Cardiology
Short Description
cardiology 5th year notes...
Description
CARDIOLOGY ANATOMY of the HEARTYYYYYYYYYYYYYYYYYYYYYYYYYYYYYY
R ATRIUM (Tricuspid valve) – R VENTRICLE L ATRIUM (Mitral Valve) – L VENTRICLE The MITRAL and TRICUSPID (atrioventricular valves). Valves prevented being everted during systole (into atria) by chordae tendinae and papillary muscles that contract in systole. Pulmonary semilunar valve- Pulmonary artery. Aortic semilunar valve – Aorta (passively close at the end of systole- ventricular pressure now less than in arteries). Atria and ventricles separated by ANNULUS FIBROSUS A band of fibrous connective tissue- provides skeleton for attachment of muscle and insertion of the valves. Prevents conduction between atria and ventricles except at AV NODE. AV node near the inetratrial septum and mouth of the coronary sinus. During diastole, ventricles fill. At initiation of systole, atria contract and complete ventricular filling. As ventricles contract, pressure rises sharply, and AV valves close. When ventricular pressure exceeds pulmonary/aortic pressure, semilunar valves open, and ejection occurs. Semilunar valves closed by backflow from aretries. Force of contraction generated by MYOCARDIUM. Ventricles have thicker myocardium than atria. Inside of heart lined with ENDOCARDIUM (thin cell layer)- Thin, slick sheet of connective tissue located on the inner surface of the myocardium. It is continuous with the blood vessels. Outer surface of myocardium lined with EPICARDIUM (Visceral layer of serous pericardium) Heart enclosed in PERICARDIUM (sac) o Fibrous Pericardium o Serous pericardium (visceral and parietal layer, in-between is the pericardial cavity) PERICARDIAL CAVITY, enclosed in the serous pericardium, contains interstitial fluid as lubricant. Myocardium made of cardiac myocytes (muscle cells) Connected together by network of intercalated disks The disks provide a structural attachment (glue together at dermosomes) and electrical connection through GAP JUNCTIONS. Myocardium acts as a FUNCTIONAL
CIRCULATIONYYYYYYYYYYYYYYYYYYYYYYYYYYYYYY
SUPERIOR and INFERIOR VENA CAVA. PULMONARY TRUNK R. and L. PULMONARY ARTERIES L. and R. PULMONARY VEINS AORTA o BRACHIOCEPHALIC ARTERY o COMMON CAROTID ARTERY o LEFT SUBCLAVIAN ARTERY o DESCENDING AORTA Blood supply from LEFT and RIGHT CORONARY ARTERIES BOTH have descending and marginal… just the left also has a circumflex. Arise from the aortic sinus, at the base of the aorta. Remain patent throughout cardiac cycle, and not blocked by cusps of aortic semilunar valve. RIGHT CORONARY- runs between pulmonary trunk and R. Atrium, to AV sulcus. Then descends to lower heart, dividing into posterior descending and right marginal LEFT CORONARY, runs behind pulmonary trunk and forward between it and L. Atrium, divides into the 3 further trunks. Anastamosis between L and R Marginal branches. Anastamosis between anterior and posterior descending branches. Blood returns via coronary sinus and anterior coronary veins LEFT CORONARY ARTERY o Left Atrium o Left ventricle o Interventricular septum o Anterior wall of right ventricle RIGHT coronary artery o Right Atrium o Right Ventricle o (in most people) supplies AV and SA NODE o Arterial disease here can cause AV block or slow HR. Coronary perfusion pressure: difference between the diastolic pressure in aorta and diastolic pressure in RA, which creates the perfusion pressure (coronary arteries fill in diastole) In tachycardia, less time spent in diastole- inc risk of ischemia
CIRCULATIONYYYYYYYYYYYYYYYYYYYYYYYYYYYYYY LEFT CORONARY ARTERY
The left main coronary artery (LMCA) arises from the left aortic sinus,
It quickly divides into the anterior interventricular branch also known as the left anterior descending (LAD) artery and the circumflex artery.
The LAD runs along the anterior interventricular sulcus, (groove in the anterior surface of the heart that separates the left and right ventricle) down towards the apex.
LAD runs around to the posterior surface of the heart in another groove called the posterior interventicular sulcus.
The LAD artery supplies blood to the walls of both the left and right ventricles.
The circumflex, follows a different course to the LAD. It runs along the atrioventricular groove, which seperates the atria from the ventricles, giving rise to the left marginal branch in the process.
The circumflex then continues around the heart, terminating on its posteroinferior aspect, to supply blood to both the left and right atrium.
RIGHT CORONARY ARTERY
The right coronary artery (RCA) arises from the right aortic sinus, and along the right atrioventricular groove.
From here, it curls around towards the inferior surface of the heart, forming the posterior interventricular branch, more commonly known as the posterior descending artery (PDA).
The PDA runs along the posterior interventiculas sulcus, to supply blood to the walls of both the left and right ventricle.
However, before turning towards the diaphragmatic surface of the heart the RCA gives rise to the right marginal branch, that runs along the right margin, to supply the wall of the right ventricle.
Important branches from the RCA include, the conus branch and the sino-atrial node artery.
As an aside, compared to the left ventricle the right ventricle has a greater ratio of muscle fibres to capillaries: it is more likely to suffer toxic damage but less likely to suffer ischaemic damage.
CORONARY BLOOD FLOW
Small arteries and arterioles are key players in altering vascular resistance and thus regulating myocardial blood flow.
Myocardial blood flow is closely linked with oxygen demand, with an increase in cardiac activity resulting in an increase in demand for oxygen.
This is achieved by an increase in myocardial blood flow, involving autoregulation.
Whenever there is a change in coronary perfusion pressure, through changes in aortic pressure, the process of autoregulation ensures that myocardial blood flow is always maintained.
Adenosine and nitric oxide (NO) are important mediators in the regulation of coronary blood flow as well as the involvement of the sympathetic and parasympathetic nervous system.
QUICK RELATION TO EGC
ISCHEMIA: ST depression and T-wave inversion
INJURY: ST elevation
INFARCTION: ST elevation
PREV INFARCTION: Q waves SEPTAL: ANTERIOR:
V!, V2 V3, V4
LATERAL:
V5, V6, V1,
INFERIOR:
II, III, aVF
aVL
THE CARDIAC CYCLE- VENTRICLE AP YYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYY
What is an action potential? It is when a cell transiently depolarizes, due to ion channels. CARDAC ACTION POTENTIAL is a lot longer than those in nerves or skeletal muscle. Because of a PLATEAU PHASE in cardiac muscle, lasting 200-300ms.
I aVL II V2 V5
V1
V4
VENTRICULAR MUSCLE ACTION POTENTIAL
(4) -90 RESTING POTENTIAL The membrane at rest is most permeable to K+ ions, so the RESTING POTENTIAL is most dependent on the K+ gradient. (K+ out) There is transmission from an adjacent cell through intercalated disks. An action potential is initiated when the membrane is depolarized to a THRESHOLD POTENTIAL. o (0) RAPID DEPOLERISATION: Rapid Na+ channels are stimulated to open, flooding the cell with positive Na+ ions. Transmembrane potential is the is the difference in voltage inside, compared to outside the cell. Positive change. The Na+ going in is large enough to overcome the outward current through K+ channels. This causes further depolarization, and activates more Na+ channels. Depolarization becomes self-generating, so has a rapid upstroke. ARTERIAL OCCLUSIONYYYYYYYYYYYYYYYYYYYYYYYYYYYYYY Depolarisation of one cell triggers the Na+ channels in surrounding cells to open as well, causing the depolarizing wavefront to propagate cell by cell throughout the heart. Very fast conduction velocity- ie. The slope of 0 is very steep. LAD: the LEFT ANTERIOR from left coronary After this, theDESCENDING, cell begins to repolarize and return to the resting state, as it cant o V1 (septal) again until its in its resting state. depolarize V2Initial(septal) o o (1) phase of repolarization. o V3 (anterior) Rapid inactivation of Na+ channels. V4PLATEAU (anterior) o o (2) STAGE o V5 (lateral) The membrane potential goes down slowly, followed by a more rapid repolarization o V6 (lateral) phase. Rate of repolarization is slowed by the INFLUX OF Ca2+ ions into the cell. L. Circumflex They activate relatively slowly, when the membrane potential starts getting more o 1 (all lateral) positive (over 35). o aVL Ca2+ ions enter the cell slower than the Na+ ions, and help prevent the cell o V5 andrepolarizing V6 (maybe)too quickly- extending the REFRACTORY PERIOD (cant respond to a new stimulus) R. Coronary Artery The refractory period and length of AP, means that the cardiac muscle cannot be o II (inferior) tetanized. o III (inferior) The length of the plateau is related to slow inactivation of Ca+ channels. o aVF (inferior) Ca2+ entry in the plateau is vital for contraction (calcium channel blockers reduce force) o (3) Critical period where a strong signal may trigger depolarization and cause VT or VF It’s the later stages of repolarization. o (4) o Repolarization is complete. o K+ outward current becomes dominant o
III aVF V6 V3
HYPERKALAEMIA (K+) o Plasma K+ can be increased in RENAL FAILURE TISSUE DAMAGE o Can cause dangerous arrhythmias eg. VF, as the membrane depolarizes (positive) and becomes closer to threshold potential. o MORE K+ outside cell, so less wants to move out, so resting potential is more positive. o Also slows and weakens the upstroke of the action potential, as it partially inactivates the Na+ channels, and slows conduction. o Above 8, this leads to complete cessation of conduction- and heart block. HYPOKALAEMIA o Hyperpolarises the membrane, making it difficult to reach threshold.
THE CARDIAC CYCLE – SA NODE Action PotentialYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYY
SA NODE INITIATING THE HEART BEAT o SA node is primary heart pacemaker. o Innervated by Parasympathetic VAGUS CNX (dec Heart rate, not contraction) Sympathetic T1- T4 Spinal nerves (innervate atria and ventricles too so can increase contraction force as well as HR) o The SA node cells have no ‘resting potential’- regular spontaneous Action Potentials are generated. o SA node cells are special, as slow Ca2+ channels carry the current, rather than the fast Na+ channels. o Relies on CALCIUM influx, rather than SODIUM. o In terms of how fast they depolarize, the action potentials are much slower than in eg. Skeletal muscle or cardiac muscle. o Can be referred to as ‘slow-response action potentials’- the curve doesn’t go up sharp. o Conduction velocity is slow- slower conduction cell to cell. o An action potential in the SA node is generated at -40- (rather than -60 in cardiac myocytes)- ie… the cell has to get even more positive before an action potential is created- its harder. o The Ca2+ channels activate in a more positive environment than the Na+ ones. o The rate of decay of the resting potential, (to make an action potential) determines the heart rate. o Initially, an outward K+ current, slows over time, so more positive.
SA nodal action potentials are divided into:
Phase 4 o
The spontaneous depolarization (pacemaker potential) that triggers the action potential once the membrane potential reaches threshold between -40 and -30 mV).
o
(K+ out slower and slower, Na+ in) slow decline in the outward movement of K + as the K+ channels close- that were open in phase 3.
o
At the end of repolarization, when the membrane potential is very negative (about -60 mV), ion channels open that conduct slow, inward (depolarizing) Na + currents.
o
These currents are called "funny" currents and abbreviated as "If".
o
These depolarizing currents cause the membrane potential to begin to spontaneously depolarize- initiating Phase 4.
o
As the membrane potential reaches about -50 mV, another type of channel opens (transient or T-type Ca++ channel)
o
As Ca++ enters the cell through these channels down its electrochemical gradient, the inward directed Ca++ currents further depolarize the cell.
o
When the membrane depolarizes to -40 mV, a second type of Ca ++ channel opens (long-lasting L-type Ca++ channels)
o
Opening of these channels causes more Ca ++ to enter the cell and to further depolarize the cell until an action potential threshold is reached (usually between -40 and -30 mV).
Phase 0 is the depolarization phase of the action potential. Action potential threshold has been reached!
Phase 3 repolarization. (calcium channels close) o
A hyperpolarized (very negative) state is necessary for pacemaker channels to become activated again
THE CARDIAC CYCLE – CARDIAC MUSCLE CONTRACTIONYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYY
Between the ends of adjacent cardiac muscle cells are specialised intercellular junctions called INTERCALATED DISCS.
These are irregular transverse thickenings of the sarcolemma that contain structures called DESMOSOMES.
Desmosomes are like spot-rivets, that hold adjacent cardiac muscle fibres together.
The intercalated discs act as points of anchorage for the contractile proteins, and they contain channels called GAP JUNCTIONS.
These connect the cytoplasm of adjacent cardiac muscle fibres and permit the extremely rapid lowresistance spread of action potentials from one cell to another.
Adjacent fibres are caused to contract almost simultaneously
Three types of cardiocytes are found in the myocardium.
o
1. AUTORHYTHMIC CELLS: Cells found at the junction of the great veins and the right atrium have the fastest intrinsic rhythm (this is the sinoatrial (SA) node or 'pacemaker' of the heart).
o
Spontaneously discharge about 100 times per minute.
o
Nervous and hormonal input can alter the rate of this automatic discharge so that the normal heart rate is about 70 beats per minute.
o
2. PURKINJE FIBRES (conduction fibres) allow fast conduction of action potentials around the heart.
o
3. MYOCYTES (contractile cells)
CONTRACTION- depends on CALCIUM! o Remember: calcium induced calcium release. In the absence of external Ca2+, there can be no contraction. o Cardiac muscle contraction occurs by utilising the sliding filament model already described for skeletal muscle. o The action potential spreads from the cell membrane into the T tubules. o Calcium enters the cell from the ECF (this doesn't happen in skeletal muscle). o This triggers the release of even more calcium from the SR. (the amount released depends on the amount previously stored and on the size of the inward current from the ECF) o Intracelllular calcium increases. o Calcium binds to the troponin/tropomysin complex, and tropomysin moves out of the way of the active site on the actin filament. o Actin and myosin bind, and the thick and thin filaments slide past each other o The myocyte contracts. o Relaxation occurs when calcium is actively transported back into the SR (by calcium-ATPase pump) or out of the cell into the ECF. IONTROPES- Iron- iron man- strong contraction o Alter the CONTRACTILITY of cardiac muscle o POSITIVE IONOTROPE: Increases contractility o E.g. high plasma Ca2+ increases contractility, as calcium entry is increased during the action potential. o NORADRENALINE and ADRENALINE Physiological positive ionotrope. (from sympathetic nerve endings) Also positive chronotropes (increase HR)- Chrone- clock – HR Bascially, the noradrenaline binds to beta1-adrenoceptors on the sarcolemma, and inreases cAMP, this causes more calcium channels to be phosphorylated, which
THE CARDIAC CYCLE – THE ACTUAL CYCLEYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYY
The sequence of mechanical events that occur during a heart beat
Ie. Diastole, Systole, and the Pause.
Cycle begins when SA node initiates a heart beat
o
It’s the end of diastole
o
Atrium and ventricles are relaxed
o
Mitral and Tricuspid (atrioventricular valves) are open
o
Pulmonary and Aortic (semilunar valves) are closed- as the arterial pressure- both pulmonary and aortic pressure is greater than the relaxed ventricular.
1. ATRIAL SYSTOLE (ATRIAL contraction) o
Blood from Atrium - Ventricles
o
Fills the ventricles and completes ventricular filling
o
AV valves open
o
Semilunar valves closed
o
Ventricles are already partially filled from when the whole heart was relaxed.
o
Ventricles receive the last 30% blood- final vol of approx. 130ml.
2. ISOVOLUMETRIC CONTRACTION (VENTRICLES CONTRACT) o
Ventricles filled with blood contract
o
Tricuspid and Mitral valves close as pressure now high in ventricles
o
Ventricular volume unchanged, but the pressure rockets.
o
Semilunar valves still closed.
3. VENTRICULAR EJECTION o
Pressure in ventricles now higher than in pulmonary arteries and aorta, so semilunar (arterial) valves open.
o
Blood into arteries
o
Pressure in aorta is 80mmHg, and pulmonary artery 10mmHg- ventricular pressure is above this.
o
Ejection is rapid, and slows down as systole progresses
THE CARDIAC CYCLE – SOUNDS and CONDUCTIONYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYY Heart Sounds HS I-II+0 o
o
o
S1: Closure of AV Valves o
Lub
o
Normally close together, if split- might indicate delayed conduction
o
In L or R bundle of HIS.
o
AV valves close during ventricular contraction, so ie. A ventricle is contracting a bit late
S2: Pulmonary/aortic valve closure o
Splits in young people due to inspiration of exercise- longer ejection period in right ventricle.
o
Lungs are lower pressure, want to keep blood, less returns to Left ventricle
o
Increase in blood into Right ventricle from vena cava, as sucked into Right Atrium, and wants to go into the lungs.
o
Takes longer to empty Right ventricle as more blood, pulmonary valve stays open a bit longer than aortic.
o
Aortic closes slightly earlier, as less blood.
S3: Rapid refilling, S4: atrial systole (S3 and S4 togther produce a gallop rhythem)- HF.
Electrical conduction pathways
CARDIAC MUSCLE o
Muscle cells connected by intercalated discs
o
On the intercalated disc connections are GAP JUNCTIONS, where membranes of cells are very close, consist of low resistance proteins: CONNEXONS
o
Allow transfer of small ions, therefore ELECTRICAL CURRENT.
o
Cardiac muscle is a FUNCTIONAL SYNCTIUM: as its electrically connected.
o
If Action Potential is initiated in one cell, local currents via gap junctions will cause adjacent cells to depolarize, initiating their own action potential.
o
A wave of depolarization, will conduct cell-cell throughout the myocardium.
o
(Rate of conduction is related to gap junction resistance and size of depolarizing currentrelated to upstroke of action potential).
o
Drugs that slow this phase (0).. slow conduction
THE CARDIAC CYCLE – THE BASIC LAWSYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYY
HEART BLOCK o
Complete heart block (third degree) occurs when conduction between atria and ventricles abolished.
o
Ischemic damage to nodal tissue/ Bundle His.
o
AVN and Bundle of His then generate HR of around 40bpm
o
Abnormally slow conduction through AV Node- causes incomplete (1 st degree) Heart Block- delay is greater than normal- extended P-R interval on ECG.
o
2nd degree heart block when only a fraction of impulses from atria are conducted- eg. Ventricular contraction only initiated every 2nd or 3rd atrial contraction (2:1 or 3:1 block)
o
Wencheback (Mobitz2) is another type of 2nd degree block- P-R interval progressively lengthens, until no transmission from atria to ventricles, and a QRS is missed.
