Saint-Frances Guide to Inpatient Medicine

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SAINT-FRANCES �: GUIDE TO :I------J INPATIENT MEDICINE

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Sanjay Saint,

M.D.

Chief Medical Resident, 1995-96 University of California, San Francisco San Francisco. California V I I

Craig Frances,

M.D.

Chief Medical Resident, 1996-97 University of California, San Francisco San Francisco, California

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8 :x: 0 0.. 061

SAINT-FRANCES GUIDE TO INPATIENT MEDICINE

8 C') I=[ ::r:: -:t: u :>, � II! :s: 0 0.. OJ III :x: 0 :: 1 1 mm (> 13 mm if left anterior fascicular block is present) 2. R wave in lead aVL + S wave in lead V3 > 20 mm in a woman or 28 mm in a man 3.

S wave in lead VI + R wave in leads VS or V6 (whichever is larger) > 35 mm

Electrocardiogram (EKG) Interpretation

Chapter 4

28

B. Right ventricular hypertrophy. Criteria for the diagnosis

of right ventricular hypertrophy are also highly specific but insensitive. 1. R : S wave ratio in lead VI greater than or equal to 1 2. R wave in lead VI greater than 7 mm 3. R : S wave ratio in lead VS or V6 less than I C. Left atrial abnonnality was formerly called left atrial enlargement, but the name was changed because the EKG findings may actually represent dilatation, in­ creased atrial pressure, or hypertrophy. 1. Lead II. Notched P waves greater than 0.04 second apart (1 small box) indicate left atrial abnormality. 2. Lead VI. If the P terminal force (the negative deflec­ tion that represents left atrial depolarization) is equal to or greater than one small box by one small box (0.04 sec by 1 mm), left atrial abnormality is diagnosed. D. Right atrial eulargement 1. Lead II. A P wave greater than 2.5 mm high indicates

right atrial enlargement.

2. Lead VI or V2. A P wave greater than 1.5 mm high

indicates right atrial enlargement.

Q WAVES simply indicate that forces are moving away from their respective leads. A. Normal Q waves. Sometimes Q waves are normal and expected. For example. the interventricular septum is depolarized left to right, and so a Q wave is expected in lead V6 (reflecting forces moving away from this left­ ward lead). B. Pathologic Q waves signify that forces are moving away from the area more than would normally be expected. A pathologic Q wave indicates an old myocardial in­ farction, and is only diagnosed when the Q wave is at least 30 msec (close to one small box) in duration and one third the height of the ensuing R wave. 1. Inferior wall myocardial infarction. Leads II, III. and aVF evaluate the inferior surface of the left ventricle. Therefore, Q waves in these leads denote an inferior wall myocardial infarction. 2. Posterior wall myocardial infarction. Sometimes an inferior wall infarction is accompanied by a posterior wall infarction, producing a large R wave in lead VI (i.e., forces move away from the posterior wall anteriorly). Differential diagnoses for a large R wave in VI include:

, .

29

Posterior wall myocardial infarction Posteroseptal accessory pathway Right ventricular hypertrophy Right interventricular conduction delay Right bundle branch block Duchenne's muscular dystrophy Limb lead reversal h. Dextrocardia i. Normal variant 3. Anterior myocardial infarction. Q waves in the pre­ cordial leads (Vl-V6) imply an old anterior myocar­ dial infarction. a. b. c. d. e. f. g.

m 5T/T WAVE CHANGES A. Canses. The most common causes of STfT wave changes are: 1. Myocardial ischemia, injury, or infarction 2. Ventricular enlargement 3. Abnormal ventricular depolarization (e.g., with bun­

dle branch block) 4. Electrolyte disturbances

B. Findings 1. T wave inversions often indicate myocardial ischemia. 2. ST elevations or depressions often indicate myocar­ dial injury. 3. ST elevations with the appearance of Q waves usually indicate myocardial infarction. C. Tenninology. Clinicians often refer to ST depressions

and elevations as ischemia and infarct, respectively, rather than simply "injury." This is because ST depres­ sion is caused by injury to the subendocardial (inner) region that is often the result of a supply/demand mis­ match caused by ischemia. ST elevation implies transmu­ ral injury that usually occurs as a result of complete coronary occlusion during an infarction.

1

5. Syncope

a INTRODUCTION

A. Definition. Syncope is a transient loss of consciousness

B.

and postural tone that is caused by inadequate cerebral blood flow. Epidemiology. Syncope is extremely common, account­ ing for approximately 5% of medical admissions and 3% of emergency room visits. The lifetime incidence ap­ proaches 50% in some groups.

III CAUSES OF SYNCOPE.

There are many causes of syncope, but the most important can easily be remembered using the mnemonic, "SYNCOPE."

31

Sy ncope

Obstructive disorders. Aortic, mitral, or pul­ monic stenosis, idiopathic hypertrophic subaortic stenosis. atrial myxoma, and pulmonary embo­ lism interfere with cardiac output and can precip­ itate a syncopal attack. b. Arrhythmias. Disorders that lead to bradycardia [e.g., sick sinus syndrome, second- and third-de­ gree atrioventricular CAY) block] or tachycardia [e.g., ventricular fibrillation, ventricular tachycar­ dia, torsades de pointes, supraventricular tachy­ cardia] also interfere with cardiac output. c. Ischemic disorders can precipitate an episode of syncope. 5. Orthostatic hypotension can cause syncope. 6. Psychogenic syncope is a diagnosis of exclusion. a.

7.

Everything else a. Medications (e.g., vasodilators, hypnotics, seda­

tives, nitrates, diuretics,

a

blockers)

b. Drugs (e.g., cocaine, hypnotics, sedatives, al-

cohol) Causes of Syncope ("SYNCOPE") Situational Vasovagal (the V looks like a Y) Neurogenic Cardiac Orthostatic hypotension Psy chiatric Everything else

1. Situational causes include mictuntlOn, defecation, swallowing, coughing, subclavian steal, and carotid sinus sensitivity. 2. Vasovagal syncope, also known as the "common faint," is the most common cause of syncope in young patients and is often preceded by a painful or emo­ tional stimulus. 3. Neurogenic causes inclUde autonomic insufficiency and transient ischemic attacks (TIAs). a. Transient ischemic attacks (TIAs) are extremely rare causes of syncope. For syncope to occur, the vertebrobasilar circulation must be involved. b. Autonomic insufficiency is common in elderly patients and patients with diabetes. 4. Cardiac causes 30

IIII ApPROACH TO THE PATIENT.

The evaluation of a patient with syncope must be approached in a rigorous. stepwise fashion to avoid missing life-threatening disease. A. History and physical examination. A thorough history and physical examination is a very important aspect of the evaluation and may establish the diagnosis in many patients. 1. Situational. Was the episode preceded by urination, defecation, swallowing, coughing, exertion of arm muscles (subclavian steal), or manipulation of the neck (carotid sinus hypersensitivity)? 2. Vasovagal. Did a painful or emotional stimulus pre­ cede the event? 3. Neurogenic. Did anyone witness convulsions, bowel or bladder incontinence, or signs suggestive of a post­ ictal state? A seizure is not syncope but could result in a loss of consciousness and therefore must be considered in the differential diagnosis. 4. Cardiac. A cardiac cause is more likely if the patient has any history suggestive of cardiac disease. Has the patient complained of feeling lightheaded during exercise (suggestive of an obstructive cause)? Has the patient complained of "palpitations" (suggestive of an arrhythmic cause)? Patients may also complain of symptoms suggestive of cardiac ischemia.

32

Chapter 5

5. Orthostatic hypotension. Does the patient report that he "got up too quickly"? Always check or­ thostatic vital signs in patients admitted with syncope. 6. Psychogenic. A psychogenic cause for the syncope (e.g., hyperventilation) should be considered after all other causes have been excluded. 7. Everything else. What prescription, over-the­ counter, or illicit drugs might the patient have ac­ cess to? B. Electrocardiogram (EKG). All patients should have an EKG, although fewer than 10% of the causes of syncope can be identified by this test. Look for evidence of acute or remote myocardial infarction, preexcitation syn­ dromes, arrhythmias, and conduction system disease. C. Risk assessment. Patients should be separated into two groups: those without evidence of heart disease, and those who may have heart disease. 1. No evidence of heart disease. Patients who meet all of the following criteria after a thorough history, physical examination, and EKG are at low risk for a cardiac cause, and additional cardiac testing may not be indicated. However, some patients may re­ quire additional evaluation and treatment. The crite­ ria are: a. Yonnger than 60 years of age

2.

b. No history or evidence of coronary artery disease or congestive heart failnre c. Normal EKG Evidence of heart disease. Anyone who does not

meet all of the criteria in III C 1 is included in this group. If there is suspicion of an ischemic or arrhyth­ mic cause, admission and EKG monitoring are indi­ cated. Additional diagnostic tests to be considered in­ clude: a. Ambulatory EKG monitoring. This test is widely used, but it establishes a diagnosis in only a small percentage of patients. Event or loop recorders may improve the diagnostic yield. b. Exercise treadmill testing can rule out exercise­ or ischemia-induced syncope. c. Echocardiography allows assessment of valvular disease, as well as left ventricular size and function. d. Electrophysiologic testing is especially useful in patients at high risk for arrhythmia (i.e., those

l

33

Syncope

with poor left ventricular function) when a diag­ nosis cannot be established using noninvasive methods. e. Tilt table test. This test can be useful in docu­ menting vasovagal syncope, but it has poor speci­ ficity. f. Signal-averaged EKG (SAEKG). The utility of this test in patients with syncope is controversial.

TREATMENT is cause-specific. A. The treatment of any correctable cardiac abnormality

should be the first consideration. B. Patients with frequent vasovagal syncope may benefit

from a trial of f3 blockers.

PREVENTION A. Medications and the use of alcohol or illicit drugs should

be carefully reviewed. B. Education about likely precipitants can help prevent re­

currences.

6.

I

Arrhythmias

Arrhythmias

35

TABLE 6-1: Classification of Tachyarrhythmias'

Narrow QRS

a

INTRODUCTION A. Bradyarrhythmias usually do not pose a diagnostic di­

lemma and have relatively few treatment options (e.g., atropine, pacer device). B. Tachyarrhythmias may pose a significant challenge in diagnosis and often are treated very differently. All tachyarrhythmias can be classified according to whether they are regular (same distance between successive R waves) or irregular, and whether their QRS complex is narrow « 0.12 second) or wide (> 0.12 second). Making these two determinations and consulting Table 6-1 can significantly narrow the diagnostic possibili­ ties:

III

Wide QRS

Regular Rhythm

Irregular Rhythm

Sinus tachycardia AVNRT AVRT AT Atrial flutter

Atrial fibrillation Atrial flutter with vari­ able bloek Multifocal atrial tachy­ cardia Frequent premature atrial contractions Atrial fibrillation with

Ventricular tachycardia

Supraventricular tachy­ cardia with aber­ rancy

aberrancy* Ventricular tachycardia (monomorphic or polymorphic)

AT atrial tachycardia; AVNRT atrioventricular nodal reentrant tachycar­ dia; AVRT atrioventricular reentrant tachycardia. * Because all arrhythmias characterized by an irregular rhythm and a narrow QRS camplex can become irreg ular with a wide QRS complex in the presence of aberrant conduction, atrial flutter with variable block and multifoeal atrial tachycardia must also be considered here, although they are much less common than atrial fibrillation. =

=

=

NARROW, REGUlAR TACHYARRHYTHMIAS A. Differential diagnosis L Sinus tachycardia a. Etiologies. Sinus tachycardia is usually a physio­ logic response to stress. Important etiologies in­

clude: (1) Low stroke volume states (e.g., from intra­ vascular volume depletion or myocardial dys­ function) (2) Hypoxia (e.g., from pulmonary embolus) (3) Hypercatecholamine states (e.g., from pheo­ chromocytoma, pain, anxiety) (4) Drugs (e.g., inhaled f3 agonists, theophyl­ line, caffeine) (5) Systemic causes (e.g., fever, anemia, hyper­ thyroidism) (6) Myocarditis and pericarditis b. Electrocardiogram (EKG) appearance. Upright P waves in leads II, III, and aVF are always followed by a QRS complex. 34

HOT The maximum heart rate in sinus tachycardia

minus the patient's age.

