is advisable to observe the facial coloration of patients during the maneuver. At no time should the patient feel ill at ease. In addition, the following elements call for circumspection before vascular pulmonary manipulations: • fever • weight loss • subcutaneous emphysema
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The practice of visceral vascular manipulation • • • • • • • • •
retroclavicular and axillary lymph nodes unexplained cough change in a pre-existing cough dysphonia dysphagia dyspnea without precise cause unusual palor tachycardia when resting costal pain on a deep inhalation (without previous trauma) • intercostal cutaneous vesicles • sudden onset of expectoration • cervicobrachial neuralgia without mechanical cause. If there is ever the slightest doubt, do not hesitate to refer the patient to their physician.
12.5 PULMONARY VASCULAR MANIPULATION
12.3 CONTRAINDICATIONS
Before manipulating the pulmonary vascular tree: • perform the Adson–Wright test • evaluate the pleural cervical attachments • test the subclavian arteries.
The main contraindications to manipulation are the following: • accidental or spontaneous pneumothorax • cardiac material (i.e. ‘material medica’) • pacemakers: these are frequently placed beneath the right clavicle, where one would exert the action of the palm. It is best to abstain from this maneuver, to avoid moving the pacemaker. Among thoracic pains, it is important to emphasize that spontaneous pneumothorax can occur during exertion or without reason. We have seen this in athletes practicing windsurfing and skiing, whose only complaint was neck pain or scapular discomfort. The most common symptoms are a sudden sharp chest pain, sometimes accompanied by suffocating dyspnea, bouts of dry coughing, and unaccustomed anxiety.
12.4 INDICATIONS
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The indications for manipulations are the following: • pleural pulmonary pathology • chronic bronchitis, asthma, dyspnea • frequent stitch in the side • allergies (treat in conjunction with the liver and pancreas).
The thoracic cage prevents direct palpation of the pulmonary vessels. As we are unable to evaluate their pulses, we apply our manipulations on the larger axis of the vascular trunks. Whereas the main vascular axis of the heart is virtually vertical, those of the lung, except for the initial portion of the pulmonary artery, are transverse. Our techniques are applied transversely to affect the large elastic trunks, and sagittally for the innumerable small arterioles, which are very sensitive to viscoelastic manipulation (Fig. 12.1).
12.5.1 Comments
12.5.2 Position The patient is in decubitus, hands crossed over the stomach (Fig. 12.2). You are standing behind the patient, your palms placed on the thorax of the patient. • On the right side: the right border of the heart is about one fingerwidth lateral to the edge of the sternum. The main right bronchus lies obliquely along a line running from the right second rib to the left fourth rib. To fine-tune your contact over the lungs, place your right palm in alignment with the right mid-clavicular line. • On the left side: the left border of the heart is just inside the vertical left midclavicular line: position your palm outside this line.
12.5.3 Techniques Pulmonary arteries As indicated above, most of our thoracic techniques do not concern the hard frame of the
The pulmonary vessels Brachial plexus
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Left internal jugular vein
Brachiocephalic trunk Right brachiocephalic vein
Left subclavian artery Trachea
Superior lobe of the right lung
Aortic arch
Right pulmonary artery
Left pulmonary artery
Right superior pulmonary vein
Left pulmonary vein
Superior vena cava
Pulmonary trunk
Right inferior pulmonary vein Medial lobe
Inferior lobe Diaphragm
Stomach
Fig. 12.1 Pulmonary vasculature.
thorax and the muscles attached to it. To reach the deep structures, such as the heart, it is necessary to pass through different barriers. • At the beginning of palmar sagittal compression, you will first feel the strong resistance of the hard frame of the thorax. Continue softly and gradually without ever releasing your pressure, as you go past this barrier. You will then feel a second, less marked, impression of resistance. Here it feels like a soft pillow under your pressure. You are now in contact with the lung. • Without releasing your pressure, move your palms laterally, maintaining the pressure for about 15 s. Keeping the sagittal pressure, allow the tissues to return medially, and smoothly commence
another round of lateral pressure. Repeat this several times. It is as though you want to separate the lung from its hilum. It is important to have a mental picture of the lungs and their pulmonary roots so as to exert the pressures in the correct direction.
Pulmonary arterioles To affect the arterioles, work with the pulmonary viscoelasticity of each lung individually. Palm over palm, sink to the level of the lung in a sagittal direction. Take care to return to the starting position very slowly and gradually following induction. It is at this level that the hand has the sensation of a sponge that you are squeezing and releasing several times. You can also place one hand posterior in relation to the anterior hand to perform a
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Fig. 12.3 Manipulation in lateral decubitus position.
Manipulation in lateral decubitus Fig. 12.2 Manipulation of the pulmonary arteries.
double compression–induction. Be sure that the posterior hand has passed through the posterior osteocartilaginous barrier (hard frame) of the thorax.
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Make two points of contact, one anterior and one posterior, directly opposite each other (Fig. 12.3). Together, the two hands will stretch the thorax and the lungs laterally and cephalad. During this movement you must have the impression of lifting the hemi-thorax laterally.
Vessels of the breast
13.1 BREAST PAIN AND THE ROLE OF ESTROGEN Women frequently complain of breast pain in connection with their menstrual cycle, or sometimes more randomly. It is almost always due to hormonal imbalance involving excess estrogens, notably estradiol. Estradiol is the predominant estrogen. It circulates in the blood and is linked to a specific globulin. Estrogens stimulate breast development during puberty and ensure the proliferation and implantation of subcutaneous fat. They cause renal water and salt retention, which favors cutaneous edema. In addition they contribute to increased osteoblast activity. This is why, after menopause, women can become osteoporotic. Estrogens also diminish the concentration of low density lipoprotein (LDL) and increase high density lipoprotein (HDL) levels, reducing the incidence of atherosclerosis in premenopausal females. Estrogen thins and softens the skin. The techniques that we use for the breast do not act on the causes, but on the consequences, of hormone disturbance. However, it often seems to us that the techniques have a central effect, perhaps by way of the vascular and fat system. Remember that fat tissue undoubtedly has a central hormonal role that is still largely being explored. Women who are too thin suffer amenorrhea in large part because of a lack of fat tissue. ©
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13.2 BREAST CANCER According to statistics, presently more than one woman in ten has breast cancer, treated by surgery, radiation, and/or chemotherapy. In addition to cancerous lesions, the breasts are subject to numerous mechanical insults due to upright posture, as well as significant variation in hormone production during breastfeeding and menopause. Surgery and radiation treatment leave traces in all the soft tissues that compose and surround the breast. The surrounding tissues include the skin, adipose tissue, glands, nerves, vascular system, lungs, pleura, heart, mediastinum, and skeletal structure. Even with the great progress that has been made in radiotherapy, all the soft tissues have a tendency to become fibrotic and the skeleton decalcifies. Promoting renewed circulation of fluid around the breast anatomy helps tissues to rebuild and become less fibrotic. Should one perform vascular techniques on a breast when cancer is active? This is a frequently asked question. Manipulation of the vascular system does not increase the neoformation. According to a dearly held osteopathic concept, the stimulation of an organism’s defense mechanisms requires good circulatory function. We are confident about one thing: at the end of cancer treatment one must help the circulatory system of the breast. In a general way, various components of the organism always benefit from
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The practice of visceral vascular manipulation good circulation. However, we must be very careful after irradiation (X-ray therapy), as this causes the artery walls to be very fragile.
13.3 ANATOMY 13.3.1 Container The breasts, located between the third and seventh ribs, are supported by collagen fibers called the suspensory mammary ligaments (of Astley Cooper) (Fig. 13.1). The ligaments are found between the dermis and the connective tissue of the breast. They can extend towards the axillary fossa, overlying the pectoral muscle. The suspensory ligaments of the breast are comprised of numerous septa,
joining the pre- and post-mammary fascia. These fibrous strands of connective tissue are more developed in the upper part of the breast. The breast is mobile, thanks to its posterior part which is filled with celluloid adipose tissue that glides on the myofascial planes. Here, in the submammary space behind the breast, we find superficial and deep myofascial layers. • In the superficial plane, two-thirds of the mammary gland rests on the pectoralis major muscle, and the remaining third on the external oblique and rectus abdominis muscles. The superolateral quadrant is related to the axillary fascia
Deltoid muscle
Biceps brachii muscle
Coracobrachialis muscle Triceps brachii muscle Teres major muscle Subscapularis muscle Axillary process of breast Serratus anterior muscle Mammary lobe Latissimus dorsi muscle
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Fig. 13.1 The container of the breast.
Pectoralis major muscle
Suspensory (Cooper's) ligaments (interlobular septum)
Vessels of the breast by its lateral process, where it contacts the fifth and sixth digitations of the serratus anterior muscle. • The deep plane is made up of the subclavian and pectoralis minor muscles, which are ensheathed in the clavipectoral aponeurosis.
approximately 15 sweat and sebaceous glands. Each lobe has excretory ducts leading to the terminal duct, which is the functional milk secretory component. With age, the glandular lobes become filled with fat tissue and the suspensory ligaments weaken and lose their ability to support.
13.3.2 Contents
13.3.3 Innervation
The breast is composed of glandular lobes and adipose tissue surrounded by connective tissue (Fig. 13.2). The adipose tissue makes up the shape and size of the breast. Surrounding the areola are
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Intercostal nerves The breast is innervated by the third to the sixth intercostal nerves (Fig. 13.3). The lateral cutaneous branches innervate the lateral
Suspensory ligaments of the breast Subclavian muscle
Clavipectoral fascia Endothoracic fascia
Parietal pleura
Pectoralis minor muscle
Pectoral fascia Superficial thoracic fascia
Premammary fascia Retromammary fascia Mammary lobule
Pectoralis major muscle
Suspensory ligaments of the breast (Cooper's)
Nipple Areola Lactiferous sinuses Premammary fat
Fig. 13.2 Contents of the breast.
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Medial cutaneous nerve of arm
Anterior cutaneous branches of intercostal nerves
Intercostobrachial nerve Lateral cutaneous branches of intercostal nerves
Fig. 13.3 Innervation of the breast.
breast, whereas the anterior cutaneous branches pass through the pectoralis major muscle to reach the medial breast.
Nerves of the autonomic system These nerves derive from the internal and lateral plexus of the internal and lateral thoracic arteries. The plexus of the internal thoracic artery arises from the subclavian plexus, consisting of nerve fibers coming from the stellate ganglion (cervicothoracic ganglion).
Tegumentary innervation
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The areola and nipple have a dense nerve plexus, carrying genital corpuscles. These mechanoreceptors are nerve endings in the skin. Once called Golgi and Vater–Pacini corpuscles, these receptors are responsive to
pain and especially to gross changes in pressure.
13.3.4 Vascularization We emphasize again the fact that vascular manipulations will involve the venous system. The breast has a rich venous supply (Fig. 13.4).
Arteries of the breast The breasts are essentially supplied by the subclavian artery and its extension, the axillary artery. The areola is the vascular center of the breast. Subclavian artery (see Chapter 11) This is an artery of great importance. It supplies, either directly or indirectly, the
Vessels of the breast
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Right subclavian artery
Axillary artery
Left external jugular vein Afferent mammary vein
Brachiocephalic trunks
Lateral thoracic artery Lateral mammary branches
Medial mammary branches Internal thoracic artery Thoracodorsal artery
Circular areolar plexus Internal thoracic vein
Fig. 13.4 Vascularization of the breast.
cerebellum, medulla oblongata, spinal cord, breast, and arm. Internal thoracic artery
Origin The internal thoracic artery arises from the anterior surface of the first part of the subclavian artery, opposite the thyrocervical trunk, one fingerwidth lateral to the sternoclavicular joint. Pathway Posterior to the sternal end of the clavicle, the internal thoracic artery descends posteriorly to the costal cartilages, close to the lateral sternal border.
Interesting relationship As it enters the thorax, the phrenic nerve crosses the internal thoracic artery obliquely from its lateral side. Collaterals • The anterior intercostal arteries perforate the intercostal muscle and pectoralis major at the third, fourth, and fifth intercostal spaces. These branches then reach the mammary gland, becoming the medial mammary arteries. • Posterior branches go to the thymus and the pericardium. • Lateral branches, which form the anterior arteries, are distributed in pairs in each intercostal space.
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The practice of visceral vascular manipulation Terminal branches Posterior to the sixth rib, the thoracic artery divides into branches: • Thoracic – giving off the anterior intercostal arteries for the last six intercostal spaces • Diaphragmatic – musculophrenic branches • Abdominal – the abdominal branch of the internal thoracic anastomoses with the superior epigastric artery, which originates from the iliac artery. The abdominal branch exits the thorax at the level of the xiphoid. • The thoracic and peritoneal tissues communicate across the xiphoid fascicles as they penetrate the diaphragm. Axillary artery
Origin The axillary artery, a continuation of the subclavian artery, begins inferior to the clavicle at the outer border of the first rib. Pathway The axillary artery descends caudally and laterally. Termination The axillary artery ends nominally at the insertion of the latissimus dorsi muscle, where it becomes the brachial artery.
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Relations The pectoralis minor muscle is the most important landmark for the axillary artery. The muscle crosses the artery and divides it into three parts: • Proximal to the pectoralis minor muscle: The axillary artery runs between the clavicle and the first rib anterior to the brachial plexus. Lying against the anterior wall of the axilla, the artery runs anterior to the serratus anterior, where it is covered by the clavicular fibers of pectoralis major and the clavipectoral fascia. The pectoralis minor muscle crosses the artery at right
angles. Note that the vein is often three times the size of the artery. • Posterior to the pectoralis minor muscle: The axillary artery departs the ribcage and is ensheathed in the pectoralis minor aponeurosis. It is here that one finds the trunk of the median nerve, formed by the medial and lateral cords of the brachial plexus. • Distal to the pectoralis minor muscle: This is the longest and most accessible part of the artery. Still covered by the pectoralis major muscle, the axillary artery rests on the tendons of the latissimus dorsi and teres major muscles. The coracobrachialis muscle is lateral. The median nerve is satellite to the axillary artery. It descends anteriorly and just laterally to it. The median nerve is located between the artery and the coracobrachialis muscle.
Collaterals Thoracoacromial artery The thoracoacromial artery arises from the second part of the axillary artery immediately posterior to the pectoralis minor muscle. The superior thoracic artery sometimes arises from it. Superior thoracic artery This artery derives from the first part of the axillary artery and passes between the pectoralis major and pectorals minor muscles, near the lower border of the subclavius. It anastomoses with the internal thoracic artery and the first intercostal artery. Its pulse can be felt two fingerwidths beneath the clavicle on the mid-clavicular line. It reaches the breast at the level of the third intercostal space. Lateral thoracic artery The lateral thoracic artery curves between the pectoralis major muscle and the serratus anterior as far distally as the fifth intercostal space. It anastomoses with the intercostal arteries and distributes branches to the mammary gland. It projects on the thorax on a vertical line passing one thumbwidth outside the coracoid process.
Vessels of the breast
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Premammary arterial plexus Cutaneous arterial plexus Intercostal artery
Areolar network
Deep mammary branch
Mammary plexus
Fig. 13.5 Anastomoses of the arteries of the breast.
Comments All of these branches have shared anastomoses in the adipose layer of the breast, forming an arteriovenous net. This rich perimammary network gives off very fine cutaneous branches and more important glandular branches. Numerous branches divide in the interlobular connective tissue to supply the tiny acinar glands (Fig. 13.5).
Posterior drainage The intercostal veins drain into the azygos veins on the right and the accessory hemiazygos veins on the left. This is the metastatic route to the lung, bone, and ovaries. The azygos vein drains the vertebral, pelvic, shoulder, and proximal femur veins.
Deep venous network
We concentrate our breast techniques around the pectoralis minor and its tendinous insertion. The goal is to softly and gently to free up all the elements superior, inferior, and posterior to this tendon and muscle.
The medial and posterior venous drainage passageways are clinically significant as potential routes of metastatic spread. Medial drainage Medial drainage flows into the internal thoracic veins, which also drain the parietal pleura, and constitute potential metastatic pathway to the lung.
13.4 MANIPULATIONS
13.4.1 Preamble Before any vascular breast manipulation, be sure to have freed up any mechanical constraints in the surrounding structures:
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The practice of visceral vascular manipulation • the sternochondral, costochondral, costovertebral, sternoclavicular, acromioclavicular, and coracohumeral articulations • the subclavian muscle and its aponeurosis • the coracoclavicular ligaments, especially the conoid and trapezoid • the pleural cervical attachments • the mid-cervical aponeurosis • the pleura and pericardium.
13.4.2 Internal thoracic artery Pulse evaluation This pulse is sometimes difficult to feel because of the shape of the thorax. On a large chest, it is palpable at the third, fourth, and fifth anterior intercostal spaces, and one fingerwidth from the lateral border of the sternum. More laterally, the more superficial internal mammary branches can be felt.
Manipulation Position In decubitus, the person’s hands are placed either on the abdomen or behind the lower back, to open the intercostal spaces.
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Technique Begin at the lateral edge of the sternum. Place your fingerpad facing the lower border of the upper rib and the upper border of the lower rib, in turn. Feel for the pulse and perform a gliding induction technique in a lateral direction, along the cephalad and caudad borders of the ribs. Teach your patient how to massage their own intercostal spaces, from medial to lateral. Massaging in this way ten times a day for 10 days is sufficient.
13.4.3 The axillary artery The treatment consists of releasing myofascial fibers that accompany the artery. Treatment for the axillary artery can begin once the subclavian muscle has been released.
Manipulation of the subclavian muscle This muscle is located between the clavicle and the first rib. To release the muscle and stretch its fibers, as well as those that extend from it to join the conoid and trapezoid ligament, mobilize these bony relationships (Fig. 13.6).
Fig. 13.6 Manipulation of the axillary artery (via the subclavian muscle).
Vessels of the breast Position In lateral decubitus, the patient rests on the side opposite the muscle to be treated. One hand is placed under the head, the other rests on the table with the palm up and facing the patient’s face. Technique Place two fingers of one hand on the upper part of the clavicle to be able to direct them posteriorly and caudally. Place your thumb under the clavicle. To gain access and avoid pain, first bring the shoulder forward and only then move it cephalad. Encircle the clavicle to find the fixation of the muscle. With the goal of enlaging the cost clavicular space, move the shoulder on the clavicle following the Listening.
Manipulation of pectoralis minor muscle (posterior part) Still in lateral decubitus, place one thumb in the axilla, deep to the pectoralis major muscle, until you feel the tendon of the pectoralis minor at the coracoid process (Fig. 13.7). Softly play the tendon, trying to bring it forward. The fingers of the other hand are placed behind the clavicle to bring it anterior while you release the tendon of the pectoralis muscle.
Fig. 13.7 Manipulation of the posterior part of pectoralis minor.
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Remember that the brachial plexus is lateral in relationship to the artery, and it is important not to compress it.
13.4.4 Superior thoracic artery Locate the superior thoracic artery pulse, about one fingerwidth below the mid-clavicle. With your fingerpad on the pulse, allow the artery to draw your finger in a caudal direction.
13.4.5 Lateral thoracic artery Feel for the lateral thoracic artery on the lateral part of the thorax, below the latissimus dorsi muscle. With a perfectly flat contact on the artery, draw it in a caudal direction, without allowing the finger to slip.
13.4.6 Brachial artery (see Chapter 11) Via this artery as intermediary, one can have an effect on the axillary artery.
13.4.7 Viscoelasticity treatment of the breast The breast is filled with small arterioles, venules, and lymphatic channels. It is an
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The practice of visceral vascular manipulation performed directly on the skin, without her hand as intermediary. And so we proceed.
Position The patient is in decubitus, with both hands around the breast to be treated. Through their hands, compress the breast several times to wake up its mechanoreceptors. Then carry out the induction technique until the Listening ceases. It is possible at the outset to do these compression–decompression techniques without the patient’s hands to free the breast from its thoracic attachments. Show the patient how to do the technique herself, 20 times once a day for 1 month, and repeat if need be.
13.4.8 Traction–induction of the breast
Fig. 13.8 Viscoelasticity treatment of the breast.
organ that frequently has circulatory problems. A breast bruise or hematoma takes a long time to resorb. In our experience with infrared scanners, we find the breast is an organ of lower temperature than the others. The two coldest regions in the body are the buttocks and the breasts, from where hematoma and bruises are the slowest to disappear. The breast is a veritable sponge and responds well to our viscoelasticity technique (Fig. 13.8).
Precaution To remove any ambiguity about this technique, we begin by working over the patient’s own hands placed on the breast. Very often the patient herself asks whether the viscoelasticity technique would not be more efficient 130
It is useful to manipulate the breast in the gliding space underlying the mammary gland. In this retromammary space are numerous short vessels that play a significant role in the return circulation of the breast. This maneuver can be done in two ways.
First method Contact the periphery of the breast with the fingerpads of both hands (Fig. 13.9). Place your thumbs together in line with the nipple to create a fixed point between your hands, and find a comprehensive contact. Exert light compression towards the center of the breast to delicately to contact the mammary gland. Maintain this contact as you traction the breast as though gradually and lightly ‘ungluing’ the breast from the chest wall. Be alert for small spontaneous movements of the mammary gland as you mobilize it, and slowly amplify these movements with induction. Generally, when the Listening stops, the consistency of the mammary gland changes. As a rule, it becomes more yielding and more fluid between your fingers.
Vessels of the breast
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This technique is very effective for venous and lymphatic drainage. It can rapidly and markedly reduce congestive pain following radiotherapy or surgery. It helps with the resorption of contrast agents injected into the breast to diagnose sentinel ganglia. These agents are often the underlying cause of longstanding inflammation, especially when the drainage of the breast is weak or deficient to begin with. It is possible to teach patients to do the same maneuver themselves. Have them circumscribe their breast and bring it softly anterior (Fig. 13.10).
Second method
Fig. 13.9 Traction–induction of the breast (first method).
The second method addresses specifically the superior lateral quadrant, which is situated towards the axilla (the axillary tail). Place two thumbs on the superior lateral quadrant (Fig. 13.11). First spread your thumbs apart, and then push the gland anteriorly and medially. This technique can also be done in sidelying position.
Fig. 13.10 Self breast manipulation.
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Fig. 13.11 Traction–induction of the breast (second method).
Fig. 13.12 Manipulation of the intercostal pedicle.
13.4.9 Manipulation of the intercostal pedicle The patient is in lateral decubitus, and you are standing behind them. Place the pad of your
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index finger against the caudal border of the cephalad rib. Direct your pressure first a little medially to better contact the pedicle better, and perform a gliding induction in a posterior and then anterior direction (Fig. 13.12).
SECTION 2 VESSELS OF THE HEAD AND NECK
The common carotid artery
14.1 ANATOMY REVIEW 14.1.1 Origin The common carotid arteries (Fig. 14.1) arise: • on the right, from the brachiocephalic trunk • on the left, directly from the arch of the aorta, which makes the left carotid longer.
14.1.2 Pathway The common carotid artery ascends along the tracheoesophageal axis, inside the sternocleidomastoid muscle. It follows a more or less straight line from the sternoclavicular joint to a point just behind the condyle of the mandible.
14.1.3 Termination The common carotid artery ends where it bifurcates into internal and external branches, between the hyoid bone and the thyroid cartilage, between C3 and C4. Note that: • 67% of bifurcations occur cephalad of the thyroid cartilage at C4 • 20% appear at the level of the hyoid bone, approximately C3.
14.1.4 Relations The common carotid arteries are covered by the following muscles: • omohyoid • sternohyoid ©
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• sternothyroid • sternocleidomastoid • platysma of the neck.
14.1.5 Carotid triangle At the level of the carotid triangle, the common carotid artery is covered only by skin and superficial cervical fascia (Fig. 14.2). The triangle is bounded by these muscles: • sternocleidomastoid • omohyoid • posterior belly of digastric.
14.1.6 Features The common carotid artery, internal jugular vein, and vagus nerve are enveloped in a common fibrous sheath. Because of this, it is difficult not to include the nervous system in carotid artery manipulation, especially knowing the sympathetic fibers neighboring the vagus nerve are in the direct vicinity.
14.1.7 Terminal branches The common carotid arteries have no collaterals, but simply bifurcate into the internal and external carotid arteries.
14.2 MANUAL APPROACH 14.2.1 Palpation The patient is in decubitus, hands on the abdomen. The patient turns their head slightly
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Internal jugular vein
Sternocleidomastoid muscle
Hyoid bone Common carotid artery
Thyroid cartilage
Trachea
Thyroid gland
Fig. 14.1 Common carotid artery.
towards the artery being palpated. Palpate the artery with two or three fingerpads. The sternocleidomastoid muscle crosses the common carotid artery like an X. Palpation varies depending on whether your fingers are cephalad, medial, or caudad in relation to this muscle crossing (Fig. 14.3).
Caudad part
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At this level the common carotid artery can be palpated between the two heads of the sternocleidomastoid muscle by pushing the clavicular head laterally just above the clavicle. Place two or three fingerpads immediately outside the trachea, inside the sternal head of the sternocleidomastoid. Due to the obliqueness of this muscle, the common carotid artery approximates its anterior border.
Progressively glide your fingers cephalad to check the pulse of the artery.
Medial part The medial part is palpated two to three fingerwidths from the lateral border of the trachea, outside the sternal head of the sternocleidomastoid. Do not hesitate to mobilize this muscle to better perceive the carotid pulse better. In the carotid triangle, the common carotid artery is covered only by skin, platysma, and superficial fascia. Here the carotid artery relates: • medially to the trachea, esophagus, larynx, and thyroid • laterally to the internal jugular vein and vagus nerve.
The common carotid artery
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Parotid gland Digastric muscle Stylohyoid muscle Internal jugular vein Sternocleidomastoid muscle
Submandibular gland Common carotid artery
Trapezius muscle Brachial plexus Sternohyoid muscle
Inferior jugular vein
Fig. 14.2 Carotid triangle.
Fig. 14.3 Palpation of the common carotid artery.
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Cephalad part The common carotid artery ascends free of the sternocleidomastoid 2 cm beneath the upper border of the thyroid cartilage. Feel for the carotid pulse below the hyoid bone. Remember that the common carotid divides at the level of C3 or C4.
What to look for in evaluating the artery Spread and glide your finger pads to appreciate: • the consistency of the artery • possible variations in its caliber • a clear and frank pulse along the length of the artery • any lack of smoothness on the artery wall as you spread and glide your fingers. NB: Compare both carotid arteries. For best results, manipulate the areas where the pulse is least perceptible and the artery surface is somewhat rough. Remember to explore these qualities where the sternocleidomastoid muscle crosses the artery. This is often where rough areas are discovered. Note that the common carotid artery may become compressed against a prominent transverse process of the sixth cervical vertebra and cause discomfort.
14.2.2 Precautions
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It is advisable to proceed with caution in these instances: • significant arterial hypertension • atheromatous plaque • raised cholesterol levels • unexplained vertigo or instability. Pay attention with female smokers who are taking contraceptive hormones and who have high cholesterol levels. Adenopathy is very common at the neck. Often benign, these ganglia are indicators of an immune response to serious disease challenges. Some things to keep in mind include: • Small riziform (rice-shaped) and easily mobilized ganglia at the back of the neck
•
•
•
• •
often indicate a respiratory or food allergy. Small retrocervical or laterocervical ganglia the size of a hazelnut, often more evident on one side, are the result of infection or inflammation. It is usually on the side where they are more developed that a gingival, dental, or ear, nose, and throat (ENT) problem exists. Always be prepared to ask the patient when they last visited the dentist, especially when they have neck pain of nontraumatic origin. Submental and maxillary ganglia arise with infections of the face and mastication system. In adolescents, multiple ganglia often appear at the neck and cervical region. Usually, they signify a general state of exhaustion. Nevertheless, consider mononucleosis in the presence of tonsillitis, sizable adenopathies, and ganglia that are painless, firm, and smooth.