BUNDLE BRANCH BLOCK o
When one branch of bundle of His doesn’t conduct.
o
The part of the ventricle it serves will still be stimulated by conduction through the myocardium from unaffected areas.
o
Conduction is slower, activation is delayed and QRS broadened (ventricular systole takes longer)
ARRYTHMIAS o
Caused, promoted, potentiated by defects in conduction system/ ischemia/ damage
WOLF-PARKINSON WHITE SYNDROME o
AV NODE normal, but a separate extra congenital conduction pathway (bundle of Kent) between atrium and ventricle.
o
Atrial impulses conducted to ventricles by AV NODE and Bundle of Kent.
o
Bundle of Kent faster, so part of ventricle stimulated before the rest- wide QRS COMPLEX. (preexcitation).
o
A premature impulse can set up a re-entry circuit and bad and fast arrhythmia.
HAEMODYNAMICS DARCYS LAW:
Flow =
Pump Pressure resistance
CARDIAC OUTPUT =
Mean Arterial BP−Centra l Venous Blood Pressure(0) Total Peripheral Resistance
THE CARDIAC CYCLE – THE BASIC LAWSYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYY
BLOOD VISCOSITY o
Viscosity is caused by frictional forces in a fluid that resist flow.
o
Blood is 4x as viscous as water because of erythrocytes.
o
ANAEMIA: haematocrit (cell concentration) is low, viscosity and vascular resistance decrease, Cardiac Output rises.
o
POLYCYTHEMIA: vascular resistance and blood pressure are increased.
LAMINAR FLOW o
As liquid flows through a tube, frictional forces are exerted by the tube wall.
o
These, and viscous forces in the tube, set up a velocity gradient across the tube.
o
Flow velocity is greatest at tube centre. (LAMINAR FLOW)
o
Occurs in the microcirculation.
o
Erythrocytes move away from vessel wall, and sit in the middle flow, aligned.
o
Reduces the viscisoty of the blood in the microcirculation, reducing the resistance (FahraeusLindqvist effect)
WALL TENSION (TRANSMURAL PRESSURE) o
The wall has a pressure exerted on it: Pressure inside the vessel, minus the interstitial pressure.
o
This distends the blood vessel wall (ie, the pressure of the blood pushes it out)
o
This is the FRANK/LAPLACE LAW
Wall Tension = Transmural Pressure
vessel rad ius wallThickness
o
In the aorta, where the transmural pressure (blood pushing wall out) is high, atherosclerosis may cause thinning of the blood vessel wall, and the development of a bulge/anyeurysm.
o
This increases the vassel radius, and decreases wall thickness, which sets up a viscious cycle of increasing wall tension, which if not treated may lead to rupture.
CARDIAC OUTPUT LAWS
What is the cardiac output?
CARDIAC OUTPUT = (STROKE VOLUME) x (HEART RATE)
I.e. is the Vol blood pumped through heart per minute
In a normal 70kg man, about 5 L.min, exercise can be 25L/min.
THE CARDIAC CYCLE – THE BASIC LAWSYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYY
WHAT IF THE AFTERLOAD (BP) IS HIGH? WILL SV DECREASE? o
Starlings law means that even if the afterload (blood pressure) increases, the stroke volume can be maintained.
o
The resistance to outflow increases, the left ventricle has to pump against a higher resistance, and the amount of blood ejected is reduced.
o
This means the EJECTION FRACTION has decreased, and the proportion of the END DIASTOLIC VOLUME pumped out falls.
o
The end systolic volume is larger than the beat before.
o
So when the ventricle is being filled again in diastole, there is already more blood than usual in the ventricle.
o
The end diastolic volume is now larger! Ventricle wall is stretched more, so STROKE VOLUME INCREASES.
o
When BP increases, the ENP and EDV increase too, so CO can remain the same, despite pushing against greater force.
AUTONOMIC NS o
Externally regulates CO
o
So very important in controlling BP.
o
Sympathetic stimulation (adrenaline) causes an increase in HR and contractile force.
Positive IONOTROPE, and CHRONOTROPE
o
The ventricular function curve is shifted upwards
o
Nor-adrenaline inc this too.
o
Negative ionotropes decrease force o
Acidity
CVP and Autonomic NS are prime determinants of CO.
Heart Rate
Stroke Vol
Positive Chronotropes, eg. SYMPATHETIC NS
END DIASTOLIC VOLUME - Compliance - CVP (pessure pushing it) and so EDP (how much fills with blood before contracts)
Negative Chronotropes, e.g. PARASYMPATHETIC NS
END SYSTOLIC VOLUME - Arterial pressure - Contractility (both of which affected by symp stimulation and tissue health - o2, pH etc
CARDIAC REFLEXESYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYY
REFLEXES o
Fluctuations in MABP (Mean arterial BP) and volume need to be minimized, to maintain adequate cerebral and cardiac perfusion.
o
There are autonomic reflexes and local mechanisms.
o
Intrinsic reflexes (respond to stimuli in CV system)
Baroreceptor
Cardiopulmonary
Chemoreceptor
Extrinsic reflexes- Cardiac responding to stimuli elsewhere.
o
Eg. Pain/temp changes
o
Cardiovascular reflexes involve
o
o
RECEPTORS: Afferent nerves- sense change, communicate to brain
o
BRAIN: Processes and responds to info, so later activity of efferent nerves
o
EFFERENT NERVES: control cardiac, vascular and renal function- homeostasisreverse change.
THE BARORECEPTOR REFLEX o
Minimizes fluctuations in moment-moment MEAN ARTERIAL BLOOD PRESSURE (MABP)
o
Afferent (sensory) nerve endings in CAROTID SINUS (dilations at the origin of the carotid arteries and aortic arch).
o
They are MECHANORECEPTORS
o
Sense alterations in wall stretch caused by pressure changes.
o
Change the frequency they send action potentials- more pressure, more frequent.
o
MABP decreases…Baroreceptors fire less,
Brain reduces vagal supply to SA node… TACHYCARDIA.
Brain inc sympathetic supply to heart and blood vessels.. CONSTRICTION VEINS+ARTERIES, INC CONTRACTILITY.
Brain increases stimulation of renal sympathetic nerves… RENIN is released.. so angiotensin II production inc, and aldosterone… Fluid retention.
BP increased by fluid retention, tachycardia, vasoconstriction, and contractility.
CARDIAC REFLEXESYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYY
CNS ISCHAEMIC RESPONSE o
Generalized peripheral vasoconstriction
o
Stimulated by brainstem hypoxia.
o
During severe hypotension
o
Helps maintain bloodflow to brain in shock
o
Also causes the CUSHING REFLEX: Brainstem hypoxia due to a tumor which is causing increased CSF pressure: vasoconstriction and hypertension develop.
EXTRINSIC REFLEXES o
Moderate pain causes increased MABP and tachycardia.
o
Severe pain has opposite effect.
o
Cold causes cutaneous and coronary vasoconstriction- can precipitate angina.
HOW IS THIS ALL CENTRALLY REGULATED!? o
Cardiovascular autonomic control arises when areas of the brainstem, hypothalamus, cortex and cerebellum interact.
o
Afferent nerves carrying the stimulus from the receptors terminate in the NTS (NUCLEUS TRACTUS SOLITARIUS) of the medulla.
o
Neurones from here (NTS) project to areas of the brainstem which control parasympathetic and sympathetic outflow.
o
The nucleus ambiguous and dorsal motor nucleus contain the cell bodies of the pre-ganglionic vagal parasympathetic neurons- slow the heart when NTS says theres an increased BP.
o
Neurons from NTS project to areas of ventro-lateral medulla.. blah blah its complicated.
o
Higher centres eg. Limbic system in cortex modify the action of the brainstem centres, integrated and appropriate responses are generated.
AUTONOMIC CONTROL OF THE CV SYSTEM o
Help maintain appropriate MABP in response to the reflexes and receptors.
o
Homeostatic adjustment to postural changes.
o
Change in heammorhage and blood gases.
o
Can override local vascular control- serves body as a whole.
o
Regulated by brain signals to- so reacts to EMOTIONAL STRESS/ENVORONMENT
o
Brain can selectively override /modify the CV reflexes, behavioral responses and CV adjustments
CONTROL OF BLOOD VOLUMEYYxxxxxxxxxxxxxxYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYY
BLOOD VOL CONTROL o
Baroreceptors measure short term fluctuations in BP.
o
Long term, body needs constant blood volume, to sustain constant BP.
o
Alterations in blood vol affect venous return, and CO.
o
Changes in CO lead to adaptive effects of the vasculature that : Increase peripheral resistance and therefore BP.
o
Volume of blood affected by changes in total body contents of o
Water
o
Na
o
These are both controlled by kidneys.
o
Maintain a stable BP relies on adjusting renal excretion of Na and Water.
PLASMA VOLUME: Na and Osmoregulation o
Water content in body altered by sweating/ fluid intake
o
Changes the plasma osmolarity
o
Any deviation from normal sensed by HYPOTHALAMIC OSMORECEPTORS o
Activate thist
o
Release ADH from pituitary
o
ADH is a peptide that suppresses renal water excretion
o
ADH acts on DISTAL NEPHRON- to increase its reabsorption of water: reducing loss water in urine.
o
Opposite happens if less osmolarity- more water excreted and less ADH.
o
THEREFORE PLASMA VOLUME mainly controlled by Na+ content of EXTRAVELLULAR FLUID (in blood).
o
95% of the osmotic solute in the ECF is Na+… with Cl- and HCO-
o
After eg. Eating a salty meal, the plasma osmolarity is changed and the body will adjust the water content (plasma vol)
CONTROL OF TOTAL BODY Na CONTENT
CONTROL OF BLOOD VOLUMEYYxxxxxxxxxxxxxxYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYY
ANP: ATRIAL NATRIURETIC PEPTIDE o
Released from atrial myocytes when stretched by INCREASED ATRIAL VOL.
o
Response to Volume Overload.
o
Causes DISURESIS and NATIURESIS by
INCREASING GFR
Decreasing Renin and Aldostreone Secretion
Reducing Na+ reabsorption throughout nephron- loose Na+ and therefore water.
Dilates arterioles
Increases capillary permeability
CARDIAC MONITORING -
Trends more important than single readings
-
Non invasive techniques better (less risks eg. Pneumothorax/ line infection)
-
BLOOD PRESSURE
-
o
Measured intermittently using automated sphygmomanometer
o
BP doesn’t reflect CO.. BP can be high, but CO low if peripheral vasoconstriction raises peripheral vascular resistance (SVR)
o
Vasodilated septic patients, with low SVR may have a high CO, but still be hypotensive.
CENTRAL VENOUS PRESSURE (CVP) o
Reflects RIGHT ATRIAL PRESSURE
o
Measured with internal jugular/ subclavian vein catheters
o
Useful means of assessing circulating blood volume- determine rate to administer fluid.
o
Increased venous tone can act to maintain CVP, and mask volume depletion during hypovoluemia/heamorrhage.
o
CVP isn’t as important as the response to a fluid challenge
o
High CVP indicates
Fluid overload
BASIC CHEST PAIN HISTORYiix ONSET and PROGRESSION
Cardiac ischemia builds up over few mins
Brought on exercise, exertion, cold weather, emotion
Angina- resolves with rest/GTNreproducible.
Unstable angina- pain at rest/ inc severity/ inc frequency
MI- severe, nausea, vomiting, sweating, lasts at least 30mins, not fully relieved by GTN
Spontaneous pneumothorax or PE cause sudden onset pleuritic pain and dyspnoea (patient usually remembers exactly what doing at time)
SITE & RADIATION
BASIC CHEST PAIN DIFFERENTIALSiix
Cardia ischemia, and pericarditisretrosternal pain.
Ischemia- pain tight and crushing- radiates to neck, back, jaw, arms
Pericarditis is pleuritic, relieved sitting forwards, worse laying flat.
PLEURITIC o
Sharp pain
o
Worse on deep inspiration, coughing, movement
Dissecting AA: tearing pain radiating through the back
o
Pneumothorax
Pulmonary disease- unilateral pain that the patient can locate specifically
o
Pneumonia
Oesophageal disease- retrosternal pain- may mimic cardiac pain
Referred pain from vertebral collapse/ shingles- dermatomal pattern
o
PE
o
Pericarditis: Retrosternal
CENTRAL o
Angina (crushing, tightness)
ASSOCIATED SYMPTOMS
DYSPNOEA:
RISK FACTORSiix
IHD o o
smoking, family, hypercholesterol, hypertension, diabetes. (SF C HD Sausage Fest Causes HD!)
PE travel history, immobility, surgery, fam hist, pregnancy, malignancy o wells score (Pist FM ) Pneumothorax o spontaneous- (young, thin men), trauma, emphysema, asthma, malignancy o
LOOK FOR? abnormal lipids: o xantholasma o tendon xanthoma CHEST PAIN INVESTIGATIONS ix Tar stained fingers (IHD) Hot, oedematous calf: DVT (IHD) GP,Hypertension (non-acute chest pain) Marfans syndrome Diabetes (IHD)
CHEST PAIN INVESTIGATIONSix
ECG (ACS)
FBC (to exclude anaemia).
o
New onset LBBB
Renal function tests and electrolytes.
o
T wave changes
TFTs. (arrhythmia from hyper T)
o
ST depression/elevation
CRP.
Fasting lipids and glucose.
o
Sinus Tachycardia
Resting ECG. Note: a resting ECG is normal in over 90% patients with recent symptoms of angina. If an urgent ECG is considered necessary on clinical grounds, admission to hospital is usually required.
o
AF
o
R. heart strain
o
R. Axis deviation
o
RBBB
o
S1Q3T3 (deep S wave in 1, Q wave in 3, T-wave inversion in 3)
Additional tests if a non-cardiac cause is suspected - eg,
o
ECG (PE)
CXR,
o
LFTs and amylase,
o
abdominal ultrasound.
ECG (pericarditis)
PRESENTING WITH PALPITATATIONSx
Palpitation s PALPITATIONS HISTORY kkkkkmmmmm REGULAR REGULAR • • • •
CAUSES ooo IRREGULAR IRREGULAR
Non- Cardiac causes TACYCARDIA: What the patient means by palpitations. SLOW It should mean an awareness of the heart beating. SLOW FAST FAST It may really be a pulsatile tinnitus or a carotid bruit. FAST PACE!!!! Ask the patient PERSISTANT o how often it happens, PERSISTANT OCCASIONAL OCCASIONAL o VT how long it lasts and SINUS BRADY Fever VT SINUS BRADY o any precipitating or relieving factors. Sometimes people are only aware of it whilst lying down AF ECTOPIC at night. AF ECTOPIC Anaemia AFof block block Determine whether the rate is regular or irregular. AF- degree degree of TACHYCARDIA TACHYCARDIA Ask the patient to tap out the beat. ECTOPIC AF This may be regular or irregular. It may be a normal rate AF ECTOPIC Sympathomimetic drugs COMPLETE HEART S (paroxysmal) or fast. COMPLETE HEART S (paroxysmal) AF BLOCK BLOCK Try toAF estimate the rate. ATRIAL Establish whether there are any symptoms that ATRIAL Thyrotoxicosis accompany the palpitations, such as sweating or FLUTTER (with FLUTTER (with breathlessness. SVT SVT block) block) These may be organic or psychosomatic in origin. Pregnancy Associated chest pain?.sinister significance! Enquire about consumption of caffeine. Palpitations may be related in time to consumption but assess daily intake Anxiety (pain) Arteriovenous too fistulae Ask about alcohol consumption. Ask about smoking. The level of nicotine in cigars tends to be rather higher than in cigarettes. In young people ask about use of illicit substances, Cigrettes, alcohol, caffeine especially cocaine, 'ecstasy' methylenedioxymethamfetamine (MDMA) - and amfetamines. Exercise OTC and prescribed meds! High levels of anxiety can also result from withdrawal of sedatives such as benzodiazepines. Causes of Bradycardia Ask about general health and well-being. There may be great anxiety in the individual's life at present. There may be shortness of breath on exertion, loss of Athletes weight or gain in weight, with ankle oedema. Symptoms of thyrotoxicosis- can cause sinus tachycardia, AF / Atrial flutter. Hypothyroidism History of:
PALPITATIONS- EXAMINATIONx
If the patient currently has the palpitations then it is easy to assess the rate and regularity of the pulse and to get an ECG to confirm the diagnosis.
Consider the following:
o
Does the patient look well?
o
Does the patient look anxious?
o
Is there exophthalmos to suggest thyrotoxicosis?
o
Are the fingers stained with nicotine?