=

220

KEY

2.

tt: I=: 1:1: ()) :r:

I

V I I

Atrioventricular nodal reentrant tachycardia (AVNRT) accounts for more than 50% of all supra­

ventricular tachyarrhythmias. [All narrow, regular tachyarrhythmias are supraventricular, but the term supraventricular tachycardia is classically used for AVNRT, atrioventricular reentrant tachycardia (AVRT). and atrial tachycardia (AT).] a. Characteristics include:

Chapter 6

36

(1) A heart rate of 180 beats/min (::'::10%) (2) Isolated R waves, pseudo S waves. or in­ verted P waves on the EKG b. Mechanism. Many people have a dual atrioven­ tricular (AV) node that contains a fast pathway with a long refractory period and a slow pathway with a short refractory period. (1) Sinus rhythm. During sinus rhythm, the im­ pulse is conducted down the fast pathway to the ventricles. Conduction down the fast pathway is also able to traverse the A V node retrograde and block impulses on the slow pathway (Figure 6-1 ). (2) Excitation loop. The incidence of premature atrial contractions (PACs) increases with age. A PAC may be blocked at the fast path­ way secondary to its long refractory period; the impulse is then conducted down the slow pathway, which has a short refractory period. The impulse may then enter the fast pathway, which is no longer refractory, and activate the atria by retrograde conduction (Figure 6-2). c. EKG appearance

SA node

Slow pathway (short refractory period)

AV node

Fast pathway (long refractory period)

Arrhythmias

PAC

Slow pathway (short refractory period)

I I I

1 o 0. J:j

FiGURE 6-1. ular; SA

=

Dual atrioventricular node. sinus rhythm. AV sinoatrial.

=

atrioventric­

AV node

Fast pathway (long refractory period)

His-Purkinje fibers

� I

I His-Purkinje fibers

37

FIGURE 6-2.

Atrioventricular nodal reentrant tachycardia (AVNRT) from premature atrial contractions (PACs). Following conduction down the slow pathway , the fast pathway is no longer refractory and may conduct retro­ grade, forming an excitation loop. AV atrioventricular. =

(1) In typical AVNRT (90% of cases), a PAC begins the loop of excitation. The P wave is inverted and occurs simultaneously with the QRS complex; only R waves are seen on the EKG. (2) In atypical AVNRT (10% of cases), a prema­ ture ventricular contraction (PVC) initiates the conduction of an impUlse up the slow pathway and down the fast one (Figure 6-3). Because the retrograde P waves are formed from the slower pathway, they occur slightly later and can be seen as pseudo S waves in the inferior leads (II, III, avF) or as inverted P waves following the QRS complex. 3. AVRT accounts for more than 30% of all supraven­ tricular tachyarrhythmias. a. Characteristics. AVRT is characterized by a short RP interval on the EKG. b. Mechanism. AVRT involves an accessory path­ way, an abnormal tract of fast conducting tissue between the atria and ventricles that bypasses

38

Arrhythmias

Chapter 6

Slow pathway (short refractory p er iod)

AV node

39

�

Fast pathway (long refractory period)

/

/�

/

I I

1I Bypass tract \ It,

-,,,'fI("

/

AV node

'�-

fiGURE 6-4.

Orthodromic conduction leading to atrioventricular reen­ trant tachycardia (AVRT). AV atrioventricular. =

from AT. The QRS complex remains nar­ row because the ventricle is depolarized normally (i.e., via the His-Purkinje system). (b) Antidromic conduction occurs when the impulse is conducted ante grade down the bypass tract. Antidromic conduction pro­ duces a wide QRS complex because the tract terminates on ventricular muscle fibers. (Conduction from fiber to fiber is slow.) 4. AT accounts for 15% of all supraventricular tachy­ cardias. a. Characteristics (1) The atrial rate (as reflected by the P waves on the EKG) is usually less than 250 beatsl min. (In atrial flutter, the atrial rate is approx­ imately 300 beats/min.) (2) A long RP interval is noted on the EKG. b. Mechanism. Enhanced automaticity of atrial tis­ sue or atrial reentry with a focus usually located in the lower portion of the atrium is thought to be the mechanism. (1) Patients often have structural heart disease. (2) Because digitalis increases atrial and ventricular automaticity and depresses conduction tissue, AT with variable degrees of AV nodal block is a common presentation of digitalis toxicity. c. EKG appearance. A retrograde P wave, pro­ duced by depolarization of the atria from below, is followed by a narrow QRS complex (produced

PVC FIGURE 6-3.

Atypical atrioventricular nodal reentrant tachycardia (AVNRT). AV atrioventricular; PVC premature ventricular con­ traction. =

=

the AV node. Accessory pathways often conduct in both an anterograde and retrograde direction. c. EKG appearance (1) Sinus rhythm (a) During sinus rhythm. anterograde con­ duction results in ventricular preexcita­ tion, manifested as a short PR interval and a delta wave on the EKG. (b) If only retrograde conduction is possible (as is the case in approximately 25% of patients), no abnormality is seen during sinus rhythm (concealed bypass tract). (2) Excitation loop (a) Orthodromic conduction occurs when an impulse is conducted through the AV node and then up the accessory pathway in a retrograde direction (Figure 6-4). Be­ cause the loop is longer than that of AVNRT, the retrograde P wave is easily seen (i.e., it is not buried in the R wave). The interval from the R wave to the ensu­ ing retrograde P wave will be less than that from the P wave to the next R wave (short RP or RP < PR tachycardia). This characteristic helps distinguish AVRT V I I

Chapter 6

40

by conduction of the impulse down the AV node). The preceding P wave is linked to the R wave, and the PR interval is shorter than the RP interval (long RP or short PR tachycardia).

HOT The supraventricular tachycardias can be classified according to the RP interval: Short RP AVRT and, occasionally, AVNRT long RP AT =

=

No RP

KEY

=

AVNRT

5. Atrial flutter a.

Characteristics (1) The atrial rate is often 300 beats!min, and the ventricular rate is approximately 150 beats! min. (In other words. a 2 : 1 AV block is com­ monly seen.)

HOT Whenever the ventricular rate is 150 beats/min (::+:: 5 ), think of atrial flutter.

KEY

(2) Atrial flutter is frequently transient and may degenerate to atrial fibrillation or return to sinus rhythm. In general, the causes of atrial flutter are similar to those of atrial fibril­ lation. b. Mechanism. Waves of organized depolarization move through the atria. c. EKG appearance. Because the waves often move in a superior-inferior direction, flutter waves are best seen in the inferior leads (i.e., leads II, III, and avF).

Arrhythmias

41

B. Treatment 1. Acute treatment depends on the patient's hemody­ namic stability. a. Hemodynamically unstable (or ischemic) pa­ tient. Determine if the patient is in sinus rhythm. (1) If the patient is not in sinus rhythm, initiate electrical cardioversion immediately. (2) If the patient is in sinus rhythm, treatment is aimed at the underlying cause. b. Hemodynamically stable patient (1) Carotid sinus massage may increase vagal tone and block impulses at the level of the AV node. Carotid sinus massage is contrain­ dicated in the presence of a carotid bruit and should be performed with continuous EKG monitoring and a crash cart available. (a) AVNRT and AVRT, tachycardias that involve reentrant loops through the AV node, may terminate. (b) AT is usually unaffected by carotid sinus massage, but may terminate abruptly. (c) Sinus tachycardia. Carotid sinus massage may slow the atrial rate. (d) Atrial flutter usually becomes more obvi­ ous as the AV block increases and flutter waves appear; the tachycardia will not terminate. (2) Administer adenosine in incremental doses of 6 and 12 mg if carotid sinus massage is ineffective. (Halve the dose if administration is via a central line.) Adenosine is contraindi­ cated in patients with acute bronchospasm, and heart transplant patients and patients on dipyridamole have an increased sensitivity. The effects of adenosine occur within 15-30 seconds of administration and last for 10-20 seconds. Adenosine has effects similar to those of carotid sinus massage. but they are more pronounced. (a) AVNRT and AVRT. More than 90% of these tachycardias will be terminated with a 12 mg dose. (b) AT rarely terminates. Intravenous ad­ ministration of verapamil or diltiazem is preferable for arresting atrial tachycardia -

42

Chapter 6

c. Atrial tachycardia. Calcium channel blockers or

and may decrease the ventricular re­ sponse, even if the tachycardia persists. (c) Sinus tachycardia transiently slows. Ad­ ditional treatment should be aimed at the underlying cause. (d) Atrial flutter. AV block increases and flutter waves are more evident. The heart rate returns to its previous accelerated rate as the effects of the adenosine wane. Additional treatment may involve AV nodal blockade with digitalis, {3 blockers, or calcium channel blockers, followed by either chemical (e.g.. procainamide) or electrical cardioversion. (i) Often, AV nodal blocking agents will be unsuccessful at controlling the heart rate and doses are limited by their toxicity.

{3 blockers are often the drugs of first choice. If pharmacologic therapy fails, ablation may be in­ dicated. d. Atrial flutter usually degenerates to atrial fibril­ lation or reverts to sinus rhythm.

III

In atrial flutter, la agents should not be given prior to the administration of AV nodal blocking agents be· cause type la agents may slow atrial conduction suffi­ cienrly to permit 1 : 1 conduction through the AV node, thereby increasing the ventricular response.

(ii) Electrical cardioversion starting at 25 J is a reasonable alternative to AV nodal blocking agents. 2.

A. Differential diagnosis. In general, the members of this

VIOUS.

Chronic treahuent a. AVNRT. If the patient experiences sporadic epi­

sodes, control may be possible using vagal ma­ neuvers. For patients who experience frequent or symptomatic episodes, AV nodal blocking agents or radiofrequency may be used. b. AVRT. Symptomatic patients with evidence of preexcitation on a baseline EKG should proba­ bly receive radiofrequency ablation. Patients with symptoms but no evidence of anterograde conduction (i.e., concealed bypass tract) can be treated with ablation or an initial trial of an AV nodal blocking agent.

