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Cardiac pacing and pacemakers I. Indications for pacing bradyarrhythmias
Appraisal and reappraisal of cardiac therapy Edited by Arthur C. DeGraff and Julian Frieden
Cardiac pacing and pacemakers I. Indications for pacing bradyarrhythmias Seymour Furman, M.D. Bronx, N. Y.
A wide variety of cardiac arrhythmias has become permanently controllable by electrical cardiac stimulation since Zoll's initial treatment 1 of complete heart block with an external transcutaneous pacemaker in 1952, later wired transthoracic pacing, 2 external transvenous, ~ and finally implantable transvenous ~ and transthoracic pacing2 Though our incomplete understanding of the nature of heart block 6 tended to raise the question of the fixed or intermittent n a t u r e of heart block, t h e development of non-competitive (demand, standy, ventricular inhibited and ventricular synchronous) pacemakers about 19657~ s resolved the problem by enabling the implant of devices which would be capable of allowing sinus r h y t h m to exist and to stimulate the heart whenever the cardiac rate fell below a predetermined interval between QRS complexes. By 1965 to 1967 the basis of modern cardiac pacing for bradyarrhythmias had been established. The three factors were: (1) the development of an implantable device, (2) the transvenous approach, and (3) the ability of the pacemaker to sense cardiac activity and respond to the cardiac chamber being stimulated. The future of pacing for cardiac arrhythmias other than heart block could have been foretold by the initial clinical description of transvenous pacing in which the patient with bradycardia, asystole and recurrent Adams-Stokes seizures did not have classic complete heart block but rheuFrom the Department of Surgery, Cardiothoracic Division, Montefiore Hospital and Medical Center, 111 East 210th St., Bronx, N. Y. 10467. Supported in Part by United States Public Health Service Grant No. HE-04666-16. Received for publication Nov. 29, 1976. Reprint requests to: Seymour Furman, M.D., Montefiore Hospital and Medical Center, 111 East 210th St., Bronx, N. Y. 10467.
April, 1977, Vol. 93, No. 4, pp. 523-530
matic heart disease, mitral valvular disease, and chronic atrial fibrillation with a markedly reduced ventricular rate2 The immediate cause of asystole was hypopotassemia, unrecognized in significance at that time but later found to be a profound causative agent for ventricular bradycardia and interruption of A-V conduction. From the preliminary treatment of heart block, a far wider group of arrhythmias has been treated. In 1975, at Montefiore Hospital and Medical Center, a total of 200 initial pacemaker implants were performed., Of these 36.5 per cent were for sinus node dysfunction with brady-tachy syndrome, sinus arrest, or sinus bradycardia. Eighteen per cent were for complete heart block and 35 per cent for intermittent or partial heart block, the balance for a variety of ventricular arrhythmias and reentry tachycardias, drug induced bradycardia, etc. Fixed complete heart block, the classic arrhythmia, accounted for less than 20 per cent of all arrhythmias (Table I). The patients are a diverse group, over half with arteriosclerotic heart disease, one-fifth with hypertension and one-tenth with diabetes mellitus. Rheumatic heart disease or an acute myocardial infarction as the immediate cause for the heart block accounted for another 10 per cent and 1 per cent of patients required pacing as a complication of cardiac surgery at the time of implant or at some later time, in at least one case two years later (Table II). Until about 1970 most physicians and surgeons would have considered carefully whether to implant a pacemaker in the absence of demonstrated Adams-Stokes seizures. Gradually a variety of minor neurologic lapses and prophylactic indications have become dominant. For purposes of clarity and utility in comprehending Adams-Stokes seizures they should be thought of,
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Table I. P a c e r i m p l a n t s (1975): R h y t h m distur-
bance Sinus node dysfunction Brady-tachy syndrome Sinus arrest Sinus bradycardia Atrial fibrillation with ventricular rate below 50 Complete heart block Acquired Congenital Intermittent heart block Wolff-Parkinson-White syndrome Other ventricular arrhythmia Drug-induced bradycardia Malfunction of implanted pacer
Table
36.5% 20.2% 11.3% 5.0% 4.2% 17.9% 16.7% 1.2% 35.1% 1.2% 2.4% 1.2% 1.2%
]]. P a c e r i m p l a n t s (1975): C o n c o m i t a n t
factors Arteriosclerotic cardiovascular disease Hypertension Diabetes mellitus Rheumatic heart disease Congenital heart disease Postcardiac surgery {recent) Postcardiac surgery {old) Acute myocardial infarct {recent)
57.4% 19.7% 9.6% 4.2% 3.2% 0.5% 0.5% 5.3%
"as t h e result of all cardiac conditions which produce episodic cerebral ischemia due to diminution of o u t p u t of the left ventricle ''1~ and as "every d i s t u r b a n c e of the action of h e a r t t h a t begins and ends a b r u p t l y a n d causes such interruption of t h e circulation t h a t m o r e or less c o m p l e t e cerebral ischemia results. ''1~ S y m p t o m s m a y include dizziness, lightheadedness, brief lapses of consciousness, and fainting, with or w i t h o u t c o n v u l s i o n s - a l l based on i n t e r r u p t i o n of cardiac o u t p u t . T h e s e definitions are useful as they direct m o d e r n t h e r a p y to the circulatory arrest a n d its consequence, with only s e c o n d a r y a t t e n t i o n to the u n d e r l y i n g cardiac r h y t h m . 1'-' T h o s e definitions, as early as 1940, r e m a i n e d especially p e r t i n e n t as t h e y b r o a d e n the useful definition a w a y f r o m c o m p l e t e loss of consciousness, with or w i t h o u t convulsions a n d t a k e it to a group of lesser b u t t r o u b l e s o m e neurologic manifestations. F r e q u e n t l y the d e t e r m i n a t i o n of w h e t h e r a p a t i e n t has h a d an A d a m s - S t o k e s seizure, especially where it entails lesser neurologic m a n i f e s t a t i o n s , can be m o s t difficult.