PALPITATIONS- WORKING OUT DIFFERENTIALSx
Anxiety: diagnosis of exclusion: It may be part of a panic attack. There may be an occasional 'missed beat'. This is really a misnomer, as what happens is a premature beat, usually from an ectopic source and this leads to a weak beat followed by a prolonged refractory period during which the ventricles fill more than usual and, when ejection occurs, it is more forceful than usual and so is noticed. Occasional ectopics are fairly common and usually of no sinister significance. They are more likely with a slow pulse. AF or atrial flutter is often paroxysmal before AF becomes established. It is often quite fast but can be slow. T he crucial feature is the random irregularity but this is more difficult to discern with a faster rate. AF is often associated with shortness of breath on exertion, as it tends to reduce cardiac output by about 20%. As a general rule, o ventricular tachycardia (VT) has a rate of 120 to 160 BPM o supraventricular tachycardia (SVT) a rate of 160 to 200 BPM. Paroxysmal tachycardia can result from a junctional re-entry phenomenon. This tends to produce a very fast rate, often in a young person: Wolff-Parkinson-White (WPW) syndrome is well documented. A hyperdynamic pulse may occur with anaemia and thyrotoxicosis. Thyrotoxicosis may produce AF, especially in the elderly where that may be the only feature. Drugs that reduce the resistance in the circulation may also be responsible. These can include nitrates and calcium-channel blockers. Excessive use of a beta agonist inhaler will cause palpitations. Irregularities of rhythm may occur with cardiomyopathy. Bradycardia may produce palpitations, as a high stroke volume is required to meet the necessary
PALPITATIONS- INVESTIGATIONSx
The gold standard is a full 12-lead ECG taken at the time of palpitations. It should, however, be performed even if the palpitations have resolved. Shows o irregular rate and it is easy to deduce the type. o abnormalities suggestive of ischaemia, hypertrophy or cardiomyopathy. o occasional ectopics that are not currently causing symptoms. o incomplete heart block. o short PR interval in WPW syndrome. Basic blood tests HEART MURMURS x HEART MURMURS Hx x o FBC, o U&Es EJECTION oSYSTOLIC No real symptoms- so need to find out TFTs. (A and P area) cause/ consequences. A 24-hour ECG should be arranged (many GPs now have direct access to this). (a Rheumatic feverwhich (mitral Originate either is ventricle tractsofor 24 hours o Thein patient given a outflow device to wear Holter monitor) is valve) returned to the either hospital around the or the IHD (mitral regurg) for pulmonary analysis thearteries following day. aorta o The time that palpitations start and finish shouldbe noted so this can disease be correlated with the Congenital heart They’re either before the valves (in the ECG recording. Hypertension (flow murmus) heart), in athe valves, oran in the arteries. o As refinement, event recorder can be used for patients IVDU whose palpitation frequency is Reach less a crescendo mid-systole, die down than daily. Family Hx hypertrophic cardiomyopathybefore second heart sound (semilunar o For added convenience, leadless monitors have beenautosomal developed. dominant. shutting) If the problem is related to exercise then a treadmill ECG is AORTIC required. Sometimes there is with) an REGURG (associated - irregularity Causes in AORTIC AREA.. either valvular / at rest that is suppressed on exercise. These tend to be ofRheumatoid rather less sinister significance o arthritis supravalvular / subvalvular o Seronegative arthropathies o Coactation of aorta HEARToMURMURS x (ankloysing spondylitis, reiters Supra-aortic stenosis syndrome, psoriatitic arthritis o Aortic sclerosis o Coarctation of aorta o Hypertrophic obstructive Murmurs are vibrations due t turbulent blood flow in heart. MiTRAL REGURG cardiomyopathy (subvalvular) Non valvular causes o Lupus o Hyperkinetic Cardiac Output states o Innocent flow murmurs in children o Rheumatoid arthritis Causes in PULMONARY AREA o High CO: fever, thyrotoxicosis, pregnancy. o Ankylosing spondylitis o Pulmonary arterial stenosis o Congenital heart diseases: ASD, VSD, PDA, Coarctation ofoaorta. Marfans o Pulmonary valve stenosis CLASSIFICATION o Ehlers-Danlos o Flow murmurs, hyperkinetic states, o Osteogenesis imperfect. left-Right shunts (ASD)- left side EJECTION SYSTOLIC biggerremember Consequences PANSYSTOLIC o Aortic valve disease and mitral DIASTOLIC regurg may be asymptomatic. PANSYSTOLIC MURMURS (T and M area) CONTINUOUS o LOW CO- fatigue and weakness o Paliptations- AF Same intensity o Angina (aortic stenosis) Heard throughout the whole of systole and o Symptoms of RV failure merge with the 2nd heart sound (semilunar Anorexia valves shutting) Ankle and leg oedema Causes at APEX (mitral) o Mitral Regurg Hepatic pain o Mitral valve prolapse Intestinal mucosal Causes at TRICUSPID area congestion o Tricuspid regurg o Symptoms of LV failure o VSDs- left side bigger/louder Breathlessness exertion remember Cough Haemoptysis (mitral stenosis) DIASTOLIC MURMURS *always pathological, Orthopnoea always hard to hear. Paroxysmal nocturnal dyspnoea When blood ejected from the ventricles o Syncope (poor CO)- eg, severe and the heart relaxes, Atria are filling. aortic stenosis. Causes at PULMONARY area o Emboli- TIA/Stroke- mitral stenosis o Aortic regurg (early diastolic) o Infective endocarditis o Pulmonary regurg (early diastolic) o Symptoms of enlarged LA, Causes at APEX (MITRAL) area o Mitral stenosis- think in pressing on other structures, especially in mitral stenosis isovolumentic relaxation- ventricles Recurrant laryngeal nerveare filling through here. o Carey Combs murmus (acute horseness- Ortner’s syndrome rheumatic fever, mitral valves
MITRAL STENOSIS
x
-
MITRAL REGURGITATION
x -
x
Mitral valve doesn’t close properly Blood leaks back into LA when LV contracts, instead of going into the body. Due to infective endocarditis, Ehlers Danlos, Marfans, SLE, scleroderma, acute rheumatic fever SYMPTOMS o If acute, you get rapid backpressure into lungs and acute pulmonary oedemaemergency valve repair! o Chronic- eventually, dilation of Left ventricle, HF. EXAMINATION OF A MURMUR o Progressive exertional dyspnoea o (Systemic emboli/stroke, chest pain AF, less common than Inspection, palpation, auscultation stenosis)note when maximum Time a murmur, o . and radiation intensity COMPICATIONS SYSTOLIC o o AFdue to faulty LA Pansystolic? o o HF: orthopnoea, PND Ejection systolic? o Stroke/emboli- due to AF DIASTOLIC o o Fatigue and cold (start hands-from low CO Early diastolic? SIGNS 2nd sound) oo Bibasal crackles- pulmonary Mid diastolic? oedema o LA enlargement- parasternal heave o LV dilation- thrill at apex o Look for things eg. Rheumatoid arthritis, EhlersDanlos, oesteogenesis imperfect (blue sclera) MURMUR o PANSYSTOLIC MURMUR at
Narrowing of the mitral valve (when LALV) Backpressure builds up behind the narrowed valve Reduced amount of blood ejected from LV. Backpressure into lungs. Most caused by past Rheumatic feverfollows a bacterial infection with streptococcus- body makes autoantibodies to clear infection, but also attack mitral valve- inflammation, damage and thickening. Can also be calcification, congenital, endocarditis. More effort form LA to pump into LV- get a hypertrophy of the LA. SYMPTOMS o SOB during exercise o Fainting, dizzy o Tired o Chest pains (reduced flow coronary arteries) o Chest infections- due to bronchial vein ruptures, congention, pulmonary infarction. o Coughing up bloody sputum. COMPICATIONS o AF- due to faulty LA o HF: orthopnoea, PND o Stroke/emboli- due to AF o Fatigue and cold hands- low CO SIGNS o Malar flush o Pulse: small vol/ AF o Evidence emboli- ischaemic bowel/ leg etc o JVP raised o Swollen liver MURMUR o MID DIASTOLIC (blood from A to V, before V contract- blood fills ventricles in diastole, as in systole, pumps to body.) o At APEX (M area)
AORTIC STENOSIS
AORTIC REGURG
x
-
x
-
Aortic Sclerosis is the precursor of calcified, degenerative aortic stenosis Congenital or calcified from aging. Blood harder to pump into body at ventricular systole. SYMPTOMS o Usually none until late o Angina o Exertional dyspnnoea o Syncope o . Triad- chest pain, HF, syncope COMPICATIONS o Sudden death- ventricular dysrrythmia. SIGNS o BP- narrow pulse pressure (less difference between systolic and diastolic, as systolic lower. o LV hypertrophy as more force needed to pass valve- small decrease in radius, massively more resistance. o Small volume, slow rising pulse. o Ventricular heave. MURMUR o EJECTION SYSTOLIC o at AORTIC area (A) o RADIATES TO carotids o Loudest at expiration Investigations o CXR: enlarged heart /
Usually asymptomatic, until ventricle fails! Ventricles make up and make up to pump the body, loosing a bit every time, then can enlarge and keep up no more. After rheumatic fever, infective endocarditis, collogen vascular diseases, SLE, lupus, marfans, ehlers-danlos, ankylosing spondylitis, reiters, bechets. SYMPTOMS o Heart failure when ventricle fails SIGNS o Low diastolic BP o Wide pulse pressure- large difference between systolic and diastolic, as diastolic is even lower. o Collapsing pulse- sharp rise and fall (historical) o Head bobbing with each pulse (hist)- de mussets sign o Corrigans sign: visible pulsation arterial in neck o Traubes sign- pistol shot femoral artery MURMUR o DIASTOLIC o (T) Lower L sternal edgeEXPIRATION, LEAN FORWARDS AND HOLD BREATH o no radiation Investigations
TRICUSPID REGURG -
x
Mitral Stenosis, can cause pulmonary hypertension, which can cause Tricuspid regurgitation Trauma or infective endocarditis Rheumatic fever Blood goes from RA to RV, but in systole, RV is meant to squeeze it into the lungs and it goes back into RA, pressure on venous system of body- portal hypertension. -ISCHAEMIC IVDU? Infective endocarditis? HEART DISEASE- Basics x SYMPTOMS o Fatigue Result of imbalance Myocardial oxygen supply and demand o anOedema andbetween ascites (peripheral) Term covers o Hepatic pain- liver capsule stretched. o Angina MURMUR o ACS o PANSYSTOLIC MURMUR o Anything that reduces blood edge supplyintoinspiration heart! o Loudest at L sternal (T) Due too No radiation o Atherosclerosis of coronary arteries (COMMON) o Investigations o Coronary artery spasm o Emboli o Aortic stenosis (supplies coronary arteries) o Hypertrophic obstructive cardiomyopathy o Arrythmias- cause dec coronary perfusion. o Anaemia o Syndrome X- normal coronary arteries- but abnormal small vessels. Risk Factors o Age- Raised cholesterol, hypertension, cigarettes over time. o Male / post-menopausal women o Family Hx- below 50 / hypercholesterolemia. o Cigarettes (x3)- after 10 years same as non-smoker o Blood lipids- HDL protective, LDL and Triglycerides inc risk o Hypertension- (also a risk of stroke and renal failure)- drugs decrease risk heart disease by 16% o DM – (2x risk major ISH event) o Race- Asian- more DM. o Weight: overweight 2x risk IHD. (increased BP, total cholesterol, insulin resistance, decreased HDL, dec exercise) IHD Investigations o EGC- ACS o Exercise ECG- look for 1mm ST depression o ECHO: assess ventricular function- an exercise stress echo can be used to look at areas of ‘hibernating myocardium- where reduced bloodflow in exercise, as decreased coronary reserve in a territory- if improve at rest- good for intervention. o Nuclear Imaging- Radioactive isotope (thallium) injected during exercise and image after. Isotope taken up by healthy myocardium- infarction are cold spots. Adenosine can give pharmatological stress instead.
PATHOLOGY OF ATHEROSCLEROSIS- Basic TREATING IHD (Basic) x
x
Slowly progressive, focal proliferation of connective tissue in arterial intima. Begins in early life. High lipid GENERAL levels. o Inc exercise, (better collaterial circulation heart, and for VD) smoking stop, diet, LDL – main athrogenic lipid weightloss Plaques- mostly made of COLLOGEN synthesized by smooth muscle cells. oDRUGS 1. ENDOTHELIAL DYSFUNCTION- associated with high cholesteriol, inflammation, and shear forces. 2. MACROPHAGES – enter arterial wall, between endothelial cells, take up lipids and become FOAM - oANTIPLATELET CELLS. o All patients ASPIRIN 75mg Daily- lowers risk subsequent MI and death o 3.o FOAM ACCUMULATE subendothelial zone- forms FATTY STREAKS RiskCELLS of GI bleedmelena,intake with food, PPI o 4.o FOAM CELLS/MACROPHAGES release toxic productslead to aggregation)PLATELET ADHESION, MUSCLE CLOPIDOGREL if aspirin contraindicated (inhibits platelet mostly used postCELL PROLIFERATION, THROMBUS FORMATION NSTMI/angioplasty. 5. Becomes organized- ATHEROSCLEROTIC CAP with FIBROUS CAP. - oBETA-BLOCKERS o 6.o Progressive enlargement, and narrowing of lumen- exertional angina. Reduce Sympathetic tone. o 7.o RUPTUREsudden(reduce thrombus Negativecause ionotropes contractility)- reduce oxygen demand o Neg Chronotripoc (HR)- reduce oxygen demand o is Increase of ischaemic area- decreasing HR, increases time Atherosclerosis initiatedperfusion by inflammatory processes in the endothelial cells of diastolethe vessel wallfor in coronary response to retained (LDL) blood flow. o Contraindications? Asthma, PVD with skin ulceration, 2 nd and 3rd degree heart block. Lipoproteinsoin the blood survival vary in size. Some data suggests that small dense LDL particles are more prone to Improve post-MI pass between endothelial cells, going behind the cellular monolayer of endothelium. o the Good in chronic heart failureshouldn’t be given in acute. NITRATES LDL particles and their content are susceptible to oxidation by free radicals- risk is higher while in the wall than o Cause peripheral vasodilation- especially in veins while in the bloodstream. o Reduces venous return, and ventricular pre-load. o Reduction in a heart wallof distensiondecreases o2and demand of heart(LDL wall-particles angina relief. However, LDL particles have half-life only a couple of days, their content typically carry o fat Nitrates are converted NO- which phospholipids, results in an increased intracellular cyclic guanosine 3,000 to 6,000 molecules, including:to cholesterol, cholesteryl esters, tryglycerides & all other in smooth This stimulates calcium processes and LDL fats in the watermonophosphate outside cells, to cGMP the tissues of themuscle. body) changes with time. Oncebinding inside the vessel wall, free calcium vaaliable to trigger muscle contraction is reduced. particles can become more prone to oxidation. o Nitrates and rest relieve angina in minutes. Endothelial cells respond by attracting monocyte white for blood cells, causing them to leave the blood by stream, o Longer acting nitrates can be effective hours. (isosorbide dinitrate, metabolized penetrate into the arterial walls and transform into liver to isosorbide mononitratethemacrophages. main active metabolite- helps avoid bad 1 st pass metabolism. o Adverse effects due to arterial dilation- headaches, flushing, hypotension, fainting CALCIUM CHANNEL BLOCKERS o Calcium antagonists inhibit influx of calcium into myocyte during action potential and relax peripheral smooth muscle. o Reduced afterload (so less myocardial oxygen demand), reduce HR, increase coronary vasodilation. o Therefore reduce angina o Useful in coronary artery spasm o Dihydropyridines (Nifedipine) may be combined with a beta blocker, as they cause peripheral vasodilation and reflex tachycardia. o Diltiazem has slight neg iontropic and chronotropic effect- if on betablocker- needs monitoring for bradycardia o Al CCB are net iotrope to a degree- be careful in impaired LV function (even through amilodipine good in HF) o Headache, dizziness, flushing, constipation, gravitational oedema. K CHANNEL ACTIVATORS o Nicrorandil- has arterial and venous vasodilating properties o Useful if refractory to other anti-anginal agents. STATINS o HMG-CoA REDUCTASE INHIBITORS o Lipid lowering therapy o Help stabilize plaques- reduce freq of acute coronary events. o If IHD, and cholesterol normal, still should be on statin.