NARROW, IRREGULAR TACHYARRHYTHMIAS category are able to be differentiated easily on the basis of a 12-lead EKG. It is most difficult to distinguish atrial fibrillation from atrial flutter with variable block. 1. Atrial fibrillation is discussed in detail in Chapter 7. This arrhythmia is characterized by irregular atrial fibrilla tory waves at a rate of 350-600 beats/min and a ventricular rate of usually 120- 160 beats/min. 2. Atrial flutter with variable block. To help differenti­ ate atrial flutter with variable block from atrial fibril­ lation: a. Look at the inferior leads (II, III, avF). With atrial flutter, flutter waves can often be "marched out" at a rate of approximately 300 beats/min. Variable block will produce a ventricular rate in proportion to the atrial rate (i.e.. the ventricular response to 2 : 1, 3: 1, and 4: 1 AV block will be 150 beats/min, 100 beats/min, and 75 beats/ min. respectively). b. Increase AV block by massaging the carotid sinus or administering adenosine. Flutter waves that may have been hidden will often become ob­

HOT

KEY

43

Arrhythmias

(J) :Ii

I

vi I I

3. Multifocal atrial tachycardia a. Mechanism. In approximately 60% of patients, multifocal atrial tachycardia is associated with pulmonary disease. For example, cor pulmonale causes right atrial stretch, producing different foci of atrial contractions. Multifocal atrial tachy­ cardia may also be caused by hypokalemia or hypomagnesemia. b. EKG appearance. Diagnosis requires the pres­ ence of three distinct P wave morphologies in the same lead and three separate PR intervals. As a result, the RR interval varies (i.e., it is irreg­ ularly irregular).

Chapter 6

44

4.

Frequent PACs. When frequent, PACs may give the appearance of an irregular rhythm.

B. Treatment 1. Hemodynamically unstable (or ischemic) patients with atrial fibrillation, atrial flutter with variable block, or multifocal atrial tachycardia should un­ dergo immediate electrical cardioversion. 2. Hemodynamically stable a. Atrial fibrillation. Treatment is discussed in

45

Arrhythmias

impulse is conducted down the faster bundle and then from fiher to fiber, producing a wide QRS. c. An accessory pathway. These tracts terminate on ventricular muscle, necessitating fiber-to-fiber con­ duction. B. Differential diagnosis. The differential is ventricular tachycardia versus supraventricular tachycardia with ab­ errancy.

Chapter 7 VI. b. Atrial flutter with variable block. Treatment is

the same as that for atrial flutter without variable block [see II B Ib]. c. Multifocal atrial tachycardia. The underlying condition (usually related to bronchospasm, hyp­ oxia, or metabolic derangements) should be treated. Intravenous verapamil is often tried, but this is a difficult arrhythmia to treat.

HOT Patients with cardiac disease should be assumed 10 have ventricular tachycardia until proven otherwise.

KEY

II WIDE, REGULAR TACHYARRHYTHMIAS The Bmgada criteria can help you distinguish between ventricular tachycardia and supraventricular tachycardia with aberrancy.! The precordial leads (Vl-V6) are exam­ ined on a 12-lead EKG. Each criteria is extremely spe­ cific, but not particularly sensitive, for ventricular tachy­ cardia; therefore, if a criterion is met. you should initiate treatment for ventricular tachycardia, and if the criterion is not met, you continue to the next.

A. Mechanism.

Normally, the impulse is conducted from the sinoatrial (SA) node to the A V node, through the bundle of His, and through the left and right bundle branches (the Purkinje fibers). The bundles conduct rap­ idly and ventricular depolarization is efficient, producing a narrow QRS complex « 100 msec in duration). 1. If one bundle is blocked, conduction will spread down the remaining bundle and then from muscle fiber to muscle fiber. This is a slow process that pro­ duces a wide QRS complex (> 120 msec in duration). A QRS complex between 100 and 120 msec in dura­ tion represents an incomplete bundle branch block and is often termed an interventricular conduction delay. 2. The QRS complex will be wide if the impulse starts in the ventricle and spreads fiber to fiber (as is the case with ventricular tachycardia) or if it starts above the ventricle but eventually spreads fiber to fiber (as is the case with supraventricular tachycardia with aberrancy). There are three mechanisms of aber­ rant conduction: a. A preexisting underlying bundle branch block b. A rate-related bundle branch block. As the heart

rate increases, one bundle (usually the right bun­ die) is unable to keep up with the other. The

1.

Absence of a true RS pattern in all of the precordial leads. An S wave is a discrete negative deflection. A

broad negative deflection is an inverted T wave (as opposed to an S wave). If there is a monomorphic pattern (no RS), the arrhythmia is ventricular tachy­ cardia. 2.

RS complex (from start of R to nadir of S) is greater than 100 msec. Ventricular depolarization takes

more time if it starts in the ventricle, rather than if it begins supraventricularly and is conducted aber­ rantly. If the RS complex is greater than 100 msec. then the arrhythmia is ventricular tachycardia. 3. Evidence of A V dissociation includes P waves 1 Brugada

P, Brugada J, Mont L, Sweets J, Andreis EW: A new approach

to the differential diagnosis of a regular tachycardia with a wide QRS complex.

Cire

83(5): 1649-59, 1991.

46

Chapter 6

marching through at different points of the wide complexes and fusion or capture beats. Although these clues are difficult to discern, they are diag­ nostic of ventricular tachycardia. If a diagnosis has still not been reached. morphologic criteria (given in several texts) can be used to arrive at a diagnosis.

HOT All members of the irregular, narrow categary will appear irregular and wide with aberrant conduction.

C. Treatment L Hemodynamically unstable (or ischemic) patients should undergo cardioversion, starting with 200 J. 2. Hemodynamically stable patients a. Ventricular tachycardia (1) Lidocaine. The initial dose is 1- 1.5 mg/kg

KEY

1.

a. Preexisting underlying bundle branch block. If,

upon comparing a previous 12-lead EKG with a current one, there is evidence of an old bundle branch block that has the same morphology as the present one. this diagnosis is extremely likely. b. Rate-related bundle branch block will usually have a right bundle branch block pattern on the EKG because the right bundle is usually slower than the left bundle. c. Accessory pathway. If there is evidence of preex­ citation during sinus rhythm (i.e., a short PR in­ terval, delta waves) on a prior 12-lead EKG, this diagnosis is extremely likely. Another clue to an accessory pathway is bizarre conduction (e.g., lead VI suggests a left bundle but the nearby V2 lead suggests a right bundle). An accessory pathway is a dangerous situation because fibril­ latory waves occur at rates of approximately 600 beats/min and the accessory pathway allows much faster conduction than does the AV node. Very fast ventricular rates (i.e., 200-300 beats/ min) can be generated; this arrhythmia can quickly degenerate to ventricular fibrillation.

b. Supraventricular arrhythmias with aberrancy. Carotid sinus massage and adenosine should be

employed as described in II B Ib. c. Undiagnosed (1) Lidocaine. The patient should be given a lido­

cain e trial. trials in 6- and 12-mg increments (half doses if administered centrally) should be tried. If the patient has a history of cardiac disease, ventricular tachycardia is likely and needs to be treated expediently. (3) Procainamide. If the patient still fails to respond, a procainamide trial may be indi­ cated.

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II WIDE, IRREGULAR TACHYARRHYTHMIAS A. Differential diagnosis. The differential diagnosis is atrial fibrillation with aberrancy versus ventricular tachycardia

(monomorphic or polymorphic).

Atrial fibrillation with aberrancy. There are three

possible mechanisms of aberrant conduction.

administered intravenously. followed by a second dose of 0.5-0.75 mg/kg after 5-10 minutes. (2) Procainamide should be considered in pa­ tients who do not respond to lidocaine. Procainamide is probably more effective at terminating ventricular tachycardia. but hy­ potension is common.

(2) Adenosine. If there is no response, adenosine

47

Arrhythmias

HOT Whenever you see a patient with a wide, irregular tachyarrhythmia with a rate greater than 200 beats/ min, consider atrial Fibrillation with an accessory pathway.

tJ:! I=.: 1:1: I

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48

Arrhythmias

Chapler 6

2.

heart rates may be better served with car­ dioversion. b. AV nodal blocking agents ({3 blockers, calcium channel blockers, or digitalis) should only be con­ sidered when the patient shows strong evidence of atrial fibrillation with an underlying bundle branch block (i.e., a prior EKG shows the same bundle branch block during sinus rhythm). Oth­

Ventricular tachycardia a. Monomorphic ventricular tachycardia. In ven­

tricular tachycardia. the rhythm may be irregular for the first 50 beats. A persistently irregular rhythm after 50 beats essentially rules out mono­ morphic ventricular tachycardia. b. Polymorphic ventricular tachycardia. Because the impulse is originating from different foci in the ventricle, the rhythm is irregular. Torsades de pointes is a type of polymorphic ventricular tachycardia that undulates around the isoelec­ tric point.

erwise, AV nodal blocking agents should not be administered to patients with wide, irregular tachycardias because if the patient has an acces­

sory pathway, AV nodal blocking agents will pro­ mote conduction down the tract, thereby increas­ ing the heart rate.

B. Treatment 1. Hemodynamically unstable (or ischemic) patients should undergo cardioversion starting at 200 J. 2. Hemodynamically stable patients a. Procainamide is the drug of choice. (1) If the rhythm is atrial fibrillation with aber­

rancy, procainamide may convert the patient to sinus rhythm. If the cause of the patient's aberrant conduction is an accessory path­ way, procainamide will slow conduction through the pathway, decreasing the ventric­ ular rate, even though conversion may not occur. (2) Procainamide also treats ventricular tachy­ cardia. However: (a) Procainamide is contraindicated in the setting of torsades de pointes. If a mor­

phology consistent with torsades de pointes is present or there are strong epi­ demiologic factors suggestive of torsades de pointes (e.g., an increased baseline QT interval, use of quinidine or tricyclic anti­ depressants, or electrolyte disturbances such as hypokalemia or hypomagnese­ mia), procainamide is contraindicated because it will increase prolongation of the QT interval and promote further tor­ sades. Torsades should be treated with intravenous magnesium or overdrive car­ diac pacing. (b) Procainamide frequently leads to hypo­ tension, so patients with borderline blood

pressures (i.e., 90-100 mm Hg) and fast

49

(l)

J

51

Atrial Fibrillation

7.

Atrial Fibrillation

Dyspnea Chest pain 3. Palpitations 4. Dizziness or syncope S. Fatigue B. Physical examination findings 1. Irregularly irregular pulse. An irregularly irregular pulse is the hallmark of atrial fibrillation. 2. Pulse of varying intensity and pulse deficit. Because I.

2.

...............................................................................................................

a INTRODUCTION A. Epidemiology 1.

Atrial fibrillation is the most common chronic ar­ rhythmia, occurring in 2% of the general population.

Of all patients admitted to the hospital, 7% will have atrial fibrillation. 2. The incidence varies with age: a. Rare in people younger than 50 years b. One out of 20 people older than 60 years of age c. One out of 10 people 80-89 years of age B. Terminology. There are a number of terms used in associ­ ation with atrial fibrillation. L "Valvular" refers to atrial fibrillation that is second­ ary to valve disease, most commonly rheumatic mi­ tral valve disease. In the past, rheumatic heart disease accounted for the majority of cases of atrial fibrilla­ tion, but currently accounts for fewer than one-third of cases. Atrial fibrillation unaccompanied by rheu­ matic or other valve disease is termed "nonvalvular." 2. "Isolated" refers to atrial fibrillation that is second­ ary to another illness (e.g., hyperthyroidism, pneu­ monia, pulmonary embolism) and resolves when the illness is treated. 3. "Paroxysmal" refers to intermittent episodes of atrial fibrillation unrelated to an acute illness. 4. "Chronic" refers to atrial fibrillation when it is the predominant rhythm. S. "Lone" refers to atrial fibrillation in the absence of structural heart disease [e.g.. left ventricular hyper­ trophy, congestive heart failure (CHF), valve disease, cardiomyopathy].

diastolic filling varies in length and is often reduced, pulses are of varying intensity and not all audible ventricular beats are palpable peripherally. 3. Absent a waves in the jugular venous pulse 4.