14.2.3 Contraindications The contraindications for manipulation of the common carotid artery are: • arterial hypertension higher than 150/90 mmHg • drop attack (sudden fall caused by vertebral basilar insufficiency) • vascular fragility (diabetes, connective tissue disease, and other systemic illness). If in the slightest doubt, refer the patient to a physician • an aneurysm of the common carotid artery feels like a large pulsation that lifts the sternocleidomastoid muscle slightly. It is fairly soft and compressible. The enlargement is longitudinal and easily mobilized transversely. The dilation increases in size with distal compression of the artery, and diminishes with proximal compression. Aneurysm of the common carotid artery can accompany a bitonal voice (laryngeal compression), irritating cough, or neck pain.
The common carotid artery
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Fig. 14.4 Manipulation of the common carotid artery (bidigital stretch).
Often our colleagues question us about the risk of dislodging atheromatous plaque. Those who have done cadaver dissection know that such a plaque is generally very hard and not easily detached – certainly not by our technique.
14.2.4 Indications Due to the large territory supplied by the common carotid artery, there are many treatment indications: • headache • vertigo • instability • arterial hypertension • tachycardia • cardiac arrhythmia • precordial pain • gastroesophageal reflux • pain in the solar plexus region • vagotonia • sympathicotonia • thyroid dysfunction • ocular dysfunction • hemiplegia • cerebral deficiency • following craniofacial trauma • after surgery.
14.2.5 Manipulations One position for three techniques The subject is in decubitus, hands placed on abdomen, elbows on the table, head turned slightly to the side opposite the artery in question. Position yourself on the treatment side.
Bidigital technique We perform these techniques either by stretching or by using induction. With one thumb, lightly take a fixed point on the carotid artery, within the triangle separating the two heads of the caudal insertion of the sternocleidomastoid muscle (Fig. 14.4). With the other thumb, take another fixed point lightly on the medial part of the carotid artery at its cephalad part. Several times, traction the areas where you felt a less distinct pulse during the initial evaluation. Next stretch the carotid artery by following the Listening and encouraging the Listening with induction. NB: It is always good to do this technique on both common carotid arteries to obtain a central stimulating effect.
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Fig. 14.5 Manipulation of the common carotid artery (multidigital stretch).
Multidigital stretch technique Place two or three fingers, pads flat on the sections of the artery above and below the sternocleidomastoid muscle (Fig. 14.5). Perform a spreading–gliding action with your fingers. Like nerves, arteries must be stretched to restore their elasticity. They love elongation and hate compression. This maneuver can also be performed with one hand while rotating the cervical spine with the other hand to increase the stretch.
Glide–induction technique Glide your fingerpads lightly along the length of the artery. Your fingers should
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slide smoothly. On any areas that appear to scrape or rub your fingers, execute a glide–induction. The fingers are placed on the artery as above. Encourage and amplify the movements you feel with Listening. The objectives of the technique are: • to balance the vascular tone of the two common carotid arteries • to release hardened zones impeding the harmonious and balanced arterial flow • to affect the fibers of the glossopharyngeal nerve in order to provide central benefit.
The external carotid artery
The external carotid artery is very much the true artery of the neck. Manipulation of this artery and its branches (studied in subsequent chapters) improves the function of the thyroid, parotid, trachea, face, and the entire mastication system, once the other tissue fixations are resolved.
15.1 ANATOMY REVIEW 15.1.1 Origin The external carotid artery (Fig. 15.1) begins at the bifurcation from the common carotid, lateral to the upper border of the thyroid cartilage, between C3 and C4. The external carotid is situated anteromedial of the internal carotid.
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Only the lingual and pharyngeal arteries are omitted from our description. They are difficult to access and respond poorly to our manipulations.
15.2 MANUAL APPROACH 15.2.1 Palpation At its origin, the external carotid is covered only by skin, the platysma, and the superficial cervical aponeurosis. Leaving the carotid triangle it is covered by the digastric and stylohoid muscles and is crossed by the hypoglossal nerve. It is lateral in relation to the pharynx and anterior to the internal carotid artery.
15.1.2 Course
15.2.2 Precautions
The external carotid artery is initially oblique, adopting a vertical course after the angle of the mandible.
Be careful and do not hesitate to direct patients to medical care in case of: • recurrent vertigo without antecedent trauma • instability • unsteady gait.
15.1.3 Terminal branches The external carotid artery ends at the neck of the mandibular condyle.
15.1.4 Collaterals The external carotid artery has six collateral branches: • three anterior: superior thyroid, lingual, and facial • two posterior: occipital and posterior auricular • one medial: pharyngeal. ©
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15.2.3 Contraindications Contraindications to treatment of the external carotid artery include: • drop attack (sudden fall without loss of consciousness, generally due to vertebral basilar insufficiency) • sudden, localized, and unexpected headache alerts you to the possibility of aneurysm
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Superficial temporal artery
Vertebral artery Internal carotid artery
Thyrocervical trunk
Subclavian artery
Fig. 15.1 External carotid artery.
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External carotid artery
Superior laryngeal artery
Common carotid artery Thyroid gland
The external carotid artery • areas where the external carotid pulse is barely perceptible • vascular fragility (systemic disease such as diabetes) • atheromatous plaque (medically diagnosed). Be especially alert to cases of vertigo or instability in smoking women on the contraceptive pill with raised cholesterol levels. These factors can be indicative of carotid or vertebral basilar vascular fragility.
15.2.4 Indications The indications are the following: • headache • facial paralysis • thyroid dysfunction • problems affecting the face, alveolar dental and pharyngeal laryngeal junction • cervical trauma with associated functional signs such as vertigo, instability, tinnitus, and headache.
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Bidigital stretch technique Place one thumb just outside the upper border of the thyroid cartilage. This will serve as a fixed point (Fig. 15.2). Place the other hand under the digastric muscle by the mandibular apex, stretch the external carotid artery cephalad and slightly medially. Finish as usual, with induction.
Gliding–induction technique The initial point of contact is the same as above, at the level of the thyroid cartilage. The other thumb or index finger carries out the gliding–induction technique, departing along the artery from the fixed point. It is important to feel all small sections where you have the impression that the finger does not glide as well. This technique has an effect on the wall of the external carotid artery and also on the fibers of the hypoglossal nerve.
Digital spreading–gliding technique 15.2.5 Manipulations Common position for three techniques The patient is in decubitus, elbows on the table, hands resting on the abdomen. The head is turned slightly away from the external carotid artery in question. Keep to the treatment side of the patient.
Fig. 15.2 Manipulation of the external carotid artery (bidigital stretch).
Carry out this maneuver with two or three fingerpads of each hand, positioned as described in the palpation test above (Fig. 15.3). Focus the action of the fingers where the gliding is not smooth. Remember that gliding is the key component, and any compression must be minimal. The maneuver is complete
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Fig. 15.3 Manipulation of the external carotid artery (digital spreading–gliding).
when the fingers can move over the artery easily without any sense of roughness along the vessel wall. In addition to affecting the elasticity of the artery itself, the fingers act on the periarterial nervous system (cervical sympathetic, hypoglossal, and glossopharyngeal fibers). At
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the end of treatment you should feel a regular, smooth arterial pulse, with no weak areas. NB: Remember to examine the part of the external carotid artery located where the sternocleidomastoid muscle crosses the vessel. Fixations of hypoglossal nerve fibers are common here.
The facial artery
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16.1 ANATOMY
16.1.5 Function
16.1.1 Origin
The facial artery supplies the palatine tonsils, soft palate, pterygoid, mylohyoid, and digastric muscles, the submandibular gland, and all of the face.
The facial artery arises between the hyoid bone and the base of the mandible. It winds its way in front of the external carotid, from which it originates (Fig. 16.1).
16.1.2 Course The facial artery winds its way forward and upwards towards the submandibular gland, passing onto the face where its pulse can be felt as it crosses the mandible. It courses over the face, emerging by the edge of the lips and ascending between the nostril and cheek.
16.1.3 Termination The terminal branch of the facial artery is the angular artery, at the inner corner of the eye.
16.1.4 Collaterals The facial artery supplies eight branches: • In the cervical region: – ascending palatine artery – pterygoid artery – submental artery – submaxillary artery. • Its named branches on the face are the: – masseteric artery – superior labial artery – inferior labial artery – lateral nasal artery. ©
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16.1.6 Anastomoses The facial artery is joined with the internal carotid via the intermediary of its terminal branch, the angular artery.
16.2 MANUAL APPROACH 16.2.1 Pulse landmarks The easiest pulses by which to gauge the success of your technique (Figs 16.2, 16.3, & 16.4) are as follows: • Beneath the mandible, locate the pulse where the artery crosses the inferior border, midway between the angle and the mental tubercle. • On the nasal bone, the angular artery can be palpated at the junction of the nasal bone and the maxilla. It is easily confused with the supratrochlear branch of the internal carotid artery. Test the angular artery with the pad of one finger. Glide the fingerpad caudad and cephalad to try to differentiate the two pulses.
Comments The facial artery serves as an indicator of the effect of our manipulation of the common carotid and external carotid arteries.
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Supraorbital artery Supratrochlear artery Angular artery Dorsal nasal artery Lateral nasal artery
Occipital artery Maxillary artery
Facial artery
Labial branches Internal carotid artery
Submental branch External carotid artery
Fig. 16.1 The facial artery.
Fig. 16.2 Locating the pulse of the facial artery at the mandible.
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Common carotid artery
The facial artery
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Supratrochlear artery Supraorbital artery Superficial temporal artery Dorsal nasal artery
Angular artery
Facial artery
Internal carotid origin External carotid origin
Fig. 16.3 The angular artery.
Fig. 16.4 Locating the pulse of the angular artery.
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The practice of visceral vascular manipulation Differences in arterial pulsation are most easily palpated as the artery crosses the mandible.
16.2.2 Indications Indications for manipulation of the facial artery are: • facial paralysis • chronic rhinopharyngeal infection • cerebral lesions
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• following facial surgery • dental apparatus.
16.2.3 Supratrochlear–angular anastomoses The compression–decompression viscoelasticity technique is applied to achieve a double effect on the external carotid by way of the angular artery and on the internal carotid via the supratrochlear artery, which we will study later.
The occipital artery
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17.1 ANATOMY
17.1.4 Terminal branches
17.1.1 Origin
The occipital artery has two terminal branches: • a lateral branch anastomoses with the posterior auricular artery • a medial branch running to the top of the skull to anastomose with its counterpart before joining the superficial temporal artery.
The occipital artery arises in the neck anterior to the mastoid protuberance from the posterior aspect of the carotid. It branches from the carotid just a little above the facial artery (Fig. 17.1).
17.1.2 Course The occipital artery passes posteriorly, parallel and deep to the posterior belly of the digastric muscle, and passes in a groove on the temporal bone medial to the mastoid process. It then runs towards the external occipital protuberance where it ascends the scalp. It perforates the trapezius muscle and the nuchal fascia between the cranial insertions of the trapezius and sternocleidomastoid muscles.
17.1.3 Collaterals The occipital artery has these branches: • muscular branches supplying the sternocleidomastoid, digastric, splenius capitis, and semispinalis capitis of the head • stylomastoid artery that accompanies the facial nerve in the stylomastoid foramen to run in the tympanum and mastoid cavities, as well as the semicircular canals • meningeal artery supplying the dura mater of the mastoid and the diploë. The artery penetrates the mastoid foramen, usually accompanied by an emissary vein. ©
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17.2 MANUAL APPROACH 17.2.1 Palpation Palpate midway between the external occipital protuberance and the occipital squama. The occipital artery can be felt through the nuchal fascia and the trapezius muscle at the superior nuchal line.
17.2.2 Indications Indications for manipulation of the occipital artery are: • aftereffects of otitis • tinnitus • facial paralysis • hearing dysfunction • cranial trauma (especially posterior) • following ‘rabbit punch’ – blow to the back of the head • cervical pain • cerebellar problems.
17.2.3 Manipulations Position It is possible to treat in decubitus or procubitus.
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Epicranial aponeurosis
Occipital belly of occipitofrontalis muscle
Third occipital nerve
Occipital artery Semispinalis capitis muscle Posterior auricular artery
Greater occipital nerve Sternocleidomastoid muscle Trapezius muscle
Fig. 17.1 Occipital artery.
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Lesser occipital nerve Splenius capitis muscle
The occipital artery
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Technique With one or two fingers, palpate the occipital arterial pulsations mid-distance between the external occipital protuberance and the lateral border of the occiput (Fig. 17.2). Alternately compress and decompress to create a viscoelastic suction phenomenon. Next contact the occipital artery as it emerges from the trapezius muscle attachment. Take a second contact on the artery a little medially or laterally, depending on the direction of the Listening. Begin by releasing the fascia that surrounds the artery, as well as the fascial ring surrounding the emissary vein. Then treat the artery itself with induction.
Comment When you do this technique, you obtain an effect on the greater occipital nerve. Moreover, thanks to the emissary vein that connects the interior of the skull with the extracranial veins, our manipulation extends to the occipital and mastoid dura mater. Fig. 17.2 Manipulation of the occipital artery.
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The posterior auricular artery
The posterior auricular artery is not the most important branch of the external carotid. However, because of its anastomoses, treating it improves the results on the occipital and superficial temporal arteries.
18.1 ANATOMY 18.1.1 Origin The posterior auricular artery (Fig. 18.1A,B) arises from the dorsal side of the external carotid artery, just above the occipital artery. These arteries sometimes share a common trunk. It is the most superior of the posterior branches of the external carotid artery.
18.1.2 Pathway The posterior auricular artery penetrates the parotid gland, and ascends between the auricle and the mastoid process.
18.1.3 Collaterals The posterior auricular artery supplies branches to the parotid gland and the skin covering it. The stylomastoid branch orginates from the posterior auricular artery.
18.1.4 Terminal branches
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In the groove between the auricular cartilage and the mastoid process, the posterior auricular artery gives off: ©
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• an auricular branch supplying the medial and lateral cranial surfaces of the auricle • a mastoid branch.
18.1.5 Anastomoses The posterior (mastoid) branch anastomoses with the occipital and superficial temporal arteries.
18.2 MANUAL APPROACH 18.2.1 Palpation Posterior auricular artery pulsations are felt mainly below the external auditory meatus, against the mastoid process. Place one fingerpad between the angle of the mandible and the mastoid process, or in the auricular mastoid angle.
18.2.2 Indications Indications are similar to those for the occipital artery: • sequelae of otitis • tinnitus • facial paralysis • auditory problems • following posterior cranial trauma • ‘rabbit punch’ blow (to the back of the head).
The posterior auricular artery
Parietal artery
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Frontal artery Supraorbital artery Nasal artery
Occipital artery
Posterior auricular artery Facial artery Internal carotid artery A
External carotid artery Common carotid artery
Perforant branches
Posterior auricular artery Contouring branches Posterior auricular branch
Mastoid process Posterior auricular artery B
Fig. 18.1 (A) Posterior auricular artery. (B) Arteries behind the ear pavilion.
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18.2.3 Manipulations Treatment is with viscoelasticity and then stretch–induction. This same technique (Fig. 18.2) serves to evaluate changes in the pulse following manipulation of the occipital and superficial temporal arteries.
18.2.4 Position The patient is in lateral decubitus, on the side opposite the artery concerned.
18.2.5 Technique Place one or two fingers (space permitting) on the pulse of the posterior auricular artery. Stretch the artery in induction.
Fig. 18.2 Manipulation of the posterior auricular artery.
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The maxillary artery
19.1 ANATOMY The maxillary artery (Fig. 19.1) cannot be palpated at its origin, as it is located behind the mandible. Of interest is its terminal infraorbital branch that accompanies the maxillary nerve and, to a lesser degree, its mental branch, which accompanies the mandibular nerve.
19.1.1 Origin The maxillary artery is the largest branch of the external carotid, arising just above the posterior auricular artery. It is hidden behind the zygomatic arch.
19.1.2 Pathway The maxillary artery runs between the two heads of the lateral pterygoid muscle to penetrate the pterygopalatine fossa.
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ophthalmic artery, arising from the internal carotid. • Descending branches: – The inferior alveolar artery gives off alveolar dental branches, before passing through the mental foramen as the mental artery. The mental artery serves as an indicator of the effects of maxillary and mandibular manipulations. It can also be used to evaluate the impact of dental apparatus. When braces are too tight, for example, the mental pulse on the side of the mechanical tension is either strained or diminished.
19.2 MANUAL APPROACH 19.2.1 Palpation Test the infraorbital and submental pulses.
Position 19.1.3 Collaterals Among its important collaterals are: • Ascending branches: – the anterior tympanic supplying the lining of the middle ear – the middle meningeal artery enters the skull through the foramen spinosum. It gives off branches for the dura mater surrounding the trigeminal ganglion. This is the main source of blood for the dura mater – the orbital branches form anastomoses with the lacrimal branch of the ©
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The patient is in decubitus, hands crossed over the abdomen. Position yourself at the patient’s head in order to compare the left and right arteries.
Infraorbital artery The infraorbital foramen is familiar to us as the location where we manipulate the maxillary nerve, the second branch of the trigeminal nerve. It is not really possible to separate treatment of the maxillary nerve and the maxillary artery. Palpate the artery in the infraorbital foramen found beneath the orbital rim,
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Superficial temporal artery Supraorbital artery Supratrochlear artery Transverse facial artery Angular artery Infraorbital artery
Middle temporal artery Occipital artery Maxillary artery
Facial artery Internal carotid artery External carotid artery
Common carotid artery
Fig. 19.1 Maxillary artery.
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The maxillary artery about two to three fingerwidths from a vertical line passing through the nose and dividing the face in half. This foramen is near the zygomatic maxillary suture. Always be sure to compare both pulses. Generally, the side with the weaker pulse indicates the problem side.
Mental artery Take the mental pulse at the mental foramen, in line with the second premolar. The mental foramen is approximately on the extension of an imaginary vertical line passing through the infraorbital and supraorbital foramina.
19.2.2 Indications The indications for the maxillary artery are:
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• after craniofacial trauma (remember this artery vascularizes the dura mater) – following maxillofacial surgery – headache – migraine • mastication problems.
19.2.3 Infraorbital artery technique The infraorbital artery responds well to manipulation (Fig. 19.2). Treat it with viscoelasticity–induction technique. First compress the artery and then, during the decompression phase, follow the return with induction. This technique also benefits the infraorbital nerve. At the end of the maneuver, compare the left and right infraorbital pulses to gauge the effectiveness of your technique.
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The superficial temporal artery
20.1 ANATOMY
20.1.5 Features
20.1.1 Origin
The superficial temporal artery, a branch of the external carotid, anastomoses with the supraorbital artery, a branch of the internal carotid. Here, once again, is an example of the entanglement of these arteries. Moreover, the orbital branch of the superficial temporal artery anastomoses with a branch of the internal carotid artery.
The superficial temporal artery (Fig. 20.1) is the smaller terminal artery of the external carotid. It arises at the neck of the mandibular condyle and has several named branches.
20.1.2 Pathway The superficial temporal artery passes over the zygomatic tubercle and the external pore, to run up the scalp in the temporal region. At the zygomatic arch it is covered by the parotid gland.
20.1.3 Collaterals The principal branches of the superficial temporal artery are: • a transverse artery that courses across the cheek • an anterior articular branch supplying the temporomandibular joint • branches for the side of the face and the ear pavilion • an orbital branch supplying muscles of the eyelids and anastomosing with the superior palpebral artery, arising from the ophthalmic artery (a branch of the internal carotid).
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The terminal branches are the frontal and parietal arteries. ©
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20.2 MANUAL APPROACH Among the superficial temporal artery branches we have selected four that respond best to our technique: • the transverse facial artery • the zygomatico-orbital artery • the frontal branch • the parietal branch.
20.2.1 Position The patient is in decubitus, hands on the abdomen, with the head turned slightly away from the side of the manipulation.
20.2.2 Transverse facial artery The transverse facial artery is perceptible just beneath the zygomatic process, in the mandibular notch, between the coronoid and condylar processes.
Technique Perform this technique where you best perceive the facial artery pulse as described above (Fig. 20.2).
The superficial temporal artery
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Parietal branch Superficial temporal artery
Lateral branch
Medial branch Frontal branch Middle temporal artery Transverse facial artery Facial artery
Labial branches
Occipital artery Maxillary artery
Vertebral artery Internal carotid artery
Submental branch
External carotid artery Common carotid artery
Lingual artery Superior thyroid artery
Fig. 20.1 Superficial temporal artery.
Fig. 20.2 Manipulation of the transverse facial artery.
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20.2.3 Zygomatico-orbital artery This artery runs close to the upper border of the zygomatic process. It is the most clearly palpable of all the superficial temporal branches. Feel for it in the middle of the zygomatic process, towards the sphenosquamous suture by the lateral orbital angle. This artery is important to manipulate in cases of temporal migraine pain. Patients often instinctively rub this region.
Technique Treat this artery with a small stretch–induction (Fig. 20.3).
20.2.4 Frontal branch The frontal branch passes superiorly towards the frontal tuberosity. Palpate it about four fingerwidths above the superior orbital rim.
Technique Treat with maneuvers.
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small
stretch–induction
Fig. 20.4 Manipulation of the parietal branches.
Fig. 20.3 Manipulation of the zygomatico-orbital artery.
The superficial temporal artery
20.2.5 Parietal branch
20.2.6 Comments
The parietal branch is accompanied by a parietal emissary vein that penetrates the diploë. Manipulate this artery to have an effect on the parietal dura mater following cranial trauma.
All the arteries have their contralateral partners, allowing us to compare pulses on both sides. Often the problem artery is on the side where the pulse is weakest or most tenuous. More rarely the problem side is indicated by a bounding or stretched (tense or pulled) pulse. Cranial suture fixations often affect the pulse of the neighboring artery. Finally, it is helpful to show your patients how to do skin rolling over hardened or sensitive cutaneous areas of the temporal fossa.
Technique Undertake microstretch–induction movements, using two or more fingers (Fig. 20.4).
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The internal carotid artery and its branches
The internal carotid artery is very difficult to feel at its origin and impossible to palpate along its intracranial course. Happily, some of its terminal branches appear on the face where they are fairly easily palpated. These branches serve mainly to direct us to the side of reduced cerebral blood flow, and enable us to evaluate our results.
21.1 ANATOMY 21.1.1 Origin The internal carotid (Fig. 21.1) begins at the bifurcation of the common carotid, between the hyoid bone and the superior border of the thyroid cartilage, at the level of C3 or C4. It is located lateral and posterior to the external carotid artery as it ascends the neck.
The ophthalmic artery provides an indication of the internal carotid dysfunction.
21.1.5 Relations In the neck, the internal carotid artery has the same positioning as the external carotid, although it is slightly lateral and posterior to it. The internal carotid is initially superficial, covered only by skin, the platysma, and the superficial cervical aponeurosis. At the base of the skull the glossopharyngeal, vagus, and hypoglossal nerves are positioned posterior to the internal carotid artery. They then circumvent it and are lateral to the internal carotid artery.
21.2 MANUAL APPROACH
21.1.2 Pathway
21.2.1 Precautions
The internal carotid runs superiorly and medially towards the pharynx. It enters the skull through the carotid canal in the petrous part of the temporal bone (foramen lacerum).
Use caution in cases of: • hypertension • atheromatous plaque.
21.1.3 Terminal branches
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21.1.4 Comment
The terminal branches of the internal carotid artery are the: • ophthalmic artery • anterior cerebral artery • middle cerebral artery (Sylvian) • posterior communicating artery • choroidal artery • circle of Willis. ©
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21.2.2 Contraindications The contraindications are: • violent and random headache • general vascular fragility • cerebral hemorrhage.
21.2.3 Indications Indications for manipulation are cerebral disorders in general, such as:
The internal carotid artery and its branches
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Internal carotid artery Vertebral artery
External carotid artery
Fig. 21.1 Internal carotid artery.
• • • • • • •
Parkinson’s disease arteriosclerosis cerebrovascular accidents motor deficits consequences of paralysis vertigo instability.
21.2.4 Palpating the pulse Palpation of the carotid bifurcation It is not always easy to distinguish between the internal and external carotid pulses (Fig. 21.2).
Palpation of the supraorbital foramen The supraorbital artery exits the cranium through the supraorbital notch, located in the supraorbital rim of the frontal bone (Fig. 21.3). The foramen sits about three fingerwidths from the glabella. To feel this pulse, search along the orbital rim lifting the soft tissue and the eyebrow. Execute a small compression at the foramen. Release your pressure slightly and you will feel the pulse. Compare left and right supraorbital pulses.
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Glossopharyngeal nerve
Internal carotid artery External carotid artery Carotid glomus Nerve of the carotid sinus
Carotid glomus
Carotid sinus
Common carotid artery
Fig. 21.2 Carotid bifurcation.
Supraorbital artery
Supraorbital nerve
Supratrochlear artery Supratrochlear nerve
Orbital septum Lacrimal gland Superior tarsus Lateral palpebral ligament Inferior tarsus
Ophthalmic artery Angular vein Medial palpebral ligament Angular artery Lacrimal sac
Infraorbital artery Facial vein
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Fig. 21.3 Supraorbital and supratrochlear arteries.
Facial artery
The internal carotid artery and its branches
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Palpation of the supratrochlear artery The supratrochlear artery perforates the orbital septum at the frontal notch together with the supratrochlear nerve (see Fig. 21.3). Place the pad of your index finger beneath the trochlea. Moving from caudad to cephalad, you will easily feel the supratrochlear pulse. This artery anastomoses with the angular artery, a branch of the facial artery, which takes its origin from the external carotid artery. It is possible to confuse the two pulses. Be sure your fingerpad is well above the trochlea.
21.2.5 Manipulation of the ophthalmic artery Anatomy The ophthalmic artery arises from the anterior clinoid process and passes through the orbital fissure. This artery is winding and flexible, affording great mobility to the eye. It enters the optic canal, inferiorly and laterally to the optic nerve, which it eventually crosses over or sometimes under, as it turns medially. It runs along the inferior border of the superior oblique muscle as far as the trochlea, at the medial end of the upper eyelid. Over a very short distance the ophthalmic artery gives off several branches, two of which are the supraorbital and the supratrochlear. As it impossible to palpate this vessel directly, we manipulate it using the eyeball as intermediary.
Manipulation Position The subject is in decubitus, eyes closed. Technique Place the pad of one index finger on the eyeball (Fig. 21.4). Superimpose the other index finger. With the overlaid finger creating the movement, delicately push the eyeball posteriorly and medially. Release your pressure and allow its gradual viscoelastic return. This is the same technique we apply to the optic nerve. It has the effect of pleating and then unpleating the artery.
Fig. 21.4 Manipulation of the ophthalmic artery.
As a preliminary assessment, take the supraorbital and supratrochlear pulses. Apply the technique on the side of the weaker pulse. Afterwards verify your treatment with the same pulses. In any event, always treat both left and right arteries. This general rule applies to all paired organs. The ophthalmic artery follows the trajectory of the superior oblique muscle. To stretch it, draw the eyeball laterally and caudally. Normally the pulse is more marked when this muscle is stretched. This technique can be combined with induction of the supraorbital artery, described below.
