Diagnosis and management of cardiac arrhythmias

DIAGNOSIS AND MANAGEMENT OF CARDIAC ARRHYTHMIAS CHARLES FISCH

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Editorial Board (clockwise from top): W. Proctor Harvey, James J. Leonard, William C. Roberts, Robert A. O'Rourke, Frank I. Marcus and Antonio C. de Leon, Jr.

EDITOR'S PREFACE Dr. Charles Fisch is recognized as one of the world's authorities on the diagnosis and management of cardiac arrhythmias. His presentation in this issue of CURRENT PROBLEMS IN CARDIOLOGY is a typical example of his talents and expertise. He has just completed a 2-year term as President of the American College of Cardiology. Despite his numerous duties associated with this honor, in addition to his commitments to his busy schedule at Indiana University School of Medicine, he still was able to write this monograph for us. Many thanks, Charlie! Take some time off for a well-deserved rest.

SELF-ASSESSMENT QUESTIONS 1. Mobitz Type II AV block frequently is characterized by: a. Prolonged QRS. b. RBBB and LAD block. c. Adams-Stokes disease. d. Infra His block. e. All of the above. 2. For a given ventricular rate and rhythm, the most likely arrhythmia is (match the rate with the diagnosis): i. 150 regular. ii. 220 regular. iii. 180 grossly irregular. iv. 180 slightly irregular. a. Ventricular tachycardia. b. Atrial flutter. c. Atrial fibrillation. d. PAT. 3. Automaticity or latent automaticity is the property of the following cardiac tissues: a. Purkinje fibers. b. Atrial myocardium. c. AV junctional tissue. d. Sinoatrial node. e. Ventricular myocardium. 4. Asynchrony of conduction due to ischemia may result in: a. Automaticity. b. Re-entry. 5. The primary determinant of an action potential (AP) that initiates a series of changes resulting in depression of conduction is: a. Low-amplitude AP. b. Reduction of dV/dt of phase 0. c. Increased negativity of phase 4. d. Reduction in overshoot of AP. e. Reduction of phase 4 negativity. 6. Atrioventricular dissociation implies independence of atrial and ventricular activity and may result from or be found in: a. Organic "transection" of the conduction system. b. Acceleration of AV junction rhythm by digitalis. c. Bradycardia due to vagal influence. d. Individuals with normal hearts. e. All of the above. 7. A definitive diagnosis of ventricular tachycardia is indicated by: a. Bizarre QRS. b. Bizarre QRS with a slightly irregular tachycardia. c. Bizarre QRS, tachycardia and AV dissociation.

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d. Intra-atrial electrogram demonstrating independent P waves. e. Evidence of ventricular activation preceding H spike. Palpitations can be a symptom of: a. Tight mitral stenosis. b. Cardiomyopathy with failure. c. Aortic insufficiency. d. Anatomically normal heart. e. All of the above. Palpitations usually are indicative of heart disease and most often require drug therapy. True? False? Presence of cannon waves, changing intensity heart sounds and pulse may be seen in: a. Adams-Stokes disease. b. Complete AV block. c. AV dissociation due to severe bradycardia. d. Ventricular tachycardia. e. All of the above. A patient with chronic atrial fibrillation treated with digitalis is found to have a regular rate of 100. The most likely diagnosis is: a. Sinus tachycardia. b. Atrial flutter with 2:1 block. c. Nonparoxysmal junctional tachycardia. d. PAT. e. Atrial tachycardia with block. The treatment of this arrhythmia is: a. Quinidine. b. Procainamide. c. Discontinuation of digitalis. d. Cardioversion. e. Vasopressors. Given a patient with ventricular arrhythmias, which of the following is the correct answer? a. Prognosis of ventricular arrhythmias is clear. b. Currently available drugs for long-term use are highly effective. c. Currently available drugs have minimal side-effects. d. There are a number of drugs available for long-term suppressive therapy. e. None of the above. In the following disorders, the indications for treatment are clearly established: a. Mitral prolapse with VPC. b. Unifocal VPC in normal individuals. c. VPC in acute myocardial infarction.

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d. More than 6 VPC per minute. e. R on T phenomenon in absence of heart disease. A patient with atrial fibrillation and a resting ventricular rate of about 70 receiving digitalis may require additional digitalis because the effect of digitalis is: a. Extravagal. b. Direct on the cell membrane. c. Vagal. d. On the transport system of the cell. For a patient with episodes of giddiness due to bradycardia the therapy of choice is: a. Atropine. b. Pacing. c. Adrenalin. d. Mecholyl. e. None. Patients with chronic RBBB and extreme left axis deviation frequently become symptomatic because of complete AV block. True? False? A patient with acute myocardial infarction who develops RBBB and left axis deviation often proceeds to complete AV block and should be paced. True? False? In which of the following conditions can atrial fibrillation be expected not to respond in a predictable manner to digitalis with slowing of the ventricular rate? a. Fever. b. Thyrotoxicosis. c. Pulmonary embolization. d. Pneumonia. e. All of the above. Initial treatment of atrial arrhythmias complicating W-P-W should include the following: a. Digitalis. b. Digitalis, quinidine. c. Quinidine, lidocaine. d. Quinidine. e. Dilantin, propranolol.

A n s w e r s on p. 57.

TABLE G E N E R A L PRINCIPLES

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E l e c t r o p h y s i o l o g i c B a s i s of A r r h y t h m i a s His Bundle Electrocardiography

F u n c t i o n a l C l a s s i f i c a t i o n of A r r h y t h m i a s Diagnosis

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E t i o l o g y of U n d e r l y i n g H e a r t D i s e a s e a n d P r e c i p i t a t i n g Factors . . . . . . . . . . . . . . . . . . . P r i n c i p l e s of T h e r a p y

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SPECIFIC ARRHYTHMIAS

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Accelerated Rhythms Bradycardias

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A t r i o v e n t r i c u l a r (AV) B l o c k .

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D i s o r d e r s of A t r i o v e n t r i c u l a r

Conduction .

Atrioventricular Dissociation COMMENTS .

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is Distinguished Professor of Medicine and Director, Cardiovascular Division and Krannert Institute of Cardiology, Indiana University School of Medicine. Doctor Fisch received his medical education at Indiana University. Member of a number of professional organizations including the Association of American Pathologists and the ABIM Cardiovascular Board, he served as President of the American College of Cardiology from 1975-1977. Cardiac arrythmias are of special clinical interest to Dr. Fisch.

DISORDERS OF RHYTHM are clinically important because of their frequency, their association with both normal and abnormal hearts and their potential for significant cardiovascular and psychologic consequences. They often appear in otherwise normal individuals and may remain asymptomatic or may cause a severe state of anxiety and incapacity. In patients with heart disease, identical arrhythmias may result in severe depression of cardiac function, with resultant cardiac failure or impairment of regional blood flow or both. Arrhythmias are a manifestation of disordered function and do not comprise a complete cardiac diagnosis. The etiology, pathophysiology and functional classification of the underlying heart disease should be determined when possible. 1, 2 Cardiac arrhythmia results from abnormality of impulse formation, impulse conduction or a combination of these. 3-5 In contrast to an almost infinite number of permutations of mechanisms of arrhythmias of interest largely to those concerned with electrocardiography and mechanisms of complex arrhythmias, 6 the clinically relevant types of rhythm disorders comprise a relatively small group and the principles of diagnosis and management are comparatively few in number. The discussion that follows is divided into two sections. Section I, entitled General Principles, will include (1) a brief review of electrophysiology (EP), (2) functional classification, (3) factors influencing therapeutic decisions, including diagnosis, immediate prognosis, etiology, precipitating factors, long-term prognosis, and (4) general therapeutic principles. Section II, entitled Specific Arrhythmias, will deal with selected, clinically relevant arNOTE: This work was supported in part by the Herman C. Krannert Fund; by Grants HL-06308, HL-05363, HL-07182, HL-18795 and HL-18538 from the National Heart, Lung and Blood Institute of the National Institutes of Health; and by the American Heart Association, Indiana Affiliate, Inc. 7

rhythmias. The inclusion of arrhythmias in this section may be somewhat arbitrary but is based largely on my experience.

I. GENERAL PRINCIPLES ELECTROPHYSIOLOGIC BASIS OF ARRHYTHMIAS

The cellular mechanisms responsible for the genesis of arrhythmias are complex and at times difficult to translate to the intact organism, particularly to the human with a diseased heart. Despite these limitations, a grasp of the basic concepts is necessary for a better understanding of clinical arrhythmias and the literature dealing with arrhythmias?, 5 Arrhythmias are a manifestation of disturbed function of the specialized tissues of the heart. 4 In the clinical setting, arrhythmias probably do not originate in the myocardium, be it atrial or ventricular, normal or diseased. The specialized conducting tissue includes the sinoatrial node (SAN) located at the opening of the superior vena cava into the right atrium, the AV node, the bundle of His, right and left bundle branches (RBB and LBB) and the Purkinje system. 7 The impulse leaves the SAN and traverses the atrium, giving rise to the ECG P wave. The impulse then is delayed in the AV node and the P - R segment of the ECG is inscribed. Once the inpulse leaves the AV node it is conducted along the bundle of His, the RBB and LBB and the ECG registers a QRS. Despite the difference of opinion regarding the existence of discrete anatomic fascicles in the human heart, it is useful from the standpoint of clinical electrocardiography to accept the concept of anterior (LAD) and posterior (LPD) division (fascicles) of the LBB. Whereas the surface ECG reflects the electrical properties of the myocardial cells, arrhythmias are a manifestation of disordered function of the specialized tissues. The function of the specialized tissues is not reflected in the ECG. It becomes clear, therefore, that the problems and difficulties connected with ECG analysis of arrhythmias stem to a large extent from the fact that the electrocardiographer has to analyze and define the largely "invisible" behavior of the specialized conduction tissue from the ECG, which mirrors the electrical properties of the myocardium. The SAN rate may vary in response to a variety of physiologic and pathophysiologic stimuli and result in sinus tachycardia, sinus bradycardia or sinus arrhythmia. These should be thought of in a light different from the "truly" pathologic ectopic arrhythmia due either to (1) ectopic automaticity or (2) re-entry. The concept of automaticity, conduction and re-entry can best be presented and understood in the light of the EP behavior of a single cell?, 4 8

When a cell membrane is penetrated with a microelectrode, a voltage difference is registered across the membrane, with the inside of the cell being negative. The magnitude of this voltage difference varies from tissue to tissue, being approximately minus 90 millivolts in the Purkinje fiber and approximately 60 millivolts in the SAN. This negative transmembrane voltage is a function of potassium effiux during the resting phase 4 of the action potential (AP). When the cell is stimulated there is a sudden influx of sodium and this reverses the intracellular polarity from the previously negative to a positive overshoot of about 15-20 millivolts. The rapid upstroke and overshoot are phase 0 and 1 respectively of the AP and correlate with the QRS of the ECG. Following the overshoot there is a slow phase of repolarization (plateau or phase 2), probably related to slow inward calcium-carried current. The phase 2 of the AP equates with the ST segment of the surface ECG and is followed by a relatively rapid effiux of potassium from the cell. This effiux of potassium results in repolarization, phase 3 of the AP and the T wave of the ECG. The efflux of the positively charged potassium during phase 3 restores the negative transmembrane resting potential of phase 4 (Fig. 1). Activation of a cell and generation of a propagated AP can be initiated either by stimulation or, as in the case of the SAN, AV node and Purkinje fiber, the cells may exhibit a spontaneous gradual reduction of the resting potential, which, on reaching the threshold potential, results in a propagated AP. This ability to generate spontaneously a propagated AP defines automaticity Fig 1.-Correlation of the electrocardiogram with the transmembrane action potential. For details see text.