HOT Patients in atrial fibrillation never have an 54.

KEY

C. Electrocardiography

50

L

The electrocardiogram (EKG) may show f waves (fine fibrillation of the atria at a rate of 350-600 beats/min) that are best visualized in lead VI.

2.

P waves are absent.

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MANIFESTATIONS OF ATRIAL FIBRILLATION III CUNICAL A. Symptoms are due to loss of the atrial kick and an in­ creased heart rate, which results in decreased ventricular filling, decreased cardiac output, and an increase in car­ diac demand. The most common symptoms reflect these processes.

Variation in the intensity of the first heart sound (SI)

(I) :Ii V I I

3. The ventricular response will be irregularly irregular, although this may be difficult to appreciate at higher heart rates.

OF ATRIAL FIBRILLATION. Because many of the III CAUSES causes of atrial fibrillation are correctable, an effort should be made to pinpoint the cause of the arrhythmia. A. Idiopathic. In approximately 10% of patients, no etiology can be found; these patients are said to have "lone" atrial fibrillation. B. Cardiovascular disorders, including sick sinus syndrome, Wolff-Parkinson-White syndrome. coronary artery dis­ ease, congestive heart failure, cardiomyopathy (hyper­ trophic and dilated), myocarditis, hypertension, and con­ genital heart disease

Chapter 7

52

C. D. E. F.

Atrial Fibrillation

Pulmonary disorders, including pulmonary embolism Pericardial disease Metabolic disturbances, including hyperthyroidism Infiltrative diseases, including amyloidosis. sarcoidosis,

Risk Factors for Stroke in Patients with Atrial Fibrillation ("CHASE") CHF (Within 3 months)

and hemochromatosis

Hypertension Atrial size> 5 cm Stroke in past

G. Intoxication (e.g., alcohol, theophylline, (3 agonists) H. Infection (e.g., endocarditis) I. Stress-induced (e.g., post-surgery)

Causes of CHILD")

Atrial

Fibrillation

53

Ejection fraction reduced

("SWAMP

A. In patients with no risk factors, the risk of stroke is

Sick sinus syndrome, Stress WoIff-Parkinson-White syndrome

approximately the same as the risk in the general popu­ lation. B. If the patient has one or two risk factors, the risk of stroke is approximately 5% per year. C. If the patient has three or more risk factors, the risk increases to roughly 20% per year.

Alcohol (intoxication, withdrawal, "holiday heart") Myocarditis, Metabolic abnormality Pericardial disease, Pulmonary disease CHF, Coronary artery disease, Congenital heart disease Hypertension, Hyperthyroidism, Hypertrophic

II TREATMENT

cardiomyopathy Infiltrative disease, Infection Lone (idiopathic) Dilated cardiomyopathy, Drugs V I I

APPROACH TO THE PATIENT. A knowledge of the differ­ ential will help direct diagnostic tests. All patients should undergo an EKG, a chest radiograph (to rule out pneumonia and other intrathoracic processes), a complete blood count (C8C), electrolyte studies, and thyroid function testing. An echocardiogram is usually obtained to examine cardiac func­ tion and atrial size, and to rule out valve disease.

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COMPUCATIONS. The risk of stroke in all patients with atrial fibrillation is approximately 5% per year, five times the risk in those without atrial fibrillation. It is important to "CHASE" after five important factors that can allow you to further define your patient's risk for stroke:

(I) :Ii V I I

A. Acute treatment. The goal of the acute treatment of a patient with atrial fibrillation is rate control. 1. Cardioversion a. Indications. Cardioversion is indicated for any patient with rapid atrial fibrillation and life­ threatening problems (e.g., ischemia, severe hy­

potension, or severe pulmonary edema). You may begin with 100 J in the synchronized mode, but 360 J may be necessary. b. Contraindications. Unless there is an emergent indication. no patient with atrial fibrillation should be cardioverted until anticoagulation therapy has been initiated or until atrial throm­ bus has been excluded using transesophageal echocardiography. This usually includes patients who are thought to have "new onset" atrial fi­ brillation because it is difficult to estimate the length of time the patient has been in atrial fibril­ lation from the patient history. Patients who are cardioverted without undergoing anticoagula­ tion therapy have a 3%-5% risk of stroke within 30 days.

Chapter 7

54

2.

Atrial Fibrillation

Pharmacologic therapy a. Atrioventricular (AV) node blocking agents. There

are several options for controlling heart rate: (1) Digoxin (0.5 mg intravenously followed by 0.25 mg intravenously every 6 hours to a total dose of 1 mg) (2) Diltiazem [15-20 mg (U.25 mg/kg) intrave­ nously over 2 minutes; repeat in 15 minutes at 20-25 mg if necessary; maintenance infu­ sion is 5-20 mg/hr intravenously] (3) Verapamil (2.5-5.0 mg administered as an intravenous bolus over 1-2 minutes' if needed, repeat with a dose of 5-10 mg in 15-30 minutes; maximum dose is 30 mg) (4) Esmolol (500 /Lg/kg intravenously over 1 minute. followed by an intravenous mainte­ nance infusion of 50-200 /Lglkglmin) b. A V node blocking agents are contraindicated in patients with irregular, wide complex tachycardia until atrial fibrillation with conduction down an accessory pathway (e.g. Wolff-Parkinson-White syndrome) has been excluded. If Wolff-Parkin­ son-White syndrome is present, these agents can precipitate fatal ventricular fibrillation. B. Chronic treatment. The goals of the chronic treatment of atrial fibrillation are minimization of symptoms and reduction of the risk for stroke. L Rate control. The goal is a resting heart rate lower than YO beats/min. Treatment should be selected after considering the patient's other medical prob­ lems. For example: a. I� patients with hypertension or coronary artery dIsease, a {3 blocker is a good choice because it addresses these problems as well as the atrial fibrillation. However, in patients with asthma or chronic obstructive pulmonary disease (COPD), a {3 blocker may not be a good choice because it induces bronchoconstriction. b. In patients with CHF, digoxin can control the heart rate as well as improve symptoms of CHF. However, in patients with chronic renal insuffi­ ciency, digoxin levels should be monitored very closely. 2. Rhythm control. Theoretically, conversion to normal sinus rhythm returns the risk of stroke to baseline and relieves all rate-related symptoms.

Cardioversion should be undertaken only after atrial thrombus has been excluded, unless there is an emergent indication. b. Pharmacologic therapy. Rate must be controlled prior to the initiation of any antiarrhythmic medi­ cation. (1) Procainamide and quinidine increase the time to relapse in treated patients, but both agents are proarrhythmic and have been as­ sociated with increased mortality rates. Most patients should not be treated with these agents. (2) Amiodarone appears to be as effective as procainamide and quinidine for maintaining sinus rhythm without causing proarrhythmic effects. Amiodarone is likely to become the drug of choice. although there are significant side effects. c. AV node ablation with pacemaker implantation is used only under special circumstances. 3. Clot control. Stroke is the major cause of morbidity and mortality in patients with atrial fibrillation. Anti­ coagulation therapy is time consuming and bother­ some to patients, and the risks and benefits must be assessed on an individual basis. a. Wadarin treatment reduces the risk of stroke by 40%-90%. The target international normalized ratio should be 2.0-3.0. There is a small increase in the risk of major bleeding. b. Aspirin alone is a consideration for patients at low risk for stroke. c. Lower dose anticoagulation [i.e., a target interna­ tional normalized ratio (INR) of 1.0-2.0] and combination therapy (e.g., aspirin plus wadarin) is currently being studied. a.

.

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55

57

Chest Pain

8. Chest Pain

HOT

4 Killer Chest Pains Myocardial infarction or ischemia Pulmonary embolism

a comfort") is common and its etiologies range from a life­

INTRODUCTION. Because chest pain (including "dis­

Aortic dissection Spontaneous pneumothorax

KEY

threatening myocardial infarction to benign musculoskeletal pain, a simple and reliable approach to the patient is nec­ essary. Because chest pain may represent one of these emergencies, the usual order of evaluation (e.g., history, physical examina­ tion, diagnostic tests) may hinder critical early intervention. The first step should be a quick screen for the four killer chest pains, followed by a more in-depth evaluation if the etiology of the chest pain is still unclear.

OF CHEST PAIN. One way to remember the III CAUSES causes of chest pain is to use an "outside-in" approach. A. Skin. Varicella-zoster virus infection (shingles) often

B.

C.

D.

E.

causes pain before vesicular lesions are noted. The pain usually occurs in a dermatomal distribution. Chest wall. Musculoskeletal pain may result from shoul­ der arthritis or bursitis, intercostal injury, metastatic dis­ ease to the bones or chest wall, or costochondritis. Breast pathology (e.g., tumors, fibrocystic disease) and nerve root compression (from cervical disk herniation) may also lead to chest pain. Lungs. Inflamed pleura from spontaneous pneumothora­ ces, pulmonary emboli, infections, malignancies, and connective tissue disorders can all cause chest pain, which is usually pleuritic (i.e., it worsens with inspiration or coughing). Heart and great vessels. Pericarditis. myocardial isch­ emia and infarction, and aortic dissection can all cause chest pain. Gastrointestinal tract. Esophageal disorders (including esophagitis, spasm, and rupture) are common causes of chest pain. Other gastrointestinal causes of chest pain include gastric and duodenal ulcers, pancreatitis, and biliary disease.

A. Screen for the killer chest pains. 1. "Eyeball" the patient. A patient who is clutching his

chest, diaphoretic, and ashen can be presumptively diagnosed as suffering from myocardial infarction from across the room. Even if the presentation is not so classic, you can often decide on who looks "sick," and may need a more rapid evaluation in a more monitored setting. 2. V I I

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EstabHsh intravenous access and cardiac rhythm monitoring immediately in patients who appear ill

or who have cardiac risk factors. 3. Evaluate the patient's vital signs

HOT Any abnormality of the vital signs should alert you to the possibility that the chest poin has a potentially serious cause.

KEY

TO THE PATIENT. Although the outside-in IIII APPROACH approach is useful for remembering the differential diagno­ ses for chest pain, it fails to highlight the four acutely life­ threatening causes: 56

(I) :r: V I I

a.

Check the blood pressure in both arms. Although a difference in pressure of 10 mm Hg or more may be seen in patients with aortic dissection,

58

local atherosclerosis can also produce pressure differences. Therefore, the blood pressure read­ ing is neither sensitive nor specific for aortic dis­ section. b.

5.