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T h e diagnosis of acquired i n t e r m i t t e n t or partial c o m p l e t e h e a r t b l o c k , 2:1 or Mobitz I I block can be m a d e e l e c t r o c a r d i o g r a p h i c a l l y Y ~ Once m a d e t h e r e are few who would dispute the need for cardiac pacing. U n f o r t u n a t e l y , c a p t u r e of the m o m e n t of A-V dissociation m a y n o t be easy and a careful neurologic e v a l u a t i o n m a y still be required. T h e presence of bifascicular block, while strongly suggestive of a cardiac basis for a c c o m p a n y i n g syncope, does n o t preclude the possibility of neurologic disease. T h e p r o b l e m becomes even m o r e complex w h e n dealing with b r a d y c a r d i a s u n r e l a t e d to h e a r t block. For e x a m ple, how often d o e s atrial fibrillation with a v e n t r i c u l a r r a t e below 50 in a p a t i e n t 70 years of age or older cause s y m p t o m s of a n y sort and in the specific instance, is pacing required to p r e v e n t f u r t h e r b r a d y c a r d i a ? T h e a n s w e r is p r o b a b l y t h a t the relatively a s y m p t o m a t i c p a t i e n t with t h a t complex should be paced and m e d i c a t i o n s such as digitalis a n d diuretics should be continued as needed. H o w slow a b r a d y c a r d i a is pathologic in an elderly person with a sinus m e c h a n i s m and A-V conduction? H o w slow is sinus b r a d y c a r d i a t h a t requires t r e a t m e n t and w h a t complex of s y m p t o m s should be considered as indicating the need for pacing? Clearly elderly p a t i e n t s can t o l e r a t e as benign a sinus r a t e of 40 to 50 per m i n u t e apparently without deleterious effect. An " a s y m p t o m a t i c " sinus r a t e of 40 per m i n u t e or above in the older p a t i e n t argues against pacem a k e r implant. B u t if so, w h a t d u r a t i o n of sinus arrest and a s y s t o l e becomes pathologic? We would p r o b a b l y all agree t h a t a sinus arrest of 3.0 seconds d e m a n d s t r e a t m e n t , b u t does an episode of L5 to 1.8 seconds during an otherwise m o r e rapid r a t e a n d w i t h o u t s y m p t o m s require pacing? T h e decision concerning p a c e m a k e r i m p l a n t a tion is often difficult and careful e v a l u a t i o n is required. H o l t e r monitoring, carried out a r o u n d the clock, o b s e r v a t i o n with c o n t i n u o u s m o n i t o r i n g in the c o r o n a r y c a r e unit, and provocative tests such as b u n d l e of His studies ~4 and sinus node recovery t i m e ~ after rapid atrial pacing a n d p r o g r a m m e d cardiac s t i m u l a t i o n m a y be required. E v e n w i t h all of these techniques a definitive answer concerning w h e t h e r to pace or n o t to pace m a y not be available. I f necessary, t e m p o r a r y cardiac pacing, 1~ u n d e r observation, m a y be
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required to resolve the uncertainties of control of the sick sinus s y n d r o m e or to resolve the problem of whether increase in a sinus bradycardia rate from 40 per m i n u t e to 60 to 70 per m i n u t e changes a patient's mentation, cardiac compensation, or feeling of well being. Often only such an approach, with assessment by colleagues, the patient and family will enable a decision to be made. Sick sinus syndrome Subgroups of w h a t would now be called the "'sick sinus s y n d r o m e " have been described for m a n y years. In 1909 Laslett 17 described a w o m a n of 40 years of age who had "'syncopal attacks. associated with prolonged arrest of the whole h e a r t " and distinguished by a slow irregular pulse 32 to 40 per m i n u t e p u n c t u a t e d by pauses to 2 to 5 seconds in duration and on jugular pulse tracing d e m o n s t r a t e d t h a t the "auricles as well as the ventricles participate in the stop" and that, " T h e condition is therefore quite different from what is known as h e a r t block. '''7 L a t e r a patient was reported with Adams-Stokes seizures because of A-V block with P waves and absent ventricular response and on other occasions sinus arrest w i t h o u t the escape of a lower pacemaker. 1S This case too foretold the combination of A-V block and sick sinus syndrome. In 1954 S h o r t ~9reported on four patients with syncope who a l t e r n a t e d between sinus bradycardia and "auricular t a c h y cardia." T h e sinus rate lay between 30 to 50 per m i n u t e and during the auricular phase the ventricular rate sometimes reached 200 per minute. 1~ In 1968 Ferrer ~ n a m e d the three varieties of the condition of sinus node dysfunction, the "Sick Sinus S y n d r o m e " and recognized t h a t there were major components: ~1) severe bradycardia, often persistent b u t sometimes episodic, (2) sinus arrest for brief or prolonged periods, with or w i t h o u t replacement by an A-V j u n c t i o n a l r h y t h m . (3~ SA block not related to drug therapy, (4) episodic atrial fibrillation, flutter, or paroxysmal atrial tachycardia alternating with a n o r m a l sinus rate or sinus bradycardia, and ~5} the slow recovery of sinus function after cardioversion. In addition, during sinus arrest or severe bradycardia, symptoms are based on the absence of a satisfactory junctional escape so t h a t disease of the AV node as well as of the conduction system is present. ~~
American Heart Journal
T h o s e with sick sinus s y n d r o m e are of the same age group as those with h e a r t block and indeed the two conditions co-exist in a b o u t 60 per cent. TM -~ A single group of patients deserve special mention. T h e s e are y o u n g men, well below the age of 50, w i t h o u t known associated disease of any sort who, with only sinus arrest and syncope and w i t h o u t t a c h y c a r d i a have suffered m a j o r syncopal episodes and required therapy. Six such patients have been t r e a t e d at Montefiore Hospital and Medical Center, all have remained vigorous and well after pacing. T w o are in their early twenties, two in the mid-thirties, and one aged f o r t y but w h o had had r e c u r r e n t dizziness and syncope since age 15, and a n o t h e r implanted at age 45 but who had been s y m p t o m a t i c since age 35. T h e pharmacologic t r e a t m e n t of sinus arrest and syncope has been unsatisfactory from the first descriptions, with response to parenteral atropine17.1~ b u t w i t h o u t significant response to oral atropine. T h e experience with s y m p a t h o m i metics is t h a t they increase the rate of a bradycardia b u t f r e q u e n t l y produce a tachycardia. ~3 Procainamide 19 and propranolol m a y increase the episodes of sinus arrest and syncope. M a n y patients with sick sinus s y n d r o m e have congestive h e a r t failure and require digitalis a n d / o r diuretics. T h e digitalis is helpful in reducing the tachycardia and treating the congestive h e a r t failure b u t m a y depress the cardiac rate. In light of the ineffectiveness of pharmacologic therapy, pacing the a t r i u m or the ventricle has been widely used. ~ Atrial pacing ~ m a y be considered a logical a p p r o a c h and indeed has been successful, but because of the incidence of associated A-V conduction disease and the possibility of late development of A-V block and the ineffectiveness of n o r m a l - r a t e atrial pacing in the presence of atrial fibrillation or flutter, atrial pacing is not usually used. Ventricular pacing is a p p a r e n t l y equally effective. T h e technical difficulties associated with atrial pacingl the f r e q u e n t poor amplitude or the P wave for adequate p a c e m a k e r recycle, and the high rate of difficulty with all atrial pacing approaches m a k e t h a t route less desirable. Despite the effectiveness of a r r h y t h m i a control by atrial, ~ or the more c o m m o n ventricular pacing, three disturbing features exist. T h e first is the frequency with which neurologic symptoms,