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(Fig. 2). The rate with which phase 4 of an automatic fiber reachesthreshold potential results in either a tachycardia or a bradycardia. The difference in voltage between the resting potential (phase 4) and the threshold potential determines excitability of a cell. Normally, an AP originates in the SAN and stimulates the adjoining cells, which respond with an AP. This AP, in turn, acts as a stimulus for the surrounding cells. This process of stimulus-response results in impulse propagation. Since the AP is the stimulus, it follows that the integrity of the AP will determine the speed of conduction. The integrity of the AP is, in turn, dependent on the magnitude of the resting potential at the moment the cell is activated. The more negative the transmembrane resting potential the more rapid the upstroke of phase 0 and the higher the amplitude of the AP the more rapid the impulse propagation. This relation between the "takeoff' potential of the resting, or phase 4, transmembrane potential and the AP and conduction implies that the "healthier" the action potential the more rapid the propagation. On the other hand, as the resting potential (phase 4) declines (becomes less negative), the rate of upstroke (phase 0) also declines, the amplitude of the AP is lowered, such an AP becomes a poor stimulus and slowing of conduction or block may result (Fig. 3). Re-entry, in contrast to automaticity, is the result of conducFig 2.-Automaticity manifested by a gradual loss of resting membrane potential (phase 4), which, on reaching the threshold potential, generates a propagated action potential, is shown at the left. Re-entry: An impulse arrives at an area of unequal conduction. It conducts normally along one pathway and takes part in ventricular activation, which gives rise to the normal QRS. After a critical delay, the impulse traverses the depressed area, re-enters the heart and, finding the ventricle recovered, gives rise to an ectopic QRS (left). Re-entry can also, and most likely does, result from localized complete unidirectional block (right). In such a setting, forward conduction is blocked completely. Following excitation, however, the impulse enters the blocked area in a retrograde manner and re-enters the tissue via the more rapidly conducting pathway, giving rise to the second, re-entrant ectopic complex. Reproduced with permission, s 1125

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tion. When an impulse reaches an area of nonuniform propagation, "part" of an impulse may be blocked whereas the "remainder" is propagated through an adjoining normal or less-depressed tissue and contributes to activation of a given chamber. This more rapidly conducting impulse then may return through the unidirectionally blocked area and re-enter and re-excite the heart for the second time, giving rise to an ectopic impulse (see Fig. 2). Perpetuation of this circular, re-entrant activity results in a variety of tachycardias. HIs BUNDLE ELECTROCARDIOGRAPHY

His bundle electrocardiography (HBE), a relatively new method of study of arrhythmias, coupled with atrial or ventricufar stimulation, has contributed considerably to our understanding of the mechanisms of arrhythmias and, on occasion, defined previously unrecognized mechanisms (e.g., Wolff-ParkinsonWhite with unidirection, ventriculoatrial conduction via the anomalous bypass). However, its application to the clinical, everyday care of patients with arrhythmias is yet to be defined. It m a y well be that the clinical utility of this technique will be limited to a small group of patients where information gained from H B E m a y be absolutely essential for proper management 11

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of an arrhythmia (Fig. 4). For the time being, HBE remains in the hands of those especially interested in this procedure. 8 FUNCTIONAL CLASSIFICATION OF ARRHYTHMIAS

Classification of arrhythmias may be based on anatomy, EP mechanism, therapeutic approach, prognosis, ventricular rate or the etiology of the underlying heart disease. For the purposes of our discussion, the classification of the arrhythmias is based on clinical considerations. Thus, the classification may not necessarily appear as logical as one based, for example, on the site of origin of the arrhythmia or its EP mechanism.

Accelerated rhythms Supraventricular Sinus arrhythmia Sinus tachycardia Atrial premature complexes (APC) Atrial paroxysmal or junctional tachycardia (PAT, PJT) Atrial tachycardia with block (AT with block) Atrial flutter 12

Atrial fibrillation Nonparoxysmal junctional tachycardia (NPJT) Wolff-Parkinson-White (W-P-W) Ventricular Ventricular premature complexes (VPC) Ventricular tachycardia (VT) Accelerated idioventricular rhythm Ventricular flutter Ventricular fibrillation Ventricular parasystole

Bradycardias SA node disease Sinus bradycardia Sinoatrial arrest Sinoatrial block Tachycardia-bradycardia syndrome AV block Prolonged AV conduction Second degree AV block Wenckebach (Type I) Mobitz (Type II) Complete AV block AV dissociation Escape DIAGNOSIS

Two problems deserve special consideration because they are common, because a correct'diagnosis m a y be important yet difficult to make and because prompt therapeutic intervention frequently is indicated. The two problems include: (1) differentiation of supraventricular tachycardia with aberrancy from ventricular tachycardia (VTP and (2) differentiation of A V dissociation due to slowing of primary pacemaker or acceleration of subsidiary (AV dissociationdue to functional refractoriness)from pathologic A V block.TM In addition, in the latter, a differentiation between block above the bundle of His (supra His) and below the bundle of His (infra His) is important. II It is clear that supraventricular tachycardia with aberrancy and V T will have different immediate and long-term prognoses, and the therapy will differ also. This differential diagnosis is most important, for, on one hand, V T m a y be life-threatening, with sudden death a possibility whereas, on the other hand, sudden death practically never is due to supraventricular arrhythmias. Furthermore, the long-term prognosis of the two arrhythmias is entirely different. In a significant number of patients, a differentialbetween the two based on the E C G alone is 13

impossible. Occasionally, when a definitive differential diagnosis is imperative (e.g., when surgery or pacing is considered for control of refractory arrhythmia), one might have to resort to atrial pacing and HBE in order to determine the site of impulse formation. The former may lead to captures of the ventricles with a normal QRS (Fig. 5), and the HBE will record the onset of the QRS before the inscription of His bundle potential (H), thus identifying the ventricular origin of the a r r h y t h m i a (see Fig. 4). The ECG usually is more helpful in ruling out a VT t h a n in making a definitive diagnosis of the arrhythmia. When a tachycardia is accompanied by a normal QRS, one can assume, for all practical purposes, that a supraventricular a r r h y t h m i a is presFig 5 . - D i f f i c u l t y of differentiating VT from supraventricular tachycardia with aberrancy is demonstrated in this figure. Inferior myocardial infarction (top row) is complicated by a bizarre tachycardia (row 2). Intra-atrial electrogram (HRA) does not resolve the problem. Each broad and negative QRS is followed by an upright deflection that could represent a retrograde P wave due to junctional or ventricular rhythm. With atrial pacing (row 4), the ventricles are captured and the QRS is of normal duration, ruling out aberrancy and confirming presence of VT. VT is terminated with low-energy countershock (bottom row). IUMC 57]959 - ]766 ii!!!~iiiiiii!!i::ii::ii::::-i]":::~::ii::ii::ii~

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AV dissociation due to changing rate of the primary (SAN) or subsidiary pacemakers (AV dissociation due to functional refractoriness) must be differentiated from complete pathologic heart block (Fig. 6). In the former, the QRS usually originates above the bifurcation of the bundle of His, is normal in duration, the rate is relatively rapid (usually 40 or faster), the focus is stable and the rhythm is regular. The arrhythmia most often is benign, producing few, if any symptoms and frequently is transient in nature. The most common causes of AV dissociation due to refractoriness are acute myocardial infarction, digitalis poisoning and open heart surgery. Occasionally, AV dissociation may be present in young, normal individuals with a strong vagal influence. TM Once the cause for the bradycardia is shown to be AV block, a differentiation between AV block at the level of the AV node (supra His) and that at the level of bundle branches or their divisions (infra His) becomes clinically important. ~ Fig 7.-AV

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In complete AV block, particularly acquired, the focus may be below the bundle of His (see below), the QRS is prolonged, the rate usually is considerably slower (40 or less) and the pacemaker frequently unstable (Fig. 7). The bradycardia frequently is complicated by ventricular arrhythmias, ventricular standstill with clinical manifestations of Adams-Stokes disease and requires prompt and definitive therapy. CLINICAL DIAGNOSIS

Arrhythmias produce symptoms because of awareness of heart action (palpitations) or hemodynamic impairment. In the vast majority of patients, symptoms are absent or, if present, are manifested by occasional palpitations. In the case of tachycardias with rapid ventricular rates, the patient may feel giddy or become dizzy but rately will lose consciousness. Patients with rapid rates and underlying heart disease may experience chest pain due to ischemia or dyspnea secondary to heart failure. Symptoms due to bradycardia may include changing behavior, memory loss, dizziness and occasionally lightheadedness, momentary lapses, syncope and, rarely, seizures, all a manifestation of decreased cerebral blood flow (Adams-Stokes). Not uncommonly, the symptoms are annoying and out of proportion to the seriousness of the underlying disorder. This is particularly true in the case of supraventricular arrhythmias. The frequent lack of a relationship between the severity of symptoms and their prognostic significance makes evaluation and selection of patients for therapy difficult. The presence or absence of heart disease, its severity and history of drug ingestion are most important to assess. History coupled with a careful assessment of the pulse, heart rate and rhythm, neck vein pulsations, heart sounds, response to carotid stimulation and presence or absence of pulse deficit often will permit a bedside diagnosis of arrhythmias with a high degree of accuracy. The diagnostic sensitivity is improved further when clinical findings are correlated with the ECG. ANTONIO C. DE LEON, JR.: An example of the value of clinical correlation with the ECG is in some patients with premature, wide QRS complexes, where there is some question as to whether they represent premature ventricular contractions or premature supraventricular beats with aberrancy. The bedside observation of cannon A waves in the jugular venous pulse occurring with these premature beats would indicate ventricular rather than supraventricular origin.

Ventricular tachycardia TM can be suspected in the presence of a heart rate of 150-200 (occasionally the rate may be lower or higher), either regular or slightly irregular rhythm and signs of 17

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e n u m e r a t e d above, if accompanied by significant b r a d y c a r d i a and r a t e below 40, with a r e g u l a r r h y t h m , indicate the presence of complete AV block. Obviously, in the absence of sinus r h y t h m , the signs of AV dissociation cannot be elicited because of lack of atrial contraction. li~ W. PROCTOR HARVEY: Multiple sounds, if present, in a number of patients having ventricular tachycardia provide an immediate clue as to the diagnosis. This is illustrated in Figure A. Other tachycardias (Fig. B) do not show these multiple sounds. This auscultatory finding, plus the lack of response to carotid sinus pressure, can lead to a quick diagnosis. It is especially useful when an electrocardiogram is not available. Early recognition and treatment of this arrhythmia, of course, can be lifesaving.

Fig 8 . - E f f e c t of arrhythmia on arterial blood pressure (BP). Pressure in mm Hg is shown on the ordinate. Atrial pacing (A) and s p o n t a n e o u s AV junctional tachycardia (B) with a p p r o x i m a t e l y the same ventricular rate result in a relatively minor drop in BP. In atrial fibrillation (C) at a rate of 1 4 0 - 1 5 0 there is a significant negative effect on the arterial pressure. A n u m b e r of the QRS c o m p l e x e s are not followed by arterial pressure curves (pulse deficit). /

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The heart rate and r h y t h m alone often can point to a correct diagnosis. ~3 A regular rate between 180 and 200 or higher suggests PAT whereas a rate of 150 and regular points to atrial flutter. The diagnosis of the latter can be confirmed by a characteristic response to carotid stimulation (see under Atrial flutter). An untreated tachycardia with a rate of 130-180, with a grossly irregular rhythm, a pulse deficit and a varying intensity of heart sounds clearly identifies atrial fibrillation (Fig. 8). In patients with acute myocardial infarction or with digitalis intoxication or following open heart surgery, the appearance of a regular r h y t h m varying from 70 to 130, particularly in a patient with atrial fibrillation, suggests the emergence of NPJT. ROBERT A. O'ROURKE: Cannon A waves are observed in the jugular venous pulse whenever atrial contraction occurs with the tricuspid valve closed during right ventricular systole. Thus, cannon waves are observed frequently in patients with ventricular tachycardia or complete heart block.