DIAGNOSING ACSx -
-
After acute MI o Up to 18hrs: No macroscopic or microscopic changes o 24-48hrs (2 days): Pale oedematus muscle (macro), (micro) oedema, acute inflammatory cell infiltration, necrosis of myocytes. o 3-4 days: yellow rubbery centre with haemorrhagic border (macro), (micro) Obvious necrosis and inflammation, early granulation tissue. o 3-6 weeks: Silvery scar becoming rough and white, (micro) dense fibrosis. Cardiac Enzymes o Intracellular enzymes that leak out of infarcted myocardium into bloodstream o CREATININE KINASE (peak 1 day) Peaks in 24hrs Cardiac enzyme, also produced by skeletal muscle and brain. CK-MB can be requested if in doubt- a myocardium-bound isoenzyme, specific heart muscle damage. Site of infarct related to serum level of enzyme. Used to assess reinfarction in patients who have elevated troponin from a previous MI o ASPARTATE AMINOTRANSFERASE (peak day 1-2) o LACTATE DEHYDROGENASE (peak day 1-2) o TROPONIN I or T (8-12hrs) Good markers of cardiac damage Proteins involved in myocyte contraction 8-12hrs post MI most reliable
MANAGEMENT HYPERTENSION- Basic
THIAZIDE DIURETICS o Lower body sodium stores- BP falls as dec in blood vol, venous return and CO. o Gradually the CO returns to normal, but the hypotensive effect remains as peripheral resistance decreases o Side effects: GOUT, impaired glucose tolerance. o Low doses (2.5mg bendrofluthiazide) cause little biochemical disturbance without loss of anti-hypertensive effect. High doses not usually needed. POTASSIUM-SPARING DIURETICS o Diuretic induced hypokalaemia. BETA-BLOCKERS o Decrease CO, so initially cause fall in BP o CO returns to normal, but peripheral resistance is ‘set’ to a new lower level so BP remains low. o Renin levels are reduced. o Side-effects: Provokes asthma, and heart block. Neg ionotrope. Cold hands and fatigue. CALCIUM CHANNEL BLOCKERS o Calcium antagonists. ACUTE CORONARY SYNDROMES: (Nifedipine)- good vasodilating drugs that can cause reflex tachycardia. o Dihydropyridines Pathophysiology o Diltiazem- neg ionotrope, and chronotrope- contraindicated in HF o Amlodipine- safe in HF ACUTE CORONARY SYNDROMES: o Flusing, headache, oedema, constipation Affects 7% population Pathophysiology o Don’t use verapamil with beta-blocker. Increases with age, males, post-menopause ACE INHIBITORS RF: smoking, hypertension, diabetes, o Inhibit renin-angiotensin-aldosterone axis Affects 7% population cholesterol, family. o Increase in vasodilating bradykiin Increases with age, males, post-menopause About 20% all deaths in UK o ofMore effective in yonger patients with higher levels- best in young white renin RF: smoking, hypertension, diabetes, cholesterol, After MI-o30-60% hospital, 10% Gooddeath in HF,before proteinurig nephropathy, diabetes family. in hospital, years (HF to or bradykinin), MI) o 20% Dry within cough 2 (secondary Hyperkalaemia, Transient worsening in serum About 20% of all deaths in UK Variant Angina? Vasospasm creatinine (GFR)- as intraglomerular pressure falls, Acute renal failure (if sepsis, After MI- 30-60% death before hospital, 10% in Stable angina? Fixed Plaque renal artery stenosis) hypovolumeia, hospital, 20% within 2 years (HF or MI) ACS: thrombosis overelectrolytes ruptured complex o Monitor until dose titrated. Variant Angina? Vasospasm plaque ANGIOTENSIN II RECEPTOR BLOCKERS Stable angina? Fixed Plaque o Block rein angiotensin system- similar to ACE ACS: thrombosis over ruptured complex plaque CONSEQUENCES oOF CORONARY ARTERY OCCLUSION Good if chronic cough on ACE- don’t effect bradykinin production o CV protective effect CONSEQUENCES OF CORONARY ARTERY OCCLUSION o LEFT CORONARY ARTERY MINOXIDIIL o Potent vasodilator, dec Major PVR- can cause reflex tachycardia- use beta-blocker Supplies LAD and Circumflex: o LEFT CORONARY ARTERY o Fluid retention diuretic) contribution to LV and (use RV perfusion Supplies LAD and Circumflex: Major o RIGHT CORONARY ARTERY o Hirsutism contribution to LV and RV perfusion Occlusion causes inferior MI. o RIGHT CORONARY ARTERY Main Supply to RV and AV node Occlusion causes inferior MI. o LAD ARTERY Main Supply to RV and AV node Occlusion causes Anterior MI o LAD ARTERY Supplies LV, Septum and RV Occlusion causes Anterior MI o CIRCUMFLEX ARTERY Supplies LV, Septum and RV Causes lateral MI o CIRCUMFLEX ARTERY Causes lateral MI FACTORS LIMITING OXYGEN SUPPLY
Artery NARROWING: Vasospasm and complex plaque thrombosis Reduced FLOW: Hypotension, tachycardiareduces diastolic time, inc LV end-diastolic pressure, LV hypertrophy. Reduced OXYGEN CARRYING capacity: Anaemia, hypoxaemia.
FACTORS LIMITING OXYGEN SUPPLY
FACTORS LIMITING OXYGEN DEMAND
Increased HR: (anxiety/ exercise) Inc LV AFTERLOAD / MASS: (increases myocardial wall stress eg. Hypertension and
Artery NARROWING: Vasospasm and complex plaque thrombosis Reduced FLOW: Hypotension, tachycardia- reduces diastolic time, inc LV end-diastolic pressure, LV hypertrophy. Reduced OXYGEN CARRYING capacity: Anaemia, hypoxaemia.
FACTORS LIMITING OXYGEN DEMAND
Increased HR: (anxiety/ exercise)
CLINICAL FEATURES OF MI Crushing/ heavy retrosternal pain Radiates to o Neck o Medial L arm o Right chest or shoulder blades Atypical: Burning, localized eg. Only jaw, absent. STABLE ANGINA o Precipitated by exercise/anxiety o Relieved in 5 mins by rest/sublingual nitrates. UNSTABLE ANGINA and NSTEMI o Frequent, unpredictable, over 15mins ACS INVESTIGATION o Respond less to nitrates o New pain? Pain with less exertion? 1st you need to differentiate ACS form other Autonomic manifestations eg. Nausea and life threatening conditions e.g. Aortic sweating? Radiation to new sites eg. Jaw? dissection and benign things e.g. Reflux, Indicate increasing coronary artery musculoskeletal. ACUTE CORONARY SYNDROME CHRONIC STABLE (exertional) occlusion and NSTEMI(ACS) ANGINA o Typically: Crescendo angina: inc freq INVESTIGATIONS of prolonged, freq angina. Angina in which Spectrumperiods of increasingly life-threatening conditions ischemia at rest/minimal exertion (and myonecrosis) follows sudden artery occlusion due to thrombosis Fixed stable coronary artery o Both have ST depression and T wave ECG (and vasoconstriction). occlusions limit blood flow inversion ECG. o Site and Size infarct. Initiated by STRESSon – INDUCED RUPTURE (hypertension) of small causing predictable, reversible o NSTEMI- high risk of coronary artery o ST Elevation (immediate eccentric (non-circumferential), non-occluded (under 50%) COMPLEX cardiac ischemia during occlusion and cores deathand (in 4-6 revascularization) plaques, with lipid-rich thinweeks) fibrous plaques. exercise. o rupture 8% hospitalized die in 30 days, 8% reo ST Depression and T inversion: NSTEMI Plaque stimulates Stenosis are caused by infarction. formation doesn’t benefit from thrombolysis. o Thrombus smooth circumferential INCREASED RISK OF FUTURE EVENTS o Survival at 6 months is similar for a with o Vasospasm atherosclerotic plaques o ST depression NSTEMI, and STEMIeven though early to o Arterial Occlusion thick fibrous caps: unlikely o Elevated troponin in STEMI. rupture. Length of time and extent of the occlusion determine severity of mortality higher o Recurrent angina o Serial ECGS diagnose. toThick fibrous cap, small lipid ischemia: defines the syndrome, ECG changes, symptoms, degree of o Diabetes o INFERIOR: RCA, II, III, aVF core. myocardial necrosis (cardiac enzyme release). o Previous o ANTERIOR: l, aVL, often V2, V3, V4, V5 LAD, Ischemia sub UNSTABLE ANGINASTEMI Impaired artery LV INTEROSEPTAL: LAD, V2, V3, endocardial, as V4 systolic oo Coronary occlusion of limited extent/duration. o HF o ANTEROLATERAL: LAD, V3,greater V4, V5 than compression oo Ischemia, not necrosis o (send High for risk!? Early cardiac angiography. o APICAL: LAD, endocardial II, III, aVF, V5, V6 epicardial than NSTEMI PCI!) No risk factorsExercise ECG incomplete/ alleviated by o LATERAL: Circumflex/diagonal, I, aVL, V6 aretries. oo Occlusion may be temporary/ MI collateral vessels Right/Circumflex, VARIANT- PRINZMETALS o POSTERIOR: R wave in NSTEMI and (cardiac enzyme uncommon, caused V1,-2 with ST ANGINA: depression. oo Ischemia andSTEMI necrosis limited to SUBENDOCARDIUM positive) by transient coronary artery ENZYMES o Myocardial damage: cardiac enzymes. o (send Thrombolytic vasospasm due enzymes to over- in o A twofold increase in plasma STEMI for PCI!) therapy is only beneficial on reactivity (to noradrenaline)/ STEMI myocardial damage. o Occlusion causes transmural ischemia impaised flow-mediated o MI: abrupt onset severe, prolongued pain, o Cardiac Troponins at 12hours are o Q-waves Often near unrelieved by nitrates. sensitive and vasodilation. specific for necrosiscan o Autonomic symptoms: Cold, clammy, detect MI after surgery, and when ECG sweating, nausea, vomiting. non-specific eg. LBBB. o Dyspnea, anxiety CXR o Only 25% have preceding unstable o Heart Failure angina. o Aortic disssection o Pain might not occur in elderly/diabetic ECHOCARDIOGRAPHY patients presenting with collapse, o Assesses contractility. confusion, HF, metabolic dysfunction. o Reveals dyskinesia o TACHYCARDIA: Anterior MI o Mural thrombus o BRADYCARDIA + HEART BLOCK: Inferior MI o Septal defects (conducting tissue damage) o Papillary muscle rupture. o Hypotension (systolic under 90): indicates INCREMENTAL EXERCISE STRESS TESTS a large MI, ie over 40% LV damage and o Reveal cardiac ischemia as angina. heralds cardiogenic shock. o Failure of BP and HR appropriate o Ascultation may show 3rd and 4th heart responses. sound (gallop rhythem) and systolic o EST= Bruce protocol murmur. st MYOCARDIAL PERFUSION SCANS o EARLY COMPLICATIONS MI (1 week) o Detects reduced isotope uptake in poorly Arrythmias perfused myocardium using a gamma Pericarditis camera. Papillary muscle/ free wall rupture o Alternative to exercise stress test in bed VSD
ACS GENERAL MANAGEMENT
MANAGEMENT OF STABLE ANGINA
NITROVASODILATORS o Efective, but tolerance develops BETA-BLOCKERS o First line therapy o Improve prognosis o Increase myocardial perfusion in diastole- slow HR and reduce pre-load and afterload so reduce LV tension. CALCIUM CHANNEL ANTAGONISTS o Useful when beta-blockers contraindicated. o Relive coronary vasospasm. o Nifedipine, can cause reflex tachycardia, and exercerbate HD (neg ionotrope) REVASCULARISATION o Needed if symptoms deteriorate. o Needed if positive exercise stress test o Needed if angiography revelas over 70% stenosis in all 3 main, left main or proximal LAD arteries.
Treatment aims to reduce MYOCARDIAL OXYGEN CONSUPMPTION, whilst increasing supply. By DECREASING o HR (beta-blockers) o AFTERLOAD: (antihypertensives) Risk Factor Reduction o Smoking, diet, weightloss, treating hypertension and DM. Antiplatelet (aspirin) and lipid lowering MANAGEMENT UNSTABLE ANGINA/ drugs (Statins) NSTEMI ACE inhibitors- reduce atherosclerosis
Thrombolytic therapy not beneficial. Nitrates, Beta blocker, CCA and…… ANTIPLATELET THERAPY o All patients 300mg Aspirin immediately o 75mg a day o Irreversible cyclo-oxygenase inhibition prevents platelet aggregation within 15mins chewing aspirin- preventing MI/sudden death by 50% o Clopidogrel inhibits its ADPStimulated platelet aggregation, reduces mortality when combined with aspirin after 30days. GLYCOPROTEIN IIb/IIIa ANTAGONISTS o Most effective platelet inhibitorsUsed after PCI to prevent stent thrombosis. ANTICOAGULANT THERAPY o IV unfractunated heparin.
MANAGEMENT OF INFARCTION/STEMI
Early reperfusion after MI limits infact size and mortality. IMMEDIATELY o Pain relief CONTRAINDICATION TO THROMBOLYTIC o Monitoring THERAPY o Oxygen Therapy o Aspirin o Beta-Blockers Absolute o Clopidogrel o (Heparin) Active Bleeding (GI heamorrhage) o Revascularisation with PCI/TT Aortic Dissection OPIATES Neurosurgery/ head injury o Morphine Recent CNS disease (tumor) under o Pain, reduces pre-load, lower myocardial oxygen 6months consumption, lower anxiety induced catachlomine CVA in last 2 months release. Recent operation (under 4 weeks) ASPIRIN Recent Trauma (under 4 weeks) o Reduces 35-day mortality by 23% when with TT. Diastolic Hypertension BETA-BLOCKADES Coagulopathy (less platelets) o Reduces size of Infarct o Reduces arrhythmias Relative o Reduces Mortality- espesh if tachy/ Hypertensive o CONTRAINSICATED: Asthma, HF, Bradycardia Previous CVA/TIA NITRATES Recent CPR o Under 24hrs Systemic Hypertension o Reduce pain, infarct size, HF Recent Central lines ACE INHIBITORS Intracardiac thrombus o Over 24hrs, improve LV remodeling AAA o Reduce HF in high risk patients. IONOTROPIC SUPPORT o In cardiogenic shock PCI o If under 90mins, is the preferred method of revascularization. o Primary PCI- under 6hrs, re-opens over 90% occluded arteries o Significant mortality of unsuccessful. THROMBOLYTIC THERAPY (TT) o Dissipates thrombus o Reverses Ischemia o Limits myocardial injury o Limits complications (HF) o Most effective under 2hrs of symptom onset- until 12hrs ARRYTHMIAS STREPTOKINASE (SK) or tPA TISSUE PLASMINOGEN ACTIVATOR o Main TT agents byRate/Rhythem infusion Abnormalities of thegiven Heart o SK cheap but allergenic (single use) Due to Aberrant impulse generation / conduction (eg. Re-entry circuits) AF affects 10% of over 75s Arrythmias (VF/VT) cause 40% deaths in IHD Asymptomatic/stable rhythems can be just observed, while cause corrected eg. Hypokalaemia. Prevention o Early correction hypoxaemia o Electrolyte disturbances (hypokalaemia) o Acid-base imbalance o Cardiac ischemia o Vagal stimulation (pain) o Drugs (theophylline) o Cardiac irritants (intra-cardiac catheters) Antiarrythmic drugs o Selected due to rhythem and underlaying pathophysiology o Therapy often doesn’t work and can cause new arrhythmias. Other Therapy? DC Cardioversion, Implantable defibrillators, radiofrequency catheter ablation (destroys accessory pathways)/ ectopic pacemakers.
TACHYARRYTHMIAS
Tachy is over 100bpm Physiological (exercise) Either Supra-ventricular or ventricular Pathological (thyrotoxicosis/ HF) Detrimental if cause symptoms:- terminate immediately Stimuli which inc sympathetic tone, with cardioversion/ drugs! accelerates SA node paceing. o Hypotension TREAT? Remove case. o Pulmonary oedema o Reduce tissue perfusion ATRIAL FLUTTER Caused by o INCREASED PACEMAKER ACTIVITY BRADYARRYTHMIAS o RE-ENTRY CIRCUITS An anticlockwise atrial re-entry circuit. Increased pacemaker: faster spontaneous membrane Causes rapid, co-ordinated Under 60bpm depolarization, lower thresholds and oscillations during redepolarization. Due to Delayed conduction. polarisation trigger early APs. 300bpm If symptomatic treat with Re-entry circuits:A depolarization wave travels around a Ventricular rate depends on AV Node ATROPINE circle of myocardial tissue. If the tissue is not refactory o refractoriness, with conduction of o BETA – AGONISTS when the impulse returns, it will depolarize again producing every 2nd, 3rd or 4th depolarization. a recurring circuit (paroxysmal tachys). o PACING (2:1, 3:1, 4:1 block) BP and CO fall if stroke volume cant increase due to Tachycardia with rate of exactly DIAGNOSIS reduced compliance / contractility. 150bpm suggests Atrial Flutter. o NARROW QRS TACHYCARDIAS SINUS BRADYCARDIA Treat? Adenosine bolus HEART BLOCK o Class 1a, 2, 3, 4 drugs / To assess/ terminate o FIRST digoxin. Usually SVT. o SECOND: MOBITZ 1+2 o Class 1a may cause VT, so o WIDE COMPLEX TACHYCARDIAS o COMPLETE Usually VT AF Hard to tell if its unusal conduction of SVC SINUS BRADYCARDIA Exclude AV node block. Spontaneous, chaotic, atrial If haemodynamically unstable, treat as VT Normal ECG p waves, and Av node conduction depolarization. DC Cardioversion Treated by addressing causes eg. Vagal reflexes Over 300bpm Doesn’t work? Probably SVT- use adenosine (pain), Drug Toxicity (beta-blockers), Atropine. Refractory AVN conductions limits Ongoing treatment amiodarone. ventricles to under 200bpm. VAGAL STIMULATION (eg. Carotid sinus massage) HEART BLOCK Ineffective atrial contraction slows HR and may cardiovert some SVT predisposes to atrial thrombus and Due to AV node or Conducting tissue ischemia. thromboembolism. SUPRAVENTRICULAR TACHYARRYTHMIAS (SVT) Treat?! Common after inferior MI (RCA supplies the AV node) o Originate above the AV Node o anterior Anticoagulation (stroke) Heart Block after an MI suggests a large o Dizziness, palpitations, breathlessness o Digoxin (controls resting HR) infarct… requires early pacemaker insertion. o Rarely life-threatening. Can be sudden death. o Beta-blockers (control exercise SINUS TACHYCARDIA st HR) 1 DEGREE HEART BLOCK ATRIAL FLUTTER AF VENTRICULAR FIBRILLATION AVN RE-ENTRANT TACHYCARDIA Slows AV node conduction PRE-EXCITATION SYNDROMES Prolongued P-R (over 0.2 secs) Chaotic ventricular rhythm An early warning of worse heart block later. VENTRICULAR TACHYARRYTHMIAS Follows Acute MI VENTRICULAR TACHYCARDIA o Arise in ventricles, in patients with IHD, 2nd DEGREE HEARTBLOCK Treat?! Immediate DC cardioversion! cardiomyopathy, congenital disease. o Class 2/3 drugs/ implant defib Seriouscircuits eg. Scar tissue from Due oto re-enry (recurs) Some Atrial beats are not conducted to the ventricles VF MI, with uniform QRS MOBITZ1: WENKEBACH Or focal ectopic automaticity (drugs or o Progressive P-R lengthening, then failure of metabolic) with irregular or phasic impulse (don’t really treat) TORSADE DE POINTES QRS (polymorphic MOBITZ2: VT)- unstable and may progress to VF. o Below the AVN in the His Purkinje system Ventricular rate 150 – 250 o Eveny 2nd or 3rd artrial impulse initiates Treat!? Terminate with cardioversion ventricular contraction (2:1 block etc) Or class 1a/1b drugs o (need pacemaker, as complete heart block Use class 2 or 3 to prevent initial often follows) reoccurance
AV RE-ENTRANT TACHYCARDIAS
SINUS TACHYCARDIA
PAROXYSMAL SVT! Re-enrant circuits between atria and ventricles. Or between atria and AV Node- ie in the AV NODE Treat!? Vagal Stimulation Drugs slowing Av node conduction (Adenosine), class 2, class 4
3rd DEGREE COMPLETE HEART BLOCK
Conduction between atrium and ventricles ceases AV Node pacemaker action produces nonconducting junctional escape rhythems (asymptomatic) Infranodal WC pacemaker escape rhythms are unstable, slower (30 bpm), symptomatic. Essentail to insert pacemaker.