Check the respiratory rate and oxygen satura­ tion. A low oxygen saturation may accompany

spontaneous pneumothorax, pulmonary embo­ lism, and myocardial infarction (with pulmo­ nary edema). (1) A low oxygen saturation (e.g., < 92%) is of­ ten an indication that an arterial blood gas should be ordered immediately. (2) A normal oxygen saturation may still be ac­ companied by a significant alveolar-to-arte­ rial (A-a) oxygen gradient during hyperventi­ lation. Therefore, arterial blood gas testing to evaluate the possibility of pulmonary em­ bolism may still be necessary if the rest of the evaluation is unrevealing. 4. Look at the electrocardiogram (EKG). The EKG leads are often placed while the vitals are obtained. a. EKG abnormalities that suggest myocardial in­ farction or ischemia are always grounds for ad­ mission. Make sure the patient has intravenous access, a cardiac rhythm monitor, supplemental oxygen, and has been administered an aspirin (usually 325 mg) orally. (The emergent treatment of myocardial infarction and ischemia is dis­ cussed in more detail in Chapter 10.) b. Normal EKG. Because a normal EKG does not rule out myocardial infarction or ischemia, nitro­ glycerin (0.3-0.6 mg sublingually or via aerosol) may be administered and the dose repeated every 3-5 minutes as both a diagnostic challenge and as potential therapy.

HOT In patients with a history of coronary artery disease or cardiac risk factors and no alternative explanation for the chest pain after careful evaluation, an admission

KEY

59

Chest Pain

Chapter 8

to rule out myocardial infarction (ROMI) is usually ap­ propriate.

6.

7. V I I

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8.

B.

Take a preliminary history. a. Cardiac history and risk factors. First, ask about

any prior cardiovascular problems. (1) If there is a history of coronary artery disease, the patient has ischemia until proven other­ wise. (2) With a negative cardiac history, you can quickly establish the pretest probability of myocardial infarction by assessing cardiac risk factors (i.e., age, male sex, smoking, dia­ betes, hypertension, high cholesterol, and positive family history). h. Other risk factors. The preliminary history can also help elucidate any predisposing factors to the other killer chest pains. For example, a his­ tory of cancer or inactivity may contribute to pulmonary embolism, and uncontrolled hyper­ tension may increase the likelihood of aortic dis­ section or myocardial infarction. Perform a preliminary physical examination. Fre­ quently, you will have a few brief moments between tests where you can look at the neck veins, listen to the heart and lungs, palpate the upper abdomen for tenderness, and evaluate the pulses in the arms and legs. Evaluate the chest radiographs. Always compare the new films to old films, if they are available. a. Spontaneous pneumothorax can be subtle and you need to look carefully, especially in the apices. b. Esophageal rupture may lead to air in the medi­ astinum (pneumomediastinum). c. Myocardial infarction or aortic dissection may be accompanied by enlargement of the heart or mediastinum, respectively; however, these struc­ tures are often exaggerated on anteroposterior films. The presence of pulmonary edema may also be suggestive of myocardial infarction. Order an arterial blood gas. If not performed earlier, an arterial blood gas analysis with the patient breath­ ing room air is usually necessary.

Further define the cause of the chest pain. L Take a more detailed patient history. a. Type of chest pain. Pulmonary embolism fre­

quently presents with pleuritic chest pain, myo­ cardial infarction may present with "crushing"

I I 1\

60

Chapter 8

b.

c.

d.

e.

chest pain or only a mild "discomfort," and aortic dissection often is characterized by a ripping pain that radiates to the back. Radiation of chest pain. Pain that radiates to the neck or left arm should be considered cardiac until proven otherwise. (1) Atypical patterns may still indicate ischemia and include pain, tingling, or numbness in the left fingertips unaccompanied by arm pain and pain in the outer left shoulder. (2) It is wise to consider any neck, upper abdomi­ nal, or upper back pain as cardiac in origin until proven otherwise. Onset of chest pain. Spontaneous pneumothorax, aortic dissection, and pulmonary embolism usu­ ally present with abrupt pain, whereas pain from myocardial infarction or ischemia may build more gradually. Spontaneous pneumothorax and pulmonary embolism often occur while the pa­ tient is at rest, whereas aortic dissection and myo­ cardial infarction may occur with rest or exertion. Duration of chest pain. Pain that only lasts sec­ onds or that has been constant for more than 24 hours is usually not caused by one of the four killer chest pains. A myocardial infarction is almost always associated with more than 20 minutes of chest pain. Associated symptoms. Dyspnea, diaphoresis, or lightheadedness should alert you to a probable serious cause of chest pain.

:» P-

.

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f. Aggravating and mitigating factors (1) Deep inspiration often aggravates pain from

the pleura or pericardium (e.g., pleurisy from a pulmonary embolism or pericarditis). (2) Exertion may worsen the pain from myocar­ dial infarction or aortic dissection. Rest may ease the pain from cardiac ischemia, usu­ ally gradually. (3) Position. Patients with pericarditis often feel worse when supine, and better sitting up. Pa­ tients with musculoskeletal pain may feel worse in certain positions. The pain of myo­ cardial infarction is usually unaffected by changes in position, but this is not always the case. (4) Food intake. Pain on swallowing localizes the

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61

Chest Pain

problem to the gastroint�tinal tract. Ch� t . . pain after a meal may mdIcate gastrOJnte�tI­ nal pathology, but it also may occur WIth myocardial infarction. . (5) Nitroglycerin. If chest pain decreases WIth nitrates, (e.g., sublingual nitroglycerin), a car­ diac etiology should be presumed; howeve�, esophageal spasm may also respond to thIS therapy. 2. Perform a complete physical examination. Pay extra attention to the following parts of the exam. a. Jugular venous pressure. An elevated jugular ve­ nous pressure should alert you to t? e possib�lity of a serious disorder (e.g., myocardIal mfarctIOn, pulmonary embolism, or tension pneumothorax), but a normal jugular venous pressure does not exclude these disorders. b. Cardiac examination (see Chapter 3) (1) Heart sounds. Listen carefully for a third heart sound (83) or fourth heart sound (S4) gallop. which may indicate �mpaired ven�ic­ ular contractility or ventncular relaxation, respectively. Both impaired ventricular con­ tractility and impaired relaxation can accompany cardiac ischemia. . (2) Murmurs may also increase th� hkelIhood . of a cardiac etiology of chest pam. A mItral regurgitant murmur may accompany a �yo­ cardial infarction with papillary muscle Isch­ emia whereas an ejection murmur may indic�te aortic stenosis or hypertrophic cardiomyopathy (both of these conditions may predispose the patient to ischemia). c. Lung examination. Listen carefully for rales (e.g., from myocardial infarction with pulmonary edema) and pleural friction rubs (e.g.. from pul­ monary embolism, infection, or other pleural processes). d. Chest wall examination. Minimal tenderness to palpation is nonspecific, but if the che�t pai� is exactly and reliably reproduced (especially m a . well-localized area), a musculoskeletal etiology is likely. Briefly inspect the skin for lesions. e. Abdominal examination. Palpate for any upper abdominal tenderness that may indicate a gastro­ intestinal cause of the chest pain. .

62

Chapter 8

f. Pulses. Check pulses in the arms and legs bilat­ era
ly. 3. Pearls a. Myocardial infarction (1) Because coronary artery disease is such a common disease, it is always better to admit patients for ROMI if there is any doubt as to the diagnosis, even in young patients. (2) More than 20 minutes of unexplained chest pain may represent a myocardial infarction, whereas chest pain that lasts less than 20 minutes but increases in frequency, duration, or occurs with minimal exertion often repre­ sents unstable angina; both patterns are indi­ cations for admission. (3) Frequently, patients with chest pain are given an antacid and lidocaine swish and swallow ("01 cocktail") to evaluate possible reflux esophagitis. Many patients who "benefit" from this "diagnostic test" may actually have ischemic pain that is improving sponta­ neously or from bed rest and oxygen therapy. b. Pulmonary embolism. Clinical suspicion is criti­ cal. There is often no evidence of deep vein thrombosis, and subtle symptoms and signs may be inappropriately rationalized away. If you have a high clinical index of suspicion, administer hep­ arin before sending the patient for diagnostic tests. c. Aortic dissection (1) The greater curvature of the aorta is the site for most dissections; the right coronary artery is the one most frequently "picked off." If the patient has pain that radiates to the back, unequal blood pressures, or other suspicious findings accompanied by evidence of right coronary ischemia (i.e., inferior or right ven­ tricular ischemia), aortic dissection should be considered. (2) Both computed tomography (CT) and trans­ esophageal echocardiography are used in the evaluation of aortic dissection. The choice of diagnostic modality depends on the patient (e.g., poor renal function may weigh against

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Chest Pain

63

a CT scan) and institutional preferences. If clinical suspicion is high, the surgeon should be consulted immediately for his or her input regarding subsequent evaluation. Transtho­ racic echocardiography is not sensitive enough to rule out aortic dissection.

Angina

9.

Angina

a INTRODUCTION

A. Definition. Angina is the symptom of chest pain that results when the oxygen supply is inadequate to meet the oxygen demands of the cardiac muscle. Although other diseases may reduce the oxygen supply (e.g., coro­ nary artery spasm, hypoxia, anemia) or increase the oxy­ gen demand (e.g., tachycardia as a result of infection, thyrotoxicosis), angina rarely occurs without underlying coronary artery disease. B. Risk factors for coronary artery disease include: 1. Age greater than 45 years (men) or 55 years (women) 2. Male sex 3. Diabetes mellitus 4. Smoking habit 5. Hypercholesterolemia 6. Family history (first degree male or female relative with premature coronary artery disease) C. Classification. Angina may be stable or unstable. 1. Stable angina usually results from a fixed atheroscle­ rotic plaque that limits oxygen delivery to the cardiac tissue. When there is an increase in oxygen demand (e.g., from physical exertion), the oxygen supply can­ not be increased to compensate. The oxygen mis­ match that results causes a predictable and stable pattern of chest pain during exertion. 2. Unstable angina usually results when an atheroscle­ rotic plaque ruptures or becomes thrombosed. As a result, the oxygen supply is inadequate at lower activ­ ity levels, and sometimes even at rest.

B.

V I I

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MANIFESTATIONS OF CORONARY ARTERY III CLINICAL DISEASE A. Symptoms 1. Angina is usually experienced beneath or left of mid­ sternum, increases with physical exertion or stress, often lasts from a few minutes up to 20 minutes, and subsides gradually with rest or nitroglycerin. a. If chest pain radiates to the neck or left arm 64

V I I

65

or is accompanied by dyspnea, diaphoresis, or lightheadedness. the likelihood of coronary ar­ tery disease is increased, but these features need not be present. b. Symptoms of stable angina occur predictably, whereas symptoms of unstable angina are in­ creasing in frequency or duration or occur with less exertion (even at rest). 2. "Anginal equivalents." Other symptoms unaccom­ panied by chest pain (e.g., dyspnea) may actually represent "anginal equivalents;" some patients with coronary artery disease may not have any symptoms at all. Physical examination findings. Because patients often have no discernible signs of illness, a normal physical examination does not rule out the possibility of coronary artery disease. Transient signs may occur during ischemic episodes, including hypertension or, less commonly, hy­ potension; ventricular or supraventricular arrhythmias; a third or fourth heart sound (S3 or S4); or a holosystolic murmur over the apex (representative of mitral regurgi­ tation as a result of papillary muscle ischemia). The pres­ ence of elevated jugular venous pressure, pulmonary edema, a gallop rhythm, pathologic murmurs, or signs of the cardiac risk factors (e.g., peripheral vascular disease from diabetes) should all increase your suspicion of coro­ nary artery disease.