HEMODYNAMIC EFFECTS

TACHYCARDIAS.-- The potential EP and hemodynamic consequences of an arrhythmia dictate the need, the urgency and the method of therapy. TM The more important immediate prognostic determinants include the site of origin of the arrhythmia, whether supraventricular or ventricular, the ventricular rate and the intrinsic state of the heart. Other factors include atrial contribution, regularity of the rhythm, vasomotor tone, catecholamines and perhaps sequence of ventricular activation. The site of impulse formation is of particular importance, because, although ventricular arrhythmias may be potentially lethal, supraventricular arrhythmias may be disabling because of symptoms secondary to restriction of circulation to the vital organs, namely, heart, brain and kidneys, but rarely are a cause of sudden death. The heart rate is an important determining factor of hemodynamic consequences of an arrhythmia. Normally, the ventricles fill rapidly during the first third of diastole, and during this period the major share of ventricular filling is accomplished, l' ~3 Relatively little filling takes place during the last two-thirds of diastole. Shortening of the cardiac cycle with acceleration of the heart rate is at the expense of diastole. However, only with encroachment on the early rapid filling phase does the cardiac output begin to decline significantly. In normal individuals there is some decline when the atria are paced at about 150, and a clear drop of cardiac output is seen at pacing rates of 1 7 0 - 1 8 0 per minute. Although in the normal an increase in paced heart rate of 140 2O

or 150 is not accompanied by major hemodynamic effects (see Fig. 8), this is not the case in patients with heart disease and myocardial impairment. It may have a significant depressing effect on ventricular function, the depression being more marked with ventricular stimulation, and the depression is directionally related to the severity of the underlying disease, the heart rate and rhythm as well as the duration of the tachycardia. The atrial contribution to the total cardiac output is estimated to be approximately 15-20%. Although this fraction of the output may not be important in patients with a normal ventricular function, it may be critical in patients with myocardial disease and severely depressed myocardial function. For example, rapid deterioration of cardiac function may be observed in patients with heart disease with onset of atrial fibrillation, irrespective of the ventricular rate. Sequence of ventricular activation ordinarily is of limited or no importance in maintaining integrity of cardiac output. Studies in patients with normal hearts and with heart disease show very little difference in cardiac output with atrial pacing and normal ventricular activation and atrial pacing with aberrant ventricular activation as initiated, for example, with sequential atrioventricular pacemakers. When ventricular aberrancy results from ventricular pacing, significant depression of cardiac output is noted and this is due to loss of atrial contribution. However, there is no question that in isolated cases aberrant ventricular activation per se contributes to depression of cardiac function (see below). Irregular rate such as is present in atrial fibrillation may impair cardiac efficiency further. This is due not only to the tachycardia with changing cycle length, which impedes diastolic filling and directly affects the stroke output, but also because of changing contractility. The changing contractility may be independent of the end-diastolic pressure or volume. Potentiation, in which two closely spaced contractions enhance the force of the subsequent contraction, on the other hand, may make a positive contribution to cardiac function (see Fig. 8). Vasomotor tone and circulating catecholamines also play a role in determining the final effect of tachycardia on hemodynamic function. For example, although atrial pacing may not affect the cardiac output or, in fact, may cause it to decline, exercise to the same ventricular rate will result in an increased cardiac output. Similarly, although in a normal individual atrial pacing to a heart rate of about 130 frequently induces AV block, a physiologically induced tachycardia to rates as high as 180 and 190 rarely, if ever, produces AV conduction disorders. With exercise there is an inhibition of the vagal effect and a parallel release of catecholamines. The above examples are rather simplistic but do stress the need to evaluate the total environment 21

of an arrhythmia. Additional factors such as blood volume, drugs, electrolytes, metabolic and hormonal milieu influence the effect of arrhythmias on hemodynamics. The sequelae of VT may include sudden death due to ventricular fibrillation or severe hemodynamic deterioration. Patients with VT may show marked hypotension, fall in cardiac output and evidence of impairment of flow to the vital organs at heart rates that are not excessive, rates at which a supraventricular pacemaker may not impair cardiac function. It is clear, therefore, that although the heart rate and the severity of underlying disease play an important role in potential hemodynamic deterioration, these are not the only factors. In some, lack of atrial contribution and asynchrony of ventricular activation contribute significantly to the functional deterioration (Fig. 9). In summary, the severity of the hemodynamic impairment due to the tachycardia may be the result of increased oxygen Fig 9.-Striking deterioration of hemodynamics due to ventricular arrhythmias. The depression is not only a function of accelerated rate, for it is also seen clearly following a single PVC occurring late in diastole (top row). The deterioration probably is related to loss of atrial contribution and aberrancy of intraventricular conduction.

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demand of the myocardium, compromised coronary flow, reduction in diastolic filling time, loss of atrial contribution, irregularity of contraction and, on rare occasions, abnormal sequence of ventricular activation. The effect of any one or a combination of these variables varies from patient to patient. If hemodynamic deterioration becomes severe, circulation to the vital organs, namely, the heart, brain and kidneys, becomes compromised and the patient will exhibit clinical evidence of impaired cerebral flow, shock, angina or heart failure. These can be easily detected at the bedside without complex diagnostic procedures. The appearance of such symptoms indicates the need for prompt intervention designed to increase the cardiac output. BRADYCARDIAS.- Bradycardia may cause depression of cardiac function or ventricular arrhythmias or both. The ventricular arrhythmias may include VT, ventricular flutter or fibrillation. If the dominant pacemaker is ventricular in origin, a sudden cessation of the impulse formation may result in cardiac standstill. As in the case of tachycardia, the hemodynamic consequence of slow rates depends to a large extent on the state of the myocardium. For example, slow rates, which do not reduce cardiac output in the normal individual, may result in severe depression of cardiac function in the presence of acute myocardial infarction. 15 When the bradycardia is accompanied by AV dissociation, atrial fibrillation or flutter, the loss of atrial contribution may depress the cardiac function further. ETIOLOGY OF UNDERLYING HEART DISEASE AND PRECIPITATING FACTORS

The recognition of an underlying heart disease or sudden precipitating changes or both may be essential for prognosis and proper treatment. Two examples will make this point clear. In the absence of significant myocardial disease or obstruction to flow, arrhythmias with rates approaching or exceeding 200 can be tolerated well for prolonged periods. On the other hand, this same arrhythmia in the patient with significant mitral stenosis or acute infarction can result in acute heart failure or shock or both. '3 Similarly, recurrent ventricular arrhythmias due to chronic ischemic heart disease should be treated with procainamide or quinidine, but an identical arrhythmia precipitated by hypokalemia should be treated with potassium. TM The etiology of the underlying heart disease usually is more easily identifiable than are the immediate precipitating factors. The latter include, among many, hypoxia, electrolyte and metabolic disorders, fever, thoracotomy and pulmonary embolism. 23

PRINCIPLES OF THERAPY

GENERAL COMMENTS.-- Selection of a patient for definitive therapy may be difficult, often more difficult than either the diagnosis or the treatment itself. This is true because information necessary for selection of patients for therapy often is not available. Frequently, the etiology is obscure, the prognosis of a given arrhythmia remains in question and long-term administration of drugs may not be feasible. Decision to treat a patient with an arrhythmia is simple when (1) the symptoms are severe enough to interfere with the quality of life, irrespective of presence or absence of heart disease, (2) the heart rate is rapid enough to interfere with perfusion of vital organs or (3) the arrhythmia is potentially lethal. On the other hand, a decision whether or not to subject an asymptomatic patient with compensated heart disease or one without obvious heart disease to long-term suppressive therapy may prove extremely difficult. Often, hard data are lacking and the final decision depends on the physician's attitude and experience with a given arrhythmia. The goals of antiarrhythmic treatment are (1) termination of an arrhythmia (e.g., VT), (2) reduction of ventricular rate without attempting to suppress the primary mechanism (e.g., atrial fibrillation) or (3) long-term prevention or suppression of recurrent arrhythmias (e.g., VT or PAT). The urgency and method of treatment will depend on the immediate prognosis. If an arrhythmia is potentially prefibrillatory, as in the case of VPC or VT complicating MI or digitalis poisoning, prompt termination of the arrhythmia may be in order. On the other hand, in patients with atrial fibrillation, reduction of the ventricular rate may be preferable to actual termination of the arrhythmia. The final therapeutic decision is dependent on careful assessment of all the available clinical and laboratory information. For example, ordinarily the management of atrial fibrillation is directed toward slowing of the ventricular rate with digitalis. However, in a patient who recently has undergone heart surgery with replacement of a heart valve and in whom the rapid ventricular response not only may impair the cardiac output but, in addition, the ventricular rate frequently fails to respond to digitalis, cardioversion may be preferable to digitalis. Another example is the patient with PVC and heart failure. Ordinarily, and when indicated, the treatment of PVC is one of direct suppression of the ectopy. However, when due to heart failure, the PVC may respond to treatment of the heart failure without the necessity for resorting to the use of antiarrhythmic drugs. In general, the goal of therapy in supraventricular arrhythmias is to slow the ventricular rate whereas in ventricular arrhythmias the aim is suppression of the arrhythmia. There are 24

exceptions to this general rule, and these will be dealt with in the context of the specific arrhythmias. Once the basic concepts of diagnosis, prognosis and treatment are mastered, the approach to an arrhythmia proves fairly straightforward. The plan of action, however, should not be equated, or confused with, success or failure of treatment. Although the proper management depends on the physician's base of information, failure of therapy is due more often to deficiencies in knowledge of arrhythmias. Such deficiencies plague both the generalist and the specialist alike and may preclude a definitive diagnosis and/or successful intervention. Failure to recognize the fact that the best possible approach to an arrhythmia does not guarantee success of therapy may result in unnecessary insecurity on the part of the physician. Theoretically, successful response to treatment would seem ensured if the following were available: (1) correct diagnosis of the arrhythmia, (2) etiology of the underlying heart disease, if any, (3) the immediate precipitating event, (4) prognosis of the arrhythmia and (5) drugs with an acceptable risk-to-benefit ratio. However, this often is not the case, because: (1) a correct diagnosis may not be possible (e.g., supraventricular arrhythmia with aberrancy versus VT), (2) often the prognosis, thus, indication for therapy, is not clear (e.g., mitral valve prolapse with ventricular arrhythmia, the significance of some PVC in ischemic heart disease), (3) the currently available antiarrhythmic agents have serious limitations as to both their efficacy and incidence of side-effects. SPECIFIC INTERVENTION.- A glance at the past 30 years of our efforts to control arrhythmias clearly suggests that with the exception of lidocaine and perhaps propranolol little progress has been made in the area of pharmacotherapy. The basic drugs remain digitalis, quinidine, procainamide, atropine, isoproterenol and Adrenalin. Drugs that are in the experimental stage either in the United States or overseas and which hold out promise include aprindine, 17 disopyramide TM and amiodarone. TM Despite these shortcomings, considerable information has accumulated regarding the mechanism of action and pharmacokinetics of drugs, their indications and proper use. Whereas limited progress has been made in control of arrhythmias with drugs, the advent of monitoring, pacing, cardioversion and defibrillation has made a tremendous impact on our ability to manage arrhythmias. Because of the proof that symptoms are indeed due to the arrhythmia in question, the severity and frequency of recurrence of such symptoms are most important to define. At times, such information can best be obtained with continuous ambulatory recording. Current limitations of continuous taping include our 25

i n a b i l i t y to r e d u c e t h e d a t a r a p i d l y e n o u g h to m a k e it f e a s i b l e to m o n i t o r l a r g e n u m b e r s of p a t i e n t s . T h e r e a r e also r e s e r v a t i o n s a b o u t t h e a c c u r a c y of t h e d a t a r e d u c t i o n . T h e r e is l i t t l e d o u b t , however, that with modern computer technology the reduction of d a t a will be r e s o l v e d w h e r e a s i n t e r p r e t a t i o n of a r r h y t h m i a s , p a r t i c u l a r l y m o r e c o m p l e x ones, m a y p r o v e a m u c h m o r e diffic u l t t a s k . 2° It is e q u a l l y i m p o r t a n t to r e c o g n i z e c l i n i c a l d i s o r d e r s c o n d u cive to a r r h y t h m i a s a n d t h e c l i n i c a l s t a t e s in w h i c h t h e arr h y t h m i a m a y n o t r e s p o n d to t r e a t m e n t in a n e x p e c t e d a n d pred i c t a b l e m a n n e r . F o r e x a m p l e , t h e r a p i d v e n t r i c u l a r r a t e in a t r i al f i b r i l l a t i o n w i t h t h y r o t o x i c o s i s m a y n o t r e s p o n d to d i g i t a l i s , AGENTS USED TO ELICIT THE VAGAL EFFECT DRUG

DOSE A N D ROUTE OF A D M I N I S T R A T I O N

Intravenous Digitoxin

1.2- 2.0 mg

Digoxin

1.25 mg

Lanatoside C (Cedilanid) Lidocaine

1.6 mg

Quinidine Procainamide

Propranolol Diphenylhydantoin Potassium Atropine Adrenalin Isoproterenol Edrophonium chloride (Tensilon) Phenylephrine (Neo-Synephrine) Metaraminol (Aramine) Methoxamine (Vasoxyl) 26