21.2.6 Manipulation of the supraorbital artery Anatomy The supraorbital artery is more centrally located than the ophthalmic artery from
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The practice of visceral vascular manipulation Little by little you will feel the supraorbital pulse intensify. This perception comes only with experience, owing to the innately weaker quality of this particular pulse. Comment Manipulating the supraorbital artery is very worthwhile because it is indirectly a branch of the internal carotid artery. Furthermore, via its anastomoses with the angular artery, this technique affects the external carotid artery as well.
Indications Manipulation of the supraorbital artery is used for all circulatory problems involving the brain, whether of traumatic, infectious, or degenerative origin. The aftermath of vascular cerebrovascular accidents is a good indication for treatment. Fig. 21.5 Manipulation of the supraorbital artery.
Contraindication
which it originates. Keep this in mind when choosing the direction of the manipulation. The supraorbital artery divides into small branches supplying the soft tissue of the eyebrow, and also sends a branch to the diploë of the frontal bone.
There are no formal contraindications. Our techniques are so soft and respectful of the tissues that it is difficult to believe they could be iatrogenic. You have only to remember that coughing, sneezing, and straining on the toilet all increase intracranial pressure far more than any pressures we might exert with our fingers.
Manipulation This technique has two components: one directed to the supraorbital artery and the other to the optic nerve (Fig. 21.5). Step one With the pad of one finger, compress the supraorbital artery. Gently release your pressure and follow the decompression with induction.
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Step two With the index finger of the opposite hand, compress the eyeball in a posteromedial direction to manipulate the optic nerve. Allow the eyeball to gradually return to its neutral position.
21.2.7 Manipulation of the supratrochlear artery Place one middle finger over the other and perform compression–decompression and induction techniques, as shown in Fig. 21.6. The supratrochlear artery is interesting to manipulate because of its links to arteries branching from the external carotid artery. These small branches are surrounded by numerous tiny nerve fibers from the cervical sympathetic system. Through these fibers an important reflexogenic effect is achieved. This effect can act on arterial vasomotor control and the muscles around the arteries.
The internal carotid artery and its branches
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Fig. 21.6 Manipulation of the supratrochlear artery.
21.2.8 Exercise If you find a difference in the quality of the supratrochlear and supraorbital pulses, consider a possible cranial problem. This finding can be of osseous, sutural, meningeal, or encephalic origin. As a rule, the restriction will be on the side of the weak pulse.
Cranial Local Listening is the best way to detect the restriction. Effective cranial treatment often resolves the pulse difference. An overly tight dental appliance frequently manifests as a weakened supratrochlear or infratrochlear pulse, on the side of the constraint.
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Vessels of the thyroid
22.1 INTRODUCTORY NOTE This chapter, devoted to the thyroid, is fairly long. To our knowledge little coverage has been given to this organ in manual medicine texts. For this reason we have included paragraphs on its physiology and pathology.
22.2 ANATOMY AND PHYSIOLOGY The thyroid is located in the lower third of the anterior surface of the neck. The body of the thyroid comprises the thyroid and parathyroid glands.
22.2.1 Thyroid gland The thyroid is a conjoined endocrine gland, symmetrical and medial, adapted to the anterior larynx and trachea.
Shape and dimensions
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In the frontal plane the thyroid is shaped like an H or a butterfly (Fig. 22.1). In the transverse plane it has the form of a horseshoe, concave posteriorly and enclosing the trachea. The right and left lobes are approximately conical and connected by a narrow medial isthmus. Frequently larger in women than in men, the lobes generally measure: • 6–8 cm in breadth • 6 cm in height • 3 cm in thickness. The thyroid usually weighs 30 g, but this varies. It is brownish-red in color. Its ©
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consistency is rather soft, and its parenchyma is slightly granular. Its surface, when lightly palpated, appears somewhat irregular.
The thyroid Lobes The thyroid lobes have the shape of a pear or a triangular pyramid, and are largely covered by the sternothyroid, sternohyoid, and omohyoid muscles. A perfectly normal thyroid is difficult to palpate. The medial surfaces of the lobes are adapted to the lateral surfaces of the first five or six tracheal cartilages, the lateral surface of the cricoid cartilage, and the inferior part of the thyroid cartilage. Posteriorly, the lobes relate to the carotid sheath and its neurovascular contents, as well as to the parathyroid glands. Isthmus The isthmus is a flat lamina connecting the lobes, usually over the second, third, and fourth tracheal cartilages. It measures about 10 mm in width, 15 mm in height, and 5 mm in thickness. The superior border of the isthmus often gives rise to a vertical prolongation called the pyramidal lobe. This extra lobe is sometimes joined to the hyoid by a fibromuscular band, the levator of the thyroid gland.
Stability The thyroid parenchyma is surrounded by a thin fibrous capsule, a dependency of the visceral sheath of the neck. The capsule is held in place by ligaments of the trachea and the
Vessels of the thyroid
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Epiglottis Hyoid bone Thyrohyoid membrane
Thyroid cartilage Pyramidal lobe (of Lalouette) Superior parathyroid gland Thyroid isthmus Inferior parathyroid gland
Trachea
A
Anterior view
B
Posterior view
Fig. 22.1 (A) Frontal view and profile of the thyroid. (B) Posterior view of the thyroid.
vascular sheath called the thyrotracheal ligaments, one medial and two lateral. These are also referred to as the ligaments of Grüber. The thyroid compartment is in the shape of a U, open at the back. The thyroid sheath enclosing it is made up: • posteriorly by the visceral sheath medially and the carotid sheath laterally • anteriorly by the pretracheal layer of the deep cervical fascia, which also surrounds the infrahyoid strap muscles. The pretracheal lamina inserts on the inferior border of the hyoid bone and splits into two layers: • a pretracheal lamina covers the sternohyoid and omohyoid muscles • a deep lamina covers the thyrohyoid and sternothyroid muscles.
Physiology The thyroid gland secretes two hormones that stimulate cellular metabolism, and one hormone concerned with phosphate and calcium metabolism. Thyroxine and triiodothyronine Iodine is essential in the formation of the thyroid hormone thyroxine (T4) and tri iodothyronine (T3). The abbreviations T4 and T3 denote the number of iodine atoms the hormone contains. These hormones are initially synthesized as the precursor thyroglobulin. The release of hormones into the blood is controlled by TSH (thyroid stimulating hormone), secreted by the anterior pituitary gland. The secretion of TSH is stimulated by
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The practice of visceral vascular manipulation TRH (thyroid releasing hormone). Secretion of TRH is modulated by exercise, stress, malnutrition, hypoglycemia, and sleep. The rate of TSH secretion depends on the plasma levels of T3 and T4, which affect the responsiveness of the anterior pituitary to TRH. Raised T3 and T4 levels cause the secretion of TSH to drop, whereas low levels cause it to rise. T3 and T4 are necessary for normal growth and development, especially of the skeleton and nervous system. Virtually all organs and systems in the body are influenced by thyroid hormones. The physiological effects of T3 and T4 on the heart, skeletal muscles, skin, digestive and reproductive systems are more marked when the thyroid gland is hyperactive or hypoactive. These modifications and related dysfunctions are detailed in Table 22.1. Calcitonin This hormone is secreted by parafollicular cells in the thyroid. It concerns the function of the bones and the kidney by lowering blood calcium levels when they are raised. Calcitonin reduces bone resorption by osteoclasts and inhibits the resorption of calcium by the renal tubules, whereas parathyroid hormone acts to increase blood calcium and bone resorption. Calcitonin secretion is stimulated by high calcium blood levels. This hormone is important during infancy, when bones change significantly in size and shape.
22.2.2 Parathyroid glands Description
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The parathyroid glands are small endocrine glands situated on the posterior surface of the lateral thyroid lobes. They are paired glands, divided into two groups: the superior and inferior parathyroids. Each gland is commonly 8 mm long, 4 mm across, and 2 mm from back to front. Each weighs about 40 mg. The superior parathyroid glands are attached to the surface of the apex of the
Table 22.1 Symptoms of thyroid dysfunction Hyperthyroid
Hypothyroid
Symptoms Sympathicotonia
Fatigue, lethargy
Nervousness
Apathy, sleepiness
Irritability, intense emotion
Memory problems, poor hearing Peripheral neuropathy, carpal tunnel syndrome
Excessive sweating, thirst
Hypothermia, chills
Intolerance to heat
Intolerance to cold
Palpitations Frequent stools, diarrhea
Constipation
Weak muscles, fatigue
Muscle cramps, myotonia
Trembling
Arthralgia, paresthesia
Oligomenorrhea, amenorrhea Weight loss despite increased appetite
Weight gain despite decreased appetite
Signs Tachycardia
Bradycardia
Increased systolic and diminished diastolic pressure
Decreased systolic and increased diastolic pressure
Leucopenia, thrombopenia
Anemia
Hot, smooth, moist skin
Dry, rough, cold skin
Trembling, proximal muscle weakness
Edema (nonpitting)
Basedow’s disease: ocular signs (fixed gaze, oculopalpebral asynergy, exopthalmia)
Dull hair, fragile nails, hair loss
Swelling of the face, hands, and feet; puffiness around the eyes
Vessels of the thyroid thyroid, near the external branch of the superior laryngeal nerve. The inferior parathyroid glands are attached to the caudal edge of the thyroid lobes, each near an inferior thyroid artery and a recurrent laryngeal nerve.
Physiology The parathyroids secrete parathyroid hormone (parathormone) and play an important role in calcium metabolism. Secretion is regulated by blood calcium levels. When calcium concentration falls, parathyroid hormone secretion increases, and vice versa. The main function of the parathyroid hormone is to maintain a constant concen tration of calcium in the extracellular fluid. Thus, when blood calcium levels falls, parathyroid hormone: • increases the amount of calcium absorbed in the small intestine • increases the amount of calcium reabsorbed in the renal tubule.
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with specific observation such as a slight extension of the neck or on swallowing. The thyroid is sometimes visible even in the absence of pathology. In subjects with elongated graceful necks, the isthmus region can be clearly seen. Sometimes the thyroid can be noticed casually in profile, as a discrete anterior cervical bulge that moves with swallowing (Fig. 22.2). Ordinarily, everyone has a slight depression at the lower part of the neck, between the sternocleidomastoid muscles. Its spontaneous disappearance on rotation of the head is a good indication of an enlarged thyroid. Pay attention to small, unusual projections on the thyroid at the median line or behind the sternocleidomastoid muscle. Any mass that moves during the course of swallowing is highly likely located in the thyroid gland, or adhered to it. Should you observe hypertrophy, notice whether it is diffuse, like a goiter, or localized, like a nodule or thyroid cyst.
Palpation
22.3 CLINICAL EXAMINATION OF THE THYROID The evaluation and management of thyroid disorders has benefited from advancements in metabolic, hormonal, immunology, ultrasound, and isotropic exploration. Nevertheless, patient interview and examination provide information essential to diagnosing thyroid pathology. Clinical examination of the thyroid should be almost systematic, like taking blood pressure. Morphological and functional changes in the thyroid can be easily identified. Keep in mind, for example, that thyroid problems can masquerade as cervical pain.
22.3.1 Approach to thyroid morphology Inspection Visual inspection can provide precious clues. This may be noticed with a quick glance, or
The superficial location of the thyroid suggests that palpation will be easy. However, in the absence of pathology, palpation of the gland is hampered by the thickness of the infrahyoid and sternocleidomastoid muscles covering it. Ideally, palpation is done with a patient seated with their back leaning against the therapist, who stands behind the patient. To begin, either the patient’s head is in the standard neutral position or the cervical thoracic junction is slightly flexed to reduce tension on the anterior neck muscles. With practice it is possible to perform this palpation in supine. You might want to provide a glass of water for the patient if he or she needs to swallow repeatedly. Identify the cricoid cartilage and then, with the pad of your index and middle fingers, search caudally to feel the isthmus, located about 1 cm below. To palpate the isthmus from the sternal notch, glide your fingers upwards using a light touch, and short back and forth
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Subhyoid region Carotid region
Infrahyoid region
Subclavicular region
Fig. 22.2 Frontal view of the neck.
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movements. Your fingers will run into the substance of the isthmus. Have the patient swallow and feel the elastic isthmus elevate under your finger (Fig. 22.3). Move laterally to palpate the right and left lobes, which are somewhat easier to find. Palpate in a symmetrical manner using the fingers of both hands simultaneously. The palpation can be facilitated by asking the patient to swallow, in order to mobilize the thyroid cephalad, making the inferior part more accessible. To access the medial part of each lobe with precision, maintain the trachea with one hand and palpate the internal border of the lobe with the other hand. To palpate the main and lateral aspects of each lobe, glide the trachea towards the side being examined. With the other hand, encircle the sternocleidomastoid by placing your fingers and thumb around it. Ask the patient to swallow once more and palpate the whole lobe. This technique is particularly useful in cases of glandular hypertrophy.
This exploration is sometimes difficult, especially when the neck is short and thick or the person is obese. You can always ask the patient to tilt the neck toward and away from the side of the examination. If you still feel nothing, when the patient swallows make soft vertical up and down movements with the fingers just below the thyroid cartilage. Occasionally thyroid palpation requires extension and rotation of the neck towards the side being examined. This relaxes the sternocleidomastoid so that it can be moved out of the way. Palpation allows you to check the shape, size, structure, mobility, and sensitivity of the thyroid parenchyma, and to look for lymph nodes in the area of thyroid drainage. Form The lateral lobes lie anterior and lateral to the trachea and larynx, and posterior to the isthmus, which crosses the anterior surface of the trachea (Fig. 22.4). It is helpful to
Vessels of the thyroid
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Epiglottis
Hyoid bone Median thyrohyoid ligament Thyrohyoid membrane
Thyroid cartilage Pyramidal lobe (of Lalouette)
Thyroid
Trachea
Fig. 22.3 Larynx and thyroid in profile.
Anterior jugular vein Sternothyroid muscle Sternocleidomastoid muscle Omohyoid muscle External jugular vein Inferior laryngeal nerve Lymph nodes
Sternohyoid muscle Thyroid Internal jugular vein Common carotid artery Vagus nerve Inferior thyroid artery Vertebral artery and vein
Fig. 22.4 Transverse section of the thyroid.
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The practice of visceral vascular manipulation visualize the body of the thyroid as a concave horseshoe. Sometimes a narrow slender vertical extension is found on the inferior border of the isthmus ascending towards the larynx. This is known as the pyramid of Lalouette or the pyramidal lobe. This classical morphology is variable: the isthmus can be short and thick, lateral lobes can be fused in a V shape, the isthmus can be absent, the pyramidal lobe can be present in two or three parts, etc. In general, the gland is more or less symmetrical, although the right lobe is commonly a little larger than the left in a normal thyroid. Volume Remember that, in the average adult, the thyroid weighs no more than 30 g. The size of the gland is fairly variable. Generally the body of the thyroid is more developed in women than in men, and their lateral lobes are slightly more prominent. The surface of each thyroid lobe should not exceed that of the last phalange of the thumb of the patient being examined. Goiter refers to any enlargement of the thyroid body. When there are no clinical or biological signs other than hyper- or hypofunctioning, the terminology is euthyroid goiter. Not all enlargements are pathological: hypertrophy is often transitory in puberty, and the thyroid increases in size during menstruation and pregnancy.
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Structure Of firm but friable consistency, the parenchyma should feel supple and elastic when encountered by the first tracheal rings. The surface of the gland should feel somewhat lobular to superficial palpation. In slender people, the lobular constitution of the thyroid may mean that it appears to be grainy. Nevertheless, the parenchyma should always be homogeneous in texture. Any localized increase in density should make one suspicious of a nodule, whose volume and contour should be ascertained. Such densities can
easily be searched out by feeling the gland from anterior to posterior. Also palpate in the horizontal plane, by bringing the lateral lobes medially. Sometimes dense areas or nodules are easier to feel with a change in the direction of palpation. So that the caudad part of the lobes are more accessible, add a slight extension of the cervical column. This brings the gland cephalad. Mobility The gland should be able to move freely and spontaneously on swallowing, and when nudged by palpation. Sensitivity Normally palpation of the thyroid does not cause discomfort or any particular sensitivity. However, the pain referred to as ‘intrascapular hypertension’ is found in people with thyroiditis, and certain acute cancers. Lymphatic ganglia Special attention must be given to the detection of jugular, carotid, spinal, subclavicular, or subisthmic (ganglion of Delphien) adenopathies. Evaluate the size, consistency, mobility, and condition of the ganglion encountered. Be wary of enlarged, agglomerated, sensitive, fixed, or hot ganglia. Anomalies in volume and consistency Sometimes the thyroid compartment is absent (athyreosis, atrophic thyroiditis). In this case, rather than the thyroid, your fingers will feel the tracheal rings clear from the laryngeal cartilages to the sternal manubrium. Thyroid hypertrophy is easily recognized, whether diffuse or nodular. Try to differentiate an increase in volume (goiter) from single or multiple nodules. In the case of hypertrophy, percuss the top of the thorax. Any dullness should make one suspicious of endothoracic thyroid extensions. Discomfort on swallowing is common with an enlarged thyroid. According to Bates (1993), it is possible clinically to distinguish three major anomalies (Fig. 22.5).
Vessels of the thyroid
Diffuse thyroid hypertrophy
Multinodular goiter
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Isolated thyroid nodule
Fig. 22.5 Anomalies in thyroid volume and consistency (after Bates 1993).
• Diffuse hypertrophy of the thyroid. A diffusely enlarged gland or goiter engulfs the isthmus and the lateral lobes, but has no palpable nodes. This is found in Basedow’s disease, Hashimoto’s disease, and endemic goiter linked to iodine deficiency. Sporadic goiter refers to hypertrophy with no apparent cause. • Multinodular goiter. This term applies to a swollen thyroid containing two or more identifiable nodules. Multiple nodules cause more metabolic problems than does a malignant lesion. In any case, exposure to radiation in infancy, a family history of cancer, or a rapid increase in the volume of one of the nodules makes one suspicious of a malignant lesion. • Isolated thyroid nodule. An isolated nodule found during examination may be a cyst, a benign tumor, a nodule within an atypical multinodular goiter, or a malignant lesion. Again, factors such as anterior irradiation, a rapid or recent increase in nodule size, fixations to neighboring tissues, the hardness of the nodule, irregularity of contour, or enlarged cervical lymph ganglia raise the
possibility of malignancy. These isolated nodules are more common in men.
22.3.2 Functional approach to the thyroid As with every endocrine pathology, diagnosis of a dysfunctional thyroid rests largely on the inspection and observation of the patient. The first impression is often determinant: the face a little puffed up, translucent appearance of the eyelids, erythrocyanosis of the cheeks, hair loss, and cervical swelling can all make you think of thyroid dysfunction. With a minimum of attention and good powers of observation, it is possible to detect thyroid dysfunction by means of clinical findings. Among the most common are: • weight and appetite changes • water drinking habits • cardiac and vascular condition • digestive transit • neuropsychic demeanor • trophic disorders of the skin, hair, muscles, bones, etc. No symptom is specific to thyroid dysfunction; rather it is the entire group of clinical signs that is characteristic (Table 22.1).
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22.3.3 Precautions and contraindications Never hesitate to refer the patient to their physician or a specialist whenever the thyroid shows structural changes or functional disturbance, for example perceptible nodules occurring together with several of the symptoms summarized in Table 22.1.
22.4 VASCULAR MANIPULATION OF THE THYROID 22.4.1 Neurovascular anatomy As with all endocrine glands, the thyroid is a highly vascular organ, well endowed with both arteries and veins.
Arteries The arterial blood supply relies on two main trunks: 1 the superior thyroid artery, arising from the carotid artery 2 the inferior thyroid artery, a branch of the subclavian artery. These two trunks are large and, because their branches anastomose frequently, their manipulations are complementary. There is also an accessory pedicle called the middle thyroid artery. This collateral branch comes from the arch of the aorta and ascends the trachea to reach the inferior border of the isthmus. Superior thyroid artery
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Relations The superior thyroid artery passes under the omohyoid, sternohyoid, and thyrohyoid muscles. Collaterals The main branches of the superior thyroid artery are the laryngeal arteries supplying the tissues of the larynx. Function The superior thyroid artery supplies the superior two-thirds of the gland. Terminal branches The superior thyroid artery divides into three branches relating to the three surfaces of the lobes: 1 a lateral branch for the anterior lateral surface 2 a medial branch which crosses above the isthmus to anastomose with its partner on the opposite side 3 a posterior branch descending on the posterior border to supply the medial and lateral surfaces (anastomoses with the posterior branch of the inferior thyroid artery). Distinctive feature The superior thyroid artery follows the superior laryngeal nerve, branch of the vagus nerve (see Barral & Croibier 2006). Needless to say, any manipulation of the laryngeal artery has an effect on the superior laryngeal nerve. Inferior thyroid artery
Origin This is the first branch of the external carotid artery; it arises just beyond the carotid bifurcation (Fig. 22.6).
Origin The inferior thyroid artery (Fig. 22.7) arises from the thyrocervical trunk, which branches from the subclavian artery on the pleural dome, in front and a little lateral of the vertebral artery.
Pathway Beginning just below the greater cornu of the hyoid bone, the superior thyroid artery descends vertically along the lateral border of the thyrohyoid muscle, to reach the upper lobe of the gland.
Course The inferior thyroid artery has three segments: 1 A vertical part beginning just outside the vertebral artery.
Vessels of the thyroid
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Ascending pharyngeal artery
External carotid artery Suprahyoid artery Superior laryngeal artery
Internal carotid artery Superior thyroid artery Common carotid artery
Cricothyroid artery
Subclavian artery Trachea
Fig. 22.6 Superior thyroid artery.
2 A curved segment that runs medially above the transverse process of C6, passing in front of the vertebral artery and behind the carotid sheath. Here it intersects with the sympathetic cervical chain. 3 Curving again, the artery ascends obliquely in an anteromedial direction. It intersects the lateral border of the esophagus and the trachea, and passes anterior to the recurrent laryngeal nerve
(branch of the vagus) on the right, and posterior to it on the left.
Relations The inferior thyroid artery reaches the posterior surface of the thyroid gland at C5. It winds around the: • internal jugular vein • common carotid artery • vagus nerve • sympathetic trunk.
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External carotid artery Superior thyroid artery
Internal carotid artery
Vagus nerve Common carotid artery
Inferior thyroid artery
Inferior laryngeal nerve Right recurrent laryngeal nerve
Left recurrent laryngeal nerve
Fig. 22.7 Superior and inferior thyroid arteries.
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At the level of C5, the inferior thyroid artery passes anterior to the vertebral artery and posterior to the carotid sheath. Manipulation of the inferior thyroid artery at its origin affects the homolateral vertebral artery.
medially behind the carotid sheath. It supplies the adjacent muscles and gives off spinal branches to supply vertebral bodies and the spinal cord, owing to its anastomoses with the spinal arteries.
Collaterals The inferior thyroid artery divides into several branches to supply the: • esophagus • trachea • larynx. The ascending cervical artery is a small branch that arises as the inferior thyroid turns
Terminal branches The inferior thyroid artery reaches the thyroid body at the junction of the superior twothirds and inferior one-third of the gland. It divides into three terminal branches: 1 A posterior branch forms an anastomosis with the posterior branch of the superior thyroid artery, along the
Vessels of the thyroid
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Superior thyroid artery Medial branch Lateral branch
Superior parathyroid gland Supraisthmic arcade Deep branch Inferior thyroid artery
Inferior parathyroid gland
Infraisthmic arcade
Thyroid ima artery
Fig. 22.8 Intrathyroid anastomoses.
posterior medial border of the thyroid lobe. 2 A deep branch anastomoses with its contralateral partner. 3 An inferior branch anastomoses with its counterpart, along the inferior border of the isthmus (Fig. 22.8). NB: The inferior thyroid artery is subject to numerous variations from its origin and along its trajectory. To keep it simple, just remember that it reaches the thyroid body at C5.
• The middle thyroid veins are short horizontal branches that arise from the posterior surface of the lobes, drain the middle of the lobe, and empty directly into the inferior jugular vein. • The inferior thyroid veins collect blood from the inferior pole of the lobe and inferior border of the isthmus. They descend obliquely inferiorly to let into either the brachiocephalic or the internal jugular vein.
Function The inferior thyroid artery supplies the inferior third of the thyroid gland.
Nerves
Veins Three pairs of veins drain the thyroid. • The superior thyroid veins drain the superior pole of the thyroid and accompany the superior thyroid artery. They empty into the internal jugular vein via the thyro-lingual-facial trunk.
The thyroid receives nerve supply from: • parasympathetic fibers arising from the superior and inferior laryngeal nerves • sympathetic fibers from the superior and middle cervical ganglia, as well as from the superior cardiac nerve. The parathyroid nerve supply is sympathetic, from the cervical ganglion. Innervation reaches the thyroid through the periarterial plexus on the inferior thyroid
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22.5 MANUAL APPROACH 22.5.1 Taking the pulse Pick up the pulse as superiorly as possible along the common carotid artery, as far up as the superior border of the thyroid cartilage. Begin by resting your finger between the hyoid bone and the thyroid cartilage. Here you will feel two pulses: the beat of the superior laryngeal artery and of the superior thyroid artery. Superior laryngeal artery This pulse is found between the hyoid and the thyroid cartilage, one or two fingerwidths medial in relation to the lateral surface of the cartilage. This artery pierces the thyroid membrane, along with the superior laryngeal nerve, a branch of the vagus. Superior thyroid artery You are almost sure to find the superior thyroid artery between the hyoid bone and the thyroid cartilage. It is medial to the external carotid artery. In relation to the superior laryngeal artery, slide your flat fingers in a caudal and gradually lateral direction. Descend by one fingerwidth, along the medial border of the thyroid cartilage. Initially it is difficult to feel the superior thyroid pulse because of the strong pulse of the carotid. Move your finger laterally and slightly caudally of the carotid artery so as not to confuse the two.
22.5.2 Manipulations Manipulation of the superior laryngeal artery
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Position The patient is in decubitus, hands crossed on the abdomen, head turned slightly away from the artery in question (Fig. 22.9).
Fig. 22.9 Manipulation of the superior laryngeal artery.
Techniques Once the artery is perceived, compress and release it a few times. Using a very light contact, treat it with induction. One or two fingerwidths from the lateral border of the thyroid cartilage, below the hyoid bone, the superior laryngeal artery perforates the thyrohyoid membrane (Fig. 22.10). This piercing is often surrounded by a small fascial ring, which must be released for two reasons: • to free the perineurovascular tension • to obtain an effect on the superior laryngeal nerve. This, along with the external auditory canal, is a key point for manipulation of the vagus nerve. Next, locate the superior laryngeal artery where it arises from the superior thyroid artery. Stretch the artery in a superior and medial direction, with induction. It is also important to perform skin rolling in regard to this artery, both vertically and transversally.
Vessels of the thyroid
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Fig. 22.10 Manipulation of the superior laryngeal artery at the thyroid membrane.
Fig. 22.11 Manipulation of the superior thyroid artery.
Manipulation of the superior thyroid artery
Stretch maneuver With one finger fix the superior thyroid artery where it arises from the carotid. With the other fingerpad placed flatly just beneath the first finger, stretch this artery caudally and medially on the anterior surface of the thyroid cartilage. NB: Always remember to treat both the left and right inferior and superior thyroid arteries. Viscoelasticity–induction This technique is applied where the superior laryngeal artery passes through the thyrohyoid
membrane. Compress, release, and follow the Listening. Be careful to stay light with your palpation because of the superior laryngeal nerve.