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indistinguishable for those which originally indicated p a c e m a k e r i m p l a n t , persist. I n a t least one report, 14 of 39 p a t i e n t s ~7 persisted in significant s y m p t o m a t o l o g y . P a t i e n t s w i t h p a c e m a k e r s also h a v e h a d a high incidence of p e r i p h e r a l embolization, p e r h a p s f r o m p o o r atrial function a n d f o r m a t i o n of m u r a l t h r o m b i and possibly with e m b o l i z a t i o n during a change in atrial r h y t h m . T w e n t y - f o u r per cent of one series, 2~ 10 per cent of another, 2~ a n d 13 per cent in a third ~' suffered such embolization. T h e third c o m p l i c a t i o n is a d e a t h r a t e a b o u t twice as high, during the first y e a r a f t e r i m p l a n t a t i o n , t h a n those with h e a r t block. One third ~ 30 died during the first posti m p l a n t year, -~ t h o u g h in o t h e r series, the first y e a r m o r t a l i t y r a t e is a b o u t 15 per cent, ~' a figure m o r e nearly c o m p a t i b l e with usual h e a r t block pacer implants. T h o u g h it is suggested t h a t m o r t a l i t y m a y be higher for this condition, review of 352 p a t i e n t s r e p o r t e d -'~ and t r e a t e d with cardiac p a c e m a k e r s shows a m o r t a l i t y r a t e of 33 per cent over an a v e r a g e follow-up of 24 to 30 m o n t h s , a figure c o m p a t i b l e with t h a t of the general paced population. :~1 Disturbances of A-V conduction
During c o m p l e t e h e a r t block cardiac function is m a r k e d l y reduced in the following ways: 1. T h e v e n t r i c u l a r r a t e is slow, usually between 30 to 40 b e a t s per m i n u t e , ~ with episodes of even slower rates or arrest. 2. T h e cardiac o u t p u t is reduced and is maintained by m a x i m u m stroke v o l u m e so t h a t increases in r e q u i r e m e n t c a n n o t be m e t either by increases in r a t e or stroke volume. '~:~ 3. T h e a r t e r i o v e n o u s oxygen difference is increased. 3~ 4. R i g h t v e n t r i c u l a r a n d p u l m o n a r y a r t e r y systolic pressures are e v a l u a t e d and congestive h e a r t failure is c o m m o n 2 ~ 5. Left v e n t r i c u l a r a n d systemic arterial pressure systolic and, to a less extent, diastolic pressures are increased. 36 6. A-V dissociation and a s y n c h r o n y luncorrected even during v e n t r i c u l a r pacing) is associated with a cyclical reduction of systemic and p u l m o n a r y pressures a n d o u t p u t s as the atrial activity moves t o w a r d a n d a w a y f r o m a physiologic sequence. Electrophysiologic defects caused by slow cardiac rates are:
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1. All " l o w e r " p a c e m a k e r s t h a n the SA node tend to be b o t h slower a n d less reliable. 37 Acquired c o m p l e t e h e a r t block with a consistent His bundle r h y t h m a n d a n a r r o w Q R S complex is c o m m o n l y associated with A d a m s - S t o k e s seizures. I d i o v e n t r i c u l a r p a c e m a k e r s are even less reliable. 2. Slow cardiac r a t e s allow the d e v e l o p m e n t of ectopic v e n t r i c u l a r r h y t h m s in single and multifocal f o r m a t s and even allow the fall of p r e m a t u r e ventricular c o n t r a c t i o n s during the v e n t r i c u l a r vulnerable period a n d the d e v e l o p m e n t of v e n t r i c u l a r t a c h y c a r d i a a n d fibrillation as an additional r h y t h m to an idioventricular bradycardia2 ~ V e n t r i c u l a r pacing a m e l i o r a t e s all f u n c t i o n a l disturbances except the A-V dissociation and corrects the electrophysiologic disturbances. I n a p a t i e n t with A-V dissociation and a bizarre multifocal idioventricular r h y t h m the application of physiologic r a t e v e n t r i c u l a r pacing is an i m m e diate and effective t h e r a p y , far m o r e so t h a n a n y c o m b i n a t i o n of drugs. 3~ Pacing is also indicated in lesser degrees of fixed A-V block because of the possibility of i n t e r m i t t e n t c o m p l e t e h e a r t block with asystole, a n d / o r v e n t r i c u l a r t a c h y c a r d i a and fibrillation and syncope or sudden death. Because of the possibility of i n t e r m i t t e n t c o m p l e t e h e a r t block in a s y m p t o m a t i c p a t i e n t with n o r m a l sinus r h y t h m during evaluation, the diagnostic p a t t e r n of fascicular block is i m p o r t a n t . As there are three fascicles below the b u n d l e of His. the right bundle, left bundle and its two subdivisions, the a n t e r i o r a n d posterior, a n y c o m b i n a t i o n of two or m o r e m a y be in fixed or i n t e r m i t t e n t block? ~ R i g h t bundle b r a n c h block or left a n t e r i o r or posterior hemiblock with a n o r m a l P - R interval is diagnostic of monofascicular block and need not be considered for pacing unless evidence for additional block or suggestive s y m p t o m a t o l o g y , such as syncope, exists. Bifascicular block with right bundle b r a n c h block with left a n t e r i o r ~' or left posterior h e m i b l o c k ~2 (especially the latter} is m u c h m o r e ominous, a n d if associated w i t h syncope, t h e b u r d e n of p r o o f rests on the denial of cardiac origin for syncope. A prolonged P R interval as well, i.e., bifascicular block with first degree h e a r t block is strongly suggestive of block in the third fascicle unless it can be d e m o n s t r a t e d t h a t t h e delay is in t h e AV
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node only. If t h a t Cannot be demonstrated, perhaps by His bundle conduction study, the combination must be considered trifascicular block and an indication for pacing2 a The following electrocardiographic patterns can be considered bifascicular block and potentially trifascicular block, which will be associated with brief or prolonged complete heart block and asystole or ventricular tachycardia a n d / o r fibrillation. 1. Right bundle branch block with left axis deviation (caused by left anterior hemiblock). 2. Right bundle branch block with right axis deviation (caused by left posterior hemiblock). 3. Right bundle branch with llrst degree A-V block (the entire left bundle must be compromised); unless it can be demonstrated t hat the conduction delay is in the A-V node. 4. Complete left bundle branch block is in itself ominous but when associated with first degree A-V block the right bundle branch must also be compromised. 5. Alternating bilateral bundle branch block. The three fascicles are alternately blocked even during 1:1 A-V conduction. Acquired complete heart block is accepted as a reason for cardiac pacing, temporary or permanent, as a function of the patient's outlook for survival. Congenital heart block as an isolated lesion also requires pacing if the patient is at all symptomatic or if the duration of the QRS complex is beyond 0.12 second2 ~ A number of children have apparently survived to adult life, '~ and such survival is an excellent portent for their future. 4~ However, it is in infancy t hat m o s t deaths occur ~' and detection of complete heart block after early childhood has not taken into account those who have died. As the patient with congenital heart block may be asymptomatic, the needed electrocardiographic diagnosis may not be made. If symptoms cause an ECG to be performed and the diagnosis is made, the patient can be watched for the development of congestive heart failure, bradycardia, or syncope. 48 Even with adequate follow-up sudden death m ay be the first clinical manifestation2 ~ Atrial fibrillation or flutter with ventricular bradycardia may occur because of complete heart block irrespective of the atrial a r r hyt hm i a or