1 mg/kg bolus followed by 1- 3 mg/min 0.500-0.800 mg in 100 ml saline given over 10- 30 min 100-200 mg q 5 min, up to 1000 mg followed by 1 - 5 mg/min 0.5-2.0 mg q 1-3 h 3- 5 mg/kg 0.5 mEq/min as a solution of 50-100 mEq/1000 ml 1-2 mg 1-4 mg/min as a solution of 1-4 mg/1000 ml 1-4 mg/min as a solution of 1-4 mg/1000 ml 5-10 mg 0.5-1.0 mg 0.5-2.0 mg as a solution of 50-100 mg/500 ml 5-10 mg

Oral Initial Maintenance Initial Maintenance

1.2 -2.0 mg 0.05 -2.0 mg 2.0 -5.0 mg 0.125- .75 mg

200-400 mg q 2 - 6 h 250-500 mg q 6 h (up to 8 gm per day) 10-40 mg q 4 - 6 h 100-300 mg tid 40 mEq in 200 ml orange juice q h for total of 100-120 mEq

and vigorous attempts to slow the rate with glycosides may prove disastrous. 2' Once a decision is made to treat an arrhythmia, any o n e - o r a combination-of the following, may be selected: 1. Vagal stimulation. 2. Drugs. 3. Pacing. 4. Cardioversion. 5. Surgery. VAGAL STIMULATION. -- This approach most often is used to terminate PAT or paroxysmal junctional (AV nodal) tachycardia. Vagal stimulation can be accomplished with carotid sinus massage or with other, less reliable maneuvers, such as gagging and deep inspiration. The vagal effect can also be elicited by transient elevation of blood pressure to about 170 mm Hg using vasopressors, such as phenylephrine (Neo-Synephrine) 0.5 mg, metaraminol (Aramine) 0.5-2.0 mg or methoxamine (Vasoxyl) 5 - 1 0 mg given intravenously (see the accompanying table). These agents should be avoided in patients with significant myocardial disease, particularly ischemic heart disease, or hypertension.

m,* ROBERTA. O'ROURKE:To perform carotid sinus massage properly, the patient's neck should be extended with a pillow under the shoulders, the fusiform carotid artery identified below the angle of the jaw and pressure exerted on the artery in a medial and posterior direction for 1-5 seconds while listening to the heart sounds for a sudden slowing of the heart rate. D R U G S . - F r o m the practical, clinical standpoint, drugs can be divided into those used in the management of tachycardias and bradycardias. The former include digitalis, lidocaine, procainamide, quinidine, propranolol, diphenylhydantoin and potassium. For bradycardias, when pacing is either not indicated or not available, drug therapy includes atropine, isoproterenol and Adrenalin (see table). Digitalis. - This drug, probably the oldest antiarrhythmic agent known, is extremely useful and frequently is the drug of choice for the management of supraventricular arrhythmias. The glycoside has a twofold a c t i o n - v a g a l and extravagal. The latter probably combines some degree of inhibition of the sympathetics as well as a direct effect on cellular function. Recognition of this dual action of digitalis is clinically most important, particularly in atrial fibrillation, in which suppression of AV nodal conduction and slowing of ventricular rate is the therapeutic end point 2' (Fig. 10). It also is important to differentiate 27

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Fig l O . - V a g a l effect of digitalis on AV conduction and ventricular rate in atrial fibrillation. The slow ventricular response in the supine position is overcome promptly by change to a sitting position and walking. The vagal effect depressed AV conduction, prolonged AV nodal refractoriness, enhanced concealment and resulted in a slow ventricular response. However, this was not the optimal desired effect of digitalis. In order to control the ventricular rate during usual daily activities, the extravagal effect of digitalis is required. In this instance, additional digitalis had to be administered despite the supine, resting ventricular rate of 60 per minute. Reproduced with permission. 21

between the inotropic and antiarrhythmic action of the glycoside because the dose of digitalis may vary, depending on which action is desirable. For long-term control of arrhythmias, digitoxin is my drug of choice. The initial oral dose is 0.6 mg, followed by 0.4 mg in 6 - 8 hours, and 0.2 mg twice daily until the patient is "digitalized." The daily maintenance dose varies from 0.1 to 0.2 mg, with an average dose of 0.15 mg. The therapeutic blood levels vary from 10 to 20 ng/ml, with toxic arrhythmias seen at levels greater than 25 ng/ml. The oral digitalizing dose of digoxin is 2.0-5.0 mg given over 1 8 - 7 2 hours. The daily maintenance dose varies from 0.25 to 0.1 mg. For a more prompt result, especially when cardioversion is not indicated, a rapidly acting drug such as lanatoside can be given intravenously in doses of 0.8 mg followed by 0.4 mg every 4 0 - 6 0 minutes until the desired result is obtained. For intermediate action, digoxin can be given intravenously. The initial dose is 0.5-1.0 mg followed by 0.25-0.5 mg every 2 - 4 hours until the desired result is obtained. The therapeutic levels of digoxin vary from 1 to 2 ng/ml and digitalis-induced arrhythmias may be seen with levels above 2 ng/ml. More important than the type of glycoside one chooses is one's familiarity with its pharmacokinetics. The problems faced when using digitalis in prevention of arrhythmias are the. sporadic and unpredictable pattern of recurrence of the arrhythmia and lack of an easily identifiable therapeutic end point, such as, for 28

example, the ventricular rate in atrial fibrillation. Consequently, it is difficult to be certain that a given maintenance dose of the glycoside was indeed the proper "therapeutic" dose and that the therapeutic trial was indeed optimal. For example, failure to prevent PAT in an otherwise normal patient with a maintenance dose of 0.25 or even 0.50 mg of digoxin does not necessarily denote failure of the glycoside, because larger doses, equivalent to 0.15 or 0.2 mg of digitoxin, might prove effective. Glycoside levels may be, but most often are not, very useful in monitoring chronic drug administration. Although manifestations of digitalis poisoning include symptoms referable to the gastrointestinal, central nervous and muscular systems, the potentially lethal effects are related to the specialized conduction tissue of the heart. Any arrhythmia, especially if ectopic, first appearing in the course of administration of digitalis must be assumed to be due to the drug. Such arrhythmias are numerous and their specificity for digitalis poisoning varies widely. Digitalis toxicity is difficult to diagnose because identical arrhythmias appear in patients from causes other than digitalis. A diagnosis of digitalis toxicity must take into account not only the ECG but all available clinical and laboratory information. We find digitalis levels to be of very limited value in the diagnosis of digitalis poisoning. Arrhythmias suggestive of digitalis overdosage or poisoning, especially if first manifested during the administration of the drug, include PVC, AT with block, NPJT, VT and a variety of AV conduction defects. Less commonly, disorders of SAN function result. 2~ ROBERT A. O'ROURKE: In patients in atrial fibrillation on digoxin therapy, the ventricular rate rather than the serum digoxin level is more accurate for assessing the effectiveness of therapy. In many patients, the ventricular rate is controlled by a digoxin dosage that is associated with serum levels of 2- 3 ng/ml but no signs of digitalis toxicity. Potassium. - This cation is a very effective antiarrhythmic agent and probably is the drug of choice for suppression of lifethreatening arrhythmias due to digitalis. The drug can be given intravenously as KC1 in a solution containing 5 0 - 1 0 0 mEq of potassium in 1000 ml of saline or 5% glucose. Provided that there are no contraindications, such as congestive heart failure, the preferred vehicle is saline. The rate of administration is 0.5 mEq per minute and the infusion should be monitored carefully. The potassium can also be given orally in the form of a solution containing 40 mEq of potassium in 200 ml of orange juice. This dose can be repeated two or three times at 4 5 - 6 0 - m i n u t e intervals. The effect of the cation is shortlived, lasting only minutes after intravenous infusion is discontinued, or 3 - 4 hours after oral administration. Consequently, 29

the cation must be given repeatedly until the causative agent, such as digitalis poisoning, dissipates. The most serious potential toxic effect of potassium is depression of conduction, especially AV conduction. However, a considerable margin of safety exists between the antiarrhythmic and conduction depressing effects of the drug. TM

Lidocaine.- This drug usually is administered as a 50-100-mg bolus followed by an infusion of 1 - 4 mg per minute. The efl~ctive blood levels vary from 2 to 5 ng/ml, with potential toxicity at levels exceeding 5 ng/ml. The usual manifestations of toxicity include drowsiness, disorientation, paresthesia and occasionally seizures. ROBERT A. O'ROURKE: In patients with a marked reduction in cardiac output and thus hepatic blood flow, symptoms of lidocaine toxicity may occur at infusion rates (2-4 mg/min) usually not associated with toxicity.

Quinidine.- The oral dose of quinidine varies from 200 to 400 mg every 6 hours and an effective concentration varies from 2.5 to 5 ng/ml. Manifestations of toxicity may appear at levels exceeding 5 - 7 ng/ml and include QRS widening in excess of 50%, fever, diarrhea, cinchonism, thrombocytopenia, hypotension, ventricular arrhythmias and syncope. 1 Procainamide.- The oral dose of procainamide is 250-500 mg every 6 hours for a total 24-hour dose of 2 - 4 gm. Occasionally, as much as 8 gm per day can be administered. Intravenously, the drug is given in doses of 100-200 mg every 5 minutes, up to a total of 1000 mg. This is followed by a drip of 1 - 5 mg per minute. The effective blood levels usually are in the range of 4 - 8 ng/ml, and toxic manifestations appear when the level exceeds 8 ng/ml. These include QRS widening in excess of 50%, hypotension and lupus-like syndrome. 1 Propranolol.-The oral dose of this drug varies from 10 to 40 mg every 4 - 6 hours. Intravenously 0.5-2 mg can be given every 1 - 3 hours. The effective blood level of the drug varies considerably. The toxic manifestations include bradycardia, AV block, hypotension, congestive heart failure and bronchospasm. Diphenylhydantoin.-The oral dose of diphenylhydantoin may include a l-gm loading dose, followed by 100-300 mg every 6 - 8 hours. Intravenously, 50 mg can be administered every 5 minutes up to a total of 500 mg. The usual therapeutic range is 8 - 1 6 ng/ml, toxicity appearing when the level exceeds 16 ng/ ml. The toxic manifestations include ataxia, asthenia, drowsiness and hematologic disorders. The treatment of choice of chronic symptomatic bradycardia is 30

pacing. For temporary control of symptoms, atropine, Adrenalin and isoproterenol m a y prove useful. Atropine is administered subcutaneously or intravenously in 1 - 2 - m g doses. As a rule, atropine is a safe drug and should be used whenever indicated. Very rarely, atropine-induced sinus tachycardia will induce an ectopic tachycardia. The bradycardias can also be controlled with Adrenalin or isoproterenol administered in a solution of 1 - 4 mg in 1000 ml of fluid, with an optimal ventricular rate of about 40 per minute. Doses in amounts that result in ventricular rates higher than 40 per minute may also induce VT: PACING.-Pacing is the treatment of choice for symptomatic bradycardias due to sick sinus syndrome (SSS) or AV junctional disease.22, 23 This procedure is also used occasionally for overdrive suppression of refractory tachycardias 24, 25 or for termination of an arrhythmia: Of the different pacemakers currently available, the demand, QRS blocking pacemaker is used most commonly. Atrial, ventricular or sequential atrioventricular mode of pacing is also available. The pacemaker may be right ventricular transvenous or left ventricular epicardial. Occasionally, the definitive selection of a proper type of pacemaker and mode of pacing may depend on electrophysiologic studies. For example, in patients with SSS, proving the integrity of AV conduction with rapid atrial pacing may result in selection of a sequential AV pacemaker, especially if preservation of atrial contribution appears important. DIRECT CURRENT (De)COUNTERSHOCK.--This procedure has contributed significantly to our management of arrhythmias. 24 As a rule, for termination of a rrhythmias other than ventricular flutter or ventricular fibrillation, QRS synchronized countershock is used. Synchronization to the preceding R wave avoids induction of ventricular fibrillation with the shock. Anesthesia or sedation and amnesia are first induced with short-acting barbiturates or diazepam (Valium) in doses of 5 - 1 5 mg given intravenously. The energies used for cardioversion usually are of low intensity, e.g., 1 0 - 5 0 W-S. Occasionally, higher energies may be required. All measures essential for resuscitation should be available also. In patients with ventricular flutter, fibrillation and rarely other arrhythmias, when speed is of utmost essence and success or failure of therapy is measured in seconds, prompt nonsynchronized countershock is administered before any attempt is made at ECG recognition of the mechanism of the cardiac arrest.