Multidigital fanning Depending on the size of the neck, this technique is recommended because it benefits several small branches of the artery. Throughout the maneuver, keep one fingerpad on the origin of the superior thyroid artery as you spread small branches towards the substance of the gland. Pulse variations guide you in determining the optimal orientation of the fanning (Fig. 22.11).
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Fig. 22.12 Locating the inferior thyroid artery.
Manipulation of the inferior thyroid artery The inferior thyroid artery is located behind the common carotid and just above the subclavian arteries. It is very difficult, not to say impossible, to differentiate its pulse at its origin. Take the pulse as it courses superiorly along the medial surface of the scalene muscle.
Decubitus position The patient is in decubitus, elbows on the table, hands placed under the lower back to open the thoracic inlet (Fig. 22.12).
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Maneuver Locate the pulse of the common carotid artery inside the sternal head of the sternocleidomastoid. Next, direct your fingers laterally and posteriorly to the common carotid to find the second, less distinct, pulse of the inferior thyroid artery. Locate the pulse of the subclavian artery beyond the sternoclavicular junction in order to distinguish it from the inferior thyroid artery, whose caliber is clearly smaller. Place one thumb on the subclavian artery, and either fix it or push it slightly caudally. At the same time, place the other thumb in the direction of the inferior thyroid artery, and stretch it medially and a little cephalad. You can mobilize the corresponding thyroid
lobe medially at the same time, to assist the stretch. Complete the technique with induction, following the same protocol as for the superior thyroid artery, extending your action as caudally as possible to affect the anastomoses between the paired arteries.
Lateral decubitus position The patient is in lateral decubitus on the side opposite the manipulation. Place yourself directly behind the patient. Pass your arm under the patient’s forearm to support the upper extremity with your forearm. Place your thumb under the clavicle, and your index or middle finger just above the sternoclavicular junction. Your free cephalad hand pushes the shoulder anteriorly; this allows your fingers to penetrate against the pleural dome. Next, bring the shoulder cephalad. This position allows the index or middle finger easily to reach the medial surface of the anterior scalene muscle, in order to search for a small arterial pulse. Sweep your finger along the short course of this artery to discover any lack of elasticity or a hard part. Maneuver Following the same principles, carry out induction on the inferior thyroid artery by
Vessels of the thyroid
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Fig. 22.13 Manipulation of the inferior thyroid artery in lateral decubitus.
supinating the finger that is in contact with the artery (Fig. 22.13). Strumming The patient is in decubitus, hands on abdomen. This technique involves ‘strumming’ on the thyroid lobes to find small hardened areas, which are different from cysts. These hardened areas are less compressible than cysts, and have limited elasticity and viscoelasticity. By working with these parameters in mind, you will feel these zones gradually soften. Search carefully for hardened areas located behind the sternocleidomastoid, as they are often found here. In addition, with your free hand, you can bring the lateral lobe medially
to increase its thickness and make it easier to feel for, and work with, variations in elasticity and viscosity. Indications The indications for treating the thyroid are: • thyroid dysfunction • tracheal or laryngeal dysfunction • vertebral artery problems, because of the contiguity of the two arteries and the anastomoses between the cervical branch and spinal arteries. Results It is difficult to objectify our results. However, clinically, we have seen notable improvements in certain thyroid dysfunctions.
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23
Neurovascular techniques
One of the key propositions of the neck is that it allows free passage of numerous nerve fibers arising from the skull and the cervical column. These nerve fibers help to regulate the cardiovascular system, viscera of the neck such as the thyroid, and organs of the thorax, such as the heart and the lungs (Fig. 23.1). In a somewhat simplified manner, we will describe a few manipulations for the neuro vascular system of the neck. We will focus primarily on the glossopharyngeal, hypoglos sal, vagus, and sympathetic cervical chain.
23.1 GLOSSOPHARYNGEAL NERVE The glossopharyngeal nerve is of interest because it innervates the carotid glomus and sinus. This nerve forms anastomoses with the: • vagus nerve • facial nerve • sympathetic cervical chain: together with the superior cervical ganglion, it forms the intercarotid plexus. Refer to Chapter 21 for the technique.
23.2 HYPOGLOSSAL NERVE
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This nerve was described in Chapter 15, in connection with the external carotid artery (Fig. 23.2). Multiple small branches run up and down the carotid artery. We search with our fingers for hardened fibers that do not glide smoothly on the artery wall. The hypoglossal nerve forms anastomoses with the: ©
2011 Elsevier Ltd
• • • • •
superior cervical ganglion vagus nerve phrenic nerve cardiac plexus first two cervical nerves
23.3 VAGUS NERVE There are various locations where this nerve can be manipulated in the neck. It can be accessed, for example, via the superior laryn geal nerve, the recurrent laryngeal, or the auricular branch at the external ear canal. We described a technique for the superior laryngeal artery at the place where, together with the superior laryngeal nerve, it perforates the hyothyroid membrane (see Chapter 22).
23.4 RECURRENT LARYNGEAL NERVE This nerve runs along the medial surface of the lower half of the common carotid artery. We manipulate it using the glide–induction technique over the medial surface of the artery.
23.5 SYMPATHETIC CHAIN The sympathetic chain is located posteriorly and laterally in relation to the common carotid artery. It is difficult to differentiate its manipulation clearly from that of the vagus nerve. In the end it amounts to a vagosympathetic manipulation. The main thing is to focus on
Neurovascular techniques
Glossopharyngeal nerve (IX)
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Hypoglossal nerve (XII) Vagus nerve (X)
Pharyngeal plexus (IX and X)
First cervical nerve Second cervical nerve
Carotid sinus (IX)
Third cervical nerve
Hyoid bone
Fourth cervical nerve Ansa cervicalis (XII)
Superior laryngeal nerve Common carotid artery Sympathetic trunk
Recurrent laryngeal nerve (X)
Fig. 23.1 Neurovascular relationships.
feeling the precise micro-zone of neural fixa tion, and not to decide for ourselves the outcome of the technique. The organism can self-regulate, as long as the manipulation is subtle, precise, and not painful.
23.6 CAROTID GLOMUS AND SINUS Reminder: The carotid glomus and carotid sinus are two especially important structures that cause carotid manipulations to have an immediate and consequential central effect.
Carotid sinus This small dilation rich in mechanoreceptors (Fig. 23.3) is located between the hyoid bone and the superior border of the thyroid cartilage. By analyzing intracarotid pressure it responds to changes in blood pressure.
Carotid glomus The Latin word glomus means ‘pellet’ or ‘little ball.’ Located at the carotid bifurcation, this chemoreceptor monitors the oxygen, carbon dioxide, and pH of the blood.
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Hypoglossal nerve (XII)
Second cervical nerve Hyoid bone
Third cervical nerve Ansa cervicalis (XII) Common carotid artery Sympathetic trunk
Fig. 23.2 Carotid sinus.
Note that the carotid glomus receives nerve fibers from the vagus, glossopharyngeal, and sympathetic cervical nerves. With regard to manipulation, it is difficult to separate the sinus and the glomus, and so we treat them together.
23.6.1 Manipulation of the carotid sinus and carotid glomus
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We use very light pressure–induction maneu vers on the carotid bifurcation, the pulse of which is perceived behind the tubercle of the greater wing of the hyoid bone (Fig. 23.4).
As a preliminary, take the pulse at the radial artery or use a pulse-taking devise at the index finger. After several manipulations, the pulse will diminish in intensity and rapid ity, because of stimulation to the vagus and hypoglossal nerves. These manipulations cause reactive brady cardia. We like to use the skin rolling tech nique in the area of the carotid sinus. It is an effective technique with no risk of vagotonia (Fig. 23.5). NB: Be very gentle. This region of the neck is extremely sensitive. It is not the force of the maneuver that counts, but its precision.
Neurovascular techniques
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Glossopharyngeal nerve
Internal carotid artery External carotid artery
Nerve of the carotid sinus
Carotid body
Carotid sinus
Common carotid artery
Fig. 23.3 Manipulation of the carotid sinus and carotid body.
Fig. 23.4 Manipulation of the carotid sinus and carotid body.
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Fig. 23.5 Skin rolling at the carotid sinus and carotid body.
23.6.2 Indications Indications for manipulation of the carotid sinus and glomus are: • arterial hypertension • tachycardia • arrhythmia
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• • • • • • •
anxiety attack precordial pain gastroesophageal reflux pain in the solar plexus vagotonia sympathicotonia gingival or dental problems.
SECTION 3 VESSELS OF THE ABDOMEN
Major abdominal landmarks
24.1 USEFUL VISCERAL LANDMARKS Before locating the main abdominal pulses, we will look at a few key landmarks, invaluable in the manual approach to the abdomen (Fig. 24.1).
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fingerwidths above the umbilicus. This slightly variable point is more or less symmetrical with the duodenojejunal junction. Remember that the sphincter of Oddi is in the posterior medial wall of the duodenum. Manipulation of this sphincter affects both the hepatopancreatic ampulla and the major duodenal papilla (of Vater).
24.1.1 Gastroesophageal junction The area opposite T11 and inferior to the xiphoid process is an area we approach only in the seated position.
24.1.2 Gallbladder The gallbladder is located where the right mid-clavicular umbilical line meets the ninth costal cartilage. The gallbladder is only pal pable under the ribs and in the seated position.
24.1.3 Duodenojejunal junction The duodenojejunal junction is found on the left mid-clavicular umbilical line, three fingerwidths above the umbilicus. It is a dependable landmark for radiologists.
24.1.4 Sphincter of Oddi (hepatopancreatic ampulla) The sphincter of Oddi is situated on the right mid-clavicular umbilical line, three ©
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24.1.5 Pylorus The pylorus is usually found just to the right of the xiphoid umbilical line, a handswidth superior to the umbilicus. If the person is stressed or the pylorus is active, this sphincter could move more towards the right. Despite its mobility, it is easily palpated.
24.1.6 Ileocecal valve The ileocecal valve is located one-third of the way towards the umbilicus on the right umbilical–anterior superior iliac spine (ASIS) line.
24.1.7 McBurney’s point This point is two fingerwidths below the ileocecal valve. Note that it receives sensory innervation from the right 12th intercostal nerve, which anastomoses with the first lumbar nerve root.
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Left mid-clavicular–umbilical line (LMCUL)
RMCUL
1 2 5 3
6 ASIS
4
2/3
1/3 7
8
2/3
1/3 1. Gastroesophageal junction (esophagocardio-tuberosity) 2. Gallbladder 3. Sphincter of Oddi (hepatopancreatic ampulla) 4. Duodenojejunal junction 5. Pylorus 6. Ileocecal valve 7. Ovary 8. Ovary
Fig. 24.1 Useful visceral landmarks.
24.1.8 The ovaries The ovaries are located one-third of the distance from the pubis on an ASIS–symphysis pubis line. Their location varies as a function of age and hormonal activity.
24.2 PRINCIPAL ABDOMINAL PULSES 24.2.1 The abdominal aorta
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The abdominal artery is found between the xiphoid process and the umbilicus, slightly left of the xiphoid–umbilical line (Fig. 24.2). The aortic pulse is easiest to feel either superior or inferior to the border of the
pancreas. Never place your fingers in an anteroposterior direction. Commence lateral of the artery to avoid picking up the beat of the superior mesenteric artery. Proceed towards the aorta, delicately and gradually. It is only by placing your fingers on either side of the aorta that you can feel an abdominal aortic aneurysm. Beware if you have the impression that the aorta is more than 4–5 cm wide. Its normal dimension is no more than 3 cm. Sometimes, for emotional reasons, the abdominal pulse is very powerful and distinct. This can worry the patient, even though it is a normal somatic reaction. One of the first signs of aortic aneurysm is lumbago or low back pain. If the slightest
Major abdominal landmarks
Inferior vena cava
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Celiac trunk (superior border of L1)
Aorta
Superior mesenteric artery (superior border of L2)
Transpyloric plane
Renal artery (L2) Umbilicus Inferior mesenteric artery (L3) Transtubercular plane Aortic bifurcation (L4) Confluence of the common iliac veins (L5)
Pubic symphysis
Fig. 24.2 Landmarks for palpation of the abdominal aorta.
doubt arises, refer the patient to their physician. As a preliminary, compare the blood pressure of the upper and lower extremities. The systolic index normally sits at about 0.9 mmHg (see Chapter 6). Check that both femoral pulses are clearly perceptible. Some aneurysms are located higher up by the renal arteries. These are very difficult to feel manually.
24.2.2 Celiac trunk The celiac trunk lies opposite the lower part of the 12th vertebral body (T12), left of pylorus in the xiphoid hollow to the right of the ligament of Treitz (suspensory muscle of the duodenum). First locate the aortic pulse and then gently move your fingers very slightly to the right, near the lesser curvature of the stomach. The
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Left mid-clavicular umbilical line (MCUL)
MCUL
2
3
1
4 5 6
7
11
Bi-iliac line
8 9
10
1. Celiac trunk 2. Hepatic artery 3. Left gastric artery 4. Splenic artery 5. Superior mesenteric artery 6. Inferior mesenteric artery 7. Right colic artery 8. Common iliac artery 9. External iliac artery 10. Internal iliac artery 11. Left colic artery
Fig. 24.3 Abdominal pulses.
more pressure you apply, the greater your chances of mistaking the abdominal aorta for the celiac trunk. This confusion is common (Fig. 24.3). This pulse is an indicator of the vascular effects of our manipulations with regard to the liver, stomach, spleen, and pancreas.
24.2.3 Left gastric artery
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The left gastric artery lies opposite T12, a little superior and to the left of the celiac trunk. It is sometimes confused with the splenic artery, and is not an easy pulse to detect.
24.2.4 Common hepatic artery The common hepatic artery is found to the right of a xiphoid–umbilical line, close to pylorus, inferior to the gallbladder. With practice this pulse is fairly easily perceived (Fig. 24.4).
24.2.5 Splenic artery The splenic artery is located inferior and to the left of the celiac trunk. Try to find the superior border of the pancreas by gliding your fingers beneath the xiphoid process. The superior border of the pancreas can be
Major abdominal landmarks
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Fig. 24.4 Hepatic and splenic artery pulses.
mistaken for the transverse colon. This pulse is fairly easy to feel. Palpate for it to the left, beyond the abdominal aorta.
24.2.6 Superior mesenteric artery The superior mesenteric artery lies opposite L1, one or two fingerwidths inferior to the celiac trunk, slightly to the right of the duodenojejunal junction, close to the left midclavicular–umbilical line. Note that beneath the caudal border of the pancreas the superior mesenteric artery is more superficial than the inferior mesenteric artery. This pulse is a circulatory indicator of the right part of the colon. In addition to its supposed function of orienting the duodenojejunal flexure, another purpose of the ligament of Treitz is to surround and protect the superior mesenteric artery and the celiac trunk.
24.2.7 Inferior mesenteric artery The inferior mesenteric artery is about two to three fingerwidths superior and slightly to the left of the umbilicus, opposite L3 and sometimes L4. Often difficult to appreciate, this pulse serves as a vascular indicator of the left part of the colon and the small intestine.
24.2.8 Right colic artery The right colic artery is found just inside McBurney’s point.
24.2.9 Left colic artery The left colic artery is about three fingerwidths inferior to the umbilicus, and inferior and to the left of the inferior mesenteric pulse. Tip: When the pulse is difficult to perceive, there is a trick to make it stand out. Lightly compress the caudal part of the abdominal aorta. This has the momentary effect of increasing blood flux in the adjacent arterial branches.
24.2.10 Common iliac artery The common iliac arteries bifurcate from the aorta inferior to the umbilicus, between L4 and L5. These arteries diverge as they descend.
24.2.11 External iliac artery The external iliac artery separates from the common iliac artery at the level of the sacroiliac joint and descends along the lateral border of the sacrum.
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Right common carotid artery
Brachiocephalic trunk Right subclavian artery
Arch of aorta
Posterior intercostal artery Thoracic aorta
Diaphragm
Right inferior phrenic artery Celiac trunk Common hepatic artery Right renal artery Abdominal aorta Right ovarian and testicular artery Right lumbar artery Right common iliac artery
Fig. 24.5 Branches of the aorta.
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Left gastric artery Left inferior phrenic artery Splenic artery Superior mesenteric artery Inferior mesenteric artery
Median sacral artery
Major abdominal landmarks
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24.2.12 Internal iliac artery The internal iliac artery begins at the common iliac bifurcation, anterior to the sacroiliac joint, and descends along the lateral border of the anterior sacral foramina (Fig. 24.5).
24.2.13 In summary The most perceptible pulses are those of the: • aorta • hepatic artery • splenic artery • iliac arteries • superior mesenteric artery.
24.2.14 Manipulation of the abdominal aorta Place your fingers in the same position as when locating an aortic aneurysm. Surround the aorta with your thumbs and fingers to feel its right and left boundaries clearly (Fig. 24.6). The aorta is best perceived inferior to the caudal border of the pancreas. Begin by placing your fingers to the left of the xiphoid– umbilical line. Once you feel the aortic pulse, place your thumbs to the right of the xiphoid– umbilical line, to come up against the right side of the aorta. Elongate the aorta along its axis and perform several lateral stretches to stimulate
Fig. 24.6 Manipulation of the abdominal aorta.
the aortic mechanoreceptors. Complete the treatment with induction. Always think in three dimensions, picturing the aorta as a pipe that might have a fixation on any part of its contour.
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Vessels of the liver
The arteries described in this chapter serve as witnesses before and after liver lifting maneuvers. These gauges are the celiac trunk and hepatic artery.
manipulations, not only of the liver, but also of the spleen and pancreas. Because it is surrounded by the solar plexus, the celiac trunk is very sensitive to the glide–induction technique.
25.1 ANATOMY 25.1.1 Celiac trunk
25.1.2 Hepatic artery
Origin
Origin
The celiac trunk (Fig. 25.1) arises just below the aortic hiatus, at the caudal part of the 12th vertebral body, two fingerwidths below the xiphoid process.
Course The celiac trunk is 1.5–2 cm long, passing almost horizontally anteriorly and slightly to the right. It divides into the hepatic, splenic, and left gastric arteries. This is referred to as a tripod division (ad modum tridentis). Usually the left gastric artery arises cephalad of the others.
Relations The celiac trunk relates: • anteriorly and slightly to the right to the caudate (Spiegel) lobe of the liver • posteriorly to the superior border of the pancreas • on the left, to the stomach.
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The celiac trunk is an excellent indicator to verify the effects of our vascular ©
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The hepatic artery arises from the celiac trunk at the caudal border of T12, to the right of the xiphoid–umbilical line.
Course The hepatic artery passes almost horizontally anteriorly and laterally toward the pylorus. It passes between layers of the lesser omentum, medial to the common bile duct, to reach the porta hepatis.
Branches The branches of the hepatic artery are: • the pyloric artery • the right gastroepiploic artery • the pancreaticoduodenal arteries • the gastric and omental branches • the cystic artery • the proper hepatic artery.
Remarks There is an arterial interrelationship between the liver, stomach, pancreas, and spleen. As we shall see, it is not possible to select just one artery to treat an organ fully.
Vessels of the liver
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Stomach Reflected liver
Splenic artery
Proper hepatic artery
Spleen
Inferior vena cava
Gallbladder Cystic artery Portal vein Celiac trunk Common hepatic artery Right gastric artery Gastroduodenal artery Superior pancreaticoduodenal artery Duodenum
Right gastroepiploic artery
Pancreas
Left gastroepiploic artery
Fig. 25.1 Celiac trunk.
25.1.3 Lifting irrigation of the liver Preliminaries • Before embarking on these vascular techniques, free the ligamentous attachments of the liver. Evaluate the triangular and coronary ligaments, whose nerve supply derives largely from the phrenic nerve. • Take both the hepatic and the splenic pulses, in order to be able to check your technique. Numerous anastomoses between these two arteries are affected by this technique. • Direction of the manipulation: the hepatic artery follows the hepatoduodenal ligament. It runs cephalad, posterior, and
to the right. This ligament determines the axis for manipulating the liver.
25.2 MANUAL APPROACH Lifting irrigation of the liver can be done in the seated, lateral decubitus, or decubitus position.
25.2.1 Seated position The patient is seated, legs hanging free, and hands resting on the thighs. Position yourself behind them (Fig. 25.2). Place the fingers of your right hand slightly left of the hepatic flexure of the colon. Avoid the rectus abdominis muscle by starting out
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The practice of visceral vascular manipulation at its lateral border, and about a palmwidth below the costal margin. Begin by gradually penetrating your fingers anterior to posterior, and only when you can sink no further posteriorly, move them superiorly. Position the fingers of the left hand beneath the left part of the liver, just medial to the left triangular ligament. Place them a little to the right of the left nipple line. Gradually lift the liver superior, posterior and to the right, moving it on the axis of the hepatic artery. At the end of the movement, maintain the liver in position for about 20 s. This maneuver also has an effect on the phrenic, gastric, and pancreaticoduodenal arteries.
25.2.2 Left lateral decubitus position
Fig. 25.2 Lifting irrigation of the liver (seated position).
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In this position, rather than lifting the entire liver, focus the lift in the direction of the hilum (Fig. 25.3). First push the right ribcage in the direction of the umbilicus to gain easy access. Place your fingers slightly lateral to the axis of the gallbladder to direct the fingers posterior and then cephalad. Maintain the traction for 30 s. This maneuver has a somewhat greater effect
Fig. 25.3 Lifting irrigation of the liver (left lateral decubitus position).
Vessels of the liver
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on the hepatic arteries. It can also be done in seated position.
25.2.3 Decubitus position Follow the same principle: first push the right ribcage towards the umbilicus. Next mobilize the liver laterally, to the right and cephalad. At the outset, place one flat finger on the axis of the hepatic artery (Fig. 25.4). Stay in contact with the artery as best you can, while stretching it via the liver, towards the right. At the end, direct your finger cephalad. With practice, you will be able to feel changes in the hepatic pulse during the manipulation. The same technique can be done with two fingers placed on either side of the hepatic artery. NB: Remember to recheck the celiac and hepatic pulses following the manipulation.
25.2.4 Indications We have performed this technique on patients suffering from hepatitis B or C. Although biological tests did not change much, many patients felt better, often regaining appetite and experiencing a desire to be more intellectually and physically active. The most common indications for treating the hepatic vessels are: • fatty liver • aftermath of alcohol or alimentary intoxication • hepatitis sequelae
Fig. 25.4 Lifting irrigation of the liver (decubitus position).
• • • • • •
allergies eczema psoriasis following infectious disease psychasthenia (phobias, obsessions) digestive disorders.
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Vessels of the stomach
26.1 ANATOMY
Course
The vascular circle of the stomach is composed of the left and right gastroepiploic (gastro-omental) arteries, and the left and right gastric arteries. The left gastroepiploic artery is a branch of the splenic artery that passes through the gastrosplenic ligament and then the gastrocolic ligament. It anastomoses with the right gastroepiploic artery, arising from the gastroduodenal artery. The left gastric artery joins with the right gastric artery, itself a branch from the common hepatic artery.
The right gastric artery runs between the layers of the lesser omentum and crosses in front of the gastroduodenal artery.
26.1.1 Left gastric artery Origin Somewhat difficult to feel, the left gastric artery (Fig. 26.1) arises from the celiac trunk and ascends to the left of the midline, superior to the splenic artery, with which it can be confused.
Course The left gastric artery runs along the superior end of the lesser curvature of the stomach.
Termination The left gastric artery anastomoses with the right gastric artery near to the pylorus.
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Termination The right gastric artery anastomoses with the left gastric artery.
26.1.3 Left gastroepiploic (gastro-omental) artery Origin The left gastroepiploic artery arises from the splenic artery near the splenic hilum (see Fig. 26.1).
Course The left gastroepiploic artery follows the greater curvature of the stomach. Its direction varies depending on the fullness and shape of the stomach. For this reason it is fairly sinuous.
Termination The left gastroepiploic artery anastomoses with the right gastroepiploic artery.
26.1.2 Right gastric artery
26.1.4 Right gastroepiploic artery
Origin
Origin
The right gastric artery arises from the proper hepatic artery, under cover of the liver.
The right gastroepiploic artery originates from the gastroduodenal artery, which comes
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Vessels of the stomach
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Left gastric artery
Common hepatic artery Gastroduodenal artery
Right gastric artery
Left gastroepiploic artery
Superior pancreaticoduodenal artery
Splenic artery
Right gastroepiploic artery
Dorsal pancreatic artery
Inferior pancreaticoduodenal artery
Greater omentum
Superior pancreaticoduodenal artery Epiploic (omental) arteries
Epiploic arterial arch
Fig. 26.1 Left gastric and gastroepiploic arteries.
from the common hepatic artery (see Fig. 26.1).
Course The right gastroepiploic artery runs to the left, posteriorly and inferiorly to the pylorus, along the greater curvature of the stomach to anastomose with the left gastroepiploic artery.
Comment In studying the distribution of these arteries, it is clear that the arterial blood supply of the stomach is related to that of the liver and pancreas. This means that any effective
manipulation of the abdominal organs must take the entire ensemble into consideration.
26.2 MANUAL APPROACH 26.2.1 Preliminaries • Take the celiac pulse by placing your fingerpad opposite the caudal part of the 12th vertebral body. • Attempt to differentiate the left gastric and splenic pulses by orienting one or two fingers to the left of the celiac trunk, perpendicular to the aorta. Often the splenic pulse is perceived first. It is located on the cephalad border of the
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2 1
Fig. 26.2 Manipulation of the left gastric artery (decubitus position).
pancreas. The left gastric pulse is located more superiorly, toward the caudal part of the gastroesophageal junction. Confusion between the two pulses is essentially unimportant because the purpose is to feel a change in the quality of pulsation following treatment. Due to their vascular interrelationship, manipulating any of the organs brings change to any or all of the pulses in the area. • Take the pulse of the common hepatic artery, to the right of the celiac trunk, perpendicular to the aorta.
26.2.2 Left gastric artery
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mobilizing to the left. During this maneuver, place a flat finger on the splenic artery, whose pulse is easy to feel. This enables you to pick up variations in the pulse, as a function of the direction of your manipulations. Step two: Bring the lesser curvature caudad and maintain this position for about 20 s.
Manipulation in right lateral decubitus position Direct your fingerpads deeply towards the upper part of the lesser curvature. Draw it towards you (towards the left) and maintain this position about 20 s (Fig. 26.3).
Manipulation in decubitus position
Manipulation in seated position
The patient lies on the table, arms alongside the body, with a soft pillow under the thoracolumbar junction. Position yourself to their right (Fig. 26.2). Step one: Using your thumb, push the lesser curvature of the stomach to the left, on the axis of the initial part of the left gastric artery. The lesser curvature of the stomach is fairly deeply situated. To reach it, first bring the body of the stomach towards the xiphoid– umbilical line in the direction of the lesser curvature that you are simultaneously
Standing behind the patient, begin by placing your fingers a palmwidth below the xiphoid process (Fig. 26.4). Direct your fingers posteriorly and slightly left of the xiphoid–umbilical line. Next, with your fingers as deep as possible without causing pain, bring your fingers caudad to stretch the lesser curvature of the stomach. Maintain the caudal traction in induction, for about 20 s. This manipulation has an effect on the celiac trunk and its three branches.