TO THE PATIENT. Stable and unstable angina IIII ApPROACH need to be differentiated from the many other causes of chest pain (see Chapter 8). A. Patient history. In patients with classic symptoms, the diagnosis of stable or unstable angina can be made on the basis of history alone. B. Resting electrocardiography. Unstable angina can also be diagnosed in asymptomatic patients by finding evi­ dence of active ischemia on a resting electrocardiogram (EKG) [e.g., ST segment depressions and T wave inver­ sions]. C. Stress tests may be helpful both diagnostically in patients with atypical chest pain and prognostically in patients with typical angina. 1. Types a. Exercise electrocardiography. The presence of 1 mm of down-sloping or horizontal ST-segment

66

depression is considered a positive test for ischemia. b. Myocardial perfusion scintigraphy is often per­ formed in conjunction with exercise electrocardi­ ography and involves the injection of thallium 201 eOIT!) into the peripheral venous blood. Car­ diac muscle cells that are ischemic or infarcted do not take up thallium well. (1) With time, the thallium spreads from cell to cell into regions that are ischemic, but not into areas of infarction. Reversible defects, areas that lack thallium on the initial exercise images but "fill in" on later images (i.e., after 3-4 hours), indicate ischemia. Fixed defects do not change on subsequent imaging and usually denote prior infarction. (2) In patients who are unable to exercise vigor­ ously, dipyridamole, which produces vasodi­ latation in normal coronary arteries out of proportion to that produced in atheroscle­ rotic vessels, can be used to shunt thallium away from cardiac regions served by diseased vessels. Dypyridamole is contraindicated in patients with significant reversible airway dis­ ease because it may facilitate bronchospasm. c. Exercise radionuclide angiography or echocardi­ ography. If exercise results in a decrease in ejec­ tion fraction or segmental wall motion abnormal­ ities, cardiac ischemia is presumed. Intravenous dobutamine increases oxygen demand by in­ creasing heart rate and contractility and may be used as an alternative to exercise. 2. Choosing a test. Although one stress test cannot be universally recommended over the others' certain caveats apply: a. Echocardiography is more likely to be inade­ quate in obese patients. b. Elderly patients or those with other heart disease may have a higher false-positive rate on exercise radionuclide angiography or echocardiography. c. Patients with EKG abnormalities may not be evaluated appropriately with standard exercise electrocardiography alone. Scintigraphy is fre­ quently added to increase sensitivity and speci­ ficity.

67

Angina

Chapter 9

D.

Coronary catheterization is necessary to definitively di­ agnose coronary artery disease. 1. Unstable angina. Because these patients often have high-grade coronary occlusions, a cardiac catheter­ ization is often indicated to plan future therapy. Usu­ ally, catheterization is performed after 1-3 days of therapy because the incidence of adverse events, in­ cluding myocardial infarction. increases with early catheterization. 2. Stable angina. Because stable angina can usually be diagnosed on the basis of the patient history or nonin­ vasive studies, catheterization is not usually needed for diagnosis; rather, it is usually performed to help determine subsequent therapy. If catheterization demonstrates severe coronary artery disease in a pa­ tient with stable angina. revascularization with by­ pass surgery or angioplasty may be indicated.

1:1 TREATMENT

V I I

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:x:

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A. General measures. Because angina represents coronary artery disease, an indispensable part of the treatment is aimed at identifying and treating cardiac risk factors. 1. Smoking prevention 2. Regular exercise (e.g., brisk walking for 30 minutes 4 times weekly) 3. Weight loss 4. Control of hypercholesterolemia [low-density lipo­ proteins (LDL) < 100 mg/dl]; HMG-CoA reductase inhibitors may be the drugs of choice 5. Control of hypertension (systolic < 140 mm Hg, dia­ stolic < 90 mm Hg) 6. Control of diabetes 7. Treatment of other factors that may aggravate angina (e.g., anemia, hypoxia, thyrotoxicosis) B. Specific measures for the relief of angina 1. Stable angina a. Pharmacologic therapy is generally aimed at in­ creasing the myocardial oxygen supply (by coro­ nary vasodilation) or decreasing the oxygen de­ mand (by decreasing heart rate, contractility, preload, or afterload). Most patients are started on aspirin, a f3 blocker, and short-acting nitrates unless there are contraindications. Gradually, the dose of the f3 blocker may be increased until

68

Angina

Chapter 9

the symptoms are controlled, side effects develop (e.g., postural lightheadedness), the blood pres­ sure falls below approximately 100/60 mm Hg, the heart rate falls below approximately 60 beats/ min, or the maximal dose is reached. If symptoms are still not controlled, long-acting nitrates may be added and increased as needed with attention to the patient's symptoms, side effects, and blood pressure. (1) Aspirin (usually 325 mg/day) inhibits platelet aggregation and coronary thrombosis, and may therefore prevent progression to myo­ cardial infarction or unstable angina. (2) Nitrates increase oxygen supply by vasodilat­ ing the coronary arteries and decrease oxy­ gen demand by decreasing preload and afterload. (a) Short-acting nitrates. Nitroglycerin 0.30.6 mg sublingually or by aerosol may be used for angina prophylaxis (the dose is taken 5 minutes before an activity known to result in angina) or immediate therapy (the dose is administered every 3-5 mi­ nutes until the pain is relieved; if pain is not relieved in 20 minutes, the patient should get to a hospital immediately). (b) Long-acting nitrates (e.g., isosorbide din­ itrate, isosorbide mononitrate, transder­ mal nitroglycerin patChes). An interval of approximately 8-10 hours per day without nitrate therapy is needed to pre­ vent tachyphylaxis, so the last dose is of­ ten given after dinner and patches are removed overnight. Headaches may oc­ cur with the initiation of nitrate therapy; if they can be managed conservatively, they frequently resolve after 1-2 weeks. (3) f3 Blockers can decrease heart rate and myo­ cardial contractility, resulting in symptomatic control of angina. In addition, unlike other antianginals, they have been shown to have a mortality benefit in patients with coronary artery disease who have already experienced myocardial infarction. (a) Frequently used f3 blockers include pro­ pranolol (40-80 mg orally 2-4 times

V I I

I I 1\

V I I

69

daily), metoprolol (50-100 mg orally 2 times daily), and atenolol (50-100 mg orally once daily). (b) f3 Blockers are contraindicated in pa­ tients with bradyarrhythmias or overt heart failure. In patients with chronic ob­ structive pulmonary disease (COPD), a f3rselective agent (e.g., metoprolol or atenolo!) should be used; often, all f3 blockers are avoided in patients with se­ vere COPD. Patients with impaired left ventricular function may actually benefit the most from f3 blockers; however, can­ didates must be "tuned up" prior to the initiation of therapy (e.g., no evidence of pulmonary edema should be pres­ ent).The patient should be started with a low dose (e.g., 2.5-5 mg of metoprolo!), which is gradually increased with fre­ quent patient monitoring. (4) Calcium channel blockers lower oxygen de­ mand (by decreasing heart rate, contractility, and afterload) and may increase oxygen sup­ ply (by inducing vasodilation of the coro­ nary arteries). (a) Agents include verapamil, diltiazem, and nifedipine, in order of increased effect on lowering systemic vascular resistance and decreased effect on myocardial inotropy and chronotropy. Verapamil and diltia­ zem are usually preferred. (b) Calcium channel blockers have not been associated with improved survival post­ myocardial infarction, and may lead to a worse outcome; therefore, they are not the initial drugs of choice for most pa­ tients with known or suspected coronary artery disease. b. Revascularization. The indications for coronary artery bypass surgery or angioplasty are contro­ versial. Studies are underway to address the rela­ tive advantages and disadvantages of coronary artery bypass surgery compared with angio­ plasty. (1) Coronary artery bypass surgery is generally considered the treatment of choice for pa-

70

Angina

Chapter 9

tients with left main artery disease (over 50% occlusion) or three-vessel disease (over 70% occlusion) associated with decreased left ven­ tricular function (less than 50%). (2) Bypass surgery may also benefit patients with three-vessel disease and severe angina (class III or IV) and patients with proximal left anterior descending occlusion associated with two-vessel disease, but there is less of a consensus on whether bypass surgery, angi­ oplasty, or medical therapy is appropriate. (3) Patients with angina refractory to medical therapy and patients with a recent myocardial infarction or unstable angina and continuing symptoms or signs of ischemia are also candi­ dates for revascularization. 2. Unstable angina. Patients with unstable angina re­ quire admission and should undergo serial cardiac enzyme studies and EKGs to rule out myocardial infarction. Patients with active chest pain or EKG evidence of ischemia are always managed in the coro­ nary care unit (CCU). Patients who have no current chest pain or EKG evidence of ischemia are some­ times treated and monitored in a telemetry unit; how­ ever, because a recurrence of chest pain will require a transfer, it is often easier to simply admit these patients to the CCU. a. Pharmacologic therapy is aimed at improving the oxygen mismatch and inhibiting progression of the presumed intracoronary thrombus. (1) Nitmtes are generally given transdermally or intravenously so that the dose can be care­ fully titrated to prevent ischemia and control blood pressure. (a) Transdermal nitrates are often used for patients in telemetry units. Table 9-1 out­ lines a sliding scale that could be used. (b) Intravenous nitrates are often used for patients in the CCo. The initial dose is 10 p,g/min, which may be titrated upward to keep the patient symptom-free and the blood pressure at approximately 100120/60-80 mm Hg. Doses may be as high as 100-300 p,g/min. (c) Long-acting nitrates may be substituted for other forms of therapy after the pa-

71

TABLE 9- 1 : Sliding Scale f a r Use o f Nitropaste Systolic Blood Pressure (mm Hg)

> 1 60 1 40- 1 60 1 20- 1 40 1 00- 1 20 <

V I I

I I 1\

V I I

1 00

Dosage

2" every 4 hours 1 .5" every 4 hours 1 " every 4 hours

OS' every 4 hours Wipe off nitropaste

tient has stabilized (often after 24-48 hours). Approximately 20 mg of isosor­ bide dinitrate administered orally every 8 hours may be substituted for each inch of nitropaste the patient required during sliding scale therapy. (2) f3 Blockers should be administered to pa­ tients without contraindications, and are es­ pecially useful in patients with tachycardia, hypertension, or both. (a) Although oral therapy is often sufficient, intravenous administration of metoprolol (5 mg every 5 minutes, up to 15 mg) may provide faster therapy for patients with active ischemia. (b) Patients with hemodynamic instability and those with a higher risk of adverse effects from f3 blockers (e.g., a history of bronchospasm or depressed left ventricu­ lar function) may benefit from an esmolol continuous intravenous drip that allows rapid discontinuation of therapy. (3) Calcium channel blockers. Because these agents are of unproved benefit (and may be deleterious) and there are other effective modes of managing unstable angina, they are rarely used to treat unstable angina. If a pa­ tient is already taking calcium channel block­ ers, the decision to continue this therapy de­ pends on the patient's presentation, whether f3 blockers are contraindicated, and the effi-

72

Chapter 9

1 0.Myocardial Infarction (MI)

cacy of nitrates and other therapies in con­ trolling the patient's symptoms. (4) Aspirin and heparin. The decision to use aspirin, heparin, or both for unstable angina is controversial. (a) Heparin should be used in patients with active symptoms or EKG evidence of ischemia, unless there are contraindica­ tions. The routine use of heparin in pa­ tients without active symptoms or EKG evidence of ischemia may also be appro­ priate. (b) Aspirin is also usually administered be­ cause some patients with presumed un­ stable angina may later be diagnosed with infarction. Aspirin decreases mortality associated with myocardial infarction and is useful in preventing myocardial in­ farction in patients with unstable angina. b. Revascularization. After symptoms subside, pa­ tients with unstable angina are often catheterized to evaluate their candidacy for revascularization.