PRE-EXCITATION SYNDROMES An Accessory AV Pathway: BUNDLE OF KENT in Wolf Parkinson White Syndrome. Bypasses the AV node, depolarizing an area of the ventricle early, shortening the P-R interval (time for atria then ventricles to contract) Slow transmission from the pre-excited area- no conducting tissue, creates a delta wave on ECG. Treat!? Class 1a, 1c, III IV drugs And ADENOSINE
ATRIAL TACHYCARDIA Automaticity in ectopic atrial pacemakers Treat!? o ADENOSINE to terminate o Class 1c or 3 drugs o Correct underlying metabolic defect o Radiofrequency catheter ablation.
PATHOPHYSIOLOGY OF HEART FAILURE SYSTOLIC FAILURE
HEART FAILURE AND PULMONARY OEDEMA
When CO insufficient to meet the metabolic needs of the body. Or can only do so with ELEVATED FILLING PRESSURES. (pre-load) Initially compensatory mechanisms maintain CO at rest But as HF and CO deteriorates, exercise tolerance falls, and ‘downstream’ hydrostatic pressures increase Common causes: IHD and Hypertension. Volume overload can cause pulmonary oedema, despite cgood heart function. 5 year survival under 50%.
LV FAILURE
Most common Downstream pulmonary capillary ‘wedge pressure’ (PCWP) rises to 25 ish. Fluid filters into the alveoli and interstitial spaces, causing pulmonary oedema, and breathlessness. Low plasma oncotic pressure (hypoalbuminaemia) or increased membrane permeability (inflammation) can cause pulmonary oedema at lower PCWP.
DIASTOLIC DYSFUNCTION
RV FAILURE
Causes SYSTEMIC CONGESTION (e.g. ankle swelling, hepatomegaly) Usually associated with LV failure. Biventricular failure: CONGESTIVE CARDIAC FAILURE
Reduced Myocardial contractility and Ejection Fraction (under 50%) accounts for most of HF. o Due to o IHD o Cardiomyopathy o Metabolic toxicity o Valve defects o Arrhythmias Initially CO maintained by compensatory mechanisms o Inc. sympathetic drive o Raised circulating volume (renin) o Raised Filling pressures These mechanisms have detrimental effects Failing heart responds poorly to preload Subsequent pulmonary and peripheral congestion Large ventricular volumes increase cardiac work and impair function In pressure overload (aortic stenosis), compensatory hypertrophy initially improves ventricular Ejection Fraction. Reduced compliance and capillary density eventually decreases blood supply and contractility.
When LV relaxation/filling (an energy dependent process) is impaired due to o myocardial ischemia o Fibrosis o LV hypertrophy (hypertension) Poor diastolic LV perfusion Reduced LV compliance inc PWCP, and precipitates pulmonary oedema- even if normal Ejection Fraction and contractility.
MANAGE HF
CLINICAL FEATURES
Treat the o CAUSE (IHD/valve) o Pathophysiology (DD) o Precipitating events (arrhythmias) AFTERLOAD REDUCTION rapidly improves LV function and CO in the failing heart. But may cause Hypotension. PRELOAD REDUCTION: relieves symptoms (eg. Pulmonary oedema), but CO is not increased. Non-invasive monitoring and less frequently pulmonary artery catheterization- may be required to measure filling pressures, CO, vascular resistance.to optimize HF treatment.
ACUTE LEFT VENTRICULAR FAILURE Presentation depends on o Onset speed Priority: Immediate relief of breathlessness of o Underlaying pulmonary oedema. o Ventricular involvement DIAGNOSTIC INVESTIGATIONS Sitting position most comfortable. HF precipitated/ aggravated by Supplemental OXYGEN (60%) corrects hypoxaemia. o Stress Loop (furosemide IV) initially reduce LV DIURETICS Cardiac Enzymes o Acute illnesses preload, and relieve dyspneoa by pulmonary venous ECG o Drugs dilation. CXR o Pregnancy Subsequent lowers fluid loadpeptide) and cardiac Reduced CO causes fatigue, anorexia, exercise Serum diuresis BNP (b-type natrieuritic filling increased pressures.by myocardial wall stress: sensitive limitation. NITRATES (IV/sublingual) LVF and specific for HF. inc venous capacitance, and coronary arteries in ventricular IHD. CAUSES HF AND PULMONARY dilate ECHO: wall hypokinesia, o Breathlessness DIAMORPHONE decreases preload- potent OEDEMA enlargement. o Hypoxaemia venodilator effects, andreduced V02, by in relieving anxiety. Ejection fraction: HF o Orthopnoea BRONCHODILATORS (salbutamol) reduce CO and BP may be normal o PND MYOCARDIAL DYSFUNCTION bronchospasm (but aminophylline precipitates o Cough- frothy pink sputum arrhythmias). o GALLOP RHYTHEM (S3, S4 added NEW YORK HEARTand ASSOCIATION CPAP reduces hypoxaemia, work of breathingo sounds) IHD CLASSIFICCATION HF used more often in HF o CARDIOMYOPATHIES o COURSE CREPS LUNG BASES ARRYTHMIA CONTROL essential. PREGNANCY RVF o MYOCARDIAL DISEASE CLASS 1: (mild): no activity limitation, no o o Systemic congestion, raised JVP (amyloidosis) LOW-OUTPUTsymptoms LEFT VENTRICUAR FAILURE from ordinary activity. E.g. Fatigue, o Hepatomegaly If you have an inferior MI, dyspnoea, palpitations o o Ankle oedema you can have RV failure CLASS 2: (mild): Slight limitation physicalaims When pulmonary oedema controlled, treatment o Ascites isolated, as blood activity.LV Comfortable at Diastolic rest, symptoms with to IMPROVE FUNCTION, Dysfunction o Onset may be acute supply (MI) with from RCA. ordinary activity. D, PROGNOSIS. cardiogenic shock/ acute pulmonary PRESSURE OVERLOAD INHIBITORS: CLASS 3: (moderate): Marked limitation ACE Reduce afterload, increase CO, o LEFT: hypertension, aortic activity, only and comfortable restreducephysical symptoms (fatigue) lengthenat survival. stenosis (mitral stenosis minimal activity causes symptoms. Benefit most HF patients unless contraindicated doesn’t cause LV failure) (renal artery stenosis), or side effects (cough) o RIGHT: Pulmonary Selectove BETA-BLOCKERS BISOPROLOL improve hypertension due to chronic prognosis by reducing myocardial ischemia and lung disease (cor arrhythmias. May precipitate pulmonary oedema, pulmonale), pulmonary bronchospasm, heart block. stenosis. CALCIUM CHANNEL BLOCKERS: alleviate diastolic VOLUME OVERLOAD dysfunction by reducing hypotension and coronary o Excessive fluid vasospasm administration Tachycardia and impaired contractility limit use. o Retention (renal failure) DIGOXIN: no ionotropic effects, useful in HF with AF o Aortic/ mitral valve regurg PROPHYLACTIC ANTICOAGULANTS: reduce causes LVF associated thromboembolic events. o Tricuspid regurg causes RVF. IMPAIRED FILLING RIGHT VENTRICULAR FAILURE o Constrictive pericarditis (TB, rheumatic heart Diuresis reduces peripheral oedema disease, pericardial But detrimental if high RV filling pressures remain to effusion, cardiac maintain CO tamponade). Afterload reduction with pulmonary vasodilators ARRYTHMIA (CCB) usually limited by hypotension. o Impair ventricular filling: OXYGEN THERAPY relieves cor pulmonale hypotension
TACHYCARDIA o Cause myocardial ischemia-
CARDIOGENIC SHOCK
Reduced Reduced CO CO (digoxin) (digoxin)
BETA BETA SYMPATHETIC SYMPATHETIC ACTIVATION ACTIVATION (Betablockers) (Betablockers)
INCREASES INCREASES CONTRACTILITY CONTRACTILITY and HR and HR
Reduced CO Reduced CO
Reduced CO Reduced CO
ALPHA ALPHA SYMPATHETIC SYMPATHETIC ACTIVATION ACTIVATION
ARTERIAL ARTERIAL VASOCONSTRICTIO VASOCONSTRICTIO N N (arterial (arterial vasodilators) vasodilators)
INC INC AFTERLOAD AFTERLOAD
heartMore Work Work heart- More and and oxygen oxygen consumption consumption
INC INC Myocardial Myocardial Damage Damage INC Ca2+ Overload Overload INC Ca2+ INC energy deficit deficit INC energy Cardiac Cardiac Remodelling Remodelling
heartWork heart- More More Work and oxygen and oxygen consumption consumption
RENIN-ANGIOTENSIN RENIN-ANGIOTENSIN ACTIVATION ACTIVATION
ALDOSTERONE: ALDOSTERONE: (spironolactone) (spironolactone) Fluid retention retention Fluid (diurteics)....... PRELOAD (diurteics)....... PRELOAD INCREASED! INCREASED! (venodilators) (venodilators)
ANGIOTENSIN II: ANGIOTENSIN II: (angiotensinII receptor (angiotensinII receptor blockers) blockers) ARTERIAL ARTERIAL VASOCONSTRICTION...... VASOCONSTRICTION...... AFTERLOAD AFTERLOAD INCREASED! INCREASED! Renal artery... FLUID Renal artery... FLUID RETENTION RETENTION PRELOAD PRELOAD INCRESED INCRESED
heartWork and and heart- More More Work oxygen consumption oxygen consumption
INC INC Myocardial Myocardial Damage Damage INC Ca2+ Overload INC Ca2+ Overload INC energy energy deficit deficit INC Cardiac Cardiac Remodelling Remodelling
INC Myocardial Damage INC Myocardial Damage INC Ca2+ Overload INC Ca2+ Overload INC energy deficit deficit INC energy Cardiac Remodelling Remodelling Cardiac
Reduced Reduced CO CO
Reduced CO Reduced CO
Reduced Reduced CO CO
Cardiovascular compensatory mechanisms and the detrimental positive feedback effects they exert in HF.
CARDIAC EMERGENCIES: HYPERTENSIVE EMERGENCY
Severe hypertension is o Systolic 220-240 o Diastolic 120-140 Used to be called accelerated/malignant hypertension, now based on presence/absence LIFE-THREATENING END ORGAN DAMAGE. (LTOD)- e.g. aortic dissection This determines treatment urgency. If organ damage, needs to be reduced to safe levels (diastolic 100) within 2 hrs. Caution: rapid fall in BP can cause strokes, accelerated renal failure, cardiac ischemia. If NO end organ damage…. Gradual reduction over 6-72hrs preferred. Most common cause o Inadequate/discontinued therapy for benign essential HT. In under 30s or blacks, over 50% have a secondary cause o Renovascular disease o Phaeochromocytoma o Endocrine o Drug induced catachlomine release (cocaine) o Pregnancy related Most end organ damage due to ARTERIOLAR NECROTIZING VASCULITIS And LOSS OF VASCULAR AUTOREGULATION
HYPERTENSIVE EMERGENCY o o o o o o o
Clinical features of end organ damage (HTN) ENCEPHELOPATHY Decreased vascular auroregulation- cerebral oedema Headache, nausea, vomiting, blurred vision, confusion. Later: Focal neurological deficits, seizures, papilloedema, coma PULMONARY OEDEMA Due to Increased LV afterload (not fluid overload): treat by reducing afterload. PROGRESSIVE RENAL IMPAIRMENT Increased urea and creatinine, dec GFR. Haematuria, proteinuria HTN can be secondary to glomerulonephritis and renal artery stenosis- bruit? STROKE SYNDROMES o Cerebral infarctions o Cerebral Heamorrhage o SAH RETINOPATHY o Grade3: exudates and hemorrhage o Grade4: Papilloedema. AORTIC DISSECTION o Tearing chest/back pain o Arm/leg BP difference o Absent peripheral pulses ANGINA + MI o Due to inc LV afterload, inc wall stress, dec myocardial perfusion PREGNANCY RELATED
HYPERTENSIVE EMERGENCY: MANAGEMENT
Severe HTN with end organ failure: REQUIRES ADMISSION! Rarely, immediate BP reduction needed (eg. Dissecting AA) Potent, titratable, vasodilator infusions. Arterial BP monitoring Mandarory! IV Therapies: o SODIUM NITROPRUSSIDE (rapidly reversible arterio-venous dilator)administered by infusion pump to avoid hypotensive episodes. o GTN (arteriovenous dilator)- effective when Myocardial ischemia and pulmonary oedema there. o LABETALOL: alpha and beta blockergood for hypertensive encephalopathy. May exacerbate asthma, HF, heart block. Severe hypertension with no end organ damage o Use oral regimes when possible o Lower over 24-72 hrs o NIFEDIPINE (sublingual) – rapid onset, short half-life, titratable.
ACUTE PERICARDITIS Infection (most viral), MI, Uremia, Connective tissue disease, Trauma, TB, Neoplasia. Dresslers syndrome. DRESSLER’S SYNDROME o 2 weeks after an MI o Immulogically-mediated febrile pleuropericarditis Clinical features o Severe positional (relieved by sitting forward) o Retrosternal chest pain o Pericardial rub on Ascultation Investigations o ECG: CONCAVE ST-SEGMENT ELEVATION IN ALL LEADS o Cardiac enzymes may be elevated Manage o Antiinflammatory drugs (ASPIRIN)
INFECTIVE ENDOCARDITIS
o
PERICARDIAL EFFUSION
Infection, (TB), Uremia, MI, Aortic dissection, myxedema, neoplasia, radiotherapy. Clinical features o Due to cardiac tamponade- when pericardial effusion impairs ventricular filling, reducing CO. o Breathlessness o Pericarditic pain o Acute cardiovascular collapse Examination o Raised JVP- increases on inspiration. o Distant heart sounds ECG o Reduced voltage o CXR (globular cardiomegaly) o ECHO- (pericardial fluid and cardiac tamponade induced RV diastolic collapse)- diagnostic. Manage
Usually subacute Infection of heart valves / endocardium Causes a chronic illness when organism is nonvirulant (streptococcus viridans) Can be ACUTE with virulent: STAPHYLOCOCCUS Common in o Elderly with degenerative aortic and mitral valve o Prosthetic valves o Rheumatic fever o Congenital heart disease Abnormal valves more susceptible to infection after dental procedures. Normal valves occasionally infected by virulent organisms. (staphylococcal valve infection after IV drug use) CNS FEATURES o Embolic infarction o Abscesses o Meningitis GENERAL INFECTION o Low grade fever o Lethargy, malaise o Anaemia, weightloss CARDIAC o Murmurs o HF o Mycotic aneurysms LATE SIGNS o Clubbing o Splenomegaly JOINTS o Arthralgia o Septic Arthritis SKIN o Vasculitis rash SOLES OF FEET o Janeway lesion IMMUNE COMPLEX DEPOSITION o RETINAL HEAMORRHAGES (Roth spots) o SUBCONJUNCTIVAL HEAMORRHAGE o SPINTER HEAMORAGES, NAILBED INFARCTS o JANEWAY LESIONS (small, red macular) o OSLERS NODES (subcut swellings in finger/toe pulps, pain. o MICROSCOPIC HAEMATURIA o GLOMERULONEPHRITIS o LUNG: R. SIDED EMBOLIC INFARCT o LOSS PERIPHERAL PULSES o RENAL/CEREBRAL EMBOLIC INFARCTS Diagnosis initially clinical Suspected in fever, anaemia, high ESR or CRP, microscopic haematuria, new heart murmurs, flulike symptoms, weightloss. Confirmed by repeatedly positive blood cultures, and ECHO confirm diagnosis. Transthoracic ECHO detects under 50% vegetations- transoesophageal studies better.