American Heart Journal
because of multiple concealed conduction at the A-V junction. Pacing in special circumstances Postcardiac surgery. Sinus bradycardia and a variety of atrial or ventricular arrhythmias occur frequently following open heart surgery and fleeting or even permanent complete heart block occurs following complex intracardiac repair and especially t hat of the tricuspid valve in Ebstein's malformation. ~'~ Even in the absence of such arrhythmias, a sinus bradycardia relative to postoperative requirement frequently exists. ~1 As the cardiac o u t p u t is markedly rate-dependent postoperatively, rate control by atrial or, if necessary, ventricular pacing is indicated. Temporary myocardial wires in the atrium and ventricles which can be extracted postoperatively should be left routinely. 5~ Should the patient have an indication for permanent postoperative pacing or develop one intraoperatively, a permanent left ventricular myocardial lead should be left 53 and attached to a non-invasively rate-variable pulse generator2 ~ Rate can be controlled by the implanted unit. If a single rate unit is implanted, the temporary leads should be used as well, and rates above t h a t of the implant will inhibit it. If permanent pacemaker implant is considered, a permanent left ventricular electrode can be left in place and insulated in the subcutaneous tissue. Should permanent pacing be required it can be established by connecting a generator to t h a t electrode. Acute myocardial infarction. Indications for pacing in acute myocardial infarction have undergone profound change from recommendation t h a t many patients ~'~should be paced to a therapeutic nihilism which held that mortality rates are unchanged with or without pacing2 ~ The recognition that prognosis of block varies whether the infarct is anterior or inferior has caused a teassessrnent of the indications. ~ Anterior infarction with complete heart block implies massive myocardial damage, and cardiogenic shock and/ or congestive heart failure cause death in over 50 per cent of patients2 ~, ~ For the inferior infarct the collected mortality rate is about 25 to 40 per cent/~,. ~1 In the former, death may occur despite successful pacing; in the latter, survival is usual without need for pacing. Nevertheless, some patients persist in heart block, survive, and
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depend on p e r m a n e n t pacing for prolonged survival. Aside from the d e v e l o p m e n t of secondor third-degree A-V block, those with a c u t e m y o c a r d i a l infarction develop b r a d y a r r h y t h m i a s , sinus b r a d y c a r d i a S-A block in 5-20 per c e n t : "~. ~3 and t a c h y a r r h y t h m i a in a b o u t o n e - q u a r t e r of patients. ~- ~5 B o t h can be m a n a g e d with pacing a n d / o r medications as necessary and frequently better in a c o m b i n a t i o n of both. T h e indications for pacing during a c u t e m y o c a r d i a l infarction at present are: 1. S y m p t o m a t i c bradycardias, including sinus bradycardia, S-A block, and sick sinus syndrome. 2. Drug-resistant t a c h y a r r h y t h m i a s . 3. A c u t e onset of right or left bundle or bifascicular block. 4. A c u t e onset of Mobitz I I or complete A-V block with anterior infarction. 5. R h y t h m s p r o b a b l y n o t requiring pacing are Mobitz ! (Wenckebach) block or complete A-V block during inferior infarction and a rate of 40 to 50 or above w i t h o u t periods of greater b r a d y c a r dia, asystole, or escape ventricular p r e m a t u r e c o n t r a c t i o n s which are readily controlled with drugs. Of perhaps greater i m p o r t a n c e is the prognosis of the patient who develops new bundle b r a n c h block during the course of acute m y o c a r d i a l infarction b u t never develops second degree or third degree A-V block. ~r '~ Such a patient is likely to go u n p a c e d b u t early post-recovery m o r t a l i t y m a y be high. T h o s e with new right bundle b r a n c h block and left axis deviation or right axis deviation, i.e., left anterior or posterior hemiblock, carry an especially high m o r t a l i t y rate with 25 per cent of such patients dying suddenly during the first post-infarction year. T h e p r o p h y lactic m a n a g e m e n t of such patients is still in dispute, most likely because neither the techniques for detecting the severity of the persistent block nor those provocative tests now available have a d e q u a t e diagnostic specificity. Newly developed approaches to bundle of His recording with the electrode for t e m p o r a r y pacing during its removal. "pull-out His recording" have already begun ~o add to t h a t specificity. Over 80 per cent of patients can have a simple His potential recording performed during removal of a conventional ~emporary pacing electrode. ~ In these patients o m i n o u s findings such as a split His potential ~ or m a r k e d l y prolonged H-V time.
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alone or during lidocaine administration, have distinct prognostic value. 7~ Further, s y m p t o m a t ic, u n p a c e d post-infarct patients with H-V time longer t h a n 65 msec. b u t no o t h e r evidence of h e a r t block, have a m o r t a l i t y rate of 69 per cent c o m p a r e d to 20 per cent for similar patients subjected to p e r m a n e n t pacingY 1 S u c h specificity m a y well reduce the t o t a l n u m b e r of patients who, having seemingly recovered from acute m y o c a r d i a l infarction, die suddenly. Finally a c a u t i o n a r y word concerning temporary pacing during a c u t e m y o c a r d i a l infarction. T h o s e with ischemic h e a r t disease and acute m y o c a r d i a l infarction are maximally sensitive to ventricular fibrillation 72 and especially to the a n o d a l stimulus from the almost universally used bipolar t e m p o r a r y electrode falling in the vulnerable period of the cardiac cycle. ~:~ Loss of pacer sensing because of decrease in Q R S amplitude can be as high as 15 per cent TM during acute infarction. U n d e r those circumstances pacer stimuli m a y become competitive and 14 of the 30 reported and d o c u m e n t e d cases of pacemakercaused ventricular fibrillation have been from a competitive pacer during a c u t e myocardial infarction, so t h a t caution m u s t be exercised, Pacer function m u s t be frequently assessed, and the use of the unipolar c a t h o d a l stimulation with the anode out of the ventricle m u s t be consideredY 5 REFERENCES
1. Zoll, P. M.: Resuscitation of the heart in ventricular standstill by external electrical stimulation, N. EngL J. Med. 247:768, 1952. 2. Weirich, W. L., Gott, V~ L., and Lillehei, C. W.: The treatment of complete heart block by the combined use of a myocardial electrode and an artificial pacemaker, Surg. Forum 8:360, 1957. 3. Lagergren, H., and Johansson, L.: Intracardiac stimulation for complete heart block, Acta Chir. Scand. 125:562, 1963. 4. Chardack, W. M., Gage, A. A., Federico, A. J, Schimert, G., and Greatbatch, W.: Five years' clinical experience with an implanted pacemaker; an appraisal, Surgery 58:915, 1965. 5. Chardack, W, Gage, A. A., and Greatbatch, W.: A transistorized self-contained implantable pacemaker for the long term correction of complete heart block, Surgery 48:643, 1960. 6. Friedberg, C. K., Donoso, E., and Stein, W. G.: Nonsurgical acquired heart block, Ann. N. Y. Acad. Sci. 111:835, 1964. 7. Lemberg, L., Castellanos, A., and Berkovits, B.: Pacing on demand in A-V block, J.A.M.A. 191:12, 1965. 8. Parsonnet, V., Zucker, I: R., Gilbert L., and Myers, G. H.: Clinical use of an implantable standby pacemaker, J.A.M.A. 196:784, 1966.