SURGERY. -- Surgical treatment of arrhythmias is largely in the stage of investigation and the ultimate clinical application as yet is uncertain. The only exception, perhaps, is surgical in31

terruption of the bypass in W-P-W with refractory and lifethreatening arrhythmias. This procedure is complex, requiring very sophisticated preoperative and intraoperative electrophysiologic studies, and is performed in very few centers. Other surgical approaches currently used include stellate block followed by cervical sympathectomy, usually left, aortocoronary bypass and excision of ventricular aneurysms. Because these procedures still are in the stage of clinical investigation, they should be considered only in patients with life-threatening arrhythmias proved to be refractory to the accepted forms of treatment. 26 ANTONIO C. DE LEON, JR.: Our own small experience with aneurysmectomy for medically refractory, recurrent ventricular tachycardia is mixed. In some cases in which, despite multiple antiarrhythmic drugs, persistent recurrent ventricular tachycardia requiring cardioversion was a therapeutic problem, surgical excision of the ventricular aneurysm proved to be efficacious in abolishing the arrhythmia. In other instances, however, this was not the case, suggesting that the ectopic focus was located in areas other than the excised or revascularized portion of the ventricular myocardium.

II. SPECIFIC ARRHYTHMIAS This section focuses on selected, clinically important arrhythmias. It may be necessary for the reader to refer to the section on General Principles because even though effort was made in the preceding section to discuss arrhythmias in their broadest generol terms, reference to specific arrhythmias could not be avoided and, if possible, this information will not be repeated in this section. ACCELERATED RHYTHMS SINUS TACHYCARDIA.-Sinus tachycardia, defined as any rate over 100 originating in the SAN with a range from 100 to 160, although with severe stress it may be as high as 200. As a rule, it is secondary to a variety of physiologic changes. The tachycardia per se usually is of no physiologic significance, other than possibly contributing to further deterioration of function in patients with organic heart disease and impaired cardiac function. For example, when complicating acute myocardial infarction, it may increase the myocardial oxygen demand and further jeopardize the myocardium. On rare occasions, sinus tachycardia has been shown to induce ectopic arrhythmias. The treatment of sinus tachycardia should be directed toward the management of the primary disorder. When the etiology of the tachycardia is obscure, elimination of tobacco, alcohol, cof32

fee, tea or medications t h a t contain catecholamines m a y be helpful. If the tachycardia does not respond to m a n a g e m e n t of the precipitating cause and slowing is essential, sedation, reserpine or propranolol m i g h t be useful. • W. PROCTOR HARVEY: Occasionally a sinus tachycardia, the cause of which is not evident, is bothersome to the patient because of the symptoms of palpitation. Normal activities during daily life may be interfered with. Propranolol can be quite helpful in some of these patients. A physician personally examined had sudden jumps in heart rate (sinus tachycardia) with even mild effort or emotion. Carrying out the duties of her practice became difficult, and she was suspected by some of her colleagues of being neurotic. Propranolol was effective in control. • ROBERT A. O'ROURKE: It should be emphasized that persistent sinus tachycardia is not an indication for digitalis therapy unless it is associated with other evidence of left ventricular failure.

ATRIAL PREMATURE COMPLEXES ( A P C ) . - A t r i a l p r e m a t u r e complexes are common, frequently occur in otherwise h e a l t h y individuals and most often require no therapy. In older individuals, the APC frequently are n u m e r o u s and multifocal in origin. Occasionally, the ectopia m a y induce severe symptoms and m a y require suppression. At times, it m a y prove to be a precursor of a higher a r r h y t h m i a , such as atrial fibrillation, PAT or, rarely, atrial flutter. • W. PROCTOR HARVEY: This certainly is true. Recognition that atrial premature complexes might be a forerunner of more serious and complicated atrial arrhythmias is very valuable, and institution of appropriate prophylactic therapy makes good sense. For example, the appearance of atrial premature complexes in a patient with mitral stenosis often indicates the likelihood of an arrhythmia such as atrial fibrillation occurring in the near future. Prophylactic use of a drug such as oral quinidine may forestall or prevent the arrhythmia.

When t h e r a p y of APC is indicated, the drug of choice is digitalis. Less commonly, quinidine, procainamide or propranolol m a y be indicated. PAROXYSMAL ATRIAL TACHYCARDIA ( P A T ) . - T h e onset and t e r m i n a t i o n of the a r r h y t h m i a are characteristically abrupt. With the exception of the first few beats of the tachycardia, the r h y t h m is absolutely regular. The rate varies from 140 to 240 per minute. Rarely it m a y be as low as 1 0 0 - 1 1 0 beats per minute. At its lower ranges of rate, the PAT overlaps with sinus tachycardia and at its higher ranges with atrial flutter. Vagal stimulation m a y t e r m i n a t e the PAT whereas in sinus tachycardia this m a n e u v e r results in a gradual and limited slowing, with a fairly prompt resumption of the basic rate once the vagal stimulation is terminated. 33

Isolated recurrent bouts of PAT are common in individuals without organic heart disease, and, if transient and well tolerated, no therapy other than reassurance is indicated. Occasionally, prolonged episodes may impair the cardiovascular hemodynamics; in such instances, termination of the arrhythmia is indicated. Furthermore, as an individual gets older and develops organic heart disease, the episodes of PAT, previously asymptomatic and benign, now may induce angina, shock or heart failure. The decision to treat PAT, the choice of drug and the route of administration will depend on the clinical situation. As a rule, vagal maneuver, if unsuccessful, is followed by administration of digitalis. It is not unusual for the patient to respond to vagal stimulation after digitalis has been given. Edrophonium (Tensilon), pressor drugs or propranolol may prove useful. If the patient manifests evidence of significant depression of cardiac function, such as impaired perfusion of vital organs, DC countershock probably is the treatment of choice. Digitalis is the drug of choice for prevention of PAT. If digitalis alone is unsuccessful, a combination of digitalis and quinidine or procainamide or propranolol may be tried. Because of the unpredictable course, it is difficult to evaluate the effectiveness of the treatment. Before any regimen is assumed to be a failure, one must be assured that the drugs were given in sufficiently large doses and that W-P-W is ruled out. Clinically, paroxysmal junctional (AV nodal) tachycardia resembles PAT, and, in fact, these two rarely can be differentiated. The therapy of the two arrhythmias is the same. ATRIAL TACHYCARDIA WITH BLOCK (AT WITH BLOCK).-- Atrial tachycardia with block, unlike PAT, rarely is present without severe heart failure or digitalis poisoning. About half of the cases of AT with block are due to digitalis and the remainder are due to the underlying, usually severe, heart disease and not related to digitalis. Whereas PAT nearly always is associated with a I:I AV response, AT with block frequently demonstrates a variety of AV block. The atrial rate usually is between 150 and 200 per minute, but slower and faster rates are not uncommon. At higher rates, AT with block is difficult to differentiate from "slow" atrial flutter. The AV block can be increased by vagal stimulation and decreased with atropine or isoproterenol. In contrast to PAT, vagal stimulation rarely, if ever, terminates AT with block (Fig. II). The treatment of AT with block depends on the etiology and the clinical manifestations. If the ventricular rate does not compromise myocardial function, treatment may not be necessary. In cases in which therapy is indicated and the arrhythmia is not due to digitalis, the treatment of choice is digitalis, with quini-

34

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dine or procainamide or propranolol also useful at times. If these fail, cardioversion may be tried. When the AT with block is a manifestation of digitalis intoxication and treatment is indicated, potassium is a very effective agent. The use of propranolol or diphenylhydantoin may prove effective also. If all else fails and the etiology is not clear, further cautious administration of digitalis, with the assumption that the arrhythmia may not be due to digitalis, is in order. ATRIAL FLUTTER.--Atrial flutter nearly always is associated with organic heart disease. In the untreated patient, atrial flutter is characterized by a rapid, absolutely regular atrial rhythm. In the vast majority of patients, the atrial rate is 300 but may vary from 240 to 360. The AV block usually is 2" 1 and respective ventricular rates between 120 and 180, but most often the ventricular rate is 150. In the presence of AV disease or following administration of drugs, especially digitalis, the AV block varies and the ventricular response to the atrial impulses becomes irregular and at the bedside may simulate atrial fibrillation. However, careful analysis often will reveal repetitive group beating. Carotid sinus massage is very useful in diagnosis of 35

atrial flutter. The characteristic response is an increased AV block with slowing of the ventricular rate, with prompt return to prestimulation level with cessation of carotid stimulation. The drug of choice for slowing of the ventricular rate is digitalis. The drug increases the degree of AV block and slows the ventricular rate. Under the influence of digitalis, the flutter may convert to atrial fibrillation and/or sinus rhythm. Some physicians consider DC cardioversion the preferable initial treatment of atrial flutter. In the final analysis, the mode of treatment will be dictated by the total clinical picture. If cardioversion is not available or is contraindicated and the patient fails to respond to digitalis, conversion to sinus rhythm with quinidine and procainamide may be attempted. Occasionally these drugs will enhance the degree of AV block. Very rarely, when drugs fail and cardioversion is contraindicated, as, for example, in digitalis intoxication, rapid atrial pacing may terFig 1 2 . - E f f e c t of quinidine on the ventricular rate of atrial flutter and the importance of digitalis. After administration of 1.4 gm (2/4) 2:1 atrial flutter (2/1) was converted to a 1:1 flutter with prompt hemodynamic deteriorations. Up to thattime, the patient received a total of 1.3 mg digitoxin. Because of the 1:1 response following administration of quinidine, digoxin 7.5 mg and 3.2 mg of digitoxin were administered over the next 15 days followed by 3.5 mg of quinidine on 2/19. Despite a significant slowing of the atrial rate due to quinidine, a 2:1 AV conduction was maintained. , t . t ]__._1 t :1 : ....... i:t

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minate the flutter. Quinidine frequently will increase the ventricular rate by inhibiting the depressing vagal effect on AV conduction or by slowing the rate of the atrial flutter. The combination of the above mechanisms may result in a 1:1 AV conduction with extremely rapid ventricular rates and rapid deterioration of cardiac function. Occasionally, the rate becomes more rapid because of conversion to atrial fibrillation. Thus, quinidine should not be administered to patients with atrial flutter unless the patient is properly digitalized first (Fig. 12). Persistent or chronic recurrent atrial flutter is uncommon and, when present, may be quite difficult to manage. The therapy, in many respects, is similar to that of PAT. ATRIAL FIBRILLATION.-- Chronic atrial fibrillation is very common and usually is a manifestation of organic heart disease, but occasionally it may occur in the absence of demonstrable heart disease. As a transient event, atrial fibrillation may complicate, for example, pulmonary embolism, infection, fever, thyrotoxicosis, acute alcoholism and may follow thoracotomy or be present in otherwise normal individuals. In the untreated patient, the ventricular rate varies from about 90 to 190, is grossly irregular and one finds the characteristic pulse deficit, changing intensity of heart sounds and of pulse (see Fig. 8). On rare occasions, especially in the presence of W-P-W, the ventricular response may approach or even exceed 200 per minute (Fig. 13). Similarly, in individuals with diseased AV junctional tissue, the rates may be as slow as 40 or 50 per minute. Atrial fibrillation is seen most often as a complication of rheumatic valvular disease, thyrotoxicosis, cardiomyopathy or hypertensive heart disease. Occasionally it may complicate pericarditis. Atrial fibrillation may cause palpitations, impair myocardial function and predispose to pulmonary or systemic embolization, particularly in patients with valvular heart disease. The goal of therapy of atrial fibrillation is to slow the ventricular rate, and digitalis is the treatment of choice. The mechanism of slowing the ventricular rate is both vagal and extravagal. It is important to differentiate between these two modes of action, for, if the patient's ventricular rate slows due to the vagal action, minimal exertion such as imposed by ordinary daily activities will overcome this effect, a rapid ventricular rate will result and the patient may become symptomatic (see Fig. 10). However, when the ventricular slowing is due to the extravagal effect of digitalis on AV conduction, the response of the ventricular rate to exertion remains relatively fiat. The ideal end point of therapy is a ventricular rate between 70 and 80 with a fiat response when the vagal action is inhibited. Conversion of atrial fibrillation to sinus rhythm is not difficult and is successful in more than 90% of the attempts. However, 37

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Fig 13.-Extremely rapid ventricular response to atrial fibrillation in the presence of W-P-W. Type A W-P-W during sinus rhythm is shown at the right. Atrial fibrillation with a ventricular rate of about 180 during normal AV junctional conduction (QRS of normal duration) and a ventricular rate of about 285 with conduction via bundle of Kent (bizarre QRS) are shown in the left panel.