Manage -
Look for and treat underlaying infection (dental abscess?) BENZYLPENICILLIN (empirical antibiotic therapy) Adjusted when know cultures. Treat 3-6 weeks
WHAT TO DO IN CHEST PAIN EMERGENCY
AIRWAY (patent, manouvres, adjuncts) BREATHING (no resp effort.. ARREST TEAM) CIRCULATION (no pulse.. ARREST TEAM) CALL FOR SENIOR HELP: (unewell/ deteriorating) SIT UP 15L/min OXYGEN (sats under 94% / sob) MONITOR (pulse oximiter, BP, ECG, Defib) OBS: (BP both arms, ECG) BRIEF Hx, /NOTES/ STAFF EXAMINE: (chest, Rx, Abdo) ESTABLISH LIKELY CAUSES RULE OUT SERIOUS CAUSES CONSIDER o PCI / THROMBOLYSIS o ASPIRIN 300mg PO STAT o NEEDLE DECOMPRESSION INITIATE FURTHER TREATMENT (analegesia) VENOUS ACCESS o FBC, U&E, LFT, CRP, gluc, cardiac marker, D-dimer o CXR Call senior help- worsening/ no improvement No improvement? REPEAT ECG after 20MINS REASSESS… A, B, C LIFE THREATENING CAUSES
NOTES ON EMERGENCY CHEST PAIN
MYOCARDIAL INFARCTION TENSION PNEUMOTHORAX
Stable Angina Musculoskeletal
Exertion pain Lifting Radiates to L arm/ Jaw injury -Impact Under 20mins May be pleuritic STEMI Breathlessness Pneumonia onwhen rest/GTN -Worse Dec Sudden onset pain palpation/movement Productive sputum - - Radiates to L cough, arm/ jaw - Pleuritic Dyspnoea pain - - Over 20mins -- - -Resp exam normal Tachycardia Feels unwell Breathless, nausea, Tender -sweating Non-tender Normal after pain goes - - Febrile -- - Normal CXR Asymmetrical air entry Dyspnoea ECG -Normal Transient changes Corse creps ECG (unilateral?) -- - Arrythmia Troponin not elevated Dull to percussion - - -Sweating -Non-tender Positive stress ECG CORONARY ANGIOGRAPHY - - INC WCC up - - STCRP elevation CXR - consolidation New LBBB - Increase cardiac Markers
WORRYING FEATURES o Inc/dec HR o Dec BP o Inc RR o Dec GCS o Sudden onset o Sweating o Nausea & vomiting o Pain to jaw/ L. Arm / Back o ECG Changes THINK ABOUT COMMON o MI / ACS / ANGINA o PE o MUSCULOSKELETAL o PNEUMONIA o PNEUMOTHORAX (simple / tension) o PERICARDITIS o REFLUX, PEPTIC ULCER UNCOMMON o AORTIC DISSECTION o CARDIAC TAMPONADE o SICKLE CELL CRISIS. ASK ABOUT: Site, onset, radiation, quality (heavy/ aching/ sharp), intensity (1-10), time onset, duration, associated symptoms (sweating, nausea, palpitations, breathless), exacerbating or relieving factors (breathing, position, exertion, eating), recent trauma/exertion, previous episodes PMHx: cardiac/ Resp problems / DM / GORD DRUGS: Cardiac / respiratory meds, antacids FHx: IHD / premature cardiac death SH: Smoking / Exercise tolerance INVESTIGATIONS o ECG o FBC, U&E, LFT, D-dimer, Cardiac markers, ABG o CXR- portable? Standard? o ECHO/ CT if large proximal PE/ aortic root dissection. TREAT: o 15L OXYGEN o IV OPIOID o ANTI-EMETIC Diagnosis to exclude o CARDIAC ISCHEMIA (ECG, Hx, Cardiac markers) o PE (dec sats, ECG, risk, D-Dimer, CT-PA) o PNEUMOTHORAX (Mediastinal shift, dec breath sounds)
Pericarditis Pulmonary Embolism ----------
Hx viral-like illness Breathlessness Pleuritic pain PE risk factors Increased NSTEMI on lying Pleuritic chest painforwards Decreased sitting Sudden onset pain Haemoptysis Radiates to L arm/ jaw Pericardial Rub Over 20mins Oesophageal Normal exam Otherwise normal CVS and Breathless, nausea, Spasm/reflux May Hx DVT (swollen red RS exams sweating Previous indigestion/reflux leg) Hiatus herniadyspnoea Tachycardia/ Dyspnoea Saddle-shaped by antacids ST Dec BP Arrythmia on most ECG segments Sweating leads Upperoxygen abdo tender ABG: Dec Non-tender Inc CRP & ESR Normal CV and RS Clear CXR Positive D-dimer ST DEPRESSON Sinus Tachycardia ECGexclude cardiac S1Q3T3 CXR normal T-WAVE INVERSION Echo: Thrombus Antacids trial INC TROPONIN
AORTIC DISSECTION -
Sudden onset Severe inetrscapular pain Tearing in nature Breathlessness Pneumothorax Limb weakness / ACS /numbness. Unstable Angina Sudden onset pleuritic Anginal pain at rest chest pain Tachycardia Inc severity / freq / Trauma Decreased BP duration Tall and Thin Difference in brachial COPD pulses and pressures Dyspnoea Increased RR Tachycardia Mediastinal shift Limb weakness / Non-Tender Unequal airway and paraesthesia Normal after pain resolves expansion Hyper-resonance -CXR WIDENED ST depression MEDIASTINUM T waveseparated Inversion from ribs Pleura -ECHO/ CT: Aortic Troponin on CXR not elevated. dilation ANGIOGRAM: aortic
ACUTE CORONARY SYNDROME -
General term- presentations of varying levels of myocardial ischemia. Management and outcome better if you know whats going on exactly. Typical sounding chest pain lasting over 20 mins? o New LBBB / ST elevation on ECG? 12hr Troponin will be raised, but not needed for diagnosis: STEMI o Ischemia other than ST elevation on ECG? NSTEMI: (TropT: over 0.1) or (TropI over 1)
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ACS SERUM CARDIAC MARKERS TROPONINS (I or T) A protein: If they’re in the blood- very likely myocardial injury Can be raised in PE, renal failure, septicemia, after tachyarrythmias But CK not usually raised as well in these conditions. Detection can be 6hrs after injury Levels elevated for 14days Troponins used as prognostic indicator in UNSTABLE ANGINA / NSTEMI CK CREATININE KINASE Enzyme found in all muscle and released in muscle cell lysis. Not specific for cardiac muscle Peaks 24HRS post MI Returns to normal, 48-72 hrs post-MI Useful in detecting further infarction in patients with pain 3-14 days post MI. CK-MB Cardiac isomer of CREATININE KINASE enzyme More specific than total CK.
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ST ELEVATION MI
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WORRYING SIGNS: LV failure and cardiac dysrrythmia. Central crushing heavy chest pain, (over 20mins) Radiating to L arm/jaw SOB, nausea, sweating, vomiting, palpitations, anxiety RISK o Smoking, obesity, DM, Hypertension, cholesterol, family, previous IHD. SIGNS o ST Elevation (over 1mm in 2 leads, or 2mm in 1 lead) o New LBBB: subsequent Q waves, and T wave inversion o CXR: Cardiomegaly, LV failure o Cardiac markers raised. ACUTE TREATMENT (MONAC) o Rapid re-perfusion by percutaneous coronary intervention (PCI) in those UNDER 12HRS SYMPTOMS. o IE: seek senior help M: DIAMORPHINE 2.5-5mg IV O: OXYGEN 15l/min N: NITRATES: GTN: 2 puffs every 5 mins until no pain- if still pain, give IV unless hypotensive. A: ASPIRIN 300mg C: CLOPIDOGREL 300mg (ANTIEMETIC) WHEN PCI NOT AVAILABLE WITHIN 3 HRS? o Fibrinolysis o Beta blocker: Bisoprolol 10mg/PO- limits mortality and decreases infarct size- avoid in COPD, hypotension, failure. SECONDARY PROHHYLAXIS (BAN SCAR) o B: BETA BLOCKERS o A: ACEi o N: Nitrates (symptoms) o S: STATIN o C: Clopidogrel 1yr o A: aspirin lifetime o R: Risk factors (smoking, DM, obesity, BP, cholesterol) COMPLICATIONS o Dysrhythmias AV Block, Bradycardia, VF/VT LVF Valve prolapse Ventricular septal rupture Ventricular aneurysm formation Pericarditis, Dresslers syndrome (pericarditis- fever, pleuritic pain after heart injury) Recurrent Pain CARE AFTER MI o Bed rest 48hrs with continuous ECG o Daily 12lead ECG, and clinical examination o Thromboembolism prophylaxis o Beta blocker (unless contraindicated), ACEi, Statin o Discussion over modifiable risk factors, arrange cardiac rehab o PRIMARY PCI: patients at lower risk of complications,
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RISK STRATIFICATION IN ACS o o o
Estimation of death allows individualused assessment of risks and benefits interventions Careful targeting of resources to those patients who stand to benefit the most. Validated scoring algorithms o TIMI: THROMBOLYSIS IN MI RISK SCORE GRACE: ACS RISK MODEL Data from GLOBAL REGISTRY OF ACUTE CORONARY EVENTS- huge amount of info from many countries. o Risk scores calculated on admission o Predict in hospital and 6month mortality. o On discharge: to predict 6month mortality. High risk? o Patients need a coronary care unit bed. o Consider for glycoprotein llb/llla inhibitors and urgent catheterization Low/intermediate risk? o Observation to ensure pain free o Futher stratification using exercise ECG, coronary calcium scoring/ stress
NSTEMI
WORRYING SIGNS: LV failure and cardiac dysrrythmia. Central crushing heavy chest pain, (over 20mins) Radiating to L arm/jaw SOB, nausea, sweating, vomiting, palpitations, anxiety RISK o Smoking, obesity, DM, Hypertension, cholesterol, family, previous IHD. SIGNS o Same as STEMI o Patients tend to be older with more co-morbidities than STEMI o ST DEPRESSION, INVERTED T WAVES o CARDIOMEGALY , FAILURE (CXR) o ELEVATEED TROPONIN (12hrs after worst pain) ACUTE TREATMENT (MONAC) M: DIAMORPHINE 2.5-5mg IV O: OXYGEN 15l/min N: NITRATES: GTN: 2 puffs every 5 mins until no pain- if still pain, give IV unless hypotensive. A: ASPIRIN 300mg C: CLOPIDOGREL 300mg
FONDAPARINUX (anticoagulate) Beta-blocker- Bisoprolol 10mg STAT- beware in COPD, hypotension, failure RISK STRATIFY: for ones needing bed in CCU, catheterization or glycoprotein inhibotors. SECONDARY PROHHYLAXIS (BAN SCAR)- same as STEMI o B: BETA BLOCKERS o A: ACEi o N: Nitrates (symptoms) o S: STATIN o C: Clopidogrel 1yr o A: aspirin lifetime o R: Risk factors (smoking, DM, obesity, BP, cholesterol) COMPLICATIONS- same as STEMI, but less common o Dysrhythmias AV Block, Bradycardia, VF/VT LVF Valve prolapse Ventricular septal rupture Ventricular aneurysm formation Pericarditis, Dresslers syndrome (pericarditis-
STABLE ANGINA
UNSTABLE ANGINA
Retrosternal chest discomfort occurring predictably upon exertion Relieved by rest and nitrates. SYMPTOMS o Central, heavy chest pain o Lasting under 20mins- radiating to L.arm and jaw o Precipitated by exertion, relieved by rest, or GTN in under 5 mins o SOB, nausea, sweating, palpitations. o Tachycardia, cool, sweaty, clammy, pallor- normal after episode. ECG o Transient ST-depression during pain o Flat or inverted T-waves o Signs of previous MI Cardiac markers not elevated! PRIMARY PROPHYLAXIS- kind of the same. o B: BETA BLOCKERS o A: ACEi o N: Nitrates (symptoms) o S: STATIN
WORRYING SIGNS: LV failure and cardiac dysrrythmia. Central crushing heavy chest pain, (over 20mins) Radiating to L arm/jaw SOB, nausea, sweating, vomiting, palpitations, anxiety Typically, episodes of angina, occurring at rest or minimal provocation, with poor response to GTN. More frequent and painful than usual. RISK o Smoking, obesity, DM, Hypertension, cholesterol, family, previous IHD. SIGNS o ST DEPRESSION, INVERTED T WAVES o Dynamic ECG changes over time o Signs of previous MI? o Troponin not elevated. ACUTE TREATMENT (MONAC) M: DIAMORPHINE 2.5-5mg IV O: OXYGEN 15l/min N: NITRATES: GTN: 2 puffs every 5 mins until no pain- if still pain, give IV unless hypotensive. A: ASPIRIN 300mg C: CLOPIDOGREL 300mg PLUS! BETA-BLOCKERS to limit ischemia FONDAPARINUX (disrupt thrombus) o
Same further management as NSTEMI
SECONDARY PROHHYLAXIS (BAN SCAR)same as STEMI
PERICARDITIS
Pleuritic chest pain Worse on laying flat and deep inspiration Relieved by sitting forward, recent viral illness SIGNS? o May be none o Pericardial rub ECG o Saddle shaped ST segments in most leads BLOODS o High WCC Inflammatory markers ECHO o Pericardial Effusion TREAT o Acutely- reassurance and anaelgesia o Paracetamol, NSAIDS o Should settle 2-4 weeks
AORTIC DISSECTION
Aortic dissection occurs when a tear in the inner wall of the aorta causes blood to flow between the layers of the wall of the aorta, forcing the layers apart. Severe characteristic chest or abdominal pain- "tearing" with other symptoms from decreased blood supply to organs. Aortic dissection is a medical emergency and can quickly lead to death, even with optimal treatment, as a result of decreased blood supply to other organs, cardiac failure, and sometimes rupture of the aorta. More common: high blood pressure, known thoracic aortic aneurysm, Marfan syndrome, Ehlers–Danlos syndrome. The treatment of aortic dissection depends on the part of the aorta involved. Surgery in dissections that involve the aortic arch, while dissections further away from the heart treated with blood lowering BP (systolic under 100) SYMPTOMS o Sudden onset, severe chest pain o Anterior or interscapular o Tearing in nature o Dizziness, breathlessness, sweating, neurological deficits RISK FACTORS o Smoking o Obesity o DM o High BP o Increased Cholesterol o Family history o IHD SIGNS o Unequal radial pulses o Tachycardia o Hypertension/ Hypotension o Difference in brachial pressures of over 15mmHg o Aortic regurg o Pleural Effusion (left more than right) o Neurological defects from carotid artery dissection INVESTIGATIONS o ECG normal/ show LV strain or ischemia. o CXR widened mediastinum over 8cm (rare) o Blood can track down and cause irregularity of aortic knuckle and small left pleural effusion o ECHO: shows aortic root leak, aortic valve regurg, pericardial effusion o Consider MRI/CT ACUTE TREATMENT (HYPOTENSIVE? Treat as shock) o Senior help!!! o OXYGEN (15/min) o CANNULA (2 large bore) o BLOOD: X-MATCH 6units o OPIDOIDs (anaelgesia) TREATMENT o Surgery: for type A (Ascending aorta)
TACHYARRYTHMIAS… EMERGENCY!!!
AIRWAY: (patent, manouvres, adjuncts) BREATHING (no resp effort- crash team) CIRCULATION (no pulse, crash team) SENIOR HELP! If patient unstable o Reduced GCS o Systolic under 90 o Chest pain o HF SIT UP (if hypotensive, lay flat, legs up) OXYGEN (15l/min- non rebreather) MONITOR o Pulse oximiter o Defib paddles o BP o ECG leads Request full set obs and ECG Hx- BRIEF, CHECK NOTES, MEDS, ASK STAFF EXAMINE- CV, resp, Abdo LIKELY CAUSES and SERIOUS CAUSESestablish INITIATE FURTHER TREATMENT VENOUS ACCESS o Bloods o FBC o U+E o D-Dimer o Cardiac Markers o TFT Consider requesting urgent CXRportable Reassess ABC
LIFE THREATENING CAUSES
VT VF
ADULT TACHYCATRDIA WITH PULSE ALGORHYTHM UNI! unstable? narrow? Irregular? 1.
2. 3.
4.
FIRST Assess ABCDE Oxygen and IV access Monitor: EGC, BP, Sp02, 12-lead ECG Identify and treat reversible causes.. electrolytes? ADVERSE FEAUURES? Myocardial Ischemia, HF, Shock, Syncope. (My heart’s So Speedy) YES … UNSTABLE!!! (adverse features) o SYNCHRONISED DC SHOCK o Up to 3 attempts o AMIODARONE 300mg IV (10-20mins) o Repeat shock followed by o AMIODARONE 900mg over 24hrs. NO… STABLE… o IS QRS NARROW OR BROAD??
BROAD QRS
5. REGULAR / IRREGULAR?
NARROW QRS
5. REGULAR / IRREGULAR?
Regular Regular
VT (AMIODARONE) o 300mg Over 20mins o 900mg over 24hrs SVT with BBB (ADENOSINE)
Irregular
AF with BBB Pre-Excited AF (AMIODARONE) POLYMORPHIC VT eg.
Use vagal manouvres ADENOSINE (6mg rapid IV bolus, then give 12 if needed , then 12) SINUS RHYTHEM BACK?? If now sinus rhythem, was probably REENTRY PAROXSMAL SVT NO SINUS RHYTHEM? ATRIAL FLUTTER: beta blocker.
Irregular
IRREGULAR, NARROW COMPLEX TACHCARDIA Probably AF o Beta blocker o Diltazem
TACHYARRYTHMIAS TACHYARRYTHMIAS SINUS TACHYCARDIA Worrying Features
Decreased GCS Dec BP (systolic under 90) Chest Pain HF
Causes
FAST AF
Common o Sinus Tachycardia o Fast ventricular rate in AF o SVT o Atrial Flutter o Physiological: shock, sepsis Uncommon SVT o VT o Re-entrant tachycardia (Wolf-Parkinson)
Ask about
Onset Associated Symptoms (chest, SOB, dizziness, palpitations, facial flushing, headchaes) VT (pulseless/pulse) Previous PMHx: Cardiac (IHD, valve lesions, HTN), Thyroid, DM Drugs: Cradiac, Levothyroxine, salbutamol, anticholinergics, caffeine, nicotine Smoking, Alcohol, Drugs
Observations: UNSTABLE?
VFBP, Cap-refill, RR, oxygen sats, GCS, temp Pulse, Look for worrying/ unstable features (My hearts so speedy)
ECG: -
SINUS….. 100, P before QRS AF………..100, Irregular QRS with no p (new Torsades de pointes onset?) ATRIAL FLUTTER…. Sawtooth baseline SVT…. 140, Narrow (help, get drugs ready) VT…….150, Broad Complex- check for pulse (arrest team if none) FBC, U&E, TFT, CRP, (D-DIMER, Cardiac Markers, X-match)
WOLF-PARKINSON WHITE SYNDROME
A re-entrant tachycardia Due to accessory conduction pathway (bundle of kent) between atria and ventricles. SHORT P-R INTERVAL and DELTA WAVE Avoid Digoxin and verapamil Refer to cardiologist for ablation
ATRIAL FIBRILLATION WARNING SIGNS o HF o Hypotension o Decreased GCS o Chest pain SYMPTOMS o SOB o Palpitations o Dizziness o Chest Pains RISK FACTORS o Previous AF o BP o IHD o Valvular heart disease o PE o Pneumonia o Thyrotoxicosis o Alcohol (acute excess, chronic misuse, withdrawal) o Dilated cardiomyopathy o Age o Acute illness COMPLICATIONS o Thromboembolic disease (ischaemic stroke) o Drug side effects (amiodarone, warfarin, beta blockers, digoxin) SIGNS o Irregularly irregular pulse SVT o Hypotension (CV compromise) o Signs of disease (thyrotoxicosis, pneumonia) WARNING SIGNS Investigate o HF o Absent p waves o Hypotension o Irregularly irregular QRS o Decreased GCS o WCC highbloods? Infection? o Chest pain o U&E SYMPTOMS o o TFT? SOB o o Alcohol Palpitations o o D-Dimer Dizziness(PE?) o (if ischemic episode o Troponin Chest Pains responsible?) RISK FACTORS o Previous SVT o Structural cardiac anomaly o Alcohol o Increased T4 (thyroid) COMPLICATIONS o Hypotension, o Ischemia, o HF, o Deterioration into more sinister arrhythmia.