Vessels of the stomach
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Fig. 26.3 Manipulation of the left gastric artery (right lateral decubitus position).
26.2.3 Right gastric artery With a focus on the location of the origin of the right gastric artery, employ the same technique as for the proper hepatic artery, by lifting the liver cephalad and to the right.
26.2.4 Gastroepiploic artery Manipulation in left lateral decubitus position Standing behind the patient, your fingers placed on the left lateral border of the rectus abdominis muscle, sink posteriorly to a depth of about 4–5 cm (Fig. 26.5). Depending on the part of the vascular circle of the stomach whose axis you find toward the region of the pylorus, perform fanning maneuvers in a clockwise direction. Your palms are close to pylorus, your fingers spanning along the greater curvature of the stomach. Maintain each stretch at the different segments for about 20 s each, in induction. Fig. 26.4 Manipulation of the left gastric artery (seated position).
Manipulation in decubitus position Positioned to the right of the patient, your flat hands on their stomach, carry out a fanning maneuver accompanied by clockwise rotation (Fig. 26.6). Place the pad of one finger very
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Fig. 26.5 Manipulation of the gastroepiploic artery (left lateral decubitus position).
Fig. 26.6 Manipulation of the gastroepiploic artery (decubitus position).
flat on the splenic artery, whose pulse variation will allow you to fine-tune the axis of your maneuvers. Move your hands in the direction where the pulse strengthens. This technique can be combined with the maneuver for the left gastric artery (Fig. 26.7).
26.2.5 Organs and structures related to the vessels of the stomach
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The organs concerned are: • the duodenum via the gastroduodenal artery
• the spleen via the left gastro-omental artery • the liver via the right gastro-omental artery • the pancreas via the right gastro-omental artery • the esophagus and hiatal region via the left gastric artery. The structures concerned are: • the right and left vagus nerves, and the celiac plexus, in the region of the esophagus • the gastric veins • the portal vein.
Vessels of the stomach
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Fig. 26.7 Combined manipulation of the left gastric artery and the gastroepiploic artery (decubitus position). Hepatic branch of the anterior vagal trunk
Anterior vagal trunk Left gastric artery and plexus
Lesser omentum
Hepatic plexus Celiac ganglion and plexus Right gastric artery and plexus
Anterior gastric branch of the anterior vagal trunk Splenic artery and plexus
Superior mesenteric artery and plexus
Fig. 26.8 Celiac plexus.
Gastroepiploic artery
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26.2.6 Indications Indications for manipulation of the stomach vessels include: • gastric dysfunction (especially slow digestion) • gastric ptosis • hyperchloridia • sequelae of ulcers • gastroesophageal reflux • hepatopancreatic dysfunctions.
26.2.7 Nervous system The gastric and gastroepiploic arteries are surrounded by the rich celiac plexus (Fig. 26.8) that arises principally from the vagus nerve. The anterior vagus nerve exchanges fibers with the splanchnic and celiac plexuses. All vascular manipulations of the stomach involve its nervous system.
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The celiac plexus is the largest major autonomic nerve plexus. It surrounds the celiac trunk and the origin of the superior mesenteric artery near the duodenojejunal junction, in front of the aorta. The plexus is comprised of the celiac, superior mesenteric, and aorticorenal ganglia. It exchanges fibers with the vagus, and greater and lesser splanchnic nerves – indeed with all the nerves arising in the abdomen.
26.2.8 Contraindications An active ulcer and previous gastric bypass surgery are contraindications for manipulations. It is advisable to be particularly cautious with a patient suffering with stomach pain together with low systolic pressure. It is advisable to determine the color of the stools. Black stools are a sign of gastric or upper intestinal hemorrhage.
Pancreaticoduodenal vessels
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It is difficult to separate the duodenum from the pancreas because their arterial systems are intertwined. In our opinion, the duodenum merits more medical attention than it receives because, embryologically, it is the origin of the liver and the pancreas. In medicine the duodenum is rarely cited, as it is obscured by ‘gastric’ pains.
intraperitoneal and very dependent on the mobility of the liver. The second part of the duodenum is retroperitoneal and is almost always implicated in any right renal fixations. One could almost speak of a duodenorenal ‘flirtation.’ It is at the duodenojejunal flexure that the small intestine becomes intraperitoneal.
27.1 ANATOMY
27.1.3 Remarks on the pancreas
We will see that the arteries common to the duodenum and pancreas arise from the gastroduodenal artery (Fig. 27.1).
It is sometimes difficult to imagine that this gland, 15 cm long and weighing a few hundred grams, is able to produce 2 L of secretions daily. In our courses, we usually describe the pancreas in three parts: the head, the body, and the tail. Even if this division is contestable, physiologically the head relates mainly to exocrine function, whereas the body and the tail correspond to endocrine function. This classification emerged from our clinical experience, Listening Techniques and Manual Thermal Evaluation. The more serious the pancreatic problem, the more the hand is attracted towards the tail in Listening.
27.1.1 Pancreaticoduodenal arteries The common hepatic artery gives origin to the gastroduodenal artery from which arise the: • anterior superior pancreaticoduodenal artery • posterior superior pancreaticoduodenal artery • inferior pancreaticoduodenal artery. This is a branch of the superior mesenteric artery, which ascends to anastomose with the superior pancreaticoduodenal artery.
27.1.2 Remarks on the duodenum The arterial irrigation of the duodenum is the same as that of the head of the pancreas. Its cephalad part (first part of the duodenum) is ©
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27.2 MANUAL APPROACH 27.2.1 Pancreaticoduodenal arteries As we have seen, the pancreaticoduodenal arteries arise from the gastroduodenal artery and descend the second part of the duodenum.
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Esophagus
Inferior vena cava
Left gastric artery and vein
Proper hepatic artery Right adrenal gland
Pancreas Splenic artery
Portal vein
Celiac trunk
Duodenum
Left renal artery and vein
Superior mesenteric artery and vein Abdominal aorta
Inferior mesenteric artery and vein Genitofemoral nerve
Right iliac artery and vein
Fig. 27.1 Duodenum and pancreas.
Note that this artery gives off a great number of small branches, perpendicular to it.
Position The patient is seated, legs hanging free, hands on thighs. Position yourself behind the patient.
Technique
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Begin with a hepatoduodenal lift (Fig. 27.2). Place the fingers of your right hand medial to the projection of the fundus of the gallbladder (right mid-clavicular–umbilical line). Direct your fingers first posteriorly and then cephalad to capture the liver. With the thumb of the other hand, contact the second part of the duodenum, below the sphincter of Oddi.
One hand lifts the liver while the other hand pushes the duodenum towards the back. It is often easier to push back the junction of the second and third parts of the duodenum than it is to move the sphincter of Oddi. Maintain this stretch–induction position for about 20 s.
27.2.2 Perpendicular branches of the pancreaticoduodenal arteries Position The patient is in decubitus, hands alongside the body, with a small cushion positioned under the thoracolumbar region. Begin by placing the flat of one fingerpad on the hepatic artery, whose pulse variations during the maneuver will allow you to fine-tune the angle of your technique.
Pancreaticoduodenal vessels
Technique The pancreaticoduodenal arteries run along a main vertical axis and their perpendicular branches run transversely.
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The technique consists of pushing the lateral border of the second part of the duodenum across the xiphoid–umbilical line, and maintaining the push while stretching it longitudinally. Progressing from cephalad to caudad, along the tube of the duodenum. Hold each push–induction for about 20 s (Fig. 27.3). This technique is good for the pancreaticosplenic arteries, which we will learn about in Chapter 28.
27.2.3 Counter-rotation of the pancreaticoduodenal arteries Position
Fig. 27.2 Manipulation of the pancreaticoduodenal arteries.
Fig. 27.3 Manipulation of the transverse pancreatic branches.
The patient is in decubitus. Stand on their left. The index, middle finger, and ring finger of your cephalad hand are placed on the median part of the abdomen and sink gradually posteriorly in search of the aortic pulse. The thumb of your caudad hand locates the second part of the duodenum and is placed against its medial surface. Once you perceive the pulse of the aorta, release your pressure slightly and sweep your fingers to the right of the axis of the aorta, such that your fingerpads sink deeper little by little, to contact the head of the pancreas.
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Fig. 27.4 Counter-rotation manipulation of the pancreaticoduodenal arteries.
Portal vein Common hepatic artery Superior posterior pancreaticoduodenal vein Splenic artery Gastroduodenal artery
Dorsal pancreatic artery
Gastrocolic trunk (of Henlé)
Inferior posterior pancreaticoduodenal vein
Superior posterior pancreaticoduodenal artery Inferior posterior pancreaticoduodenal artery
POSTERIOR ARTERIAL ARCADE
Inferior anterior pancreaticoduodenal artery Superior anterior pancreaticoduodenal artery
ANTERIOR ARTERIAL ARCADE
Right superior colic vein
Fig. 27.5 Intrapancreatic anastomoses.
Technique
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Your two hands work simultaneously (Fig. 27.4). Exert a light perpendicular traction along the main axis of the second part of the duodenum, as if wanting softly to ‘separate’
the second part of the duodenum from the pancreas. Perform a couple of rotations on the frontal plane, clockwise and counterclockwise. While the second part of the duodenum is brought
Pancreaticoduodenal vessels clockwise, move the pancreas reciprocally counterclockwise. While performing the clockwise or counterclockwise rotations, add induction of all the tiny movements that spontaneously arise. You will be able to feel a release and often a warming of the tissues under your hands.
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This maneuver has an effect on both the inferior and inferior posterior pancreaticoduodenal arteries, their anastomoses, and the short perpendicular branches arising from them and going to the vertical part of the duodenum (Fig. 27.5).
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Pancreaticosplenic vessels
28.1 ANATOMY 28.1.1 The pancreas We have seen that the arterial supply of the pancreas derives mainly from branches of the gastroduodenal artery (via the superior anterior and superior posterior pancreaticoduodenal arteries as intermediaries) and the splenic artery (Fig. 28.1). These two arteries anastomose with the inferior pancreaticoduodenal artery, which runs transversely from the superior mesenteric artery. Remember that the vascular arrangement between the abdominal organs allows the body to compensate for any irrigation deficit.
28.1.2 The spleen
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The spleen is a retroperitoneal organ, with a mobility of about 10 cm, weighing on average 200 g (see Fig. 28.1). Unlike lymph nodes, the spleen is connected directly to the blood circulation, making it suitable for visceral vascular manipulation. The spleen articulates by way of peritoneal folds with the: • stomach • pancreas • splenic flexure of the colon • left lobe of the liver. We have often emphasized the importance of the left side of the body in relation to trauma. This is an area you must check meticulously for any possible visceral and parietal ©
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fixations, especially in the face of unusual, and sometimes disconcerting, symptoms. We have seen, for example, several cases of posttraumatic iron deficiency where the spleen is the cause.
28.1.3 The splenic artery The splenic artery is the largest branch of the celiac trunk, and its course is amongst the most tortuous in the body. It runs behind the omental bursa, along the superior border of the pancreas (Fig. 28.2). The splenic artery supplies the left gastroepiploic artery at the greater curvature of the stomach. At the tail of the pancreas it divides into several small branches before entering the hylum of the spleen. These branches are sinuous in order to adapt to the spleen’s great mobility.
28.1.4 The inferior pancreatic artery This artery is also called the transverse pancreatic artery. It links the splenic artery with the pancreaticoduodenal arteries.
28.1.5 Perpendicular branches of the splenic artery These branches connect the splenic and inferior pancreatic arteries, essentially by way of the greater and dorsal pancreatic arteries.
Pancreaticosplenic vessels
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Reflected stomach
Spleen Left gastric artery
Left and right inferior phrenic arteries Celiac trunk Common hepatic artery Proper hepatic artery Dorsal pancreatic artery Superior posterior pancreaticoduodenal artery
Superior anterior pancreaticoduodenal artery Inferior pancreaticoduodenal artery Duodenum
Left gastroepiploic artery Great pancreatic artery Inferior pancreatic artery Splenic artery Superior mesenteric artery
Inferior anterior pancreaticoduodenal artery
Fig. 28.1 Pancreas and spleen.
Comments Two things can be concluded about these arterial arrangements: 1 It is important to stretch these arteries transversely. 2 It is also necessary to carry out stretches perpendicular to the transverse arteries. Caution: Do not compress the pancreas! The pancreas is a fragile gland that cannot rebuild itself like the liver can. At all costs one must avoid compressing it anterior to posterior, against the vertebral column. This is the only organ where there is a real risk of creating a direct irritation or inflammation. Also, take
special care with diabetic patients, who might have vascular fragility.
28.2 MANUAL APPROACH 28.2.1 Right lateral traction technique To stretch both the transverse pancreatic arteries and the splenic artery, hook the medial border of the duodenum with two flat fingers. Draw the duodenum to the right, while applying a light counterpressure on the left part of the pancreas (Fig. 28.3).
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Stomach Reflected liver
Short gastric arteries Abdominal aorta
Cystic artery Inferior vena cava
Posterior gastric artery
Celiac trunk Common hepatic artery
Splenic artery
Gastroduodenal artery
Great pancreatic artery
Portal vein Superior posterior pancreaticoduodenal artery
Inferior pancreatic artery
Superior anterior pancreaticoduodenal artery
Dorsal pancreatic artery
Inferior pancreaticoduodenal artery Superior mesenteric artery Superior mesenteric vein
Fig. 28.2 Splenic artery.
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Fig. 28.3 Right lateral traction technique of the pancreas.
Pancreaticosplenic vessels
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Fig. 28.4 Transverse accordion technique of the pancreas.
28.2.2 Mechanical peculiarity of the spleen The spleen is a very mobile organ, and in the techniques described below must be firmly maintained to avoid it escaping our manipulations.
28.2.3 Transverse accordion technique This technique addresses the pancreas and the spleen at the same time (Fig. 28.4). It is worth noting that in traditional Chinese medicine the two organs are considered as one. This might be explained, in part, by their shared vascularization.
Position The patient is in decubitus, legs flexed, hands placed on the thorax. Position yourself to the right of the patient.
Technique Place your right palm against the lateral border of the second part of the duodenum, level with the sphincter of Oddi. The duodenum will serve to protect the pancreas. With your left hand, encompass the posterior
lateral surfaces of the left ribcage, ribs eight, nine, and ten. Place your thumb under the left costal margin to keep the spleen from slipping away during the manipulation. Depending on the size of your hand or the body of the patient, this may not be possible. In such a case simply clasp the abdominal costal junction with your left hand. Gradually approximate your hands to shorten the pancreas along its main axis. Then release your palms, allowing the organ to regain its original length gradually in viscoelasticity. Depending on the morphology of the patient, it is possible to perform the same technique by placing a fingerpad on the splenic artery. The pulse variations allow you to monitor the effectiveness of the maneuver.
Think in three dimensions It is important to ‘think’ in three dimensions. Nothing in the body is flat. Incorporating three dimensions brings finesse to the manipulations. Imagine the shape of the pancreas criss-crossed by its arteries, which initially shorten and eventually elongate. Allow some time between the compression– decompression cycles, so that the pancreatic
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The practice of visceral vascular manipulation tissues and arteries can store up some elastic force that will remain with them. Likewise, the mechanoreceptors will be able to stimulate their central receptors for a long time after the treatment. A sponge is the best image to keep in mind. Picture it longer than it is wide; shorten it and allow it gradually to regain its original form. The pancreas passes like a bridge over the lumbar spine, presenting a concavity posteriorly. Respect this concavity in your manipulation. Compress the pancreas transversely and then continue transversely, but in a more posterior direction.
Predominantly pancreatic version of the accordion technique In this version of the technique it is mainly the hand on the second part of the duodenum that exerts pressure. It is as if you wanted to bring the tube of the duodenum and the spleen together. The hand on the spleen serves essentially as a counterbalance. The success of this technique depends on practice and the finesse of your pressure. Bring the duodenum towards the pancreas by the intermediary of your right thumb. NB: This technique also affects the excretory ducts of the pancreas that run in the same transverse direction.
Predominantly splenic version of the accordion technique
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This maneuver involves not only the spleen, but also the organs that are anatomically and physiologically linked to it. In effect, the left kidney, the tail of the pancreas, the attachments of the splenic flexure, and the left triangular ligament are included in this maneuver. Experience shows that a problem with one of these structures always involves one or more of the others. This time the thumb on the duodenum will serve as the counterforce, and the left costal hand actively brings the ribs and the organs nearer to the duodenum.
With practice, you will clearly feel the differences in compression, especially possible fixations at the head and the tail of the pancreas. In a healthy subject in decubitus, it is difficult to distinguish the spleen from neighboring structures. By stacking up all the various tissues towards it, the spleen is not able to escape from under your fingers, which enables it to be manipulated.
28.2.4 Left lateral decubitus technique The patient is sidelying. Stand behind the patient. The protocol is the same as in the decubitus position. To focus on the spleen, bring the left 9th and 10th ribs in the direction of your duodenal thumb. To focus on the pancreas, bring the duodenal thumb towards the spleen (Fig. 28.5). The sidelying position allows you to appreciate the different visceral layers in the sagittal plane. Remember that the greater omentum, the stomach, and the small intestine all lie in front of the pancreas.
28.2.5 Cephalad to caudad technique This technique affects the arteries that course perpendicularly to the main longitudinal axis of the splenic and inferior pancreatic arteries (Fig. 28.6): • the anterior superior pancreaticoduodenal arteries • the posterior superior pancreaticoduodenal arteries • the dorsal pancreatic arteries • the great pancreatic arteries.
Position The patient is in decubitus, hands alongside the body with a pillow placed under the thoracolumbar region. Position yourself either behind the patient or to the side, to be able to stretch the superior border of the pancreas in a caudad direction.
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Fig. 28.5 Manipulation of the pancreatic arteries in left lateral decubitus position.
Fig. 28.6 Cephalad–caudad manipulation of the pancreatic arteries.
Technique For the left part, place your thumb against the most lateral portion of the transverse colon. For the right part, place your other thumb as cephalad as possible on the second part of the duodenum. Delicately direct your thumbs posteriorly to find the upper part of the pancreas. Using your thumbs, gently stretch the upper border
of the pancreas caudally. Maintain the stretch for about 20 s. This technique, of course, affects the transverse mesocolon, which is firmly attached to the pancreas. The difference in this version is that pressure is applied to the right side of the duodenum, whereas for the mesocolon technique the right hand contact is close to the hepatic flexure of the colon.
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The practice of visceral vascular manipulation NB: Remember that the techniques for the pancreas do not involve any posterior compression. Our action must always be exerted transversely or longitudinally.
28.2.6 Associated organs Other organs affected by these manipulations are the: • stomach • duodenum • kidneys: the renal arteries run perpendicular to the abdominal aorta and very close to the axis of the splenic artery.
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The accordion technique affects the renal arteries.
28.2.7 Indications The indications include: • digestive problems • allergies • asthma • psoriasis • faintness • postprandial fatigue • immune system deficiency • hyperhidrosis.
Vessels of the intestine
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29.1 ANATOMY
Hormonal control
29.1.1 Generalities
The more that is learned about the physiology of the small intestine, the more complex it appears to be. In addition to local autonomic nervous system control, hormones regulate the organ as it adapts to the workings of the digestive tract. For example, vasoactive intestinal peptide (VIP) releases the smooth muscles and increases circulation. Acetylcholine levels rise considerably in the circulating blood after eating.
Irrigation At rest, intestinal irrigation represents 27% of total body irrigation. This percentage is very important considering that the heart, for example, draws on only 3–4% of total blood flow.
Intrinsic innervation of the intestine The innervation of the intestine is monitored by local reflexes of the autonomic nervous system. About 100 million nerve fibers constantly inform the brain about the functioning of the small intestine. The vagus nerve innervates the digestive tract from the esophagus to halfway along the transverse colon. Beyond the halfway mark, the transverse colon is supplied by the sacral sympathetic nerves. We will refer to this part of the colon where the innervation changes, as the Cannon–Böhm zone. The vascular system itself is under the control of the sympathetic system.
Endogenous reflexes of the intestine Peristaltic reflexes are triggered by tension receptors, chemoregulators, and mechanoreceptors of the digestive tract. There are many pacemaker cells in the transverse colon, making the organ particularly interesting to manipulate (Fig. 29.1). ©
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Immune defense function Peyer’s patches provide local intestinal immune protection, as well as helping to defend the whole body. They secrete immunoglobulins A. In newborns, the mucosa of the digestive tube is protected by the immunoglobulins in the mother’s milk.
29.1.2 Vascular anatomy The vascularization of the small intestine and colon is derived from both the superior and the inferior mesenteric arteries. The change occurs beyond the duodenojejunal junction. We will begin with a description of these two arteries.
Superior mesenteric artery The superior mesenteric artery (Fig. 29.2) nestles against the medial surface of the duodenojejunal junction, at the level of L1. This
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Celiac ganglion and plexus Aorticorenal plexus Superior mesenteric ganglion Intermesenteric (aortic) plexus Middle colic plexus Superior mesenteric artery and plexus Mesenteric branches
Fig. 29.1A The enteric nervous system.
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Vessels of the intestine
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Subserous plexus Myenteric plexus Longitudinal muscle layer Circular muscle layer
Muscular
Submucosa Epithelium Connective tissue
Epithelium Lamina propria Muscularis mucosae
Serous
Mucosal
Submucosal plexus
Fig. 29.1B The enteric nervous system (longitudinal view).
Reflected liver Left gastric artery Proper hepatic artery Portal vein Gastroduodenal artery Right colic artery
Ileocolic artery
Splenic artery Abdominal aorta Left renal artery Superior mesenteric artery Jejunal arteries Ileal arteries
Posterior cecal artery Anterior cecal artery
Fig. 29.2 Superior mesenteric artery.
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Greater omentum Superior mesenteric artery
Transverse colon Right colic artery
Duodenum Descending colon Abdominal aorta
Inferior vena cava
Inferior mesenteric artery Left colic artery
Right common iliac artery Ileocolic artery
Sigmoid artery
Posterior cecal artery Anterior cecal artery
Aortic bifurcation Superior rectal artery Sigmoid colon
Fig. 29.3 Anastomoses of the superior and inferior mesenteric arteries.
junction projects on the mid-clavicular– umbilical line, about three fingerwidths above the umbilicus.
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Termination The superior mesenteric artery terminates by innumerable arterioles that irrigate the small intestine and colon. These arterioles often run perpendicular to the various parts of the small intestine and colon they perfuse.
Origin and course The superior mesenteric artery: • originates from the abdominal aorta opposite L1 • is about one vertebral body height lower than the celiac trunk • runs beneath the caudal border of the pancreas, where it is easily located • is situated higher and to the right of the inferior mesenteric artery • is more superficial than the inferior mesenteric artery, and thus easier to palpate.
Comments The superior and inferior mesenteric arteries anastomose with the middle colic and left colic arteries (Fig. 29.3). The first jejunal artery, branching from the superior mesenteric artery, anastomoses with the pancreaticoduodenal artery. This illustrates the vascular interdependence of these organs and shows that vascular manipulation of the pancreas engages the small intestine.
Collaterals The superior mesenteric artery gives off these branches: • middle colic • right colic • ileocolic • jejunal and ileal.
Aorta mesenteric clamp In certain cases, the superior mesenteric artery can clamp the left renal vein against the aorta and produce lumbago and lumbar sciatic pain more commonly on the left (Fig. 29.4). The left kidney can also be affected by constriction of the superior mesenteric artery. In addition to local pain, lymphatic venous
Vessels of the intestine
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Esophagus
Inferior vena cava
Renal vein
Aorta Inferior mesenteric artery
Superior mesenteric artery
Fig. 29.4 Aortic–mesenteric arterial tree.
problems can involve the urogenital system. When the compression is severe, surgery is indicated.
the left. It originates at the level of the third or fourth lumbar vertebra.
Inferior mesenteric artery
Course As the inferior mesenteric artery descends from the aorta, it makes a large curve to the left. It then runs caudally and to the right, ending at the anterior surface of the sacrum, at the level of the third sacral segment. It is covered by the peritoneum and rests in succession on the:
Origin The inferior mesenteric artery arises from the left anterolateral aspect of the aorta, often just above and to the left of the umbilicus. In relation to the superior mesenteric artery, it is smaller and is situated lower, deeper, and to
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The practice of visceral vascular manipulation • aorta • psoas muscle • common iliac artery. Collaterals The principal branches of the inferior mesenteric artery are the: • left colic artery, which by its ascendant branch anastomoses with the middle colic artery, a division of the superior mesenteric artery • sigmoid arteries • superior rectal arteries. Termination The inferior mesenteric artery terminates in numerous arterioles that irrigate the colon and rectum.
artery. It brings into play the jejunoileal arteries and the right quadrant of the colon. • The other maneuver focuses on the territories supplied by the more deeply situated inferior mesenteric artery: the left quadrant of the colon down to the junction with the sigmoid colon.
29.2.2 Superior mesenteric artery Position The patient is in decubitus, hands lying alongside the body with a fairly soft cushion placed under the thoracolumbar junction. Position yourself to the right of the patient.
Preliminary pulse taking
29.2 MANUAL APPROACH 29.2.1 Generalities Arterial irrigation of the jejunoileum Unlike the caudal part of the duodenum, the jejunum and ileum are both intraperitoneal. The loops of the jejunoileum are fixed to the body wall by a mesentery, measuring about 20 cm at its peritoneal root, and up to 4 m in length at its intestinal attachment. Beyond the duodenojejunal flexure the small intestine becomes intraperitoneal. The jejunum comprises two-fifths of the small intestine, and the ileum accounts for three-fifths. Remember that the muscle of Trietz, in addition to positional and suspensory roles, serves to protect the gastroesophageal junction, the celiac trunk, and the superior mesenteric artery.
Distinctive techniques
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Because of the anatomical arrangement of the mesenteric arteries, manipulation of the small intestine and the colon are considered separately: • One technique concerns the more superficially located superior mesenteric
Locate the duodenojejunal flexure about three fingerwidths above the umbilicus on the left mid-clavicular–umbilical line. Glide one flat finger along the medial border of the duodenojejunal junction until you feel the pulse of the superior mesenteric artery. This artery is smaller than your little finger. If you go too deep you will be on the wall of the aorta. This pulse will serve as a reference (Fig. 29.5).
Manipulations Bidigital technique Standing to the right of your patient, place your flat thumb where you feel the pulsation of the superior mesenteric artery. This will serve as a fixed point (Fig. 29.6). Place your other thumb at the ileocecal valve, located on the lateral third of the right umbilical–anterior superior iliac spine line. Direct your ileocecal thumb caudally and laterally, virtually drawing a convex line between your two thumbs. The idea is to create a curved line between your thumbs, rather than to stretch in a straight line. Maintain this convex stretch for about 20 s to irrigate the small intestine, and then evaluate the difference in the pulsations of the superior mesenteric artery.
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Fig. 29.5 Taking the superior mesenteric pulse.
Fig. 29.6 Bidigital manipulation of the superior mesenteric artery.
Fanning technique Again the left thumb serves as a fixed point. The fingers of the right hand spread like a fan, following the contour of the superior mesenteric artery (Fig. 29.7).
29.2.3 Right colic and ileocolic arteries To stretch the right colic and ileocolic arteries, manipulate the ascending colon, the cecum, and the hepatic flexure of the colon laterally to the right. This stretching can be done in decubitus or in left lateral decubitus.