the sinus rhythm, once established, is difficult to maintain and tends to revert to atrial fibrillation. For this reason, conversion to sinus r h y t h m should be considered only in selected cases. This group includes patients with an a r r h y t h m i a of recent onset, arbitrarily defined as an atrial fibrillation of less ~han 6 months' duration, patients in whom the cause of the arrhythmia, such as, for example, thyrotoxicosis or mitral valve disease, has been corrected. In patients with severe heart failure in whom the ventricular rate does not respond to drugs or if the atrial contribution to the cardiac output theoretically may prove beneficial, cardioversion may be considered also. In about 15% of patients, atrial fibrillation will not respond to digitalis as expected and this group is important to identify. It includes patients with thyrotoxicosis, infection, fever of any etiology, pulmonary embolization, severe heart failure, marked anemia and other high-output states or recent chest or heart surgery. In such instances, the pursuit of an "acceptable" ventricular rate often will result in digitalis intoxication (Fig. 14). Normalization of the ventricular r h y t h m in the course of digitalis administration usually signals digitalis overdosage or poisoning. When the rate is slow and regular, a high degree of AV 38

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block is p r e s e n t (see Fig. 7); w h e n the v e n t r i c u l a r r a t e is rapid and r e g u l a r , VT or more likely N P J T is p r e s e n t (see Fig. 14). In e i t h e r event, digitalis should be discontinued. A p p e a r a n c e of sinus r h y t h m is u n u s u a l in p a t i e n t s w i t h chronic a t r i a l fibrillation. In p a t i e n t s in w h o m digitalis fails to slow the v e n t r i c u l a r rate, a combination of digitalis and propranolol or r e s e r p i n e m a y prove successful. This combination m a y be p a r t i c u l a r l y useful in thyrotoxicosis. Elective conversion to sinus r h y t h m can be accomplished with drugs such as quinidine or p r o c a i n a m i d e or DC cardioversion. The l a t t e r is the preferable approach. Occasionally, p r e c i p i t a t i n g factors such as exertion, caffeine or alcohol can be identified as the cause of r e c u r r e n t a t r i a l fibrillation in otherwise h e a l t h y individuals. Most often, however, t h e etiology r e m a i n s obscure. The t r e a t m e n t of such an a r r h y t h m i a can be most discouraging. The a t r i a l fibrillation is difficult to prevent, and w h e n it does appear, the v e n t r i c u l a r r a t e frequently is rapid despite chronic a d m i n i s t r a t i o n of drugs. W h a t m a k e s this problem so disconcerting is not the pathophysiologic effects of the a r r h y t h m i a but the severity of symptoms. 39

ROBERT A. O'ROURKE: Multifocal atrial tachycardia often is confused with atrial fibrillation. This rhythm, common in patients with severe obstructive pulmonary disease, is characterized by an irregular rhythm with a heart rate > 100 beats/rain, P waves with three or more configurations and isoelectric periods between P waves. In general, this rhythm responds poorly to treatment with any of the commonly used antiarrhythmic therapy. NONPAROXYSMAL JUNCTIONAL TACHYCARDIA (NPJT).- Recognition of NPJT is most important. This rhythm originates in the

AV nodal junction. Its ventricular rate varies from about 70 to 140 per minute and is regular. It may be irregular when associated with varying degrees of exit block from the site of impulse formation. NPJT differs from PAT in that its etiology usually is clear, the arrhythmia is transient, its appearance or disappearance often gradual. The most common cause of NPJT is digitalis excess (see Fig. 14), acute myocardial infarction, open heart surgery and occasionally acute myocarditis. In about 85% of the cases, the atria have an independent rhythm. The therapy of NPJT depends on the underlying etiology, potential hemodynamic consequences and presence or absence of other arrhythmias. When due to digitalis poisoning and definitive treatment is indicated, the drug of choice is potassium or lidocaine. Occasionally, propranolol or diphenylhydantoin may be tried. Recognition of the NPJT often is more important than its treatment, for continued administration of the glycoside because of failure to recognize NPJT may result in ventricular fibrillation. WOLFF-PARKINSON-WHITE SYNDROME (W-P-W).- Tachycardias complicating the pre-excitation syndrome (W-P-W) are of special concern because they often fail to respond to the usual therapy in a predictable manner, may compromise myocardial function and, at times, result in incapacitating symptoms. The W-P-W syndrome is an ECG diagnosis and is recognized by a short P - R interval, slur on the upstroke of the QRS, the so-called delta wave, prolongation of the QRS and secondary S T - T changes. The anomalous atrioventricular bypass (bundle of Kent), which accounts for the short P - R interval, is also available for circuitous impulse transmission between the atria and ventricles and thus predisposes to re-entrant tachycardia, seen frequently in patients with W-P-W. Equally important is the fact that when atrial fibrillation or flutter complicates W-P-W and the impulse conducts along the anomalous pathway, the ventricular response may be extremely rapid (see Fig. 13). The treatment of W-P-W syndrome is, in essence, the treatment of the complicating arrhythmias. PAT with a narrow QRS indicates that the impulse traverses the AV junction in a nor40

mal direction and re-enters the atrium through the bundle of Kent. In such cases, the accepted therapy is digitalis alone or with quinidine and propranolol if needed. When the PAT is characterized by a widened QRS complex, indicating antegrade conduction through the bundle of Kent, and since it cannot be assumed that the AV junction comprises an arm of the re-entrant path, digitalis together with quinidine or procainamide or propranolol should be administered. Cardioversion has been used with success for the termination of PAT complicating W-P-W. When W-P-W is accompanied by atrial flutter or fibrillation, digitalis along with quinidine or procainamide is indicated. Because of the complexity of AV conduction in W-P-W, with the ever-present possibility of more than one functioning bypass, the potential for re-entry within the AV junction without involvement of the bypass and the possibility of conversion of PAT to atrial fibrillation or flutter, it is reasonable and probably best to use both digitalis and quinidine or procainamide in all supraventricular arrhythmias complicating W-P-W. VENTRICULAR PREMATURE COMPLEXES

(VPC).-VPC originate

in the intraventricular specialized conduction system and activate the ventricles in an anomalous manner, giving rise to bizarre QRS complexes. The VPC can be unifocal, in which case the morphology is uniform and coupling to the preceding sinus impulse is fixed. If the coupling is short and VPC falls on the T wave, the so-called R on T phenomenon is recorded. VPC may be multifocal, in which case the morphology as well as the coupling varies. The VPC may manifest as two VPC in a row, or a socalled doublet. Often, VPC are benign and require no therapy. When VPC are a manifestation of a chronic myocardial disorder such as valvular heart disease, myopathy or hypertension, definitive, suppressive therapy may not be indicated. VPC may be a manifestation of disordered electrolyte or metabolic state or due to acidosis or hypoxia. In such situations, correction of the underlying disturbance may control the VPC. Similarly, when VPC are due to heart failure, management of the latter may eliminate VPC. In two specific clinical conditions, namely, acute myocardial infarction 27 and digitalis poisoning (see Fig. 14), the VPC may be precursors of more severe arrhythmias and prompt suppression is indicated. TM 27 When due to digitalis poisoning, the drug of choice is potassium, although lidocaine is effective also. Diphenylhydantoin and propranolol may prove useful. Quinidine or procainamide should be avoided if possible and cardioversion used as a procedure of last resort. In acute myocardial infarction, lidocaine will control the VPC in about 80-85% of the patients. If lidocaine fails, quinidine and procainamide are used. 27 41

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tive and have a low incidence of side-effects. Such drugs are essential for long-term administration. 28 The two drugs currently available are quinidine and procainamide. Neither is highly effective and both have frequent side-effects, which makes longterm suppressive therapy of VPC a most unsatisfactory situation. Drugs potentially effective or currently under study include propranolol, diphenylhydantoin, aprindine, disopyramide and amiodarone. In view of the foregoing, the answer to the question of whether or not long-term suppression of VPC in any one patient is indicated and feasible remains a matter of individual decision based on one's view of the ultimate efficacy of such therapy. VENTRICULAR T A C H Y C A R D I A ( V T ) . - VT is a serious disorder of function, often a manifestation of severe underlying organic heart disease or severely disordered metabolic environment. The mortality of untreated VT is high and may be due to depression of myocardial function or to ventricular fibrillation, or both.,2, 24, 27 The most common cause of VT is ischemic heart disease and especially acute myocardial infarction. About 85% of all instances of VT are said to be due to ischemic heart disease. Digitalis intoxication, cardiomyopathy, disturbances of electrolytes and acid-base balance and hypoxia may also result in VT. Rarely, VT is seen in otherwise "normal" individuals. Whenever assumption is made that VT is present in an otherwise normal individual, and because of the serious implications of such a 43

diagnosis, the diagnosis of VT should be confirmed with HBE. The exact electrophysiologic mechanism responsible for VT usually is obscure. Whether the VT is due to automaticity or re-entry cannot be determined from the ECG. Furthermore, at this time, electrophysiologic differentiation is neither essential nor important because our knowledge of the action of drugs is not as yet at a stage that permits selection of drugs on the basis of their antiautomatic or anti-re-entrant action. The ECG clues that VT may appear include, not necessarily in order of importance, VPC with the R on T phenomenon, frequent VPC, VPC in runs, multifocal VPC and occasionally prolongation of QT interval. As already suggested, ECG diagnosis of VT is difficult and, in fact, the purist may say, and rightly so, that short of atrial pacing or HBE is impossible. However, correlation of the clinical, bedside findings with the ECG more often than not makes a working diagnosis of VT possible and allows one to proceed with appropriate treatment. Furthermore, from the practical point of view, when in doubt, the problem can be resolved by assuming that the arrhythmia is VT. A history of heart disease, especially a recent myocardial infarction, digitalis intoxication or severe electrolyte or metabolic disturbance usually can be elicited and this often is associated with significant functional myocardial impairment. The heart rate generally is in the range of 150-180, although rates much faster than 180 and slower than 150 can be recorded and vary slightly. Other physical findings in VT are those of AV dissociation and increased number of heart sounds (see p. 17). Thus, history and physical findings coupled with wide QRS make a diagnosis of VT most likely. Rarely, the VT conducts to the atrium at a 1:1 ratio and the physical findings of AV dissociation are absent (see Fig. 5). Specific diagnostic ECG criteria of VT include ventricular captures or fusions (Fig. 17) and QRS complexes with normal intraventricular conduction at cycles shorter than the arrhythmia in question. These pathognomonic ECG signs of VT are seen rarely and, from the practical point of view, the diagnosis has to be suspected on the basis of a rapid rate, wide QRS and independent atrial rhythms. However, these cannot always be differentiated from AV junctional tachycardia with aberrancy and an independent atrial rhythm. Likewise, VT with 1:1 retrograde conduction can be mistaken for junctional tachycardia with aberrancy and retrograde P waves (see Fig. 5). It is clear from the foregoing that in a number of patients a definitive diagnosis of VT may be impossible from the ECG, and a correlation of the bedside findings and the ECG is imperative. The therapy of VT may be aimed at (1) termination of an 44

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acute life-threatening episode or (2) long-term suppression and prevention of recurrent VT. The therapeutic approach to VT is direct and prompt, and the success rate of termination of life-threatening acute episodes of VT is high. Frequently the urgency of the situation precludes spending much time on analysis of the ECG or in search for the etiology of the underlying heart disease or for the immediate precipitating cause. Usually a bolus of lidocaine is administered and, if the patient fails to respond, one may, depending on the urgency of the situation, repeat the lidocaine bolus or proceed directly with DC cardioversion. The vast majority of patients will respond to low-energy shock. In one series of 42 attempts, 41 (98%) of the episodes were terminated with energies of 10 WS or less. 24 The patient whose VT recurs following successful initial cardioversion can be treated with infusion of lidocaine, quinidine, procainamide, diphenylhydantoin or potassium. VT that is not immediately life-threatening or recurs after successful control of the initial episode calls for a careful evaluation of the underlying etiology and precipitating factors. For example, if VT appears concomitantly with heart failure and is thought to be related to the heart failure, one may consider correction of the failure in hopes of controlling the VT. Similarly, if the VT is due to digitali§~ intoxication, hypokalemia or hypoxia, correction of the underlying cause should be part of the treatment. Successful prevention of recurrent VT i n the ambulatory patient presents the same problems that were discussed in connection with the management of PVC (see Figs. 15 and 16). A patient with VT may have to be subjected to a number of different drug regimens; if all fail, the patient is considered "refractory. T M 45

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Fig 1 8 . - A c u t e m y o c a r d i a l i n f a r c t i o n c o m p l i c a t e d by atrial flutter and refract o r y VT. T h e latter is c o n t r o l l e d w i t h o v e r d r i v e s u p p r e s s i o n (rows 3 and 4).