ATRIAL FIBRILLATION- treat TREAT: -
Haemodynamically compromised? Help, shock?, oxygen, iv access, cardioversion (AMIODARONE)
CONSERVATIVE
Treat the precipitant (sepsis?) if new onset and this is obvious
RATE CONTROL
Control Tachycardia to reduce myocardial metabolic demand BETA BLOCKER / DILTIAZEM or VERAPAMIL (a rate limiting CCB) DIGOXIN (added in when the previous were insufficient- not 1st line)
RHYTHEM CONTROL
Younger patients/ those with new AFsuitable for attempted cardioversion FLECAINIDE: (if doesn’t have IHD) AMIODARONE (IV through central line if has IHD) DC CARDIOVERSION (under sedationanother option) Maintain sinus rhythm if successful, SVT with beta-blocker
ANTICOAGULATION SIGNS o Tachycardia Anxiety oIn all patients where a rate control ostrategy Hypotension (compromise) is adopted (rather than rhythem). Investigate oCanNarrow use aspirin 75mg tachycardia evey day.. or complex other drugs-have basedBBB on stroke (unless too) risk oassessment. P waves merge into the QRS Anticoagulation be achieved can be hardmust to see before any planned o4weeks Regular QRS o Rate over 140 Acute Treatment o Oxygen o 2 large bore cannula o Monitor rhythem on defib o Vagal manouvres o cardioversion o If recurrent, cardio might need to test conduction pathways.
VENTRICULAR TACHYCARDIA WORRYING SIGNS o HF o Hypotension o Decreased GCS o Chest pain o PULSELESS!!!!!!!! SYMPTOMS o SOB o Palpitations o Dizziness o Chest Pains o ARREST!!! RISK FACTORS o IHD o Trauma o Hypoxia o Acidosis o Long QT COMPLICATIONS o May deteriorate into VF or other dysrhythmia SIGNS o Tachycardia o Anxiety o Pallor o Hypotension o Decreased GCS/ shock Investigate o ECG: Broad complex tachycardia o Absence of p waves o Rate over 150 o Check U&E urgent! Especially K! and MG2+! o Cardioversion the main priority Acute Treatment o Pulseless VT? Call arrest team, commence ALS after precordial thump o Pulse? Oxygen, large bore cannula o Drugs: SOTALOL, AMIODARONE o DC CARDIOVERSION o Possible SVT with bundle branch block? Or VF? Treat as VT Chronic Treatment o Implantable cardiovertor/ defib *** NB: Torsades de pointes looks like FB but with a
BRADYARRYTHMIAS… EMERGENCY!!!
AIRWAY: (patent, manouvres, adjuncts) BREATHING (no resp effort- crash team) CIRCULATION (no pulse, crash team) SENIOR HELP! If patient unstable o Reduced GCS o Systolic under 90 o Chest pain o HF SIT UP (if hypotensive, lay flat, legs up) OXYGEN (15l/min- non rebreather) MONITOR o Pulse oximiter o Defib paddles o BP o ECG leads Request full set obs and ECG Hx- BRIEF, CHECK NOTES, MEDS, ASK STAFF EXAMINE- CV, resp, Abdo LIKELY CAUSES and SERIOUS CAUSES- establish CONSIDER o IV ATROPINE 500micrograms o Repeat every 2-3 mins o Max 3mg (6x) BRADYARRYTHMIAS… EMERGENCY!!! INITIATE FURTHER TREATMENT o Transcutaneous pacing VENOUS ACCESS THINK ABOUT Bloods o o SINUS BRADYCARDIA o FBC After an inferior MI (gets the SA o U+E node) o D-Dimer Drugs (digoxin toxicity) o Cardiac Markers Vasovagal o TFT Low thyroxine Consider requesting urgent CXR Hypothermia portable Cushings reflex (bradycardia Reassess ABC and hypertension secondary to
increased ICP) Sleep Anorexia nervosa Physical fitness
ASK ABOUT o Dizziness o Postural dizziness o Fits/faints o Weight change o Visual disturbance o Nausea and vomiting
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PMHx: Cardiac Disease (IHD/AF), Thyroid surgery, DM, Intercranial pathology/ head injury, glaucoma, eating disorder. Drug Hx: Cardiac meds, (Beta blockers, Ca2+ antagonists, amiodarone, digoxin) Social Hx: Exercise tolerance, IHD risk factors OBS LOOK
HR, BP, Postural BP RR Sats FOR Pulse rate/rhythem Volume Pallor SOB Dec GCS Drowsy Inc JVP (cannon waves in 3rd degree AV block) Signs of cardiac failure (increased JVP, pulmonary oedema, swollen ankles)
Investigate Bradyarrythmia o ECG: Sinus bradycardia/ complete heart block Evidence ischemia/infarction Evidence digoxin toxicity o Bloods FBC U&E Glucose Ca2+ Mg2+ TFT Cardiac markers Digoxin level Coagulation (if considering pacing wire) o CXR Not really helpful, but may reveal heart size or pulmonary oedema. o HEAD CT If suspect raised ICP- but would be in extremis ie. About to coneneed neurosurgeon
BRADYARRYTHMIAS ON AN ECG
VASOVAGAL ATTACKS
Sudden reflex bradycardia from unopposed parasympathetic nervous inhibition is common. Light-headedness, visual disturbance, nausea and sweating, then brief LOC, Prompt recovery of consciousness Precipitants: o FEAR o PAIN o POST-MICTURITION o NAUSEA AND VOMITING o DILATION ANAL SPHINCTER AND CERVIX o PULLING OF EXTRA-OCULAR MUSCLES o RAISED ICP (straining etc)
SINUS BRADYCARDIA o P before every QRS 1st DEGREE AV BLOCK o P-R interval over 0.2 secs (5 small squares) MOBITZ 1 (WENKEBACH) o P-R intervals lengthen from beat to beat o Until failure of AV conduction, then pattern restarts MOBITZII o Intermittent P waves fail to conduct to ventricles o But P-R does not lengthen (unlike MOBITZ1) o Typically 2:1 o 3:1 and above are considered high grade AV block DIGOXIN EFFECT TOXICITY o Down sloping ST segment- often present even when drug at non-toxic levels RATE CONTROLLED AF
SINUS BRADYCARDIA DRUGS PRECEEDING BRADYCARDIA Worrying: HF, Hypotension, decreased GCS BETA BLOCKERS (even in eye drops) Symptoms: DIGOXIN (if patients in AF revert to sinus) o None? Ca2+oANTAGONISTS that slow on HRstanding Dizziness, especially o VERAPAMIL o Recurrent falls o DILTIAZEM o Palpitations AMIODARONE o SOB can cause bradycardia A-AGONISTS: PNENYLEPHERINE o Symptoms of raised ICP used by anaethatistsincreased decreased PVR so causes o Hypothermia/ T4 reflex brady. ECG o QRS preceeded by a P-wave SICK SINUS SYNDROME o Rate under 60 o QRS narrow unless BBB o Exclude ischemia and infarction Dysfunction of the SA Node BLOODS Precipitated by ischemia/fibrosis o FBC Results in bradycardia/ arrest o U&E SA block/ SVT with alternating o Ca2+ bradycardia/asystole o Mg2+ Tachy-brady syndrome o TFT Needs opacing if symptomatic. Cardiac markers o Coagulation (if considering pacing wire)
OTHER TYPES OF BLOCK
1st Degree and MOBITZ1 o no treatment unless symptomatic or reversible cause.
MOBITZ2 and HIGH GRADE AV BLOCK o Can deteriorate into complete heart block o May need temp/permanent pacing o Espesh when associated with ACS/
COMPLETE 3rd DEGREE HEART BLOCK
ACUTE If symptomatic or dizzy (GCS under 15) Or systolic under 90bpm Monitor HR on defib Lay flat with legs elevated, as long as ICP not raised. o OXYGEN, ACCESS, BLOODS, worrying signs? ARREST Titrate 500micrograms ATROPINE Every 2-3 mins, up to 5mg Followed by large flush, until HR improves Identify correct precipitant Consider pacing wire via central line/ external pacing A precordial thump (percussion pacing) can be used in extremis, when an external pacing machine not immediately available. o o o o
CHRONIC o o o
Consider 24hr tape Frequent symptomatic episodes of bradycardia/pauses are a sign of SICK SINUS SYNDROME May need a permanent pacemaker.
COMPLICATIONS
Severe bradycardia and high vagal tone can
Worrying? o HF, Hypotension, Decreased GCS Symptoms o None? Dizzy? Palpitations? SOB? Chest pain? Causes o Underlying ischemic damage (inferior MI) o Post cardiac surgery o Drug induced (beta blockers, Ca2+ blockers) o Amyloid, Sarcoid, Myeloma, Infective (Lyme) Signs o Decreased BP / GCS o Cannon waves in increased JVP (due to asynchronous of right atria against closed tricuspid valve o HF signs/ underlaying disease Investigations o ECG: complete dissociation of p waves from QRS o Narrow QRS implies proximal lesion (responds to atropine) o Broad implies distal lesion (less likely to respond to atropine) o Look for evidence MI o FBC, U&E, Ca2+, Mg2+ TFT, markers, coagulation ACUTE: ATROPINE / external pacing CHRONIC: pacemaker/ correct precipitant COMPLICATIONS o Severe bradycardia and high vagal tone can deteriorate into asystole- prompt treatment required o Talk contunially
HYPERTENSION EMERGECNY
AIRWAY: Patent? Manouvres? Adjuncts? BREATHING: No resp effort? ARREST CIRCULATION: No pulse? ARREST DISABILITY: GCS under 8? Anesthetist o o o o
o o o o o o o
o o o
IF SYSTOLIC OVER 200, DIASTOLIC 120 Sit up OXYGEN (15l)- if SOB/ sats under 94% MONITOR Pulse oximiter BP Defib leads- if unwell Request full set OBS and ECG Bried HX / NOTES/ Ask staff Examine RS, CVS, abdo, EYE Rule out serious causes, establish likely causes- is it new?? DO NOT GIVE STAT DOSE ANTIHYPERTENSIVE WITHOUT SENIOR REVIEW Further treatment ACCESS FBC, U&E, markers, TFT, glucose, cortisol Consider urgent CXR Urinalysis and bHCG (if childbearing age) Senior advice reassess, ABC
Life threatening causes
PRE-ECLAMPSIA/ ECLAMPSIA MALIGNANT HYPERTENSION (200/120) HYPERTENSIVE ENCEPHALOPATHY PHAEOCHROMOCYTOMA
HYPERTENSION EMERGECNY
AIRWAY: Patent? Manouvres? Adjuncts? BREATHING: No resp effort? ARREST CIRCULATION: No pulse? ARREST DISABILITY: GCS under 8? Anesthetist o o o o
o o o o o o o
o o o
IF SYSTOLIC OVER 200, DIASTOLIC 120 Sit up OXYGEN (15l)- if SOB/ sats under 94% MONITOR Pulse oximiter BP Defib leads- if unwell Request full set OBS and ECG Bried HX / NOTES/ Ask staff Examine RS, CVS, abdo, EYE Rule out serious causes, establish likely causesis it new?? DO NOT GIVE STAT DOSE ANTI-HYPERTENSIVE WITHOUT SENIOR REVIEW Further treatment ACCESS FBC, U&E, markers, TFT, glucose, cortisol Consider urgent CXR Urinalysis and bHCG (if childbearing age) Senior advice reassess, ABC
Life threatening causes
PRE-ECLAMPSIA/ ECLAMPSIA MALIGNANT HYPERTENSION (200/120) HYPERTENSIVE ENCEPHALOPATHY PHAEOCHROMOCYTOMA
HYPERTENSION: 140/90
SYSTIOLIC over 140 DIASTOLIC over 90 Worrying: Altered mental state, seizures, retinal hemorrhages, acute renal failure, chest pain CRISIS!??!?? Over 200 or over 120! Think about o Is it a hypertensive crisis? 200/120, or pre-eclampsia? o Other: anxiety, pain, primary (essential) or secondary (thyroid storm, pheochromocytoma). PHMx of, and signs of disease o Previous hypertension o Phaeochromocytoma o Coarctation aorta, (Radiofemoral delay) o renal artery stenosis (renal bruits) o Thyroid disease, (Tremor, exopthalmus) o DM, o Conns syndrome, o Cushings, (Straie, central obesity) o Acromegaly (large hands, feet, face) o Pregnancy (gravid uterus) Drugs o Cardiac meds and Antihypertensives o Steroids, Contraceptive pill, Levothyroxine/carbimazole, MAOI, antipsychotics o Coke and amphetamines Family HYPERTENSIVE CRISIS o Hypertension, endocrine disease, polycystic kidney disease Social: exercise tolerance and smoking. Elevation of BP iver 200 is a END ORGAN DAMAGE? HYPERTENSION: 140/90 hypertensive retinopathy) hypertensive emergency o Fundoscopy (papilloedema, When accompanied by end-organ o LV hypertrophy: displaced apex beat of S4 damage INVESTIGATIONS o Haematuria KEY SECONDARY CAUSES Hypertensive urgency when no end o RENAL ARTERY DISEASE/STENOSIS organ damage Renal failure BP: Abnormal urine dipstick o Confirm with ambulatory END ORGAN DAMAGE Renal bruit measuring Family history may be relevant ECG: CNS o LV hypertrophy? Urine Microscopy o Decreased GCS, confusion Bloods: Renal Doppler USS o Headache o FBC, U&E, Glucose, Autoantibodies o Vomiting cholesterol, TFT Renal biopsy o New motor weakness Urine o o PHAEOCHROMOCYTOMA Seizures, coma Sweating TREATMENT o CT may show a SAH, ICH, Labile hypertensive encephalopathy Hypertension occurs with cerebral oedema Smoking cessation Palpitations following loss of vascular Regular exercise auto-regulation. Plasma metanephrines Reduce alcohol and caffeine intake EYES 24hr urine catachlomines and VMA Balanced diet o low-salt Headache (norepinephrine becomes Modifiable risk factors: DM, lipids vanillylmandelic acid) o Visual Disturbance o THYROID DYSFUNCTION o Fundoscopy shows retinal PHARMACOLOGICAL THERAPY Cold hemorrhage, and Heat intolerance, sweating Complications papilloedema. are end organ damage and malignant HEARThypertension Lack of energy o Chest pain TFTs o Orthopnea o ACROMEGALY o ECG changes, Headache o Elevated cardiac markers Visual Field disturbance o Pulmonary oedema on CXR Change in facial features AORTA IGF-1 o Sudden, tearing chest pain Pituitary hormone levels radiating to back o CUSHINGS SYNDROME o Collapse Centripetal obesity o Echo/CT may reveal oertic Skin thinning, weakness dissection Urinary free cortisol
PHARMACOLOGICAL TREATMENT
Everyone o HYPERTENSIVE 160/100 (aim for 140/90) or (150/90 if over 80) o TYPE2 DIABETES: if end organ damage aim for under 130/80- microalbuminuria, or eGFR under 60, retinopathy, Hx TIA/stroke o TYPE1 DIABETES: o HYPERTENSIVE PATIENTS: with existing cardiovascular disease/end-organ damage, or predicted 10year risk CV disease over 20% Under 55 Under 55
Over Over 55/Black 55/Black
A
C
A&C
A&C
A, C, D
A, C, D
CARDIAC HISTORY AND EXAMINATION A: ACEi / Angiotensin receptor blockers (RAMIPRIL) C: Calcium Channel Blockers (AMLODIPINE, INSPECTION OVERALL: o ECG monitor suggestive? Pain? Cannula? Malar flush? (mitral stenosis), tachypnea (HF), Cyanosis (HF), Forceful neck pulsations eg. Carotid (aortic regurg), ankle oedema (HF) HANDS: Splinter haemorrhages HYPERTENSIVE (IE) CRISIS- Treat ACUTELY Clubbing (IE or congenital cyanotic heart disease- caused by supperative disease ie that can lead to pus filled cavities- Chrohns, UC, empyema, bronchiectasis, CF, fibrosis). NO end organ damage o Pallor, o Peripheral cyanosis, Calcium or ACEi (A or C) o Channel nicotineBlocker staining o cap refill (Over 2 secs dehydration or PVD) END ORGAN o DAMAGE Asterixis- flap sign of CO2 retention (don’t confuse with tremor from b2 agonist salbutamol, or parkinsonian) NECK: Admit to HDU or ICU JVP Close omonitoring of BP, ECG, neurological state, Fluid balance FACE:line, central line, catheterization) (arterial Malar flush Rapid oreduction in BP can be dangerous due to cerebral hypoperfusion o Anaemia conjunctiva Only necessary in ACUTE MI / AORTIC DISSECTION o Central Otherwise, aim to Cyanosis reduce diastolic to 100 or by 25% (the higher one), over 24hrs o Hypercholersterolemia: Xantholasma More severe end organ damage needs IV therapy, otherwise oral is okay o Breathing difficulty No evidence LV failure? LABETALOL VLCHEST: Failure? HYDRALAZINE (vasodilator) and FUROSEMIDE o Hands on hips to expose lateral chest walls. Look at back too. ACEi helps to counteract high circulating renin o Scars: Midline sternotomy- valve replacement or bypass? If bypass, scar on leg from where artery In CVA (acute stroke), thecerebral auroregulation be backimpaired and aggressive lowering of BP taken.ischemic Thoracotomy scar: Scar left axilla diagonallycan down previous mitral stenosis (or line causes hypoperfusion and poor outcome from L breast to axilla) o Deformities: sternal depression, scoliosis, kyphosis- can displace apex beat and cause ejection systolic murmur. o Apex- look for cardiac pulsation o o
PALPATION
ARMS: o Radial pulse: rate, rhythm, character
Brady (under 60), Beta-blockers, heart block, hypothyroidism, young Tachy (over 100), anxiety, exercise, pyrexia, hyperthyroidism, beta2 agonists (salbutamol), hypovolemic shock, arrhythmia.
o
o
o
o
Radio-radial delay Aortic dissection Proximal arterial disease (atherosclerosis of axillary artery) Radio-femoral delay Co-arctation of the aorta (stricture of the aortic arch, distal to the L. Subclavian artery) Delayed and weak femoral pulse Other things pointing to co-arctation? Raised BP, continuous murmur over scapula, systolic murmur L sternal edge (P/T) Collapsing pulse Aortic regurgitation Ask if pain in shoulder BP Sitting and standing Hypertrophic obstructive cardiomyopathy.