Manipulation in decubitus The patient rests on their back, the arms alongside the body, with a soft cushion placed under the thoracolumbar region (Fig. 29.8). Place yourself to the right of the patient. Your fingers stretch the colon to the right, moving in sequence from the cecum towards the hepatic flexure of the colon. Perform a spreading–induction maneuver to open the medial and lateral sides of the colon. Do this several times, maintaining each stretch for about 20 s. You can also employ the fanning technique here.
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Fig. 29.7 Fanning manipulation of the superior mesenteric artery.
Fig. 29.8 Manipulation of the right colic arteries in decubitus.
Left lateral decubitus manipulation Position yourself to the right of the patient and lift the colon up towards you, beginning at the cecum and continuing along as far as the hepatic flexure (Fig. 29.9). At each segment, your fingers perform a stretch–induction maneuver, to open the circulation.
29.2.4 Arteries of the transverse colon 224
The transverse colon is intraperitoneal. Its location varies largely as a function of
digestion. It is highly placed when full, but found much lower in the abdomen when empty. Remember that the greater omentum hangs inferior from the greater curvature of the stomach, as part of the gastrocolic ligament that connects the transverse colon to the stomach. The variable position of the transverse colon leads us to focus our vascular manipulations near the hepatic and splenic flexures. Here, we can be certain not to make a mistake.
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Fig. 29.9 Manipulation of the right colic and ileocolic arteries in left lateral decubitus.
Marginal artery of the transverse colon This artery anastomoses with the middle colic artery, a branch of the superior mesenteric artery, and also with the ascending branch of the left colic artery, which stems from the inferior mesenteric artery. Position The patient is in decubitus, hands alongside the body, a soft cushion placed under the thoracolumbar junction. Position yourself either at their head or to one side (Fig. 29.10). Technique Place one thumb on the superomedial aspect of the right colic flexure and the other thumb on the superomedial part of the left colic flexure. In the first step, push the transverse colon caudally, attempting to spread your thumbs as far apart as possible. Maintain the stretch for about 20 s. In the second step, still spreading your thumbs, bring the transverse colon cephalad.
Fig. 29.10 Manipulation of the marginal artery of the transverse colon.
Cannon–Böhm zone This is a zone that particularly interests us, as it is the location of the anastomoses
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Liver
Splenic flexure of the colon
Cannon–Böhm zone Superior mesenteric artery Vagus nerve
Inferior mesenteric artery Sacral parasympathetic nerve
Fig. 29.11 Cannon–Böhm zone.
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between the superior and inferior mesenteric arteries. It is found midway between the mid-transverse colon and the left colic flexure (Fig. 29.11). In the Cannon–Böhm zone, the transverse colon is innervated by the vagus nerve, whereas beyond this interchange it is innervated by nerve fibers arising from the sacral parasympathetic nerves (S2, S3). In this region the left colic artery branch of the inferior mesenteric artery irrigates the left part of the transverse colon, and other
branches contribute to the descending colon and the rectosigmoid. To review: • The right half of the colon is innervated by the vagus nerve and irrigated by the superior mesenteric artery. • The left half of the colon is innervated by the sacral parasympathetic nerves and fed by the inferior mesenteric artery. This transition zone is a key area for neural and vascular manipulation of the intestines.
Vessels of the intestine Begin at the left flexure and migrate to the Cannon–Böhm area. At this place, you often find an area of the transverse colon that is firmer and denser, and also where the skin and subcutaneous tissues are thicker and more sensitive. Grasp the top and underside of the tube and carry out a compression–induction technique, stretching the tube longitudinally, focusing on the dense zone until cutaneous sensitivity is reduced and the wall of the transverse colon softens.
Next, your fingers stretch the small intestine to the left, away from the main trunk of the superior mesenteric artery. Starting from the origin of the superior mesenteric artery just medial to the duodenojejunal flexure, mobilize the loops of the small intestine to the left, progressing gradually until you reach the ileocecal valve. It is important to keep the stretch component.
29.2.5 Jejunal and ileal arteries
The patient lies on their left side. Your fingers bring the loops of the small intestine towards the right, and at the end of the stretching movement draw the loops anteriorly, as if to disengage them from back to front (Fig. 29.13). Stretch the loops of the small intestine generously and without pain; maintain the lift–induction for 20 s. Repeat the maneuver several times to ensure that no part of the small intestine is left out. This is an essential, indispensable, and pre-eminent technique to employ following laparotomy. NB: Remember to check the pulse of the superior mesenteric artery after the treatment. Normally the pulse should be strong and generous.
The superior mesenteric artery follows an oblique line, between the duodenojejunal flexure and the ileocecal valve.
Manipulation in decubitus The patient’s arms lie alongside the body, a soft cushion under to the thoracolumbar junction. Stand to the right of the patient (Fig. 29.12). Place the sides of your thumbs along the mesenteric artery. In step one, your fingers bring all the loops of the small intestine from left to right, with the goal of sinking gradually deeper with your thumbs, without causing pain.
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Manipulation in lateral decubitus
Fig. 29.12 Manipulation of the jejunal and ileal arteries in decubitus.
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Fig. 29.13 Manipulation of the jejunal and ileal arteries in lateral decubitus.
Fig. 29.14 Taking the inferior mesenteric pulse.
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29.2.6 Inferior mesenteric artery
Manipulation in decubitus
Preliminary pulse-taking
The subject is in decubitus, arms alongside the body, with a soft cushion under the lumbar region. Position yourself to the right of the patient (Fig. 29.15). The left thumb is placed on the origin of the inferior mesenteric artery with the fingers of the other hand above the symphysis pubis, very slightly to the left of the median line. The caudal fingers are located on the rectosigmoid
Due of its depth, the inferior mesenteric artery pulse is difficult to take. It can be felt two to three fingerwidths below and to the left of the origin of the superior mesenteric artery. Whereas the superior mesenteric artery is in front of the aorta, the inferior mesenteric artery is lateral to the aorta (Fig. 29.14).
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Fig. 29.15 Manipulation of the inferior mesenteric artery in decubitus.
Fig. 29.16 Manipulation of the inferior mesenteric artery in lateral decubitus.
junction. Anchor the inferior mesenteric artery with your thumb and push the recto sigmoid junction in a posterior direction. Either maintain this distal push–induction maneuver for 20 s, or separate your fingers like a fan and maintain the stretch for 20 s.
descending colon and sigmoid colon, and bring the tubes towards you, in lift–induction to increase the vascularization of the left colon. When you reach the rectosigmoid junction, stretch the sigmoid in an almost purely caudal direction.
Manipulation in lateral decubitus
29.2.7 Sigmoid vessels
The patient is in right sidelying; you are behind them (Fig. 29.16). Mobilize your fingers, migrating gradually along the
The sigmoid region can be affected by stasis, commonly in relation to hepaticocolic and genital problems.
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Fig. 29.17 Fanning technique for the sigmoid arteries.
When the liver is overworked, hemorrhoids are a frequent complaint. Apart from local discomfort, hemorrhoids have an undeniable effect on the urogenital region. In women, pelvic venous congestion can be a factor in uterine malposition and associated functional disturbances. The urogenital system is supported not only by ligaments and fascias, but also by a rich venous plexus (of Santorini). Lymphatic and venous rectal congestion contributes to absent or reduced mobility of the urogenital system. In men, the prostate suffers the most from venous disturbances and, more rarely, so does the erectile system.
Fanning technique for the sigmoid arteries The patient is in decubitus, and you are on their right (Fig. 29.17). Place the pads of your fingers on the medial sigmoid. First spread your fingers to fan out the whole sigmoid and
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then push the tube of the sigmoid colon in the direction of the iliac crest.
Advice In the case of venous problems, ask the patient to avoid pepper, mustard, peppers, cooked fats, strong sauces, and aspirin, antiinflammatory, antianxiety, and antidepressant medications.
29.2.8 Indications The indications are as follows: • postabdominal pelvic surgery • irritable bowel syndrome • constipation • chronic muscular contracture • Crohn’s disease • fibromyalgia, spasmophilia • pancreatic dysfunction • muscular cramps • postpartum constipation • bladder ptosis • pelvic lymphatic venous congestion.
SECTION 4 UROGENITAL VESSELS
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Renal vessels
30.1 ANATOMY
Method
30.1.1 Renal arteries
Your cephalad hand contacts the paraverte bral mass opposite the renal area, in the neighborhood of the 12th rib, and maintains a posteroanterior pressure throughout the duration of the search (Fig. 30.2). Place three or four fingers of your caudal hand juxta posed to the lateral border of the rectus abdominis muscle, slightly above the umbili cus. Slowly progress towards the anterior surface of the lumbar wall, first in a purely sagittal direction and then slightly oblique and medial, until you meet the anterior lateral surface of the psoas muscle. Glide your fingers longitudinally along the psoas, looking for an arterial pulse, perpen dicular to the main axis of the psoas. As a rule you will capture this pulsation under one fingerpad only. Stay sufficiently lateral to the abdominal aorta. You will feel a distinct pulse, almost perpendicular to the aortic axis. Oriented pos terior and lateral to the psoas, the artery is of a significant caliber. It is obviously larger than the pancreaticoduodenal branches of the celiac trunk and the middle colic artery accompanying the transverse colon. Palpation of the renal artery clearly illus trates the phenomenon referred to as principle of the concealing pulse. In this particular region, the hand is easily ‘dazzled’ by the pulsations of the larger vessels. Typically the biggest
The direction of the renal arteries is essen tially perpendicular to the aorta (Fig. 30.1). Due to their retroperitoneal location, these arteries are the most problematic to mobilize. The right renal artery arises from the abdominal aorta at the level of L1. The left shorter renal artery originates slightly higher up. The vessels branch laterally from the aorta, just below the origin of the superior mesenteric artery.
30.1.2 Renal vein The left renal vein is three times longer than the right, and somewhat curved. The left suprarenal, ovarian, and testicular veins all enter the left renal vein. The renal vascular system is innervated by the renal plexus, which lies very near the celiac plexus.
30.2 MANUAL APPROACH 30.2.1 Renal artery pulse Position The subject is in decubitus. Place yourself on the side of the renal artery in question. ©
2011 Elsevier Ltd
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Right inferior phrenic vein Hepatic veins Inferior vena cava
Esophagus Diaphragm Left gastric artery
Celiac trunk Right kidney Superior mesenteric artery Abdominal aorta Ovarian artery and vein Ureter Common iliac artery External iliac artery and vein
Inferior phrenic artery Left renal artery Left renal vein Left kidney Duodenum Inferior mesenteric artery Median sacral artery Internal iliac artery and vein
Fig. 30.1 Renal arteries.
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Fig. 30.2 Palpation of the renal artery.
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pulse can be felt clearly, even when it lies deep to the more slender ones.
Right–left differences Relatively speaking, the right renal artery pulse seems a little easier to perceive than the left. On the right, the renal artery is located behind the second part of the tube of the duodenum, whereas on the left it lies above and slightly lateral to the duodenojejunal junction, making it particularly difficult to feel in heavier set subjects. In cases of severe kidney ptosis, especially right ptosis, you can sometimes pick up the artery near the umbilicus. In this case it is certainly easier to feel.
Palpation limit Palpating the renal artery has taken us a good deal of time, perseverance, and patience in return for rather inconsistent results. Even today, with as many patients as we have seen, it is not always possible to be absolutely sure of our palpation. Nevertheless, in certain circumstances the pulse is relatively easy to feel and has enabled us to standardize our approach. These are: • thinness • hypotonic abdominal muscles (postpartum, old age) • diastases recti abdominis. By contrast, plumpness, abdominal fat, obes ity, and hypertonic abdominal musculature are all unfavorable to this approach.
30.2.2 Manipulation of the renal arteries in seated posture Our goal is to try to separate the kidneys transversely to have a stretching effect on the renal arteries. This stretch involves several other arteries, such as the mesenteric, splenic, pancreatic, etc. Right renal artery As the right renal artery is somewhat bound to the liver, it is via the liver as intermediary that we stretch it.
Fig. 30.3 Global manipulation of the right renal artery.
Place your fingers three fingerwidths below the right costal margin (Fig. 30.3). Direct them initially posteriorly and then cephalad. Next, draw the liver laterally, while maintain ing a cephalad traction. With this technique, you have an effect on the hepatic and duodenal arteries, as well as innumerable small nerve fibers that make up the celiac and renal plexuses. Left renal artery Place your fingers below the duodenojejunal junction. Direct them first deeply posterior and then exert a cephalad traction. At the end of the cephalad traction, stretch the entire gastric, omental, enteric, and pan creatic ensemble laterally. As with the right kidney, this is not a specific technique. Main tain traction of this viscerovascular group for about 20 s. It is difficult to prove the effect on the renal arteries, which are not directly palpable.
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Fig. 30.4 Manipulation of the renal artery.
However, before carrying out these maneu vers, take the arterial pressure of the patient in both arms. It is frequently possible to remedy a difference in blood pressure, and to lower elevated tension.
Manipulation in decubitus The patient lies on their back. Position your self to the side of the renal artery in question (Fig. 30.4). Place the index and middle finger of both hands on either side of the location where you have palpated the renal pulse. Place your
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thumbs on the posterior lateral part of the ribs and on the lumbar wall. Manipulation of the renal artery is done with two hands. Draw your fingers towards your thumbs in an obliquely posterolateral direction. Gently take the renal hilum later ally and posteriorly, distancing it gradually and progressively from the aorta in a stretching–Listening of the renal artery. Repeat a few times to be sure that you have indeed mobilized the kidney. Once the elas ticity of the renal artery seems satisfactory, maintain the stretch for 20–30 s in order to irrigate the organ.
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Iliac vessels
31.1 ANATOMY
31.1.3 Internal iliac artery
The aorta divides into the median sacral artery and the two common iliac arteries, to the left side of L4 and L5 intervertebral disc.
Course
31.1.1 Median sacral artery The median sacral artery is posterior to the iliac vessels and descends over the sacral promontory. It is difficult to palpate, and it is not of great interest to us.
31.1.2 Common iliac artery Course From the L4 and L5 intervertebral discs, the common iliac arteries diverge as they descend to divide at the sacroiliac joints. These arteries are about 5–6 cm in length (Fig. 31.1).
Noteworthy relationships The ureter crosses the common iliac arteries like an X. These small tubes are covered with peritoneum and run along the medial border of the psoas. The common iliac arteries diverge at an angle of 65° in men, and 75° in women, whose pelvis is wider.
Terminals The common iliac arteries divide into the internal and external iliac arteries. ©
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Formerly called the hypogastric artery, the internal iliac artery (Fig. 31.2) separates from the common iliac artery at the sacroiliac junction and descends posteriorly towards the greater sciatic foramen.
Pelvic collaterals At the greater sciatic foramen the internal iliac artery gives off about ten branches. We have selected the most important among them. They can be divided into two groups: • parietal branches for the walls of the lesser pelvis • visceral branches for the pelvic organs. Parietal branches Parietal branches are divided in accordance with their function. • The iliolumbar artery often sends a small spinal branch to penetrate the intervertebral foramen, between the fifth lumbar and first sacral vertebrae. • The lateral sacral artery supplies branches to the cauda equina and smaller vessels that penetrate the vertebral canal. • The obturator artery passes out of the pelvis through the obturator canal. Of special note is the acetabular branch, which enters the hip joint at the acetabular notch and sends a branch
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Aorta
Renal vein
Renal artery
Inferior vena cava
Ureter
Common iliac artery
Median sacral artery Internal iliac artery
External iliac artery External iliac vein Bladder
Fig. 31.1 Common iliac arteries.
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along the ligament of the femoral head. • The inferior gluteal artery runs in the buttock between the piriformis and adjacent muscles. Together with the comitans artery of the sciatic nerve, the inferior gluteal branch supplies the vascularization of the sciatic nerve.
Visceral branches • Uterine artery • Internal pudendal artery • Inferior vesical artery • Middle rectal artery • Vaginal artery
NB: Osteopaths are now well aware that the fascial mechanics of the lesser pelvis affect coxofemoral articulations. They cannot obscure the pelvic vascular connections, particularly the pelvic arteries that nourish the femoral head.
31.2.1 Common iliac artery
31.2 MANUAL APPROACH Palpation First way to locate the artery Begin at the abdominal aorta below the umbilicus (Fig. 31.3). Move inferiorly and,
Iliac vessels
Inferior vena cava
Right renal vein
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Aorta
Left renal artery Ureter
Common iliac artery Iliolumbar artery Superior gluteal artery Middle rectal artery External iliac vein
Median sacral artery Internal iliac artery
Uterine artery
Bladder Superior vesical arteries
Fig. 31.2 Internal iliac artery.
when you no longer feel its pulse, direct your fingers laterally at a 65–75° angle. The new pulse you feel will be the beat of the common iliac arteries. Second way to locate the artery Place your thumbs midway along the puboumbilical line (Fig. 31.4). Direct your thumbs cephalad. You will feel the aortic pulse and, from there, orient your thumbs laterally to feel the common iliac arteries.
Manipulation Position The patient is in decubitus, with a soft pillow placed beneath the lumbar spine, hands
resting on the chest. Stand near to the patient’s pelvis (Fig. 31.5).
Technique Identify the pulse of the abdominal aorta by palpating it above the umbilicus. Move your fingers caudally until the pulse disappears, and you will find yourself at the level where the aorta bifurcates into the common iliac arteries. Place one thumb beneath the umbilicus at the bifurcation, and the other thumb on the iliac vessel. Draw your distal thumb in a caudal and lateral direction to stretch the artery following induction. Recall that we
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The practice of visceral vascular manipulation stretch all the large arteries to restore the elasticity they require. NB: Even when checking the common iliac arterial pulses beforehand, it is not easy to feel the difference after manipulation, except
where a major initial disparity exists between the two arteries. Indications The indications for manipulation are the following: • urogenital dysfunctions • pelvic congestion • vascular problems in the lower extremity • coxarthrosis (hip arthritis) • lumbosacralgia. Precautions Check for the presence of the femoral pulse. Its absence can signify an aortic aneurysm. A difference in strength may be a sign of an obstruction along the arterial course (adhesions, tumors, calcification) or of autonomic disorders, which commonly have repercussions at the lower extremities.
31.2.2 Internal iliac artery Palpation
Fig. 31.3 Palpation of the common iliac arteries (first way to locate artery).
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The internal iliac artery pulse is not very easy to find, especially in heavier patients. Its cephalad part is more perceptible. Three fingerwidths below the aortic bifurcation and the common iliac artery, direct your fingers medially and caudally. At its cephalad part, the artery lies against the sacral promontory, which renders it relatively superficial.
Fig. 31.4 Palpation of the common iliac arteries (second way to locate artery).
Iliac vessels
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Fig. 31.5 Manipulation of the common iliac artery.
Fig. 31.6 Manipulation of the internal iliac artery in decubitus.
Manipulation Manipulation in decubitus The patient has a pillow supporting the lumbar spine, with both hands resting on the thorax. Position yourself next to the patient’s pelvis (Fig. 31.6). Starting at the common iliac artery, glide your fingers along the internal iliac artery, searching for fibrous or adhered tissues.
This is really a perivascular technique to release the soft tissue around the artery and veins. Manipulation in lateral decubitus This position allows easier digital penetration. Perform the same technique as above, first on one side then on the other. Begin midway along the umbilical–anterior superior iliac spine (ASIS) line.
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Uterine vessels
32.1 ANATOMY 32.1.1 Uterine artery Course The uterine artery (Fig. 32.1) arises from the internal iliac artery and travels caudally and anteriorly to reach the uterus a little above the uterine cervical junction. It ascends the border of the uterus, where its branches anastomose with the ovarian artery. The twists and turns of the uterine vessels allow them to adapt to manifold uterine movements. Keep in mind the following: • Just beyond its origin, the artery crosses the ureter anteriorly. • Along its caudal journey, the uterine artery rests on the aponeurosis of the obturator internus. • Just before reaching the isthmus, it is in line with the base of the broad ligament.
Collaterals Among the numerous arterioles arising from the uterine artery, we cite branches for the: • ureter • vagina • ovary • uterine tube.
Terminal branches
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Near the cephalad part of the uterus, the uterine artery anastomoses with the ovarian artery, which descends from the abdominal aorta. ©
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32.2 MANIPULATION OF THE UTERINE ARTERY 32.2.1 Manipulation in lateral decubitus Position A bilateral technique, the patient is in either left or right lateral decubitus, legs slightly flexed. Position yourself behind the patient (Fig. 32.2).
Technique Glide the fingers of both hands along the iliac fascia in the direction of the pubic symphysis. Try to sink as deeply and posteriorly as possible before gliding in the direction of the symphysis. Once you feel the body of the uterus, first stretch it cephalad and then medially. The uterine arteries run along a cephalocaudal longitudinal main axis, but also divide into innumerable arterioles that run perpendicular to its main axis. To stretch the small ramifications, glide the uterus bilaterally. Repeat on the other side.
32.2.2 Manipulation in decubitus Position The patient has a soft pillow under the lumbar region, with both hands resting on the belly, legs flexed (see Fig. 32.3). Position yourself to the side of the patient, with your hands against the medial aspect of the iliac bone.
Uterine vessels
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Ovarian artery and vein Ureter Common iliac artery
Common iliac vein
Internal iliac artery Internal iliac vein
Uterine artery
Uterine vein Ovary
Uterine tube
Uterus (retracted)
Fig. 32.1 Uterine artery.
Fig. 32.2 Manipulation of the uterine artery in lateral decubitus.
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Fig. 32.3 Manipulation of the uterine artery in decubitus.
Technique Following the same principle as in decubitus, endeavor to go posterior first, then medially and finally caudad. Surround the vesicouterine unit with both hands and draw it cephalad several times. Maintain the traction for about 20 s and follow the Listening with induction. Some patients feel an immediate benefit from this manipulation. ‘It is as if a weight has been lifted from my belly,’ they tell us.
32.2.3 Lifting irrigation of the uterus In the two preceding approaches, you can complete the manipulations by lifting the uterus and maintaining the lift for about 20 s, all the while following in induction. As the uterine artery is tortuous and winding, it is appropriate to treat it with the accordion technique, as employed with the pancreas. First bring in the element of compression by drawing the uterus in a caudad direction. Release and continue by lifting the uterus cephalad in induction.
32.2.4 Vesicouterine venous system 242
The uterus is vulnerable to congestion problems involving the lymphatic and venous
systems. The vesicouterine adnexa is surrounded by a rich venous plexus. For example, the venous plexus of Santorini plays an important role in bladder continence. Many women have pelvic varicosities involving pelvic and lower extremity problems. To have an effect on the venous system, stretch the vesicouterine unit superiorly and posteriorly several times. This movement is beneficial for arterial, venous, and lymphatic circulation. We advise our patients to place two feet on the wall with a large pillow supporting their buttocks, and to bring the soft tissues of the pelvis cephalad, beginning at the pubic symphysis. The technique is effective when performed for 2–3 min once a day. This maneuver is very effective for the small intestines, which play a considerable role in visceral pelvic mechanics.
32.3 PRECAUTIONS AND CONTRAINDICATIONS Most women are in the habit of visiting their physician or gynecologist regularly. They often come to us with pelvic pains or because of infertility. Regular medical checkups notwithstanding, one must always be vigilant and never hesitate to refer a woman back to her physician. The following symptoms demand caution.
Uterine vessels
32.3.1 Dysmenorrhea In women with sudden onset dysmenorrhea, consider: • • • •
genital infection endometriosis cervicouterine malposition benign or malignant tumor.
In young women, premenstrual pains are often due to spasm of uterine muscle fibers, owing to hormonal hyperstimulation. However, consider falls on the sacrum or coccyx as causative factors.
32.3.2 Secondary amenorrhea If amenorrhea occurs in a patient who normally has regular periods, always think first of pregnancy. Vascular techniques are contraindicated in pregnancy. During implantation the region requires ‘tranquility.’ Imagine if a woman were to miscarry in the days following treatment – you may well be held responsible. Although this has never happened, even in our long experience, it is necessary to observe this caution. Other possible causes of secondary amenorrhea are: • • • • • •
menopause rapid weight loss obesity endocrine disorders ovarian tumor psychoemotional problems.
32.3.3 Hemorrhages Until they are fully understood, diagnosed, or explained, hemorrhages are formally contraindicated for manipulations. Apart from occurring as pregnancy complications, other possible causes of hemorrhage are: • • • • •
fibroma endometriosis uterine polyps cervical cancer hormonal insufficiency.
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The following are strong contraindications: • undiagnosed pelvic mass • sharp pains on pelvic palpation • sudden amenorrhea • inguinal lymph ganglia coupled with edema of the lower extremities.
32.4 INDICATIONS The indications for uterine vessel manipulation are: • premenstrual syndrome • dysmenorrhea • pelvic varicosities • venous deficiency of the lower extremities • infertility • lumbago • sciatica (often worse on the left) • femoral neuralgia (cruralgia).
32.4.1 Premenstrual syndrome Many causes are attributable to premenstrual syndrome. Often commonplace functional problems manifest due to rapid hormonal change. When the pain is located throughout the pelvis and drags on into the start of the menses, consider autonomic problems. These dysfunctions are difficult to solve. These women often suffer headache, hepatobiliary sensitivity, and allergies, as well as outbreaks of herpes and eczema. With endometriosis, pain is more common between periods of menstruation. This is often called intermenstrual pain. The uterosacral ligament can become sensitive and fibrotic, causing sacral fixation. With endometriosis, usually the left uterosacral ligament is the most sensitive and fibrotic. In men Common prostate symptoms are: • dysuria (difficult urination and weak stream) • delayed urination • nocturnal urinary frequency • polyuria.
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The practice of visceral vascular manipulation The contraindications to manipulation are the following: • urethral discharge • hematuria • hemospermia • pelvic mass on palpation.
32.5 COMMON VENOUS COMPLAINTS Venous problems are common and mostly concern women. Pregnancy, childbirth, and hormonal circulatory influences are the main causes. We have noticed that varicosities of the lower extremities often accompany pelvic varicosities. Pelvic varicosities are not a contraindication to manipulation – quite the reverse. Nevertheless, be careful with patients who have had superficial venous thrombosis (periphlebitis) and deep venous thrombosis (phlebitis) that are characterized by the following:
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• Periphlebitis: – warm, painful, raised and hardened veins – mild perivenous edema – mild temperature • Phlebitis (the signs are more distinct): – rapid pulse – shivers – mild fever – tingling and cramping in the calf – edema in the lower extremity – cruralgia-type pain – generally altered state. Pulmonary embolism is the main risk of phlebitis. Several patients have consulted us for so-called mechanical thoracic pain, which turned out to be atypical pulmonary infarction. These patients complained of worrisome thoracic pain, in combination with difficulty in breathing when lying down. We are wary of this type of pain, especially when it occurs after surgery.
Ovarian vessels
33.1 ANATOMY The ovaries are irrigated by: • the ovarian arteries arising from the abdominal aorta • the ovarian branch of the uterine artery (Fig. 33.1). The left ovarian vein drains directly into the left renal vein, whereas the right ovarian vein drains into the inferior vena cava. When treating the ovary it is imperative to include manipulation of the left kidney, along with viscerovascular manipulation. Originating just below the renal arteries, the ovarian arteries descend along the psoas in an oblique lateral and caudal direction. They first cross the ureter just above the aortic bifurcation, and again in front of the sacral promontory.
33.2 MANUAL APPROACH The patient is in decubitus, legs extended, hands crossed over the stomach. Position yourself to the side (Fig. 33.2).