INTRODUcnON. Myocardial infarction (MI) is a leading a cause of death in the United States. The failure to recognize MI in the emergency room has led to inappropriate patient discharges, resulting in an abundance of malpractice claims. Many therapies have a proved mortality benefit in the treat­ ment of MI; however, studies show that patients frequently receive suboptimal therapy.

PATHOPHYSIOLOGY OF MI. MI usually results from cor­ III onary artery disease. The rupture or thrombosis of athero­ sclerotic plaques leads to inadequate blood flow and oxygen delivery, which in turn leads to myocardial cell death. Rarer causes of MI include vasospasm (usually associated with coronary artery disease), severe hypotension, emboli (e.g., from mitral valve disease), aortic dissection (usually with right coronary artery involvement), vasculitis, and cocaine use (vasospasm and platelet aggregation are presumed etio­ logies).

V I I

MANIFESTATIONS OF MI. Typical symptoms IIII CLINICAL and signs associated with cardiac ischemia are discussed in

I I 1\

Chapter 8 III B. The chest pain associated with MI may differ from that of stable angina in that it frequently begins while the patient is at rest, lasts more than 20 minutes, is more severe, and is umelieved with nitroglycerin; however, these findings are variable and pain that lasts for more than 20 minutes should be considered due to MI until proved oth­ erwise.

DIAGNOSIS. Because MI and unstable angina share similar pathophysiology, it is not surprising that they frequently cannot be distinguished by clinical criteria alone. Patients are often admitted for "unstable angina/rule out MI (ROMI)"; serial electrocardiograms (EKGs) and cardiac enzyme stud­ ies are required for a definitive diagnosis. V I I

73

74

Myocardial Infarction (MI)

Chapter 1 0

HOT The diagnosis of MI is made by the presence of typical symptams and signs, EKG changes, or elevated car­ diac enzymes. If the patient meets two of these three criteria, MI is diagnosed.

KEY

A. Patient history and physical examination. Chest pain is the most common symptom of MI, but other signs and symptoms may also signal MI (e.g., flash pulmonary edema, hypotension, dyspnea). B. Electrocardiography. Following admission of the patient, serial EKGs are usually obtained on a frequent basis until resolution of symptoms occurs and the EKG changes stabilize; a daily EKG and an EKG following reports of any symptoms are usually obtained thereafter. MI is usually associated with hyperacute (peaked) T waves, ST elevations, ST depressions, Q waves. or inverted T waves; occasionally, no EKG changes are noted. 1. ST segment depressions and elevations both reflect myocardial injury. a. The subendocardial region is the most suscepti­ ble to ischemia because it is perfused "last" (i.e., the coronary arteries course from the outer epi­ cardial surface inward). Because the subendocar­ dium is on the inner surface of the heart, away from the EKG leads on the chest wall, subendo­ cardial injury is frequently seen as ST segment depression. Similarly, the epicardial surface is near the EKG leads, so epicardial injury results in ST segment elevation. b. ST segment depressions are often called "isch­ emia." whereas ST segment elevations are called "infarct." This terminology is an oversimplifica­ tion resulting from the observation that de­ creases in blood flow frequently cause isolated subendocardial injury, whereas complete coro­ nary occlusion is usually needed for epicardial injury. Because ST depressions may occur with subendocardial infarction, and ST segment eleva­ tions may occur with transient epicardial isch­ emia (e.g., from vasospasm), ST segment changes

V I I

I I 1\

V I I

75

are more accurately thought of as representing myocardial "injury." 2. Q waves signify electrical activity moving away from the area of the heart where they are seen; they there­ fore indicate dead muscle (previous MI) in that region. a. Non-Q wave MIs represent approximately 30%50% of all MIs and presumably occur because there is still enough "alive" muscle generating electrical activity in the given area. b. Q wave MIs are usually larg 18 mm Hg) is suspected. c. High-risk patients have rales as well as cool ex­ tremities with diminished peripheral pulses. These patients are in cardiogenic shock. The presence of pulmonary edema suggests that the PCWP, an estimate of end-diastolic volume, is elevated. Normally, according to the Starling curve, a high end-diastolic volume ensures that the stroke volume will be maximized. If the heart is unable to adequately perfuse the end organs despite adequate filling (i.e., a high PCWP), car­ diogenic shock is diagnosed. 2. Management a. Low-risk patients are hemodynamically stable and have a low mortality rate. Management of these patients entails deciding whether thrombol­ ysis or PTCA is indicated, and what other forms of therapy might benefit the patient (see V B, C). b. Intermediate-risk patients have evidence of pul­ monary edema, which may decrease oxygenation while increasing oxygen demand (increased sym­ pathetic tone increases the heart rate and myo­ cardial contractility). (1) Agents frequently used in the treatment of MI (e.g., nitrates, morphine) may also treat pulmonary edema by decreasing preload. (2) Intravenous diuretics should be given as needed. c. High-risk patients have cardiogenic shock. (1) Pulmonary artery (PA) line placement is in­ dicated for monitoring cardiac output, sys­ temic vascular resistance, and PCWP. In pa­ tients with MI, only those with evidence of cardiogenic shock generally require hemody­ namic monitoring with a PA line.

77

(2) Pharmacologic therapy is dictated by the pa­

tient's blood pressure. Although cardiogenic shock is often accompanied by hypotension, the blood pressure may still be normal with low flow states due to a marked increase in systemic resistance.

HOT Do nat assume that a normal blood pressure indicates adequate end-organ now.

KEY

V I I

I I 1\

V I I

(a) Systolic blood pressure > 90-100 mm Hg (i) Dobutamine is often started intrave­ nously at a dose of 2. 5 p,g/kg/min. The dose may be increased gradually (up to 15-20 p,g/kg/min) until the cardiac output rises and the PCWP falls. Dobutamine raises the cardiac output by increasing myocardial contractility and by decreasing the systemic vascular resistance. Be­ cause blood pressure is the product of cardiac output and systemic vas­ cular resistance, it may remain sta­ ble, increase, or decrease depending on how much the cardiac output in­ creases in comparison with the de­ crease in systemic vascular resis­ tance. A decrease in blood pressure commonly occurs with dobutamine therapy, so the systolic blood pres­ sure should be greater than 90 mm Hg (and preferably greater than 100 mm Hg) before the initiation of therapy. (ii) Sodium nitroprusside is an alter­ native to dobutamine. but often requires a higher starting blood pres­ sure or the concomitant administra­ tion of an inotrope.

78

Myacardial Infarction (MI)

Chapter 1 0

B.

(b) Systolic blood pressure < 90 mm "g. In­ travenous dopamine is usually given. Do­ pamine usually causes renal artery dilata­ tion at doses of 1-2 p,g/kg/min. ("renal dose" dopamine), increased inotropy from /3!- receptor stimulation at doses of 5-10 p,g/kg/min, and vasoconstriction from a-receptor stimulation at higher doses; but significant overlap and vari­ ability exist. Once the systolic blood pres­ sure is greater than 90-100 mm Hg, dobu­ tamine is often added and the dopamine is titrated down (preferably to "renal doses") as tolerated by the blood pres­ sure. Because arrhythmias may compli­ cate dobutamine or dopamine therapy, patients require careful rhythm monitor­ ing, and electrolytes should be main­ tained in the normal range (especially the potassium and magnesium levels). (3) Emergent PTCA is the only therapy that has been shown to decrease mortality in patients with cardiogenic shock, and is clearly the treatment of choice. Is thrombolysis or PTCA indicated? Patients with chest pain of 6 hours or less duration (and possibly up to 12 hours or longer) associated with ST elevations of at least 1 mm in two consecutive EKG leads (or evidence of a new left bundle branch block) derive a mortality benefit from coronary reperfusion, and should therefore un­ dergo thrombolysis or angioplasty unless there are con­ traindications. L Primary PTCA may be favored when there are con­ traindications to thrombolytic therapy, and in centers that can perform the procedure quickly and with ex­ pertise. 2. Thrombolysis a. Contraindications (1) Absolute contraindications generally include the presence of: (a) Central nervous system (CNS) disease. Recent trauma or surgery, aneurysms, arteriovenous malformations, tumors, or a history of hemorrhagic stroke at any time or nonhemorrhagic stroke within 3

79

months are usually considered contrain­ dications. (b) Active gastrointestinal or genitourinary bleeding (c) Pregnancy (2) Relative contraindications generally include: (a) Traumatic or prolonged cardiopulmo­ nary resuscitation (b) Recent trauma or surgery (within 2 weeks) (c) Diabetic retinopathy (d) Sustained hypertension (e.g., blood pres­ sure > 180/130 mm Hg) (e) Coagulopathy, thrombocytopenia, or current oral anticoagulation therapy (f ) Noncompressible arterial or venous puncture sites b. Other considerations. Patients who have had prior coronary artery bypass grafting do not ben­ efit as much from either thrombolysis or angi­ oplasty. c. Agents. The two most commonly used thrombo­ lytic agents are streptokinase (usually 1.5 million units over 1 hour) and tissue plasminogen activa­ tor (t-PA). usually 100 mg. If t-PA is used, hepa­ rin must be given during or following therapy to decrease the high reocclusion rate: no benefit of additional heparin has been shown with strepto­ kinase. Most studies have shown no difference in outcome regardless of whether streptokinase or t-PA was used, but the recent large GUSTO trial found a 1% 30-day mortality benefit with front-loaded t-PA (2/3 of the dose given in 30 minutes and 113 given over the next 60 minutes).! Although this difference is relatively small, there may be slight advantages of one or the other agent, depending on the clinical situation. (1) t-PA. Young patients with anterior MIs who present within 4 hours of the onset of symp­ toms may benefit the most from t-PA. t-PA is also preferred for patients who have had

V I I

I I 1\

1 The GUSTO Investigators: An international randomized trial comparing

four thrombolytic strategies for acute myocardial infarction.

329:673, 1993.

V I I

N Engl J Med

80

Chapter 1 0

a recent streptococcal infection or received streptokinase within the last 6 months, and for patients with borderline low blood pres­ sure (because t-PA causes less hypotension than streptokinase). (2) Streptokinase. Overall, t-PA is associated with a slightly higher risk of hemorrhagic stroke than streptokinase (approximately 0.7-0.8% versus 0.5%). Patients who are older than 70 years and those with high blood pressure (i.e.. a systolic blood pressure > 160 mm Hg) have a higher risk of hemorrhagic stroke; therefore, streptokinase may be the preferred agent in these patients. d. General recommendations. The mortality benefit decreases drastically with delay in therapy, so speed is of the essence. Make sure a large-bore peripheral intravenous catheter (usually 16gauge) is in place prior to therapy. and limit ve­ nous and arterial blood draws. It is clear that the type of agent used is less important than ensuring that all patients who meet appropriate criteria and do not have contraindications receive throm­ bolytic therapy as rapidly as possible. e. Signs of successful reperfusion include a prompt decrease in chest pain. normalization of the ST segment, an accelerated idioventricular rhythm, or an early peak of the CK enzymes (within 12 hours). C. What other treatments may benefit the patient? Specific forms of therapy with nitrates. f3 blockers, and calcium channel blockers as well as potential contraindications are outlined in Chapter 9. The coronary care unit (CCU) is the best place to manage patients with MI. given the need for frequent vital checks and continuous rhythm monitoring. 1. General measures a. Bed rest and a stool softener are usually pre­ scribed. b. SUbcutaneous heparin (5000 units twice daily) is usually administered to prevent deep venous thrombosis. Co Analgesia. Initially, nitrates are usually given to relieve pain, but morphine sulfate (4-8 mg intra­ venously) may be used for persistent pain (care-

Myocardial Infarction (MI)

2.