NECK: o Carotid pulse (edge of adam’s apple and move back)
Pulse character- valvular lesions cause it to be abnormal Slow rising, then plateau (aortic stenosis) Fastrising (watrehammer) and fast falling (collapsing) : (arotic regurg) Bissfiriens Pulse (double impulse): Mixed aortic valve disease- both stenosis and regurg Other- character abnormalities are usually due to aortic valve problems, or things like hypertrophic obstructive cardiomyopathy. Comment on pulse volume, and how quickly it rises and falls o JVP 45deg, look to left, look just above clavicle at 2 heads sternocleidomastoid JVP is an approximate measure of pressure in RA (as right internal jugular vein communicates directly with RA) Lay at 45deg, - should be visible at level of clavicle between 2 heads of sternocleidomastoid. If elevated- pulsation seen further up neck. Carotid vs jugular: JVP cant be palpated and has a double wave waveform. Hepatojugular reflex: pressing on R Hypochondrium (liver) to try and inc visibility (JVP: Internal jugular lays between 2 heads- sternal and clavicular of SCM, external is more superficial, and lateral to 2 heads) Causes of raised JVP Right HF: common. Secondary to LHF. Fluid overload: kidney failure, excessive intake. Tricuspid regurg: Massive V wave on JVP waveform. Common heart block: Atrioventricular dissociation, and A and V contractions not co-ordinated. Giant wave produced when atria contracts when tricuspid valve closed so huge atrial pressure. SVC onstruction: elevated without pulsation. Distended. Hepatojugular reflex neg- due to mediastinal lymphadenopathy- lung cancer. AF: no atrial systole, - JVP has no A wave.
CHEST: o Palpate Apex beat (placement and character) Mitral Stenosis: Tapping, not displaced- you feel the normal apex beat plus the closure of the valve- on auscultation sounds like a loud 1st heart sound. Apex more abrupt and feels like tapping. Aortic stenosis and Hypertension: Both obstruct cardiac output. Extra strain and hypertrophy. Apex sustained and heavy, displaced down and out. Mitral and aortic regurgitation: Backflow of blood causes large L ventricle. Apex displaced down and out. Character unchanged as outflow of ventricle the same. LV dilation: heart failure, apex displaced down and out Cant palpate apex? Emphysema (overinflation) Pericardial effusion Dextrocardia Heaves and Thrills Thrills: murmur producing a palpable sensation. Aortic stenosis produces a thrill in aortic area Feel with palm of hand over 4 valve areas Parasternal Heave: 4th intercostal space, lateral to sternum LHS Mitral: 5th intercostal space, midclavicular line LHS
o
ASCULTATION o o
A, P, T, M Roll to axilla, mital area for mitral stenosis (diastolic)
Places to Listen
Altered Heart sounds
Mitral regurgitation and aortic stenosis Both Pan-systolic (aortic stenosis also classed as ejection systolic)
Aortic stenosis
Splitting of Heart sounds (LUB SPLAT): Extra sound after S2 is called P2, Normal finding in inspiration Loud S1 (LUUBB!dub) Mitral stenosis- narrowed valve, shuts quicker, louder sound Soft S1 (lubDUB) Mitral regurg, valve not completely closed Soft S2 Aortic stenosis (reduced valve movement) Wide fixed splitting of S2 ASD Prosthetic heart sounds Metallic clicking sound
Brief systolic murmurs
Aortic: 2nd intercostal space, midclavicular line RHS Pulmonary: 2nd inercostal space, lateral to sternum LHS Tricuspid: 4th intercostal space, lateral to sternum LHS Mitral: 5th intercostal space, midclavicular line LHS
More clinically severe than mitral regurg Can cause o Hypotension o LV enlargement o Congestive heart failure o Cold peripheries Heard over Aortic area, radiates to carotids (murmur in carotids but not atrial area… probs a carotid bruit) Shorter than mitral regurg, crescendo-decrescendo sound
Mitral Regurg (lubb– swoosh-dub)
A bit quiteter Heard in apex, radiates to axilla Causes o Rheumatic heart disease, IE, IHD, Post-MI, Cardiomyopathy, AF, Congenital
DIASTOLIC MURMURS
Aortic Mitral o o o o Aortic o o o
regurgitation stenosis Mid diastolic murmur (click whoosh) Associated with AF Lay on LHS, listen to mitral area Caused by rheumatic fever regurg Early diastolic murmur High pitched, starts loud and lets quitter Heard sitting up and forwards at L sternal edge, patient holding breath at end of expiration.
Extra heart sounds
Third heart sound (S3) o Low pitched o Heard with bell in mitral area o Comes right after S2 sounds like lub- dubdub o Fit and young, or pregnant (high SV) o Left ventricular failure o Mitral and aortic regurg (stroke vol high to compensate for regurg) 4th heart sound (S4) o low pitched, heard with bell in mitral area o Just before S1, lublub-dub o NEVER normal o Very non complient ventricle- atrium is having to push out the last little bit of blood Aortic stenosis Hypertension CF
NOISES
Opening snap o Mitral stenosis o High pitched snap after S2 Ejection click o Aortic valve opening o Aortic stenosis o Heard in aortic area after 1st heart sound Mid-systolic click o Mitral valve prolapsing o Halfway through systole, pressure in ventricles risen to such a level to prolapse the mitral valve Pericardial friction rub o Acute pericarditis o Scratching sound in systole or diastole o Can vary hr to hr o When inflamed, vicsceral and parietal pericardium rub together o Heard sitting forwards, expiration and hold breath.
Remember o lEEEft sided noises- heard in expiration
READING AN ECG 1. 2. 3.
Check NAME, DATE, TIME Examine ECG in relation to previous ECGs (St changes can be fixed or dynamic) Always interpret it in CONTEXT to the clinical situation.
ABOUT THE ECG
The ECG represents electrical activity, primarily from the L.Ventricle, as it has more muscle mass than the RV. The ECG therefore tells you little about the RV. This is important as RV infarcts can occur, and can be missed if you don’t request specific RHS leads. They have a high rate of death, so important not to miss them. Suspect RV INFARCTS in patients who are VERY HYPOTENSIVE with little in the way of ST CHANGES in the ECG, or minor ST CHANGES in the inferior leads. The ECG electrodes are place primarily across the anterior chest wall. The ECG is therefore very good at detecting ischemia originating from the LAD and RCA territories, as they supply they supply areas of the heart well covered by the ECG electrodes. However, they may miss ischemia originating from the Circumflex artery, which is poorly represented by ECG electrodes. Leads 1 and AVL that look at the lateral wall of the LV may give some indication… but changes are subtle. For this reason, ‘posterior infarcts’ are missed on ECG If you see ST DEPRESSION across V1-V3, ask for posterior leads, ST elevation in V4, V5, V5 will become evident. Ie. While a normal ECG in the setting of chest pain is reassuring, its NOT a definitive indication that ischemia and infarction are absent. If the history and context fit, then treat patients as if they do have ischemia- you can repeat the ECG every 20mins Remember: we often see NSTEMIS with NORMAL LOOKING ECGs.
THE QRS COMPLEX
QRS Width… represents speed of conduction through AV node and ventricle. HEIGHT represents ventricular mass (high), and impedance to conduction (low) (Impedance is the effective resistance of an electrical circuit) TALL COMPLEXES either (low impedance) o LV Hypertrophy- high ventricular mass o A thin person SMALL COMPLEXES represent a (high impedance) o Fat person, or pericardial fluid WIDTH o Any impulse that is generated from within the atrium, can only access the ventricle via the AVN o The atria and ventricles are electrically insulated from each other. o The AVN slows conduction momentarily, to allow atrial conduction to finish. o The bundles of His then speed up the conduction, to allow the ventricles to contract. o Therefore any QRS complex, that travels through the normal intact conduction system by definition is NARROW (UNDER 3 SMALL SQUARES) The causes of a broad complex rhythm are (2 things going on, fast rate, and slow conduction) ACCESSORY, BBB, VENTRICULAR! o 1. An atrial rhythm that is conducted in the presence of a BBB (bundle branch slows conduction through the bundles, and hence the ventricles- making the QRS broad)- SVT with BBB o 2. An atrial rhythm that bypasses the AV node, so enters the ventricles outside the high-speed bundles (ventricular conduction slowed, making the QRS broad)- SVT conducted via accessory pathway o 3. A rhythm that is generated outside of the normal conducting system (any ventricular rhythm/paced rhythem)- VT If you remember this, then you will have no problems dealing with any broad complex tachycardia that you come across on-call. A broad complex tachcardya can only be due to o SVT with BBB o SVT conducted via an accessory pathway o VT You don’t need to know whats going wrong… you just need to know the ONE drug that treats them.. AMIODARONE!
READING AN ECG
If you were to treat fast AF that was broad with DIGOXIN or BETA-BLOCKER, you can make AF worse. They act on AV NODE ONLY! If you block the AVNODE in the presence of an accessory pathway, the only way the beat can get to the ventricles is the accessory pathway.
BUNDLE BRANCH BLOCKS
Impulse travels down the bundle of His, and divides into o RIGHT BUNDLE BRANCH (one fascicle) o LEFT BUNDLE BRANCH (two fascicles) Left anterior fascicle Left posterior fasicle SIMPLE! You would PRICK YOUR FINGER ON A RBBB, but not a LBBB. RIGHT can be ALRIGHT… ie a normal finding. LBBB associated with Coronary artery disease, and is an indication for THROMBOLYSIS. Since the electrical impulse can no longer use the path it wants (heart disease/MI), it moves instead through muscle fibres, which slows movement, and changes the direction of the propagation of the impulses. Loss of ventricular synchrony, ventricular depolarization is prolonged, and may be a drop in CO
DIAGNOSED ON ECG, WHEN DURATION OF QRS IS over 120ms LBBB broadens the entire QRS (and may shift axis to the left)- look in V1 for a BROAD QRS!
WHAT???!??! HEART BLOCK
The first sign to look for is a p wave, they doesn’t have a QRS complex following Then decide what type If no impulse arrives in the ventricle, after a period of time, a ventricular escape response takes over, and this is ALWAYS REGULAR. Therefore, complete heart block always has a regular ventricular rhythm. 1st DEGREE o Prolonged P-R o Over 0.2secs o Fibrosis of the AVN, increases risk of further block in 20% cases o Every p wave followed by a QRS complex. 2nd DEGREE o MOBITZ 1 (WENKEBACH) PR progressively lengthens, until one P wave fails to conduct The cycling of lengthening and dropping is irregular Irregular conduction through the AV node, so ventricular rhythm irregular too. If you look at the rhythm strip, and see the ventricular rhythm is irregular, it has to be Wenkebach, after you’ve realized it must be a block because there are p waves without a QRS. o BOBITZ 2 (2:1) Regular pattern to non-conducted p-waves. P-R interval in conducted beat is always the same. Regular conduction through the AV node. Regular ventricular rhythem COMPLETE HEART BLOCK o Lack of any relationship between p and QRS o REGULAR VENTRICULAR RHYTHM In 2:1 block and Complete block are treated the same.- They are paced.
ECG and TERRATORIES I
AVR
V1
V4
II
AVL
V2
V5
III
AVF
V3
V6
INFERIOR: SEPTAL: ANTERIOR: LATERAL:
II, III, AVF (the bottom L) RIGHT CORONARY Proximal LAD V3, V4 LAD V5, V6, I, AVL Circumflex V1, V2
An occlusion of the LAD at the beginning (ie proximal) is a lot worse, as the territory is septal, then also a lot of the ventricles too- so more likely to lead to HF. V1 and V2 is bad. Occlusion distally results in a small loss of territory- so low risk of HF.
ST CHANGES Can be transient or permanent.
ST ELEVATION o MI, Pericarditis, Scarring, aneurysm. ST DEPRESSION o Ischemia ‘strain’ (LVH) o Repolarisation abnormalities (BBB) o Digitalis effect T WAVE INVERSION o Ischemia o Repolarization abnormalities (BBB) o Changes in posture ‘normal’.
DEFINITIONS
MI: ST elevation or new onset LBBB NSTEMI: Biochemical evidence of infarction (troponin) in the absence of ST elevation or LBBB. ECG may look normal!
QUICK CHECK
1. 2. 3. 4.
Name, Date, time Rate and Rhythem (strip at bottom) Check leads 1 and 3 for axis (Left alone, Right-alright) V1 check o P-R interval (0.12 sec to 0.2 sec) o If LBBB present, you CANT INTERPRET THE ECG ANY FURTHER!!! o If RBBB, you can, but any QRS and t changes might be due to BBB. 5. If no LBBB, check each lead looking for morphological abnormalities in the QRS and T waves. (LVhypertrophy defined as deepest S wave V1 or V2 added to the tallest R wave in V5 or V6. If over 25mm… LVH)
BASIC INTERPRETATION AND REGIGNITION ECG RATE RHYTHEM AXIS P WAVES P-R INTERVAL QRS COMPLEX ST Q-T interval T WAVES
RATE
Check paper speed is 25mm/sec Tiny square is 0.04 secs 5 small squares = 0.2 seconds. The ventricular rate is calculated by looking at distance between R-R NUMBER OF LARGE SQUARES BETWEEN R-R…. DIVIDED BY 300. If really fast, number of small squares between R-R, counted divided by 1500.
RHYTHEM
SINUS o P before every QRS and at fixed interval from it. P BEFORE EVERY QRS P-R NORMAL P-R CONSTANT ATRIAL FIBRILLATION o No P waves, irregular QRS ATRIAL FLUTTER o ECG shows presence of ‘flutter waves’ o Baseline adopts a saw-tooth appearance o AV flutter may occur with a fixed degree of block (3:1 block)- ie for every 3 flutter waves, a QRS o May have variable block HEART BLOCK o 1st: prolongued P-R interval (over more than 5 small squares), constant P-R interval o 2nd WENKE: P-R lengthens, then drops a QRS o 2nd MOB2: P-R might be normal, but every 2 or so, theres a p with no QRS. o 3rd p waves and QRS totally dissociated. Mark the p waves, then try to line up with QRS
CARDIAC AXIS
Describes the average direction of electrical activity in the heart. I and lll away.. LEFT (alone)…. I and III towards (RIGHT.. alright) Normal is little up, little up, little up I II III
P WAVES
P wave should be 2.5 SMALL SQUARES UP AND 3 ACROSS Tall P waves? P PULMONALE (enlarged right atrium)- p are peaked
BASIC INTERPRETATION AND REGIGNITION ECG Q WAVES
Should be 2 SMALL SQUARES DOWN and ONE ACROSS In the lateral leads, its fine for them to be big (V5, V6, AVL, 1) If they’re BIG ANYWHRE ELSE o Abnormal: scar tissue in heart after a MI
R, and S WAVES
Used to predict LV HYPERTROPHY Add together the height (mm) of o R in V6 o S in V1 If greater than 35mm- LVH present. Echo to confirm Causes of small complexes? Pericarditis, pericardial effusion, emphysematous lungs.
QRS DURATION
LESS THAN 3 SMALL SQUARES WIDE Wide- abnormal conduction through ventricles. Ie. Not through bundle of His etc.. but more slowly through non-specialized cardiac tissue. o RBBB 2 R-WAVES (upward deflections) seen in the QRS in V1 (RSR PATTERN) And a deep S-WAVE in V6 o LBBB Looks BIZARRE RSR may be seen in V6 STOP interpretation after establishing o RATE RHYTHEM o AXIS o PRESENCE OF LBBB
ST SEGMENT
ST ELEVATION: MI, pericarditis (saddle shaped- droopy in pericarditis) ST DEPRESSION: Cardiac ischemia Strain pattern: ST depression in lateral chest leads, and features of LVHypertrophy- this means marked LV hypertrophy. Down-sloping ST-depression seen on patients on DIGOXIN.
QT INTERVAL
Long Q-T predispose to cardiac dysrrythmias Shouldn’t be more than 2 BIG SQUARES Usually varies with HR- ie QT increases as HR slows Corrected QT should be less than 0.45 SECS.
T WAVE
Shouldn’t be more than 2 SQUARES TALL Inversion Normal if in o V1 and V2 together (but not V2 alone) o aVR o aVL Tall tented: HYPERKALAEMIA Flat, broad: HYPOKALAEMIA
Hyperkalaemia: TallTentedTwaves, no P waves, broad QRS, Sine waves, ARREST RHYTHEMS Hyperkalaemia: FlatBroadTwaves, STdepression, LongQT, Ventricular dysrrythmias.
BASIC INTERPRETATION AND REGIGNITION ECG CARDIAC ARREST RHYTHEMS
SHOCKABLE o VF o VT NON-SHOCKABLE- need to reverse the cause of the arrest, and start CPR o PEA o ASYSTOLE o P wave ASYSTOLE: only p waves, can respond to cardiac pacing
ATRIAL FLUTTER
WENKEBACH
1st DEGREE BLOCK
3rd DEGREE BLOCK
LBBB
RBBB
VT
VF
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