33.2.1 Technique Place one thumb on the abdominal aorta, slightly above the umbilicus, to serve as a counterbalance. Position the other thumb where the ureter crosses the common iliac artery at the level of the sacral promontory. This is on an imaginary line joining the ©
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anterior superior iliac crests. Softly direct the thumb deeply; you will clearly feel the firmness of the ureter. Bring the thumb caudally and medially, carrying out several transverse glide–induction maneuvers. To include the venous and lymphatic systems, stretch the thumb cephalad and slightly laterally. NB: This technique is meant to have both a vascular and a ureteral effect. However, it is here where kidney stones are found. Any precise, sharp pain demands that you lighten your pressure, discontinuing the manipulation if pain persists. This technique also serves the inferior mesenteric artery.
33.2.2 Ovarian branch of the uterine artery Carry out the uterine artery technique as described in Chapter 32. Stretch the uterus and the bladder cephalad, and at the end of the movement move the uterus in a lateral direction and then return to midline. The desired effect is one of unpleating the arteries. The ovarian vascular system is extremely sinuous, allowing the ovary exceptional mobility.
33.2.3 Left renal and ovarian veins The left renal vein is longer and more curved than the right. It receives the following veins:
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The practice of visceral vascular manipulation
Inferior vena cava Right kidney Superior mesenteric artery
Abdominal aorta Ureter
Left kidney Renal artery Renal vein
Inferior mesenteric artery Ovarian artery and vein
Common iliac artery
External iliac artery and vein
Internal iliac artery and vein
Ovary Uterus (reflected)
Uterine tube
Fig. 33.1 The ovarian vessels.
Fig. 33.2 Manipulation of the ovarian artery.
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suprarenal, spermatic, and left ovarian. This basic anatomical data has implications for all urogenital manipulations. The left kidney goes hand in hand with the genital system, whereas the right spermatic and ovarian
veins drain directly into the inferior vena cava. It is difficult to conceive of any effective genital manipulation without including the left kidney, and vice versa.
Internal pudendal artery
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34.1 ANATOMY
34.1.3 Terminal branches
At its origin in the pelvis, the internal pudendal artery (Fig. 34.1) crosses anterior to the piriformis and the sacral plexus. It leaves the pelvis by the inferior rim of the greater sciatic foramen below the piriformis. It then curves around the lateral surface of the ischial spine to enter the perineum by the lesser sciatic foramen. The pudendal artery accompanies the obturator internus muscle contained between it and its aponeurosis, to fix on the medial surface of the ischium. Finally it runs forward towards the genital organ. The artery can serve to locate the pudendal nerve, when this nerve is slender and difficult to palpate.
The terminal branches of the internal pudendal artery are: • the artery of the vestibular bulb or the bulb of the penis • the deep clitoral artery or deep artery of the penis.
34.2 MANUAL APPROACH 34.2.1 Indications Pudendal nerve neuralgia
Those who care for patients with pudendal nerve neuralgia are well aware of Alcock’s canal (in earlier times, the pudendal canal) (Fig. 34.2). It is configured by the aponeurosis of the obturator internus muscle. It contains the pudendal nerves and vessels. Any fibrosis or adhesion of this aponeurosis has deleterious consequences for the pudendal vascular and nervous systems.
Pudendal neuralgia is excruciating. Its etiology is poorly understood. Having seen many patients with this type of pain, we have been able to determine a few causative factors: • Falls on the coccyx: chronic coccidynia is usually due to the pudendal nerve. It takes hold a long time after the fall • After episiotomy, in cases where the pudendal nerve was affected • Dystocia (difficult labor) • Suction or forceps delivery, without regard to the phases of contraction • Epidural anesthesia • Following pelvic or lower extremity fracture • Following urogenital surgery.
34.1.2 Collaterals
At the vascular level
Many arterioles joining the rectum, prostate and bladder arise from the internal pudendal artery. Also given off are the: • inferior rectal artery • the superficial and deep perineal arteries.
The pudendal artery accompanies the pudendal nerve, and its pulsations can serve as a landmark for locating it. Pudendal artery manipulation can help genital vascularization as a whole.
34.1.1 Alcock’s canal
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The practice of visceral vascular manipulation
Internal iliac artery
Internal pudendal artery
Piriformis muscle Inguinal ligament
Iliococcygeus muscle
Internal obturator muscle
Sacrospinous ligament Pudendal nerve Inferior rectal artery
Levator ani muscle
Sacrotuberous ligament
Fig. 34.1 Internal pudendal artery.
Effects of manipulation
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• In women. The pudendal artery gives off numerous branches to the clitoris, labia majora, rectum, and the perineum in general. Thus the entire genital sphere benefits from its treatment. • In men. The perineum, scrotum, rectum, bulbospongiosus muscle, prostate, spongiosum, and the corpora cavernosa of the penis can benefit from the improved circulation provided by this technique. In any case, when there are urogenital problems, it is seldom possible to isolate any one area. The whole of the urogenital system, as well as the kidneys, must be considered. This includes osteoarticular fixations of the lumbar spine, sacrum, and coccyx.
34.2.2 Manipulation of the internal pudendal artery This artery is of great interest in and of itself, as well as in helping to locate the pudendal nerve, an important factor in the intolerable Alcock syndrome.
Position The patient is in decubitus, hands on thorax, the leg of the treatment side flexed and somewhat spread. Facing the patient, position yourself on the side of the artery in question (Figs 34.3 & 34.4).
Technique Place your fingers against the medial aspect of the ischial tuberosity.
34 Common iliac artery
Internal iliac artery
Common iliac vein
Iliolumbar artery Lateral sacral artery
External iliac artery
Superior gluteal artery
External iliac vein
Piriformis muscle
Obturator artery
Inferior gluteal artery Iliococcygeus muscle
Obturator muscle
Sacrotuberous ligament
Symphysis pubis
Internal pudendal artery Pudendal canal (Alcock’s)
Fig. 34.2 Alcock’s canal.
Vestibule of vagina Ischiocavernosus muscle Superficial perineal fascia
Central perineal tendon
Perineal artery
Superficial transverse perineal muscle
Perineal nerve
Internal pudendal artery and vein
Obturator fascia
Pudendal nerve
Pudendal canal (Alcock’s)
Inferior rectal nerve
Inferior rectal artery
Levator ani muscle
Inferior fascia of pelvic diaphragm
External anal sphincter muscle
Anus Anococcygeal ligament
249 Fig. 34.3 Landmarks for manipulation of the internal pudendal artery.
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Fig. 34.4 Manipulation of the internal pudendal artery.
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Glide along the ischial pubic ramus towards the inferior pubic ramus, as far as the attachment of the superficial transverse perineal muscle. Your fingers must stay in contact with the inferior pubic ramus. You will feel the pudendal artery when you leave the ischial tuberosity and migrate towards the pubis. Your fingers are about midway between the pubic crest and the ischial tuberosity. The pudendal artery is accompanied by the pudendal nerve and vein. Perform a glide– induction along the artery. This maneuver has a central stimulation effect, thanks to the artery’s intrinsic nervous system. This technique also works on the pudendal nerve. What’s more, the neurovascular bundle is surrounded by the fascia of the obturator internus muscle, and any fibrosis of this fascia can compress the nerve. When you feel that the soft tissues under the inferior pubic ramus are irregular and fibrotic, treat them first before attempting the glide– induction of the artery and nerve. Always be soft with your hands: the pudendal nerve is very sensitive and has an exceptional nociceptive memory.
The inguinal canal
35.1 ANATOMY We have studied the inguinal canal (Fig. 35.1) for the manipulation of the peripheral nerves (Barral & Croibier 2004). Contained within the canal are the iliohypogastric, ilioinguinal, and genitofemoral nerves. Superficial to the canal is the external pudendal artery, arising medially from the femoral artery to enter the saphenous hiatus. In the inguinal fold, above the superficial inguinal canal, the anterior cutaneous branch of the iliohypogastric nerve appears. Caudally and laterally one finds the ilioinguinal nerve, which joins either the round ligament of the uterus or the spermatic cord, accompanied by a small artery. NB: Although it is fairly easy to penetrate a finger in the male inguinal canal, this is next to impossible in the case of a woman. These techniques apply to men, for the most part. In any case, it seems the effect is greater on the intrainguinal nervous system than on the vascular system.
35.2 MANUAL APPROACH 35.2.1 Position The patient is in decubitus, the leg on the inguinal canal side extended, the other one
35
flexed. Place yourself to one side, facing the patient (Fig. 35.2).
35.2.2 Technique Place one thumb just to the side of the pubic spine and direct it laterally and cephalad to push into the inguinal canal. At the same time, the free hand brings the skin and external oblique, internal oblique, and transversus abdominis muscles to bear against the thumb in the canal. With experience, and thanks to their pulsations, it is possible to distinguish the testicular artery, arising directly from the aorta, and the artery of the round ligament from the nerves that accompany them. The maneuver consists of glide–induction and small cephalocaudad stretches, carried out with the thumb.
35.2.3 Precautions and contraindications The precautions and contraindications are the following: • colored urine or urinary infection • painful pelvic heaviness coupled with burning urination • pelvic pain radiating to the lumbar fossa • the presence of inguinal ganglia.
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The practice of visceral vascular manipulation
External oblique muscle
Inguinal ligament
Iliohypogastric nerve
Superficial epigastric artery
Deep inguinal ring
Superficial circumflex iliac artery
Superficial inguinal ring
Superficial external pudendal artery
Spermatic cord Femoral artery
Ilioinguinal nerve Genital branch of genitofemoral nerve
Fig. 35.1 Inguinal canal.
Fig. 35.2 Inguinal manipulation.
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Conclusion
We are first and foremost therapists, who work everyday in the field. There may be tens of thousands of techniques to apply to an organism, and new ones all the time. Even if one mastered them all, it is more important to ‘have soul’ in order fully to grasp osteopathic or manual therapy concepts and philosophies. The hand gives information to the head, and then the head returns information to the hand. In this way, we pass from the technique to the art, and this makes a world of difference.
For any osteopath or manual therapist to be a specialist is nonsense. In all the Listening techniques, it is the body that expresses its tensions, and you can be sure it does not specialize! All tissues deserve our attention. It is for us to understand them, and help them. Osteopathy and manual therapy are disciplines of generalists, whose foundation is anatomy. Their motto could be: the hands at the service of anatomy. Let us try to keep this spirit.
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Glossary
Adson–Wright test evaluation of the radial pulse while moving the arm in abduction and external rotation (arm and forearm in the chandelier position). The test is deemed positive if the radial pulse diminishes or obliterates. This can be due to an osseous callus on the clavicle or rib, a redundant rib, bony outgrowth, an anterior scalene muscle insertion problem, fibrosis of the pleurocervical ligaments, or a pulmonary apex tumor. Adventitia the outermost layer of a blood vessel wall, made up of connective tissue and smooth muscle fibers. Alcock’s canal a canal containing the pudendal vessels (once called the internal shame vessels). This passage is formed from the obturator internus aponeurosis, located along the inferior pubic ramus, where it is palpable externally. Aneurysm a localized dilation of the blood vessel wall. Aneurysms may fissure or rupture. A dissecting aneurysm occurs as a result of degeneration of the artery wall, creating a tear in the intima.
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Angina the word derives from the Greek ‘strangling.’ A condition marked by severe constrictive pain in the chest and often spreading to the left arm and jaw. The patient experiences anxiety and has the impression they might die. Angina is provoked by physical activity, running or exertion.
Angiogenesis the development of new blood vessels. Angiotensin this peptide maintains volume and arterial tension and thus can cause intense vasoconstriction of the peripheral arterioles (especially splanchnic) and arterial hypertension. Anisotension a difference in systolic tension (blood pressure) between the two arms, due to osseous or muscular compression in the thoracic inlet, or a cervical, brachial, or visceral restriction. Arterial tension also called arterial pressure, this is the elastic force exerted by the arterial walls on their blood contents. It represents the resistance of the vessel walls to blood pressure. Atheroma fatty deposits that form on the internal artery wall and can create calcification or ulceration. Atherosclerosis arterial scarring due to the deposit of fatty material on the intima that progressed towards the media. It promotes the proliferation, thickening, and calcification of elastic fibers. This condition is often found on large and medium-sized arteries, such as the aorta, femoral artery, coronary artery, etc. Bradycardia abnormally slow heart rate. Bradykinin a polypeptide formed in the plasma that causes contraction of smooth
Glossary muscle fibers, an increase in capillary permeability, and a lowering of arterial pressure. Carotid glomus small nerve ganglion located at the carotid bifurcation containing chemoreceptors that monitor oxygen and carbon dioxide blood levels. Carotid sinus small dilations in the carotid arteries, just above the common carotid bifurcation. They contain baroreceptors whose principal sensory innervation comes from the glossopharyngeal and vagus nerves. Catecholamine any of a class of sympathomimetic vasoconstrictive amines such as epinephrine (adrenaline), norepinephrine (noradrenaline), and their precursor dopamine, and some metabolic derivatives. These compounds are produced by the adrenal medulla and other chromaffin cells found in the coccygeal and carotid ganglia, the sympathetic nerves, and organs containing catecholamines. Circle of Willis a circular anastomosis at the base of the brain comprised of the internal carotid, the anterior and posterior cerebral, and the posterior and anterior communicating arteries. Coccygeal glomus a cluster of nerve cells with an epinephrine (adrenaline)-secreting endocrine function. They lie against the anterior surface of the coccyx, near its caudal extremity on the ansa which unites the two intermediate cords of the pelvic sympathetic chain. It is also known as the ganglion impar, and played an important role earlier in human evolution. Coronary thrombosis the formation of a thrombus in a coronary artery that can cause ischemia and myocardial infarction. Dopamine a neurotransmitter synthesized in various neurons. It is a vasodilator for the kidneys, the intestine, and the coronary arteries, and increases the force of contraction of the heart, without altering its rhythm.
Embolus an obstacle on the inner vessel wall (blood clot, fatty deposit, air bubble, bacterial growths, etc.) that can lead to an embolism. Endothelium a very thin membrane that lines the intima of blood vessels and the heart. It secretes various vasoactive substances such as angiogenesis stimulants. Epinephrine (adrenaline) a hormone released by the adrenal medulla that stimulates the sympathetic system, accelerates the heart, raises arterial pressure, and contracts the arteries (except the coronary and muscular arteries). It is responsible for mydriasis, dilates the bronchioles, lowers digestive motor control, and increases blood glucose levels. General circulation so-called ‘systemic’ circulation serving all the organs except the lungs. Hepatic steatosis excessive liver triglycerides; this is ‘foie gras.’ Histamine a substance found in almost every tissue. It is involved in the immune response and regulation of physiological function. It stimulates gastric secretion, contraction of smooth arterial fibers, and capillary dilation, and makes the vascular wall more permeable. This neurotransmitter is elicited in response to allergic and inflammatory reactions such as asthma and anaphylactic shock, for example. Inosculation the direct anastomosis of two vessels of the same caliber or the surgical joining together of two vessels of the same diameter. Intima the innermost coating of an artery or vein that allows frictionless gliding and facilitates gaseous, liquid, and oxygen exchange. Kallikrein a polypeptide enzyme present in plasma, salivary glands, sweat glands, urine, and the pancreas. It produces bradykinin. Law of Hagen–Poiseuille the resistance in a tube depends on the length of the tube
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Glossary and the viscosity of the liquid running through it. Manual induction a treatment that consists of treating the tissues in the direction of the Listening, by augmenting its force and amplitude. Manual tissue Listening manual evaluation whereby the hand is allowed to be drawn passively towards the fixation. Listening is an evaluation, not a treatment. Maximum arterial tension (or systole) this measure indicates the pressure in the arteries during systole (normal range is 120–140 mmHg). Media the intermediate arterial layer, composed of smooth muscle cells and elastic fibers. Minimum arterial tension (or diastole) arterial pressure between cardiac contractions. It depends on blood flow velocity, and thus on total peripheral resistance. Miosis excessive constriction of the pupil. Muscle of Trietz (suspensory muscle of the duodenum) a muscle consisting of smooth muscle fibers running from the duodenojejunal junction to the crus of the diaphragm and its aortic aperture. It neutralizes the pull of the duodenojejunal junction on the adjacent vessels and nerves, notably the superior mesenteric artery. We believe that this muscle also orients the duodenojejunal junction so as to facilitate transit. Mydriasis abnormal dilation of the pupil. Myocardial infarction necrosis of a part of the heart muscle, following coronary thrombosis or embolism. Nervi vasorum autonomic nerve fibers that innervate the arteries.
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Orthostatic hypotension a transient drop in arterial pressure when a person stands suddenly. A head rush or dizzy spell. Vagotonia is a possible cause.
Pulse the propagation of a shockwave along the arteries, generated by the impact of the ascending aorta on blood ejected from the left ventricle. It is a vibratory, not a fluid, event. The pulsatile wave is more rapid than the speed of blood. Reclining hypotension a transient drop in arterial pressure when moving from a vertical position to lying down. Among the numerous causes, cerebellar hypocirculation due to a vertebrobasilar artery problem can be the underlying etiology. It is interesting to note that this cerebellar hypocirculation does not occur in the prone position. Renin an enzyme produced by the kidney that, after diverse transformations, produces vasoconstriction and, as a consequence, hypertension. Serotonin (5-hydroxytryptamine, 5-HT) a substance synthesized in the cerebral tissue and in the digestive tube. Transported by blood platelets, it is vasoconstrictive and stimulates intestinal peristalsis. It also acts during immediate hypersensitivity reactions. Neurovascular chemoreceptors are located in the jugular fossa (a depression in the petrous temporal bone, behind the carotid canal, in which the beginning of the jugular vein is found). Small circulation the pulmonary circulation. Splanchnic concerning the viscera. Subclavian steal syndrome this condition arises in patients whose subclavian artery or brachiocephalic trunk is compromised by a stenosis or thrombus, often of atheromatous origin. The origin can be a mechanical obstruction such as osseous callus, clavicular malobliquity, or osteochondroma. Blood is stolen by the ipsilateral subclavian artery from the contralateral vertebral artery, to feed the upper extremity. This flow reversal deprives the cerebellum of circulation, and can result in a sudden fall during arm exercise, especially with the head thrown back.
Glossary Systolic pressure index the relationship between systolic arterial pressure in the superior and inferior limbs. Humeral pressure compared with dorsal pedis or posterior tibial artery pressure. The index must be 0.90. A reduction indicates arteriopathy of the inferior limb, arterial obliteration, or a lumbosacral problem (narrowing of the lumbar canal, for example). Tachycardia accelerated heart rate. Thrill a fine vibration felt by an examiner’s hand on an artery due to arterial restriction or narrowing, or even an intra- or periarterial obstruction. Thrombus a blood clot that forms in a vessel or in the heart. It is made up of plaque and agglutinated leukocytes.
Tract an assembly of ducts and viscera belonging to the same anatomophysiological system. Triglycerides a variety of lipids found in adipose tissues and blood serum. They are synthesized in the small intestine from digested dietary fat, and in the liver where they are converted to glucose for brain fuel. Vasa nervorum small arteries that supply blood to peripheral nerves. Windkessel effect elasticity of arteries that allows them to distend under the effect of blood pressure exerted against the vessel wall. This blood pressure is stored by the arteries during systole and returned during diastole, guaranteeing continuity of blood flow.
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Index
Page numbers followed by “f” indicate figures, “t” indicate tables, and “b” indicate boxes.