3. 4. 5.

6.

7.

8.

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ful titration of dose may be needed i n patients who have borderline low blood pressure). Aspirin (usually 325 mg orally) has been shown to have a mortality benefit, even in patients who receive thrombolytics. Active bleeding is a contraindication. Oxygen (e.g., 2-4 Llmin) is often administered, al­ though the benefit in patients with normal oxygen saturation is questionable. Nitrates are usually given unless the patient is hypo­ tensive or has evidence of a low cardiac output. f3 blockers have been shown to decrease mortality in patients with MI, and are especially useful in patients with tachycardia, hypertension, or both. Calcium channel blockers have not been shown to have a mortality benefit in patients with MI. and in some studies have been associated with increased mortality. Diltiazem has been shown to decrease the reinfarction rate in patients with non-Q wave MI, but does not decrease mortality. In general, these agents should be avoided in the acute management of M!. Angiotensin-converting enzyme (ACE) inhibitors have had mixed results in the acute treatment of MI, but are useful in the chronic management of patients with an ejection fraction less than 40% (see VII B 1 a). Heparin may not be useful for the treatment of acute MI unless it is being used with t-PA thrombolysis.

NS II COMPLICATIO Arrhythmias are A.

81

most common during the initial 12-24 hours. 1. Tachyarrhythmias are evaluated and treated as dis­ cussed in Chapter 6. Of note, prophylactic lidocaine is associated with higher rates of asystole, a poorer outcome, and is no longer recommended. Lidocaine is often reserved for patients with sustained or non­ sustained ventricular tachycardia. Prophylactic mag­ nesium is also not recommended. 2. Bradyarrhythmias are more common with inferior wall MI because the sinoatrial (SA) and atrioventric­ ular (AV) nodes are more dependent on blood flow from the right coronary artery. a. Intravenous atropine (0.5-1 mg every 3-5 minutes, up to 3 mg) is usually effective for sinus

Chapter 1 0

82

b.

Myocardial Infarction (MI)

bradycardia and symptomatic Wenckebach (Mobitz type 1) second-degree AV block. Temporary pacing is generally indicated for pa­ tients with acute MI and: (1) Symptomatic sinus bradycardia and Wencke­ bach block that is unresponsive to atropine (2) Mobitz type 2 second-degree AV block or

c.

83

necessary [or treatment. and may also be used diagnostically-an increased oxygen saturation between the right atrium and pulmonary artery is seen with ventricuJar septal defect, and both disorders may display prominent v waves. Treatment. Nitroprusside or aortic balloon counterpulsation may be used to decrease the afterload, thereby increasing the fraction of blood ejected into the aorta compared with the regurgitant fraction ejected into the right ventri­ cle or left atrium. Emergent surgical repair is

third-degree AV block (3) New bifascicuJar block, including alternating left and right bundle branch block, right bun­ dle branch block with left anterior or poste­

usually indicated for definitive therapy.

rior fascicular block, and left bundle branch block with first-degree AV block

3.

B. Recurrent ischemia following MI is usually an indication for emergent angiography and revascularization. C. Pump dysfunction. Severe left ventricuJar failure is man­ aged as outlined for cardiogenic shock. Intra-aortic bal­ loon counterpulsation and left ventricular assist devices may also be used until more definitive therapy (i.e., car­ diac transplantation) can be carried out. D. Right ventricular infarction shouJd always be suspected

Left ventricular aneurysm or pseudoaneurysm a. Left ventricular aneurysm most often occurs after large anterior wall MIs. Warfarin therapy for 3-6

months is often administered to patients with large anterior wall MIs. Left ventricular aneu­ rysms may also be associated with refractory heart failure or arrythmias, and require surgi­

b.

cal correction. Pseudo aneurysms are distinguished by a rela­ tively narrow neck and a predisposition [or an inferior-posterior location; surgical correction is generally performed to prevent delayed rupture.

when hypotension accompanies an inferior MI. Treat­ ment involves large fluid boluses to increase right-sided cardiac output and left ventricular filling. Inotropic

agents with hemodynamic monitoring may also be re­ quired.

RISK REDUCTION

E. Mechanical complications usually occur 2-7 days post­ infarction.

1. Cardiac tamponade

from free wall rupture usually

leads to abrupt hypotension and death.

2. Ventricular septal defect or papillary muscle rupture

V I I

leading to acute mitral regurgitation a. Clinical signs and symptoms

(1)

(2)

These disorders are often heralded by hypo­ tension, pulmonary edema, or both. Any abrupt change in hemodynamics should in­ crease clinical suspicion of one of these me­ chanical complications. A holosystolic murmur may be present in both conditions, but the location is usually at the left sternal border in ventricular septal

I I 1\

A. General measures include aspirin therapy (usually 325 mg/day), which has a mortality benefit, and aggressive risk factor reduction (see Chapter 9 I B). B. Additional diagnostic testing and preventive therapy. Because the major complications of MI are heart failure, recurrent ischemia, and arrythmias, diagnostic testing is aimed at identifying and treating these disorders (risk stratification).

1. Echocardiography.

The post-MI left ventricnlar ejection fraction is an excellent predictor of future complications and survival. For this reason, patients usually receive echocardiograms prior to discharge from the hospital.

b. Diagnosis. An emergent echocardiogram is the

ACE inhibitors have been shown to decrease mortality in patients who have a left ventricular ejection fraction of less than 40% post-MI. b. f3 blockers decrease post-MI mortality. Patients

quick and easy way to make the diagnosis. Hemo­ dynamic monitoring with a PA line is usually

with the lowest left ventricular ejection fractions who can tolerate {3 blockers may actually have

a.

defect and at the apex in papillary muscle rupture.

V I I

Chapter 1 0

84

the greatest survival advantage. f3 blockers may decrease the likelihood of arrythmias and pro­ gressive heart failure in these high-risk patients.

11. Congestive Heart Failure

2. Stress testing B.

b.

(see Chapter 9) Patients usually undergo a submaximal or maxi­ mal stress test approximately 1 week or 3-6

........................................................................

weeks, respectively, following the MI. Although the maximal stress test is considered more sensi­ tive, patients frequently undergo the former be­ cause it can be used to evaluate the patient's risk prior to hospital discharge. Angiography with revascularization is usually in­ dicated for patients with positive tests that show

.......................................

INTRODUC11O N D A. Definition.

Congestive heart failure (CHF) occurs when the heart is unable to pump sufficient amounts of blood at normal filling pressures to keep pace with the metabolic demands of the body.

significant ischemia (especially if the ischemia is

B. Clinical manifestations classically include fatigue, leth­

associated with non-Q wave MI or a depressed left ventricular ejection fraction).

argy, dyspnea on exertion or rest, paroxysmal nocturnal dyspnea (PND), orthopnea. weight gain. and leg swelling.

C. Arrhythmia monitoring

C. Incidence. CHF is a common disorder, primarily affect­

HO T

K E Y 1.

Ventricular arrythmias that occur within 24 hours of MI generally do not worsen the patient's long.term prognosis; however, subsequent episodes are associ­ ated with a higher mortality rate and often necessitate chronic therapy.

Patients with sustained ventricular tachycardia or

symptomatic nonsnstained ventricular tachycardia

2. 3.

(10% of the popul�tion of he . United States over 75 years of age carry thiS diagnOSIS). There are 400. 000 new cases per year.

�

ing older individuals

(three or more consecutive ventricular premature beats lasting less than 30 seconds) generally re­ quire treatment. Patients with asymptomatic nonsustained ventricnlar tachycardia may also be treated, although the benefit from therapy is less clear. The appropriate means of assessing risk in patients

D. Mortality rates. The annual mortality rate for all patients

with CHF is 20%. For patients who are symptomatic at rest, the mortality rate is 50%. For those with pure dia­ stolic dysfunction, it is

V I I

I I 1\

8%.

III ClASSIFICATION.

There are many different classification schemes. The most useful include the following:

A. New York Heart Association (NYHA) functional classi­ fication 1. Class I: Symptomatic only with greater than normal physical activity

. Symptomatic during normal activity Class III: Symptomatic with minimal activity

2. Class II: 3.

4. Class IV: Symptomatic at rest B. Left-sided versus right-sided failure. It is important to decide if patients have evidence of left-sided failure, be­ cause these patients can present with marked hypoxemia and therefore may need to be treated urgently (see IV D). The distinction between left-sided and ght-side� failure is based primarily on signs found dunng phYSI­ cal examination. 1. Left-sided failure. Signs of left-sided failure include

without ventricular tachycardia (i.e., those with occa­ sional or no ventricular ectopy) is even more unclear. While patients with a normal left ventricular ejection fraction and signal averaged EKG have a favorable prognosis, the positive predictive value of abnormal tests is generally not high enough to ensure a benefit from additional evaluation (i.e., electrophysiologic

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testing) and treatment.

V I I

85

87

Congestive Heart Failure

Chapter 1 1

86

a left-sided third heart sound (S3), rales, wheezes ("cardiac asthma," a manifestation of interstitial edema), and tachypnea. 2. Right-sided failure. Signs of right-sided failure in­ clude a right-sided S3 (i.e., one that increases with inspiration), an elevated jugular venous pressure. ab­

Common Causes of Dilated Cardiomyopathy ("PIPED") Postmyocarditis Idiopathic Peripartum Ethanol Drugs (cocaine and herain)

normal hepatojugular reflux, ascites, peripheral edema, and an enlarged liver. a. Most of the time, evidence of biventricular failure is found during physical examination because the most common cause of right-sided failure is left­ sided failure.

c.

Dilated cardiomyopathies (i.e., disorders of the

myocardium that are not caused by coro­ nary artery disease, hypertension, or valvular disease)

HO T

Occasionally, right-sided failure can lead to left-sided diastolic dysfunction because of septal deviation into the left ventricular cavity, thereby increasing the left ventricular end-diastolic pressure and causing pulmo­ nary edema.

K E Y

b.

2.

(1) Mitral stenosis

b.

pump, but its ability to relax a�d allow ade�uate filling during diastole is compromIsed. These patIents have a normal or supranormal ejection fraction. Causes of diastolic dysfunction include: a. Ischemia b. Disorders that lead to left ventrkular hypertro­ phy, such as: (1) Hypertension

Other causes of right-sided failure include:

(2) Pulmonary hypertension [most commonly caused by chronic obstructive pulmonary dis­ ease (COPD)] (3) Right ventricular infarction (usually oc­ curring in the setting of left-sided inferior wall infarction) (4) Right-sided endocarditis C. SystoHc versus diastolic dysfunction. Left ventricular fail­ ure can be either systolic or diastolic. This is the most important distinction to make because it affects treatment. I. Systolic dysfunction means that the heart's ability to pump is compromised. It implies that the ejection fraction is below normal (usually

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