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in disorders of sinus node function, AM. HEART J. 89:579, 1975. Furman, S.: The present status of cardiac pacing, Surg. Gynecol. Obstet. 143:645, 1976. Stack, M. F., Rader, B., Sobol, B. J., Farber, S. J., and Eichna, L. W.: Cardiovascular hemodynamic functions in complete heart block and the effect of isopropylnorepinephrine, Circulation 1 7:526, 1958. Levinson, D. C., Gunther, L., Meehan, J. P., Jr., Griffith, G. C., and Spritzler, R. J.: Hemodynamic studies in five patients with heart block and slow ventricular rates, Circulation 12:739, 1955. Samet, P., Jacobs, W., Bernstein, W. H., and Shane, R.: Hemodynamic sequelae of idioventricular pacemaking in complete h e a r t block, Am. J. Cardiol. 11:594, 1963. Brockman, S. K.: Cardiodynamics of complete heart block, Am. J. CardioL 16:72, 1965. Levinson, D. C., Shubin, H., Gunther, L., and Meehan, J. P.: Hemodynamic findings in heart block with slow ventricular rates, Am. J. Cardiol. 4:440, 1959. Parkinson, J., Papp, C., and Evans, W.: The electrocardiogram of the Stokes-Adams attack, Br. Heart J. 3:171, 1941. Dressier, W.: Observations in patients with implanted pacemaker III. Frequency of ventricular tachycardia as cause of Adams-Stokes attacks and rate of pacing required for its prevention, AM. HEART J. 68:19, 1964. Sowton, E., Leatham, A., and Carson, P.: The suppression of arrhythmias by artificial pacemaking, Lancet 2:1098, 1964. Narula, O. S., and Samet, P.: Wenckebach and Mobitz Type II A-V block due to block within the His bundle and bundle branches, Circulation 41:947, 1970. Haft, J. I., and Lasser, R. P.: ECG patterns useful in the diagnosis of intermittent heart block, J.A.M.A. 222:184, 1972. Steiner, C., Lau, S. H., Stein, E., Wit, A. L., Weiss, M. B., Damato, A. N., Haft, J. I., Weinstock, M., and Gupta, P.: Electrophysiologic documentation of trifascicular block as the common cause of complete heart block, Am. J. Cardiol. 28:436, 1971. Rosenbaum, M. B., Elizari, M. V., Lazzari, J. O., Nau, G, J., Levi, R. J., and Halpern, M. S.: Intraventricular trifascicular blocks. Review of the literature and classification, AM. HEART J. 78:450, 1969. Nakamura, F. F., and Nadas, A. S.: Complete heart block in infants and children, N. Engl. J. Med. 270:1261, 1964. Campbell, M., and Emanuel, R.: Six cases of congenital complete heart block followed for 34-40 years, Br. Heart J. 29:577, !967. Campbell, M., and Thorne, M. G.: Congenital heart block, Br. Heart J. 18:90, 1956. Michaelsson, J., and Engle, M. A.: Congenital complete heart block: an international study of the natural history, Cardiovasc. Clin. 4:85, 1973. Pahlajani, D. B., Miller, R. A., and Serratto, M.: Patterns of atrioventricular conduction in children, AM. HEART J. 90:165, 1975. Moltham, M. E., Miller, R. M., Hastreiter, A. R., and Paul, M. H.: Congenital heart block with fatal AdamsStokes attacks in childhood, Pediatrics 30:32, 1962. Reemtsma, K., Delgado, J. P., and Creech, O.: Heart block following intracardiac surgery; localization of conduction tissue injury, J. Thorac. Cardiovasc. Surg. 39:688, 1960. Friesen, W. G , Wo0dson, R. D., Ames, A. W., Herr, R. H., Starr, A., and Kassebaum, D. G.: A hemodynamic comparison of atrial and ventricular pacing in post-
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operative cardiac surgical patients, J. Thorac. Cardiovasc. Surg. 55:271, 1968. Litwak, R. S., Kuhn, L. A., Gadboys, H. L., Lukban, S. B., and Sukurai, H.: Support of myocardial performance after open cardiac operations by rate augmentation, J. Thorac. Cardiovasc. Surg. 56:484, 1968. Lajos, T. Z.: Pacemaker wire extension for permanent and temporary pacing, Ann. Thorac. Surg. 15:207, 1973. Parsonnet, V., Cuddy, T. E., Escher, D. J. W., Furman, S., Morse, D., Gilbert, L., and Zucker, I. R.: A permanent pacemaker capable of external non-invasive programming, Trans. Am. Soc. Artif. Intern. Organs 29:224, 1973. Bruce, R. A., Blackmon, J. R., Cobb, L. A., and Dodge, H. T.: T r e a t m e n t of asystole or heart block during acute myocardial infarction with electrode catheter pacing, AM. HEART J. 69:460, 1965. Chatterjee, K., Harris, A., a n d Leatham, A.: The risk of pacing after infarction, and current recommendations, Lancet 2:1061, 1969. Godman, M. J,, Lassers, B. W., and Julian, D. G.: Complete bundle-branch block complicating acute myocardial infarction, N. Engl. J. Med. 282:237, 1970. Norris, R. M.: Heart block in posterior and anterior myocardial infarction, Br. Heart J. 31:352, 1969. Resnekov, L., and Lipp, H.: Pacemaking and acute myocardial infarction, Progr. Cardiovasc. Dis. 14:475, 1972. Christiansen, I., Haghfelt, T., and Amtorp, O.: Complete heart block in acute myocardial infarction: drug therapy, AM. HEART J. 85:162, 1973. Hatee, L., and Rokseth, R.: Conservative t r e a t m e n t of AV block in acute myocardial infarction, Br. Heart J. 33:595, 1971. Imperial, E. S., Carballo, R., and Zimmerman, H. A.: Disturbances of rate, rhythm, and conduction in acute myocardial infarction, Am. J. Cardiol. 5:24, 1960. Lown, B., Hood, W. B., Fakhro, A. M., Kaplinsky, E., and
64. 65. 66.
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Roberge, G.: Unresolved problems in coronary care, Am. J. Cardiol. 20:494, 1967. E1-Sherif, N.: Tachycardia and bradycardia dependent bundle branch block after acute myocardial ischemia, Br. Heart J. 36:291, 1974. Hass, J.: Mechanisms of ventricular arrhythmias associated with myocardial infarction, Am. J. Cardiol. 24:800, 1969. Atkins, J. M., Leshin, S. J., Blomquist, G., and Mullins, C. B.: Ventricular conduction blocks and sudden death in acute myocardial infarction, N. Engl. J. Med. 288:281, 1973. Gould, L., Venkataraman, K., Mohammad, N., and Gomprecht, R. F.: Prognosis of right bundle branch block in acute myocardial infarction, J.A.M.A. 219:502, 1972. Fisher, J.: Unpublished data. Narula, O. S., Scherlag, B. J., Samet, P., and Javier, R. P.: Atrioventricular block: localization and classification by His bundle recordings, Am. J. Med. 50:146, 1971. Vera, Z., Mason, D. T., Fletcher, R. D., Awan, N. A., and Massumi, R. A.: Prolonged His-Q interval in chronic bifascicular block. Relation to impending complete heart block, Circulation 53:46, 1976. Altschuler, H., Fisher, J., and Furman, S.: Unpublished data. Bilitch, M., Cosby, R. S., and Cafferky, E. A.: Ventricular fibrillation and competitive pacing, N. Engl. J. Med. 276:598, 1967. Preston, T. A.: Anodal stimulation as a cause of pacemaker induced ventricular fibrillation, AM. HEART J. 86:366, 1973. Chatterjee, K., Sutton, R., and Davies, J. G.: Low intracardiac potentials in myocardial infarction as a cause of failure of inhibition of demand pacemakers, Lancet 1:511, 1968. Preston, T. A.: Temporary unipolar pacing using a dual cathode, J. Electrocardiol. 9:193, 1976.