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Abdominal aorta, 188–189, 189f, 193f Abdominal fat, 63 Abdominal landmarks, 187–193 aorta, branches, 192f pulses, 188–193 visceral, 187–188, 188f Abdominothoracic pressure, 43–45, 44f ‘Accordion’ technique, 88 Acetylcholine, 16, 34 Acidic ions, 47 Active hyperthermia, 5 Addison’s disease, 76 Adenosine diphosphate (ADP), 47 Adenosine monophosphate (AMP), 47 Adrenal medullary hormones, 53, 55f Adrenaline (epinephrine), 16, 19, 34, 52–53 Adrenomedullin, 19 Adson–Wright test, 79–80 Age arterial pressure, 28 cardiovascular risk, 61, 72–73 Alcock’s canal, 247, 249f Alcohol, cardiovascular risk, 64 Alternating pulse, 78 Amenorrhea, secondary, 243 Anastomoses, 19–20, 20f breast, 127f cerebral, 57–58 facial artery, 143 interpancreatic, 208f intrathyroid, 177f posterior auricular artery, 150 superior/inferior mesenteric arteries, 220, 220f supratrochlear-angular, 146 Anemia, 26b, 76 Aneurysms, abdominal aortic, 188–189 Angina pectoris, 65 Angiogenesis, 20 Angiogenic stimulants, 19 Angioma, 69
Angiotensin, 19 Angular artery, 145f Antidiuretic hormone (ADH) (vasopressin), 19, 53–55, 55f Antihypertensive agents, 71 Aorta, 13, 19 branches, 192f mesenteric clamp, 220, 221f narrowing, 70 Aortic arch technique, 103–105, 104f–105f Aortic receptors, 49 Aortic resistance, 34 Areola, 124 Arterial aneurysm, 66–69 complications, 68 etiology, 67 forms, 67, 67f pathological anatomy, 67 symptomatology, 68–69 treatment, 68 Arterial hemodynamics, 40–42 Arterial hypertension, 28, 28b, 62, 70–71 consequences, 70 signs, 75 treatment, 70–71 Arterial plexus, 16 Arterial pressure, 17, 27–28, 50, 79 classical measurement, 79 systolic pressure, 79 Arterial pulse, 29 Arterial receptors, 49 Arterial smooth muscle fibers, 18–19 Arterial tension, 28, 29f Arterial test, palpation, 78 Arterial valves, 7–8 Arterial waves, 41 Arteries, 19–20 arterial network, 19 elastic, 19, 40–41, 41f manipulation, 89–90 muscular, 41–42 pain and, 87 unpleating, 89
Index Arterioles, 5, 19 adaptation, 46 arteriosclerosis, 66–67 blood pressure, 21 circulatory resistance, 42, 42f pulmonary, 119–120 Arteriosclerosis, 62, 66–67 large/medium-caliber arteries, 66 small arteries/arterioles, 66–67 Arteriovenous axis, 88–89 Arterioventricular valves, 7 Atheromas (atheromatic plague), 65–66 complications, 66 etiology, 65–66 pathological anatomy, 65 symptomatology, 66 Atherosclerosis, 62 Atrial natriuretic peptide, 53 Atrioventricular (AV) node (Tawara’s node), 10, 10f, 94 Atrioventricular bundle, 10, 10f Atrium (‘oriellette’), 4, 7 Autacoids, 47–48 Autonomic nervous system, 49–53 electrical pathway, 50–51 Autoregulation cerebral, 58 mechanisms, 47–48 Axillary artery, 126–127 manipulation, 128–129, 128f Bainbridge reflex, 45 Baroflex, 53, 54f Baroreceptors, 49 Beta-blockers, 71 Bidigital stretch technique common carotid artery, 137, 137f external carotid artery, 141, 141f superior mesenteric artery, 222, 223f Blood, 23–26 composition, 25 distribution, 5–6, 5f functions, 23–25 physical properties, 26 see also Hemodynamics Blood cells, 25 Blood flow, 35–38 arterial pressure, 28 defined, 35 nature of, 38–39 output-speed relationship, 35, 35f total, defined, 35 Blood lipids, cardiovascular risk, 63 Blood pressure, 27 arterioles, 21 average, 28 blood flow and, 36, 37f Blood speed, 35 cross-section effects, 35–36, 36f output-speed relationship, 35, 35f
Blood viscosity, 26, 37–38, 37f Blood volume, 5f, 25 arterial pressure, 28 Body mass index (BMI), 63 Brachial artery, 112, 113f–114f manipulation, 129 Bradycardia, 16–17, 30 Bradykinin, 47 Brain arterial hypertension, 62 central control, 50 cerebral circulation, 57–58 Brainstem, motor centers, 50 Breasts, 121–132 anatomy, 122–127, 122f cancer, 121–122 container, 122–123, 122f contents, 123, 123f innervation, 123–124, 124f mammary pain, 87, 121 manipulation, 127–132 vascularization, 124–127, 125f, 127f Bundle of HIS, 10, 10f Calcitonin, 168 Calcium, 169 Calcium channel blockers, 71 Cannon–Böhm zone, 217, 225–227, 226f Capacitance, 4–5, 43 Capillaries, 5, 20–21 Capillary beds, 19, 21, 22f Capillary pulse, 78 Carbon dioxide, 47 Cardarelli’s sign, 78 Cardiac activity, 16 Cardiac arrest, 51 Cardiac cycle, 30–32, 30f–32f Cardiac fibers, excitability, 94–95 Cardiac insufficiency, 72 left chronic, 72 right chronic, 72 Cardiac mass, 29–32 Cardiac output, 32–34 adaptation, 34 arterial pressure, 28 with exertion, 6, 6f, 6t homeostasis, 46 lowering, 16–17 regulation, 33 at rest, 5, 6f, 6t stimulation, 16 Cardiac physiology, 29–34 terminology, 30–31, 31t Cardiac plexus, 13–16 Cardiac vessels, 4–5, 13 Cardiovascular system, 3–26 blood, 23–26 diseases, 65–73 function, 3–7 heart, 7–17
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Index Cardiovascular system (continued) risk factors, 61–64, 74 semiology, 74–81 vessels, 4–5, 13, 17–23 see also Homeostasis, cardiovascular system Carotid bifurcation, palpation, 161, 162f Carotid body, 185f–186f Carotid glomus, 183–186 Carotid receptors, 49 Carotid sinus, 95, 183–186, 184f–186f Carotid sinus nerve, 49 Carotid triangle, 133, 135f Catecholamines, 16, 34, 53, 55f Celiac plexus, 203f, 204 Celiac trunk, 189–190, 190f, 194, 195f Central nervous system see Nervous system Central venous pressure (CVP), 33, 45 Centrifugal (visceromotor) fibers, 16 Centripetal (viscerosensory) fibers, 16–17 Cephalad to caudad technique, 214–216, 215f Cerebral circulation, 57–58 Chambers, heart, 7–8, 8f Chemoreceptors, 49 Chest pain, 98 onset, 98–99 Circulatory system, 3, 4f balance, 80–81 fluid, 85 function, 27–29, 28f gradients, 36–37 time, 36 types, 6–7 see also Blood; Hemodynamics Clotting, 25 Coagulation, 25 Colic artery left, 191 right, 191, 223–224, 223f, 225f Common carotid artery, 133–138 anatomy, 133, 134f–135f contraindications, 136–137 evaluating, 136 indications, 137 manual approach, 133–138 precautions, 136 Common hepatic artery, 190, 191f Common iliac arteries, 235, 236f Common iliac artery, 191, 236–238, 238f–239f Complexion, inspection, 76 Compliance, 29 Compression, arterial aneurysm, 68 Compression-decompression technique, 88 occipital artery, 149 supratrochlear artery, 164 supratrochlear-angular anastomoses, 146 Compression-palpation, heart, 101 Conducting arteries, 19 Continuity, principle of, 35, 35f Convergence, 20, 20f
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Conversion enzyme inhibitors, 70–71 Cooper’s ligaments, 122, 122f Coronary arteries, 13, 14f Coronary circulation, 58–59 Coronary heart disease, 69 Coronary insufficiency, 69 Coronary sinus, 7 Coronary veins, 13 Costovertebral neuralgia, 99–100 Counter-rotation, pancreaticoduodenal arteries, 207–209, 208f Cranial Local Listening, 165 Cranial nerves, 49 Cranial venous sinuses, 23 Cushing syndrome, 76 Cyanosis face, 76 lips, 77 Cysts, 181 Deep vein thrombosis, 69 pathophysiology, 69 symptomatology, 69 Diabetes, cardiovascular risk, 62 Diapedesis, 25 Diastole, 31f Diastolic pressure, 28 Diffuse thyroid hypertrophy, 173, 173f Digestive system, 80 Digital clubbing (hippocratism), 78 Diseases, cardiovascular, 65–73 Dissecting aneurysm, 67, 67f Distributing arteries, 19 Diuretics, 70 Double compression, thorax evaluation, 92–93, 92f treatment, 93 Double pressure technique, heart, 103f ’Drop attack’, 136 Duodenojejunal junction, 187 Duodenum, 205, 206f vascular interdependence, 86–87 Dysmenorrhea, 243 Dyspnea, 98 Ears, inspection, 77 Edema, eyelid, 76 Elasticity, 29 arteries, 19, 40–41, 41f veins, 43 see also Viscoelasticity entries Electrochemical coupling, 18 Electromagnetic field, 85 Embolism, 68 Emotional discharge, 86 Endocardium, 10 Endocrine disease, 70 Endocrine function, 34 Endothelin, 19
Index Endothelium, vascular, 19, 48 Enteric nervous system, 217, 218f–219f Epinephrine (adrenaline), 16, 19, 34, 52–53 Ergo receptors, 49–50 Erythrocytes see Red blood cells Esophagus, precordial pain, 99 Essential hypertension, 62, 70 Estradiol, 121 Estrogen, 121 Euthyroid goiter, 172 Exhalation, 17 External carotid artery, 139–142 anatomy, 139, 140f contraindications, 139–141 indications, 141 manual approach, 139–142 precautions, 139 External iliac artery, 191 Eyelids edema, 76 inspection, 76 Eyes pupils, 76 white of, 77 Face, inspection, 76 Facial artery, 143–146 anatomy, 143, 144f indications, 146 manual approach, 143–146 pulse landmarks, 143–146, 144f–145f Fanning technique sigmoid vessels, 230f superior mesenteric artery, 223, 224f superior thyroid artery, 179, 179f Fibers, muscular, 9, 9f Fibrogen, 25 Fibrous pericardium, 10–11, 12f Flow velocities, 39, 39f ‘Fluid filet’, 38 Frank’s sign, 77, 77f Frank–Starling law, 33 Functional circulation, 7 Fusiform distensions, 67, 67f Gallbladder, 187 Gastric artery left, 190, 198, 199f–201f, 200, 203f right, 198, 199f, 201 Gastroepiploic (gastro-omental) artery, 201–202, 202f– 203f left, 198, 199f right, 198–199, 199f Gastroesophageal junction, 187 Gate control, pain, 88 Glide-induction technique, 87–88 common carotid artery, 138 external carotid artery, 141 recurrent laryngeal nerve, 182
Glossopharyngeal nerve, 49, 182 Goiter, 172 multinodal, 173, 173f Granulocytes, 25 Gums, inspection, 77 Hagen–Poiseulle law, 27–28, 42 Hand, inspection, 78 Heart, 7–17, 94–105 activity, 33 anatomy, 7–13, 94–96 conduction system, 9–11, 10f contraindications, 100 extrinsic innervation, 13–17, 15f fibrous skeleton, 8–9, 95–96, 97f, 101–102, 102f–103f form/orientation, 7 function, 3–4 great vessels, 95, 96f high blood pressure (HBP), 62 indications, 100 innervation, 13–17, 15f landmarks, 95, 97f manual approach, 100–105 precautions, 100 precordial pain evaluation, 98–100 structure, 8–9, 9f Heart rate, 16–17, 29–30 resting, 30 Hematocrit, 26 Hemodynamics, 34–45 arterial, 40–42 venous, 43–45 see also Blood Hemorrhage arterial aneurysm, 68 atheroma, 66 uterine vessels, 243 Hemostasis, 25 Hepatic arterial buffer response, 59 Hepatic artery, 194 Hepatic pulse, 78 Hepatopancreatic ampulla, 187 Heredity, cardiovascular risk, 63 Heterogeneity, 34–35 High blood pressure (HBP), 62 High compliance, 5 High density lipoprotein (HDL), 63, 72–73, 121 High pressure system, 4–5 High resistance, 4 Hippocratism, 78 Histamine, 19, 47 Homeostasis, cardiovascular system, 46–60 adaptation factors, 46–57 local circulatory adaptation, 57–60 Homeothermia, 23 Hormonal system, 53–57, 87 complementary, 57 control, 217
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Index Horton’s arteritis, 71–72 Hydraulic charge, 37 loss of, 38 Hydraulic circuit principle, 27, 28f Hydrodynamic law, 34 Hydroelectrolytic balance, 23 Hydrostatic law, 34 5-Hydroxytryptophan (5-HTP), 48 Hyperpigmentation, 76 Hyperthermia, 5 active, 5 Hypogastric (internal iliac) artery, 192f, 193, 235–236, 237f, 238–239, 239f Hypoglossal nerve, 182, 184f
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Ileal artery, 227, 227f–228f Ileocecal valve, 187 Ileocolic artery, right, 223–224, 225f Iliac vessels, 235–239 anatomy, 235–236, 236f manual approach, 236–239 Iliolumbar artery, 235 Immune defense, 23, 217 Infarction, 66 Inferior cardiac nerve, 13 Inferior gluteal artery, 236 Inferior mesenteric artery, 219f, 221–222, 228–229, 228f–229f Inferior pancreatic artery, 210 perpendicular branches, 210–211 Inferior thyroid artery, 174–177, 176f, 180–181, 180f– 181f Inferior thyroid veins, 177 Inferior vena cava, 7 Infraorbital artery, 153–155, 154f Inguinal canal, 251 anatomy, 251, 252f manual approach, 251, 252f precautions/contraindications, 251 Inhalation, 17 Innervation, vasculature and, 20 Inosculation, 19, 20f Intercostal nerves, 123–124, 124f Intercostal pedicle, 132, 132f Intermediate flow, 39f, 40 Intermittent claudication, 65 Internal carotid artery, 160–165 anatomy, 160, 161f contraindications, 160 indications, 160–161 manual approach, 160–165 precautions, 160 Internal iliac artery, 192f, 193, 235–236, 237f, 238–239, 239f Internal pudendal artery, 247–250 anatomy, 247, 248f indications, 247–248 manual approach, 247–250, 249f–250f Internal thoracic artery, 125–126, 128 Interview technique, 74–75
Intestine, vessels of, 217–230 anatomy, 217–222, 218f–221f indications, 230 manual approach, 222–230 Iron deficiency, 76 Irrigation, 88–89 intestinal, 217 jejunoileum, 222 liver, 195–197, 196f–197f organs affected, 89 principles, 88–89 subclavian arteries, 112 technique, 89 uterus, 242 Ischaemia, 5 Isolated thyroid nodule, 173, 173f Isovolumetric contraction, 31, 32f Isovolumetric relaxation, 32, 32f Isthmus, 166 Jejunal artery, 227, 227f–228f Jejunoileum, arterial irrigation, 222 Jugular pulse, 79 Laminar flow, 39, 39f Laplace’s law, 29 Large pericardial cavity, 11 Larynx, 171f Lateral elevation, thorax, 92, 92f Lateral sacral artery, 235 Lateral thoracic artery, 126, 129 Left chronic cardiac insufficiency, 72 Left colic artery, 191 Left gastric artery, 190, 198, 199f–201f, 200, 203f Left gastroepiploic (gastro-omental) artery, 198, 199f Left ovarian vein, 245–246 Left renal artery, 233–234 Left renal vein, 245–246 Leukocytes, 25 Leukotrienes, 48 Lichstein’s sign (Frank’s sign), 77, 77f Lifestyle, cardiovascular risk, 63–64, 74 Lift experimentation, 89 lateral/sagittal, thorax, 91–92, 92f liver irrigation, 195–197, 196f–197f maintained, 89 uterus irrigation, 242 Ligaments Cooper’s, 122, 122f of Grüber, 166–167 pericardial, 11, 11b–12b, 12f thyrotracheal, 166–167 Lips, inspection, 77 Liver, 194–197 anatomy, 194–195 indications, 197 manual approach, 195–197
Index Local circulatory regulation, 46–48, 48t Longitudinal anastomosis, 20f Low compliance, 4 Low density lipoprotein (LDL), 63, 72–73, 121 Low pressure system, 5 Lymphatic ganglia, 172 McBurney’s point, 187, 191 Malignant tumor cells, 20 Mammary pain, 87, 121 Manipulation see Visceral vascular manipulation Manual Therapy for the Cranial Nerves (Barral & Croibier), 87 Marginal artery, transverse colon, 225, 225f Maxillary artery, 153–155 anatomy, 153, 154f indications, 155 manual approach, 153–155 Mechanical pain, 75 Median sacral artery, 235, 236f Mediators, 51–53 Mental artery, 155 Metabolic hyperemia, 58 Metabolic waste, transport, 23 Metabolites, 47 Microaneurysms, 67 Microcirculation, 21, 42–43 Middle cardiac nerve, 13 Middle thyroid veins, 177 Migraine, 87 Mixed circulation, 7 Mobility, 85 Multinodal goiter, 173, 173f Muscarinic receptors, 16 Muscle of Trietz, 222 Muscular arteries, 19, 41–42 Muscular fibers, 9, 9f Musset’s sign, 78 Myocardium, 8–9 Myogenic stretch response, 47 Natriuretic atrial peptide (NAP), 19, 34, 57, 57f Nervi nervorum, 20 Nervi vasorum, 18 Nervous system, 49–53, 94–95 balance, 85 celiac plexus, 203f, 204 complementary, 57 enteric, 217, 218f–219f Neurological system, 80 Neurotransmitters, transport, 23 Neurovascular techniques, 182–186, 183f Nitrogen monoxide, 19, 47 ‘Nodal escape’, 51 Norepinephrine (noradrenaline), 16, 19, 34, 52–53 Nourishing circulation, 6 Nutrients, 5 Obesity, cardiovascular risk, 63 Obturator artery, 235–236
Occipital artery, 147–149 anatomy, 147, 148f indications, 147 manual approach, 147–149, 149f Ocular system, 80 Ophthalmic artery, 163, 163f ‘Oriellette’, 4 Ovarian artery, 246f Ovarian vessels, 245–246 anatomy, 245, 246f manual approach, 245–246 vein, left, 245–246 Ovaries, 188 Oxygen, 5 transport, 23 Oxygen deficiency, 47 Pain arteries, 87 chest, 98 costovertebral neuralgia, 99–100 duration, 75, 98 intensity, 98 location, 75, 98 mammary, 87, 121 mechanical, 75 onset, 98–99 precordial, 98–100 pudendal nerve neuralgia, 247 type, 75 Palmar erythema, 78 Palpation, 78–81 abdominal aorta, 189f carotid bifurcation, 161, 162f common carotid artery, 133–136, 135f common iliac artery, 236–237, 238f external carotid artery, 139 internal iliac arteries, 238 maxillary artery, 153–155 occipital artery, 147 posterior auricular artery, 150 renal artery, 231–233, 232f subclavian arteries, 112 supraorbital foramen, 161, 162f supratrochlear arteries, 162f, 163 thyroid, 169–173, 171f Pancreas, 205, 206f anatomy, 210, 211f vascular interdependence, 86 Pancreaticoduodenal arteries, 205–206, 206f–207f counter-rotation, 207–209, 208f perpendicular branches, 206–207, 207f Pancreaticoduodenal vessels, 205–209 anatomy, 205, 206f, 208f manual approach, 205–209 Pancreaticosplenic vessels, 210–216 anatomy, 210–211, 211f indications, 216 manual approach, 211–216, 212f–213f, 215f organs, associated, 216
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Index Paradoxical pulse, 79 Parasympathetic cardiomoderator tone, 51 Parasympathetic system, 13 action, 16–17 cardiovascular effects, 51, 51f Parathyroid glands, 168–169 Parathyroid hormone (parathormone), 169 Pectoralis minor muscle, 126, 129, 129f Pericardial cavity, 11 Pericardial ligaments, 11, 11b–12b, 12f Pericardium, 10–11 Peripheral resistance, vascular, 41–42, 42f homeostasis, 46 Periphlebitis, 244 Peyer’s patches, 217 Phagocytosis, 25 Phlebitis, 244 Physiological venous pulse, 79 Plasma, 25 Platelet activating factor (PAF), 48 Platelets, 25 clumping, 25 Pleurocervical attachments, 115 Plexus, 20 Polycythemia, 26b Post-charge, 33–34 Posterior auricular artery, 150–152 anatomy, 150, 151f indications, 150 manual approach, 150–152 Potassium, 47 Precapillary sphincter, 21 Precautions, 81b Pre-charge, 33 Precordial pain evaluation, 98–100 non-cardiac origin, 99–100 Premenstrual syndrome, 243–244 Pressure gradients, trunk, 43–45, 44f Pressure waves, 41 Pressure-induction maneuver, carotid bifurcation, 184, 185f Principle of concealing pulse, 231–233 Principle of continuity, 35, 35f Prostaglandins, 48 Prostate symptoms, 243b Psychoemotional factors, 100 Pudendal nerve neuralgia, 247 Pulmonary arteries, 13 techniques, 118–119 Pulmonary arterioles, techniques, 119–120 Pulmonary circulation, 59–60 Pulmonary hilum, 117 Pulmonary (small) circulation, 3, 4f Pulmonary vessels, 117–120 anatomy, 117, 119f contraindications, 118 indications, 118 manipulation, 118–120, 120f
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precautions, 117–118 veins, 7, 13 Pulse analysis, 78–79 principle of concealing, 231–233 Pupils, inspection, 76 Purkinje network, 10, 10f Pylorus, 187 Pyramidal lobe (pyramid of Lalouette), 166, 172 ‘Rabbit punch’ accidents, 112 Radiotherapy, 121 Raynaud’s disease, 71 Raynaud’s phenomenon, 71 Receptors, 49–50 α receptors, 52 β receptors, 52–53 Recurrent laryngeal nerve, 182 Red blood cells composition, 25 hematocrit, 26 increase/decrease, 26b microcirculation, 21 Reddened face, 76 Referrals, 75 Regulation, blood, 23 Renal arteries, 231–234, 232f, 234f anatomy, 231, 232f left, 233–234 right, 233–234, 233f Renal disease, 70 Renal veins anatomy, 231, 232f left, 245–246 Renal vessels, 231–234 anatomy, 231, 232f manual approach, 231–234 Renin-angiotensin-aldosterone system, 53, 56–57, 56f Reservoir vessels, 4–5 Resistance, 4–5 Respiratory pulse, 79 Respiratory sinoatrial arrhythmias, 17 Respiratory system, balance, 81 Retrosternal techniques, thymus, 109 Reynolds’ number, 39–40 Right chronic cardiac insufficiency, 72 Right colic artery, 191, 223–224, 223f, 225f Right gastric artery, 198, 199f, 201 Right gastroepiploic (gastro-omental) artery, 198–199, 199f Right ileocolic artery, 223–224, 225f Right lateral traction technique, pancreas, 211, 212f Right renal artery, 233–234, 233f Saccular aneurysm, 67, 67f Sagittal elevation, thorax, 91–92, 92f
Index Secondary amenorrhea, 243 Secondary hypertension, 62, 70 Sedentary lifestyle, cardiovascular risk, 63–64 Semiology, cardiovascular system, 74–81 Serosal pericardium, 10 Serous pericardium, 11 Sex arterial pressure, 28 cardiovascular risk, 61 Sigmoid vessels, 230, 230f Sinoatrial (SA) node, 9, 10f excitation, 94 Skin rolling, carotid sinus, 186f Small intestine, vascular interdependence, 86 Smoking, cardiovascular risk, 61–62 Sphincter of Oddi (hepatopancreatic ampulla), 187 Sphincters, 85 Splanchnic circulation, 59 Spleen, 213 anatomy, 210, 211f Splenic artery, 190–191, 191f, 210, 212f Spreading-gliding technique, external carotid artery, 141–142, 142f Starling’s curve, 42–43, 43f Stomach, 198–204 anatomy, 198–199 contraindications, 204 indications, 204 manual approach, 199–204 organs/structures, associated, 202 precordial pain, 99 vascular interdependence, 86 Stress, cardiovascular risk, 64 Stretch maneuver combination, 88 common carotid artery, 138, 138f maintained, 89 superior thyroid artery, 179 see also Bidigital stretch technique Stretch receptors, 49 Stretch-induction technique, 88 posterior auricular artery, 152, 152f Stroke volume, 33 Strumming, inferior thyroid artery, 181 Subclavian arteries, 110–116, 124–125 anatomy, 110–112, 111f contraindications, 112 indications, 112 interscalene segment, 110–111 irrigation territories, 112 manual approach, 112–116, 113f–116f postscalene segment, 111 prescalene segment, 110 Subclavian muscle, 128–129, 128f Superficial temporal artery, 156–159 anatomy, 156, 157f manual approach, 156–159 Superior cardiac nerve, 13
Superior laryngeal artery, 178–181, 178f–179f Superior mesenteric artery, 191, 217–223, 219f, 223f Superior thoracic artery, 126, 129 Superior thyroid artery, 174, 175f–176f, 178–179, 179f Superior thyroid veins, 177 Superior vena cava, 7 Supraorbital artery, 163–164, 164f Supraorbital foramen, palpation, 161, 162f Supratrochlear arteries, 162f, 163–164, 165f palpation, 162f, 163 Supratrochlear-angular anastomoses, 146 Sweeping, subclavian arteries, 114–115, 115f Sympathetic chain, 182–183 Sympathetic system, 13, 95 action, 16 cardiac nerves, 34 cardiovascular effects, 50–51, 52f Sympathicotonia, 80 Syndrome X, 63 Systemic (great) circulation, 3, 4f Systole, 31f Systolic ejection, 31–32, 32f volume, 33–34 Systolic pressure, 27–28, 79 Tachycardia, 16 Telangiectasia, 77–78 Temperature, 47 Temporal arteritis, 71–72 Tendinomuscular structure, heart, 9f Thoracoacromial artery, 126 Thorax, 91–93 container, 91 contents, 93 rigid components, 91–93 Thready pulse, 78 Thrombocytes see Platelets Thrombosis, 66, 68 Thymus, 106–109 anatomy, 106, 107f evolution, 106, 107f–108f innervation, 106 manual approach, 109 physiology, 106–109 structure, 106 vascularization, 106, 108f Thyroid, 166–181 anatomy, 166–169, 167f, 171f, 174–178, 177f contraindications, 168t, 174 dysfunction, symptoms, 168t examination, 169–174, 170f manipulation, 174–178 manual approach, 178–181 physiology, 167–168 Thyroid gland, 166–168 Thyroid hypertrophy, 172–173, 173f
267
Index Thyroid releasing hormone (TRH), 167–168 Thyroid stimulating hormone (TSH), 167–168 Thyrotracheal ligaments, 166–167 Thyroxine, 167–168 Toxicity, 76 Traction-induction technique, breast, 130–131, 131f–132f Transport blood, 23 metabolic waste, 23 neurotransmitters, 23 oxygen, 23 Transverse accordion technique pancreas, 213–214, 213f spleen, 214 Transverse anastomosis, 19, 20f Transverse colon arteries, 224–227 marginal artery, 225, 225f Transverse facial artery, 156, 157f Transverse pericardial sinus, 11 Trigeminal cervical system, 87 Triiodothyronine, 167–168 True capillaries, 21 Tubes, 85 Tucina intima, histology, 17, 18f Tucina media, histology, 17–18, 18f Tumor angiogenesis factor (TAF), 20 Tunica adventitia, 18, 18f, 20 Turbulent flow, 39–40, 39f Unpleating arteries/veins, 89 Unstable pulse, 79 Uterine artery, 245 anatomy, 240, 241f manipulation, 240–242, 241f–242f Uterine vessels, 240–244 anatomy, 240 common venous complaints, 244 indications, 243–244 precautions/contraindications, 242–243 Uterus, lifting irrigation, 242
268
‘Vagal brake’, 50 Vagal cervicothoracic depressor nerve, 95 Vagal parasympathetic nerves, 34, 95 Vagal sympathetic tone, 17 Vagosympathetic actions, 95 Vagotonia, 80–81 Vagus nerves, 13, 182 Values, blood, 28 Valves heart, 7–8 vein, 21–23 Vasa privata, 13, 14f, 117 Vasa publica, 13, 117 Vasa vasorum, 18, 20 Vascular activity, 33 Vascular axis, direction, 89
Vascular charge, 37 Vascular diversion vessels, 21 Vascular endothelium, 48 Vascular interdependence, 86–87 Vascular murmurs, 40 Vascular myocytes, 18–19 Vascular network, 3, 4f, 23, 24f Vascular resistance, peripheral, 41–42, 42f homeostasis, 46 Vascular sections, 4–5 Vascular self-regulation, 46–47 Vascular shortening, 89 Vascular supply, 86–87 Vascular walls, histology, 17–18, 18f Vasculature, innervation and, 20 Vasoconstriction, 5, 19, 47, 48t Vasodilation, 19, 48, 48t Vasodilators, 71 Vasomotor symptoms, 80 Vasopressin (antidiuretic hormone (ADH)), 19, 53–55, 55f Vasosympathetic balance, 80–81 Veins common complaints, 244 elastic, 43 manipulation, 89–90 properties, 23 unpleating, 89 Veins, histology, 21–23 capacity, 21 number, 21 valves, 21–23 walls, 21 Velocity profile, fluid, 38, 38f Vena cavae, 13 Venoatrial receptors, 49 Venous baroreceptors, 49 Venous hemodynamics, 43–45 Venous plexus, 16 Venous pulse, physiological, 79 Venous return, 43 vis a fronte, 43 vis a latere, 43 vis a tergo, 43 Venous sinus, 23 Ventricles, 7 Ventricular diastole, 27 Ventricular fibers, 9 Ventricular filling phase, 31, 32f Ventricular systole, 27 Venturi effect, 38, 38f Vesicouterine venous system, 242 Visceral vascular manipulation, 85–90 arteries and veins, 89–90 global concept, 86–87 precautions, 81b principles of, 85–86 techniques, 87–89 Visceromotor fibers, 16 Viscerosensory fibers, 16–17
Index Viscoelasticity techniques, 85 breast, 129–130, 130f capillary function, 21 posterior auricular artery, 152 supratrochlear-angular anastomoses, 146 Viscoelasticity-induction infraorbital artery, 154f, 155 superior thyroid artery, 179 Visual inspection, 76–78
Weak resistance, 5 Weight, cardiovascular risk, 63 White blood cells, composition, 25 White of eye, 77 Windkessel effect, 40–41, 40f–41f, 60 Wiry pulse, 78Xanthelasmata, 76 Zygomatico-orbital artery, 158, 158f
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Visceral Vascular Manipulations
Commissioning Editors: Sarena Wolfaard, Alison Taylor Development Editor: Fiona Conn Project Manager: Anita Somaroutu Designers: Charles Gray, Sarah Russell Illustrator: Élénore Lamoglia
Visceral Vascular Manipulations Jean-Pierre Barral
D.O. (UK), MRO (F)
Director of the Department of Osteopathic Manipulation, University of Paris School of Medicine, Paris, France Member of the Registre des Ostéopathes de France. Diploma in Osteopathic Medicine from the European School of Osteopathy in Maidstone, UK
Alain Croibier
D.O., MRO(F)
Member of the Registre des Ostéopathes de France Member of the Academie d’Osteopathie de France Lecturer in Visceral Manipulation and Osteopathic Diagnosis at the Osteopathic College, A.T. Still Academy, Lyon, France Lecturer in Visceral Manipulation and Nerve Manipulation for The Barral Institute Translated by Annabel Mackenzie, RST
EDINBURGH LONDON NEW YORK OXFORD PHILADELPHIA ST LOUIS SYDNEY TORONTO 2011
© 2011 The Barral Institute First published in French under the title Manipulations vasculaires viscérales © 2009 Elsevier Masson SAS Paris. No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopying, recording, or any information storage and retrieval system, without permission in writing from the publisher. Permissions may be sought directly from Elsevier’s Rights Department: phone: (+1) 215 239 3804 (US) or (+44) 1865 843830 (UK); fax: (+44) 1865 853333; e-mail:
[email protected]. You may also complete your request online via the Elsevier website at http://www.elsevier. com/permissions. First published 2011 ISBN 978 0 7020 4351 2 British Library Cataloguing in Publication Data A catalogue record for this book is available from the British Library Library of Congress Cataloging in Publication Data A catalog record for this book is available from the Library of Congress Notice Neither the Publisher nor the Authors assume any responsibility for any loss or injury and/or damage to persons or property arising out of or related to any use of the material contained in this book. It is the responsibility of the treating practitioner, relying on independent expertise and knowledge of the patient, to determine the best treatment and method of application for the patient. The Publisher
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Preface
The human body is incredibly complex. It is practically impossible to imagine the myriad of cells that contribute to our survival and to our good health. Each must play its note in the grand concert that is our life. The osteopathic concept is global in its approach. Each component part of the living human structure is of vital importance. The notion that an osteopath specializes in one part of the body is sheer nonsense. It is not for any of us to choose, by virtue of our education, our culture, or our life, what is important for the patient. Rather, it is the organism’s own vast memory store that must always guide our hand. Knowing how to ‘listen’ to a body is essential; the hand must design a therapeutic response according to the messages it receives. A. T. Still declared the rule of the artery to be supreme and fundamental. In order to function well, an organism requires optimal circulation. Few manual therapists concern themselves with the circulatory function directly. We acknowledge, however, that our excellent friend and colleague, Paul Chauffour, has pursued a keen interest in the vascular system. In this book we share the fruits of our research and experience. The visceral system requires especially plentiful circulation and it is therefore natural that we have, little by little, sought out ways to improve vascular function. Our endeavor has been to perfect simple and effective maneuvers for the visceral vascular network. About 100 000 km of
arteries and 250 000 km of veins run through our bodies – an impressive quantity! For an individual weighing 70 kg, this amounts to about 1500 km of arteries per kilogram. In this text we describe the precise location of the principal visceral pulses. These key pulses are a reliable witness by which to gauge the changes that treatment brings. We have studied, according to artery type the most effective techniques for increasing the irrigation of given organs. The experiments have been duplicated by way of Doppler effect tests. Even if for some deeply situated arteries we have not always been able to prove an augmentation of blood flow, clinical improvements have demonstrated the effectiveness of this type of manipulation. In the case of some arteries, only a momentary variation in circulation has been observed, with no ascertainable long-term effect. Even with that, the patient felt an improvement – and this is the essential thing. Our work is somewhat empirical and somewhat subjective, but why be ashamed of it? Our hands possess the magnificent privilege of improving the major functions of the human body. This remains true provided practitioners continually work to augment and broaden their knowledge, and to refine their manual applications. Knowledge of the anatomy and function of the vascular system is what determines the quality of care that patients receive. We hope that this book will become indispensable to you in meeting this objective. xxi
Acknowledgments
The authors would like to thank Annabel Mackenzie, RST, for her superb translation from the French version. Thanks also to Gail
Wetzler, RPT, and Dawn Langnes for their editorial support. JP Barral A Croibier
xxiii