When pharmacologic attempts at controlling recurrent VT prove to be unsuccessful and the patient is considered refractory, overdrive pacing can be tried (Fig. 18). Although the overdrive rate need not exceed the rate of the VT, very often, in order to suppress VT, the pacing rate has to exceed 100. The pacemaker tachycardias may contribute to hemodynamic complications, especially in patients with acute myocardial infarction. Pacing is most useful as a temporizing measure. The reported success rate of long-term suppression with overdrive pacing varies from study to study. The data presently available regarding the role of pacing in long-term therapy of VT should be considered incomplete.24, 25 It is hoped that as data accumulate it might prove possible to identify a subset of patients with refractory VT in whom success with long-term suppression with cardiac pacing might be expected. Preliminary reports suggest that, in selected cases, control of refractory arrhythmia might be achieved with surgery. 26The results to date vary and it seems too early to predict the ultimate role of surgery in treatment of refractory ventricular arrhythmias. VENTRICULAR FLUTTER AND FIBRILLATION.-- The ECG of ventricular flutter shows undulating waves without identifiable QRS or T waves. The rate of ventricular flutter varies from 180 to 260 per minute. The ECG of ventricular fibrillation reflects total electrical disorganization with waves that are grossly irregular and of varying amplitude and configuration. Both arrhythmias result in prompt and profound cardiovascular collapse. The only therapy is prompt electric defibrillation and resuscitation. 46

ACCELERATED IDIOVENTRICULAR RHYTHM.-- This arrhythmia originates in the ventricular specialized tissue and differs in many respects from the ordinary form of VT. Its rate varies from 50 to 110. It is seen with digitalis intoxication, but most often is due to acute myocardial infarction. The incidence of this arrhythmia in acute myocardial infarction is as high as 35%. The rhythm is intermittent, lasting from a few seconds to a minute, rarely longer. 3° It is a benign disorder and suppressive therapy rarely, if ever, is indicated. Isolated instances of deterioration to ventricular fibrillation have been documented. m,* ROBERTA. O'ROURI4E:This arrhythmia occurs most frequently in patients with acute inferior wall myocardial infarction. As mentioned above, usually no treatment is required. However, if the loss of atrial contraction is associated with hypotension, intravenous atropine usually is followed by the restoration of sinus rhythm. PARASYSTOLE.- Ventricular parasystole is clinically important because it usually denotes the presence of heart disease and should be differentiated from unifocal and accurately coupled VPC, which may be recorded without demonstrable heart disease. Parasystole requires no therapy. In contrast to ventricular parasystole, parasystole originating in the AV junction or atrium may be seen in the absence of heart disease. Ventricular parasystole is an ECG diagnosis (see Fig. 11). Two, rarely more, independent pacemakers compete for control of the ventricles. The competition usually is between the parasystolic focus and the sinus rhythm. Parasystole is characterized by changing coupling, a fixed interectopic interval or a manifest multiple of this interval and the presence of QRS fusions. Finally, whenever the parasystolic impulse fails to propagate when expected, the failure is due to physiologic refractoriness of the ventricles. Exceptions to the latter include exit block from the parasystolic focus and intermittent parasystole, both relatively rare phenomena. The parasystolic rhythm is perpetuated because the competing impulse, for reasons not quite clear, fails to "invade" and interrupt the parasystolic rhythm.

BRADYCARDIAS SAN DISEASE. - S i n u s b r a d y c a r d i a . - Sinus bradycardia defined as SAN rhythm with a rate of 60 per minute or less.

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S i n u s arrest. - S i n u s arrest, or pause, indicates the failure of the SAN to generate an impulse and absence of atrial activity for varying periods of time. If the sinus arrest is sufficiently long, the subsidiary junctional or ventricular pacemaker will escape (see below). 47

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Sinoatrial b l o c k . - S i n o a t r i a l (SA) block is manifested by failure of normally generated sinus impulses to reach and excite the atrium. Since the activity of SAN is uninterrupted, the atrial pauses (P to P) are, as a rule, a multiple of the basic SAN rhythm. Occasionally, however, the SA exit block assumes the Wenckebach structure and then the diagnosis of SA block may prove difficult. Tachycardia-bradycardia syndrome. - This disorder is characterized by alternation of rapid AV junctional or atrial arrhythmias, such as fibrillation, PAT or flutter with periods of bradycardia or atrial standstill (Fig. 19).

SICK SINUS SYNDROME (SSS) All of the above disorders of the SA nodal function, with the exception of the tachycardia-bradycardia syndrome, occasionally can be an expression of vagotonia in otherwise normal individuals. They may be due to a variety of drugs, such as digitalis, potassium, quinidine, propranolol or occasionally lithium, or may complicate acute myocardial infarction, especially inferior. Such arrhythmias usually are transient. More persistent disorders of the SAN are seen with primary disease of the SAN due to, for example, ischemia, myopathies, collagen disease or, rarely, amyloidosis. The disorders of SAN function, when chronic or recurrent and symptomatic, have been grouped as the SSS syn48

drome. SSS is most common in the elderly, and the clinical manifestations are those of diminished blood supply to the b r a i n (see p. 17). When SSS is suspected but the association with symptoms is not clear, monitoring either in the hospital or as an outpatient often will help to define the relationship of symptoms to the function of SAN. Provocative testing, namely, overdrive suppression of SA node by rapid atrial pacing, can be used. As a rough guide, a SAN pause of 1200-1400 msec after cessation of atrial pacing suggests SAN dysfunction. On occasion, overdrive will fail to suppress the SAN even in the presence of SAN disease. Thus, a false negative response can be obtained with atrial pacing. When pacing is not immediately available, the SSS can be treated with atropine or isoproterenol. However, once the diagnosis of symptomatic SSS is made, permanent pacing is the procedure of choice. The SSS often is complicated by abnormal AV conduction and intermittent rapid atrial arrhythmias. Consequently, ventricular pacing is preferable to atrial pacing. Often, recurrent episodes of tachycardia of the SSS can be treated with drugs only with concomitant pacing, because the drugs used to control the tachycardias often further suppress the SAN automaticity, SA and AV conduction. The prognosis of SSS is not known, but mortality and morbidity are sufficiently great to warrant therapy with pacing, once the diagnosis is established.

ATRIOVENTRICULAR (AV) BLOCK Conventional classification of AV block includes simple prolongation of AV conduction (first degree AV block), failure of some atrial impulses to reach the ventricles (second degree AV block), which can be either Wenckebach (Type I) or Mobitz (Type II), and, finally, failure of all atrial impulses to reach the ventricles, third degree or complete AV block (see Fig. 7). Once a diagnosis of AV block is made, it is equally important to establish, whenever possible, whether the block is supra or infra His. ~ The site of the block frequently determines the prognosis and mode of therapy. DISORDERS OF ATRIOVENTRICULAR CONDUCTION FIRST DEGREE ATRIOVENTRICULAR BLOCK.--A P - R interval exceeding 0.22 second defines first degree A V block. In the vast majority of cases, the conduction delay occurs in the A V node. First degree block is not always indicative of heart disease. Various degrees of block are c o m m o n in young, healthy individuals as the result of strong vagal influences, and such A V block can be decreased or abolished with atropine, isoproterenol or 49

with exercise. The AV block commonly seen in the early stages of the inferior myocardial infarction often is the result of vagal reflexes. Delayed AV conduction frequently is due to digitalis. SECOND DEGREE ATRIOVENTRICULAR B L O C K . - When some atrial impulses fail to reach the ventricles, second degree AV conduction block is present. The frequency with which atrial impulses fail to conduct may vary from failure of each alternate impulse to an only occasional failure to reach the ventricles. By far the most common form of second degree AV block is the Wenckebach or Type I AV block. It is manifested by a progressive prolongation of the P - R interval, until the sequence is interrupted by complete failure of the P wave to conduct to the ventricles. The first conducted P wave after the pause may demonstrate a normal P - R interval. Usually, the maximal increment in the P - R interval is seen following the second conducted P of the cycle and, although each of the subsequent P - R intervals is longer than the preceding one, the increment in the P - R is progressively smaller. Because of this, a characteristic pattern develops, with the first R - R interval following the pause being the longest and each successive R - R slightly shorter. The sequence of conducted P waves with increased P - R intervals, gradually foreshortening R - R cycles terminated by a pause that is shorter than two SAN cycles, is known as Wenckebach periodicity (see Fig. 7). Often, however, this periodicity is not recorded and the Wenckebach block is referred to as atypical. In ~atypical" Wenckebach block, the last conducted P waves are followed by greater increments in the P - R . Consequently, the last R - R before the pause is not the shortest R - R of the cycle and the characteristic Wenckebach periodicity is absent. From the clinical standpoint, differentiation between these two forms of Wenckebach block is not important. A much rarer type of second degree AV block is the Mobitz or Type II AV block. In this type of AV block, the P - R intervals of the conducted atrial impulses may be normal or prolonged but remain constant from beat to beat and failure of P wave conduction is sudden and unexpected (see Fig. 7). Whereas the Wenckebach Type I AV block is the result of conduction abnormalities in the AV node (supra His), Mobitz Type II AV block represents an intermittent intraventricular (infra His) block. The QRS complexes demonstrate either RBBB or LBBB or a combination of RBBB with extreme left axis deviation due to left anterior fascicular block. 19 Mobitz Type II second degree AV block commonly is associated with Stokes-Adams attacks, due to recurrent periods of complete heart block. Second degree AV block frequently is manifested by a 2:1 AV response and the differentiation between Wenckebach Type I 50

and Mobitz Type II AV block cannot be made, especially when the QRS is prolonged. However, it is safe to assume that the vast majority of 2:1 AV blocks are of the Wenckebach type. Rarely, a young, healthy individual with excessive vagal tone will demonstrate brief periods of second degree AV block. Wenckebach Type I AV block complicating an acute inferior wall myocardial infarction usually is a transient phenomenon and its presence is not necessarily an indication for transvenous pacing. If treatment of the AV block is indicated and provided that there are no clinical contraindications, such as myocardial ischemia or infarction, atropine or isoproterenol can be tried. If this approach fails, transvenous demand pacing can be instituted. The appearance of a Mobitz Type II AV block in the course of an acute myocardial infarction, usually anterior in location, is an indication for pacing. This form of block does not respond to drugs and it is associated with a high incidence of complete AV block and carries a serious prognosis. In contrast to Wenckebach Type I AV block, Mobitz Type II block rarely, if ever, is a manifestation of digitalis excess. COMPLETE (THIRD DEGREE) ATRIOVENTRICULAR BLOCK. -- C o m -

plete AV block is characterized by failure of all SAN impulses to conduct to the ventricles. If the block is infra His, the QRS is ventricular in origin, the rate usually is below 40 per minute and focus frequently is unstable, with a varying morphology of the QRS complexes (see Fig. 7). If the AV block is supra His, it may be either transient or permanent. The most common causes of the transient form of AV block are digitalis, myocardial ischemia or inferior myocardial infarction. Complete AV block complicating inferior infarction, which often is due to vagal effect, occasionally will respond to atropine, and spontaneous remission usually occurs within 2 4 - 7 2 hours. Less frequently, complete AV block associated with acute inferior infarction is the result of extensive infarction of the AV node or the lower portion of the bundle branch system. In such cases, the block may be permanent and require pacing. Complete AV block is less common with anterior myocardial infarction but, when present, it usually is due to extensive myocardial destruction involving the bundles and their divisions, and the prognosis is grave. These patients should be treated with pacing. At times, the complete AV block complicating anterior myocardial infarction is preceded by a Mobitz Type II AV block or by BBB fascicular block, or both, most often RBBB and LAD block. The appearance of such conduction defects should alert one to the fact that pacing may be necessary (Fig. 20). The first manifestation of AV conduction disease may be an Adams-Stokes attack. Less commonly, congestive heart failure 51

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Fig 20.-Acute anterior myocardial infarction is complicated by RBBB and LAD block (day 1) and RBBB and LPD block (day 2). Complete AV block followed (row 3) and this was treated with a transvenous pacemaker (row 4). On day 4, the intraventricular conduction normalized, but the patient died because of severe myocardial damage.