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Cardiac pacing and pacemakers I. Indications for pacing bradyarrhythmias Seymour Furman, M.D. Bronx, N. Y.
A wide variety of cardiac arrhythmias has become permanently controllable by electrical cardiac stimulation since Zoll's initial treatment 1 of complete heart block with an external transcutaneous pacemaker in 1952, later wired transthoracic pacing, 2 external transvenous, ~ and finally implantable transvenous ~ and transthoracic pacing2 Though our incomplete understanding of the nature of heart block 6 tended to raise the question of the fixed or intermittent n a t u r e of heart block, t h e development of non-competitive (demand, standy, ventricular inhibited and ventricular synchronous) pacemakers about 19657~ s resolved the problem by enabling the implant of devices which would be capable of allowing sinus r h y t h m to exist and to stimulate the heart whenever the cardiac rate fell below a predetermined interval between QRS complexes. By 1965 to 1967 the basis of modern cardiac pacing for bradyarrhythmias had been established. The three factors were: (1) the development of an implantable device, (2) the transvenous approach, and (3) the ability of the pacemaker to sense cardiac activity and respond to the cardiac chamber being stimulated. The future of pacing for cardiac arrhythmias other than heart block could have been foretold by the initial clinical description of transvenous pacing in which the patient with bradycardia, asystole and recurrent Adams-Stokes seizures did not have classic complete heart block but rheuFrom the Department of Surgery, Cardiothoracic Division, Montefiore Hospital and Medical Center, 111 East 210th St., Bronx, N. Y. 10467. Supported in Part by United States Public Health Service Grant No. HE-04666-16. Received for publication Nov. 29, 1976. Reprint requests to: Seymour Furman, M.D., Montefiore Hospital and Medical Center, 111 East 210th St., Bronx, N. Y. 10467.
April, 1977, Vol. 93, No. 4, pp. 523-530
matic heart disease, mitral valvular disease, and chronic atrial fibrillation with a markedly reduced ventricular rate2 The immediate cause of asystole was hypopotassemia, unrecognized in significance at that time but later found to be a profound causative agent for ventricular bradycardia and interruption of A-V conduction. From the preliminary treatment of heart block, a far wider group of arrhythmias has been treated. In 1975, at Montefiore Hospital and Medical Center, a total of 200 initial pacemaker implants were performed., Of these 36.5 per cent were for sinus node dysfunction with brady-tachy syndrome, sinus arrest, or sinus bradycardia. Eighteen per cent were for complete heart block and 35 per cent for intermittent or partial heart block, the balance for a variety of ventricular arrhythmias and reentry tachycardias, drug induced bradycardia, etc. Fixed complete heart block, the classic arrhythmia, accounted for less than 20 per cent of all arrhythmias (Table I). The patients are a diverse group, over half with arteriosclerotic heart disease, one-fifth with hypertension and one-tenth with diabetes mellitus. Rheumatic heart disease or an acute myocardial infarction as the immediate cause for the heart block accounted for another 10 per cent and 1 per cent of patients required pacing as a complication of cardiac surgery at the time of implant or at some later time, in at least one case two years later (Table II). Until about 1970 most physicians and surgeons would have considered carefully whether to implant a pacemaker in the absence of demonstrated Adams-Stokes seizures. Gradually a variety of minor neurologic lapses and prophylactic indications have become dominant. For purposes of clarity and utility in comprehending Adams-Stokes seizures they should be thought of,
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Table I. P a c e r i m p l a n t s (1975): R h y t h m distur-
bance Sinus node dysfunction Brady-tachy syndrome Sinus arrest Sinus bradycardia Atrial fibrillation with ventricular rate below 50 Complete heart block Acquired Congenital Intermittent heart block Wolff-Parkinson-White syndrome Other ventricular arrhythmia Drug-induced bradycardia Malfunction of implanted pacer
Table
36.5% 20.2% 11.3% 5.0% 4.2% 17.9% 16.7% 1.2% 35.1% 1.2% 2.4% 1.2% 1.2%
]]. P a c e r i m p l a n t s (1975): C o n c o m i t a n t
factors Arteriosclerotic cardiovascular disease Hypertension Diabetes mellitus Rheumatic heart disease Congenital heart disease Postcardiac surgery {recent) Postcardiac surgery {old) Acute myocardial infarct {recent)
57.4% 19.7% 9.6% 4.2% 3.2% 0.5% 0.5% 5.3%
"as t h e result of all cardiac conditions which produce episodic cerebral ischemia due to diminution of o u t p u t of the left ventricle ''1~ and as "every d i s t u r b a n c e of the action of h e a r t t h a t begins and ends a b r u p t l y a n d causes such interruption of t h e circulation t h a t m o r e or less c o m p l e t e cerebral ischemia results. ''1~ S y m p t o m s m a y include dizziness, lightheadedness, brief lapses of consciousness, and fainting, with or w i t h o u t c o n v u l s i o n s - a l l based on i n t e r r u p t i o n of cardiac o u t p u t . T h e s e definitions are useful as they direct m o d e r n t h e r a p y to the circulatory arrest a n d its consequence, with only s e c o n d a r y a t t e n t i o n to the u n d e r l y i n g cardiac r h y t h m . 1'-' T h o s e definitions, as early as 1940, r e m a i n e d especially p e r t i n e n t as t h e y b r o a d e n the useful definition a w a y f r o m c o m p l e t e loss of consciousness, with or w i t h o u t convulsions a n d t a k e it to a group of lesser b u t t r o u b l e s o m e neurologic manifestations. F r e q u e n t l y the d e t e r m i n a t i o n of w h e t h e r a p a t i e n t has h a d an A d a m s - S t o k e s seizure, especially where it entails lesser neurologic m a n i f e s t a t i o n s , can be m o s t difficult.
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T h e diagnosis of acquired i n t e r m i t t e n t or partial c o m p l e t e h e a r t b l o c k , 2:1 or Mobitz I I block can be m a d e e l e c t r o c a r d i o g r a p h i c a l l y Y ~ Once m a d e t h e r e are few who would dispute the need for cardiac pacing. U n f o r t u n a t e l y , c a p t u r e of the m o m e n t of A-V dissociation m a y n o t be easy and a careful neurologic e v a l u a t i o n m a y still be required. T h e presence of bifascicular block, while strongly suggestive of a cardiac basis for a c c o m p a n y i n g syncope, does n o t preclude the possibility of neurologic disease. T h e p r o b l e m becomes even m o r e complex w h e n dealing with b r a d y c a r d i a s u n r e l a t e d to h e a r t block. For e x a m ple, how often d o e s atrial fibrillation with a v e n t r i c u l a r r a t e below 50 in a p a t i e n t 70 years of age or older cause s y m p t o m s of a n y sort and in the specific instance, is pacing required to p r e v e n t f u r t h e r b r a d y c a r d i a ? T h e a n s w e r is p r o b a b l y t h a t the relatively a s y m p t o m a t i c p a t i e n t with t h a t complex should be paced and m e d i c a t i o n s such as digitalis a n d diuretics should be continued as needed. H o w slow a b r a d y c a r d i a is pathologic in an elderly person with a sinus m e c h a n i s m and A-V conduction? H o w slow is sinus b r a d y c a r d i a t h a t requires t r e a t m e n t and w h a t complex of s y m p t o m s should be considered as indicating the need for pacing? Clearly elderly p a t i e n t s can t o l e r a t e as benign a sinus r a t e of 40 to 50 per m i n u t e apparently without deleterious effect. An " a s y m p t o m a t i c " sinus r a t e of 40 per m i n u t e or above in the older p a t i e n t argues against pacem a k e r implant. B u t if so, w h a t d u r a t i o n of sinus arrest and a s y s t o l e becomes pathologic? We would p r o b a b l y all agree t h a t a sinus arrest of 3.0 seconds d e m a n d s t r e a t m e n t , b u t does an episode of L5 to 1.8 seconds during an otherwise m o r e rapid r a t e a n d w i t h o u t s y m p t o m s require pacing? T h e decision concerning p a c e m a k e r i m p l a n t a tion is often difficult and careful e v a l u a t i o n is required. H o l t e r monitoring, carried out a r o u n d the clock, o b s e r v a t i o n with c o n t i n u o u s m o n i t o r i n g in the c o r o n a r y c a r e unit, and provocative tests such as b u n d l e of His studies ~4 and sinus node recovery t i m e ~ after rapid atrial pacing a n d p r o g r a m m e d cardiac s t i m u l a t i o n m a y be required. E v e n w i t h all of these techniques a definitive answer concerning w h e t h e r to pace or n o t to pace m a y not be available. I f necessary, t e m p o r a r y cardiac pacing, 1~ u n d e r observation, m a y be
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Cardiac pacing and pacemakers I
required to resolve the uncertainties of control of the sick sinus s y n d r o m e or to resolve the problem of whether increase in a sinus bradycardia rate from 40 per m i n u t e to 60 to 70 per m i n u t e changes a patient's mentation, cardiac compensation, or feeling of well being. Often only such an approach, with assessment by colleagues, the patient and family will enable a decision to be made. Sick sinus syndrome Subgroups of w h a t would now be called the "'sick sinus s y n d r o m e " have been described for m a n y years. In 1909 Laslett 17 described a w o m a n of 40 years of age who had "'syncopal attacks. associated with prolonged arrest of the whole h e a r t " and distinguished by a slow irregular pulse 32 to 40 per m i n u t e p u n c t u a t e d by pauses to 2 to 5 seconds in duration and on jugular pulse tracing d e m o n s t r a t e d t h a t the "auricles as well as the ventricles participate in the stop" and that, " T h e condition is therefore quite different from what is known as h e a r t block. '''7 L a t e r a patient was reported with Adams-Stokes seizures because of A-V block with P waves and absent ventricular response and on other occasions sinus arrest w i t h o u t the escape of a lower pacemaker. 1S This case too foretold the combination of A-V block and sick sinus syndrome. In 1954 S h o r t ~9reported on four patients with syncope who a l t e r n a t e d between sinus bradycardia and "auricular t a c h y cardia." T h e sinus rate lay between 30 to 50 per m i n u t e and during the auricular phase the ventricular rate sometimes reached 200 per minute. 1~ In 1968 Ferrer ~ n a m e d the three varieties of the condition of sinus node dysfunction, the "Sick Sinus S y n d r o m e " and recognized t h a t there were major components: ~1) severe bradycardia, often persistent b u t sometimes episodic, (2) sinus arrest for brief or prolonged periods, with or w i t h o u t replacement by an A-V j u n c t i o n a l r h y t h m . (3~ SA block not related to drug therapy, (4) episodic atrial fibrillation, flutter, or paroxysmal atrial tachycardia alternating with a n o r m a l sinus rate or sinus bradycardia, and ~5} the slow recovery of sinus function after cardioversion. In addition, during sinus arrest or severe bradycardia, symptoms are based on the absence of a satisfactory junctional escape so t h a t disease of the AV node as well as of the conduction system is present. ~~
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T h o s e with sick sinus s y n d r o m e are of the same age group as those with h e a r t block and indeed the two conditions co-exist in a b o u t 60 per cent. TM -~ A single group of patients deserve special mention. T h e s e are y o u n g men, well below the age of 50, w i t h o u t known associated disease of any sort who, with only sinus arrest and syncope and w i t h o u t t a c h y c a r d i a have suffered m a j o r syncopal episodes and required therapy. Six such patients have been t r e a t e d at Montefiore Hospital and Medical Center, all have remained vigorous and well after pacing. T w o are in their early twenties, two in the mid-thirties, and one aged f o r t y but w h o had had r e c u r r e n t dizziness and syncope since age 15, and a n o t h e r implanted at age 45 but who had been s y m p t o m a t i c since age 35. T h e pharmacologic t r e a t m e n t of sinus arrest and syncope has been unsatisfactory from the first descriptions, with response to parenteral atropine17.1~ b u t w i t h o u t significant response to oral atropine. T h e experience with s y m p a t h o m i metics is t h a t they increase the rate of a bradycardia b u t f r e q u e n t l y produce a tachycardia. ~3 Procainamide 19 and propranolol m a y increase the episodes of sinus arrest and syncope. M a n y patients with sick sinus s y n d r o m e have congestive h e a r t failure and require digitalis a n d / o r diuretics. T h e digitalis is helpful in reducing the tachycardia and treating the congestive h e a r t failure b u t m a y depress the cardiac rate. In light of the ineffectiveness of pharmacologic therapy, pacing the a t r i u m or the ventricle has been widely used. ~ Atrial pacing ~ m a y be considered a logical a p p r o a c h and indeed has been successful, but because of the incidence of associated A-V conduction disease and the possibility of late development of A-V block and the ineffectiveness of n o r m a l - r a t e atrial pacing in the presence of atrial fibrillation or flutter, atrial pacing is not usually used. Ventricular pacing is a p p a r e n t l y equally effective. T h e technical difficulties associated with atrial pacingl the f r e q u e n t poor amplitude or the P wave for adequate p a c e m a k e r recycle, and the high rate of difficulty with all atrial pacing approaches m a k e t h a t route less desirable. Despite the effectiveness of a r r h y t h m i a control by atrial, ~ or the more c o m m o n ventricular pacing, three disturbing features exist. T h e first is the frequency with which neurologic symptoms,