or other manifestations of heart disease predominate. The pathology underlying complete AV block usually is one of diffuse fibrosis or scarring of the conduction system. At times, diffuse occlusive coronary artery disease is present, but more often coronary artery disease is minimal or moderate. Less common causes of complete AV block include cardiomyopathies, myocarditis, calcific mitral or aortic valvular disease and, rarely, collagen disease. Complete chronic AV block may be interrupted by periods of second degree AV block or even normal AV conduction. However, once the patient experiences symptoms due to AV block, pacing is indicated. If this is not readily available, the patient can be treated with an infusion of isoproterenol or Adrenalin in an attempt to maintain the rate of the idioventricular pacemaker between 30 and 40 beats per minute until pacing can 52

be introduced. Patients with Adams-Stokes disease, if untreated, have a 50% mortality rate within the first 6 - 1 2 months. Complete AV block may be congenital in origin. In this form, the dominant pacemaker usually is supra His and the QRS normal. The rate of the pacemaker is faster than that seen with acquired complete heart block, usually between 50 and 70 per minute. The pacemaker tends to show significant increments in rate with exercise, in contrast to acquired complete AV block, in which the heart rate remains fixed. The chronic RBBB and LAD block presents as a special problem. Although the incidence of this syndrome preceding complete AV block is high and its progression to complete AV block when the conduction defects are due to an acute process is equally high, the chronic form of BBB and fascicular block rarely is followed by complete AV block. Consequently, prophylactic pacing of patients with RBBB and LAD block for prevention of Adams-Stokes disease, of AV b l o c k d u r i n g surgery or of block following administration of drugs is not indicated. Even if the patient presents with BBB and fascicular block and syncope, assumption of cause and effect between the block and the symptoms may not be warranted. Of 186 patients with BBB and fascicular block, 30 had syncope, but in only 6 was AV block shown to be the cause of the syncope. Recurrent syncope showed the highest correlation with AV block. Determination of the H - Q interval with HBE did not prove helpful in separating patients with syncope due to AV block from those with syncope due to other causes. 23

ATRIOVENTRICULAR DISSOCIATION Recognition of this syndrome, which may or may not be due to complete AV block, is clinically important. Mistaken diagnosis of AV block as the cause of AV dissociation, when the dissociation is due to physiologic refractoriness (interference), is not uncommon. This is especially true in acute myocardial infarction, particularly inferior, and may result in unnecessary pacing. Failure to differentiate between AV dissociation due to AV block from that due to functional refractoriness is also responsible for a wide discrepancy in the reported incidence of third degree AV block and prognosis of complete AV block in acute infarction. Accurate diagnosis of the mechanism of AV dissociation is important in proper assessment of prognosis and treatment. In AV dissociation, the ventricles are activated by a lower, junctional or, less frequently, ventricular focus, while the atrial activity remains under the control of an atrial pacemaker, most often the SAN. The dissociation may be due to a physiologic in53

terference (physiologic refractoriness) between two pacemakers, without any evidence of AV block (see Fig. 6), or it may be due to pathologic AV block (see Fig. 7) or both. With AV dissociation due to refractoriness, the rate of the SAN and of the lower pacemaker may differ only slightly. The dissociation occurs because the lower focus maintains the AV conduction tissue in a state of refractoriness, thus interfering with antegrade activation of the ventricles by the SAN impulse. The QRS rhythm is regular, with P waves preceding, following or falling within the QRS. The P waves may "march" through the QRS until it falls outside the refractory period of the AV junction and is conducted to the ventricles (ventricular capture). Following such a capture, the faster j u n c t i o n a l p a c e m a k e r may resume control of the ventricles and the cycle is repeated. The mechanisms initiating AV dissociation due to refractoriness (interference) include either (1) an excessive slowing of the SAN with escape of a lower pacemaker (see Fig. 6, A) or (2) acceleration of the rate of discharge of a lower pacemaker (see Fig. 6, B). AV block is not a necessary ingredient for sustained AV dissociation, although both interference and block may coexist. AV dissociation due to physiologic refractoriness (interference) may be seen in otherwise normal individuals due to SAN slowing. Under these circumstances, it causes no symptoms and requires no treatment. AV dissociation secondary to excessive SAN slowing may also be caused by digitalis, myocardial ischemia or infarction. AV dissociation secondary to acceleration of a lower, usually AV nodal, pacemaker nearly always is a sign of pathologic function. Most often it is due to digitalis toxicity and less commonly due to acute myocardial infarction, carditis or open heart surgery. EscnPE.-Isolated escape or a sequence of three or more escape complexes (escape r h y t h m ) c o m e s into play whenever the dominant, usually SAN, rhythm is depressed. The escape is a physiologic protective mechanism against cardiac arrest. It can originate in the atrium, AV junction or ventricle, the most common site being the AV junction. The physiologic rate of the AV junctional pacemaker varies from about 40 to 50 per minute. Normally, the impulse generated by the SAN reaches the AV junctional site and suppresses the latter. However, if a SAN impulse fails to discharge and reset the AV junctional pacemaker, the latter will escape and will assume control of the ventricles for one or more cycles. Isolated AV junctional escape may occur in normal individuals with sinus bradycardia or marked sinus arrhythmia or the AV junctional escape may follow SAN arrest, SA block and AV block. In the presence of coronary artery disease, acute rheumatic carditis, digitalis excess or following open heart surgery, AV 54

junctional pacemakers may exhibit an abnormal acceleration of the rate of diastolic depolarization. Under these circumstances, the AV junctional escape complexes may appear unexpectedly early. Accelerated escapes are an indication of abnormal function and probably are a variant of NPJT. 31 AV junctional escape complexes and AV junctional escape rhythms require no specific therapy. The t r e a t m e n t should be directed to the underlying arrhythmia, which allows for the escape.

COMMENTS Clinically significant arrhythmias, their genesis, diagnosis, complications and therapy were reviewed in light of our current knowledge. This was done with the full realization that there may be a difference of opinion about some of the concepts expressed; however, this review reflects, in large measure, my personal experience. Post-World War II technology contributed significantly to our understanding of the cellular and subcellular mechanisms of arrhythmias and His bundle electrocardiography applied to the h u m a n confirmed the old concepts and brought to our attention some new, previously not recognized mechanisms. Although progress in pharmacotherapy over the past 30 years has been rather disappointing, the development of monitoring and the advent of pacing, cardioversion and defibrillation have enhanced significantly our ability to manage arrhythmias. Significant gaps exist in our knowledge of arrhythmias. These include, from time to time, inability to make a definitive diagnosis, lack of data base regarding n a t u r a l course and prognosis and unavailability of effective drugs with acceptable side-effects, all of which sometimes make therapeutic decisions most difficult. As a result, until the necessary data become available, decision to treat an a r r h y t h m i a is an individual one, based on the physician's perception of the potential threat of the a r r h y t h m i a and his acceptance of effectiveness and the benefit-to-risk ratio of currently available drugs. REFERENCES 1. Bellet, S.: Clinical Disorders of the Heart Beat (Philadelphia: Lea & Febiger, 1971). 2. Scherf, D., and Schott, A.: Extrasystoles and Allied Arrhythmias (2d ed.; Chicago: Year Book Medical Publishers, Inc., 1973). 3. Surawicz, B.: The input of cellular electrophysiology into the practice of clinical electrocardiography, Mod. Concepts Cardiovasc. Dis. 44:41, 1975. 4. Cranefield, P. F., Wit, A. L., and Hoffman, B. F.: Genesis of cardiac arrhythmias, Circulation 47:190, 1973. 5. Fisch, C.: Electrophysiologicalbasis of clinical arrhythmias, Heart and Lung 3:51, 1974. 55

6. Katz, L. N., and Pick, A.: Clinical Electrocardiography: The A r r h y t h m i a s (Philadelphia: Lea & Febiger, 1956). 7. Titus, J. L.: Anatomy of the conduction system, Circulation 47:170, 1973. 8. Fisch, C., and Zipes, D. P.: His bundle electrocardiography (editorial), Am. Heart J. 86:289, 1973. 9. Massumi, R. A., Mason, D. T., Fabregas, R. A., et al.: Intraventricular aberrancy versus ventricular ectopy, Cardiovasc. Clin. 5:35, 1973. 10. Fisch, C., and Knoebel, S. B.: Junctional rhythms, Prog. Cardiovasc. Dis. 13: 141, 1970. 11. Rosenbaum, M. E., Elizari, M. V., Lazarri, J. O., et al.: The Clinical Causes and Mechanisms of Intraventricular Conduction Disturbances, in Schlandt, R. C., and Hurst, J. W. (eds.), Advances in Electrocardiography (New York: Grune & Stratton, 1972), p. 145. 12. Fisch, C., and Noble, R. J.: Ventricular tachycardia (editorial), Am. Heart J. 89:551, 1975. 13. Noble, R. J.: An approach to supraventricular tachycardias, Heart and Lung 3:65, 1974. 14. Samet, P.: Hemodynamic sequelae of cardiac arrhythmias, Circulation 47: 399, 1973. 15. Rotman, M., Wagner, S. G., and Wallace, A. G.: Bradyarrhythmias in acute myocardial infarction, Circulation 45:703, 1972. 16. Fisch, C.: Relation of electrolyte disturbances to cardiac arrhythmias, Circulation 47:408, 1973. 17. Fasola, A. F., Zipes, D. P., and Noble, R. J.: Treatment of drug refractory arrhythmias with aprindine (abstract), Circulation 51 & 52(Supp. II):75, 1975. 18. Nichols, A. B., and Willis, P. W., III: Efficacy of oral disopyramide phosphate for long term treatment of ventricular arrhythmias (abstract), Am. J. Cardiol. 37:159, 1976. 19. Rosenbaum, M. D., Chiale, P. A., Halpern, S. M., et al.: Clinical efficacy of amiodarone as an antiarrhythmia agent, Am. J. Cardiol. 38:934, 1976. 20. Knoebel, S. B., Lovelace, G. E., Rasmussen, S., et al.: Computer detection of premature ventricular complexes, Am. J. Cardiol. 38:440, 1976. 21. Fisch, C., Zipes, D. P., and Noble, R. J.: Digitalis Toxicity: Mechanism and ...... Recognition, in Yu, P. N., and Goodwin, J. F. (eds.), Progress in Cardiology (Philadelphia: Lea & Febiger, 1975), Vol. 4, p. 37. 22. Ferrer, M. I.: The sick sinus syndrome, Circulation 47:635, 1973. 23. Dhingra, R. C., Denes, P., Wu, D., et al.: Syncope in patients with chronic bifascicular block. Significance, causative mechanisms, and clinical implications, Ann. Intern, Med. 81:302, 1974. 24. Lown, B., Tempte, J. V., and Arter, W. J.: Ventricular tachyarrhythmias. Clinical aspects, Circulation 47:1364, 1973. 25, Johnson, R. A., Hutter, A. M., Desanctis, R. M., et al.: Chronic overdrive pacing in control of refractory ventricular arrhythmias, Ann. Intern. Med. 80:380, 1974. 26. Nitter-Hauge, S., and Storstein, O.: Surgical treatment of recurrent ventricular tachycardia, Br. Heart J. 35:1132, 1973. 27. Bigger, J. T., Jr., Dresdale, R. J., Heissenbuttel, R. H., et al.: Ventricular arrhythmias in ischemic heart disease: Mechanisms, prevalence, significance and management. Prog. Cardiovasc. Dis. 19:255, 1977. 28. Jelinek, M. V., Lohrbauer, L., and Lown, B.: Antiarrhythmic drug therapy for sporadic ventricular arrhythmias, Circulation 49:659, 1974. 29. Winkle, R. A., Alderman, E. L., Fitzgerald, J. W., et al.: Treatment of recurrent symptomatic ventricular tachycardia, Ann. Intern. Med. 85:1, 1976. 30. Lichstein, E., Ribas-Meneclier, C., and Gupta, P. K.: Incidence and description of accelerated ventricular rhythm complicating acute myocardial infarction, Am. J. Cardiol. 58:192, 1975. -

56

31. Knoebel, S. B., and Fisch, C.: Accelerated junctional escape: A clinical and electrocardiographic study, Circulation 50:151, 1974.

SELF-ASSESSMENT ANSWERS 1. e

2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18. 19.

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57