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indistinguishable for those which originally indicated p a c e m a k e r i m p l a n t , persist. I n a t least one report, 14 of 39 p a t i e n t s ~7 persisted in significant s y m p t o m a t o l o g y . P a t i e n t s w i t h p a c e m a k e r s also h a v e h a d a high incidence of p e r i p h e r a l embolization, p e r h a p s f r o m p o o r atrial function a n d f o r m a t i o n of m u r a l t h r o m b i and possibly with e m b o l i z a t i o n during a change in atrial r h y t h m . T w e n t y - f o u r per cent of one series, 2~ 10 per cent of another, 2~ a n d 13 per cent in a third ~' suffered such embolization. T h e third c o m p l i c a t i o n is a d e a t h r a t e a b o u t twice as high, during the first y e a r a f t e r i m p l a n t a t i o n , t h a n those with h e a r t block. One third ~ 30 died during the first posti m p l a n t year, -~ t h o u g h in o t h e r series, the first y e a r m o r t a l i t y r a t e is a b o u t 15 per cent, ~' a figure m o r e nearly c o m p a t i b l e with usual h e a r t block pacer implants. T h o u g h it is suggested t h a t m o r t a l i t y m a y be higher for this condition, review of 352 p a t i e n t s r e p o r t e d -'~ and t r e a t e d with cardiac p a c e m a k e r s shows a m o r t a l i t y r a t e of 33 per cent over an a v e r a g e follow-up of 24 to 30 m o n t h s , a figure c o m p a t i b l e with t h a t of the general paced population. :~1 Disturbances of A-V conduction
During c o m p l e t e h e a r t block cardiac function is m a r k e d l y reduced in the following ways: 1. T h e v e n t r i c u l a r r a t e is slow, usually between 30 to 40 b e a t s per m i n u t e , ~ with episodes of even slower rates or arrest. 2. T h e cardiac o u t p u t is reduced and is maintained by m a x i m u m stroke v o l u m e so t h a t increases in r e q u i r e m e n t c a n n o t be m e t either by increases in r a t e or stroke volume. '~:~ 3. T h e a r t e r i o v e n o u s oxygen difference is increased. 3~ 4. R i g h t v e n t r i c u l a r a n d p u l m o n a r y a r t e r y systolic pressures are e v a l u a t e d and congestive h e a r t failure is c o m m o n 2 ~ 5. Left v e n t r i c u l a r a n d systemic arterial pressure systolic and, to a less extent, diastolic pressures are increased. 36 6. A-V dissociation and a s y n c h r o n y luncorrected even during v e n t r i c u l a r pacing) is associated with a cyclical reduction of systemic and p u l m o n a r y pressures a n d o u t p u t s as the atrial activity moves t o w a r d a n d a w a y f r o m a physiologic sequence. Electrophysiologic defects caused by slow cardiac rates are:
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1. All " l o w e r " p a c e m a k e r s t h a n the SA node tend to be b o t h slower a n d less reliable. 37 Acquired c o m p l e t e h e a r t block with a consistent His bundle r h y t h m a n d a n a r r o w Q R S complex is c o m m o n l y associated with A d a m s - S t o k e s seizures. I d i o v e n t r i c u l a r p a c e m a k e r s are even less reliable. 2. Slow cardiac r a t e s allow the d e v e l o p m e n t of ectopic v e n t r i c u l a r r h y t h m s in single and multifocal f o r m a t s and even allow the fall of p r e m a t u r e ventricular c o n t r a c t i o n s during the v e n t r i c u l a r vulnerable period a n d the d e v e l o p m e n t of v e n t r i c u l a r t a c h y c a r d i a a n d fibrillation as an additional r h y t h m to an idioventricular bradycardia2 ~ V e n t r i c u l a r pacing a m e l i o r a t e s all f u n c t i o n a l disturbances except the A-V dissociation and corrects the electrophysiologic disturbances. I n a p a t i e n t with A-V dissociation and a bizarre multifocal idioventricular r h y t h m the application of physiologic r a t e v e n t r i c u l a r pacing is an i m m e diate and effective t h e r a p y , far m o r e so t h a n a n y c o m b i n a t i o n of drugs. 3~ Pacing is also indicated in lesser degrees of fixed A-V block because of the possibility of i n t e r m i t t e n t c o m p l e t e h e a r t block with asystole, a n d / o r v e n t r i c u l a r t a c h y c a r d i a and fibrillation and syncope or sudden death. Because of the possibility of i n t e r m i t t e n t c o m p l e t e h e a r t block in a s y m p t o m a t i c p a t i e n t with n o r m a l sinus r h y t h m during evaluation, the diagnostic p a t t e r n of fascicular block is i m p o r t a n t . As there are three fascicles below the b u n d l e of His. the right bundle, left bundle and its two subdivisions, the a n t e r i o r a n d posterior, a n y c o m b i n a t i o n of two or m o r e m a y be in fixed or i n t e r m i t t e n t block? ~ R i g h t bundle b r a n c h block or left a n t e r i o r or posterior hemiblock with a n o r m a l P - R interval is diagnostic of monofascicular block and need not be considered for pacing unless evidence for additional block or suggestive s y m p t o m a t o l o g y , such as syncope, exists. Bifascicular block with right bundle b r a n c h block with left a n t e r i o r ~' or left posterior h e m i b l o c k ~2 (especially the latter} is m u c h m o r e ominous, a n d if associated w i t h syncope, t h e b u r d e n of p r o o f rests on the denial of cardiac origin for syncope. A prolonged P R interval as well, i.e., bifascicular block with first degree h e a r t block is strongly suggestive of block in the third fascicle unless it can be d e m o n s t r a t e d t h a t t h e delay is in t h e AV
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node only. If t h a t Cannot be demonstrated, perhaps by His bundle conduction study, the combination must be considered trifascicular block and an indication for pacing2 a The following electrocardiographic patterns can be considered bifascicular block and potentially trifascicular block, which will be associated with brief or prolonged complete heart block and asystole or ventricular tachycardia a n d / o r fibrillation. 1. Right bundle branch block with left axis deviation (caused by left anterior hemiblock). 2. Right bundle branch block with right axis deviation (caused by left posterior hemiblock). 3. Right bundle branch with llrst degree A-V block (the entire left bundle must be compromised); unless it can be demonstrated t hat the conduction delay is in the A-V node. 4. Complete left bundle branch block is in itself ominous but when associated with first degree A-V block the right bundle branch must also be compromised. 5. Alternating bilateral bundle branch block. The three fascicles are alternately blocked even during 1:1 A-V conduction. Acquired complete heart block is accepted as a reason for cardiac pacing, temporary or permanent, as a function of the patient's outlook for survival. Congenital heart block as an isolated lesion also requires pacing if the patient is at all symptomatic or if the duration of the QRS complex is beyond 0.12 second2 ~ A number of children have apparently survived to adult life, '~ and such survival is an excellent portent for their future. 4~ However, it is in infancy t hat m o s t deaths occur ~' and detection of complete heart block after early childhood has not taken into account those who have died. As the patient with congenital heart block may be asymptomatic, the needed electrocardiographic diagnosis may not be made. If symptoms cause an ECG to be performed and the diagnosis is made, the patient can be watched for the development of congestive heart failure, bradycardia, or syncope. 48 Even with adequate follow-up sudden death m ay be the first clinical manifestation2 ~ Atrial fibrillation or flutter with ventricular bradycardia may occur because of complete heart block irrespective of the atrial a r r hyt hm i a or
American Heart Journal
because of multiple concealed conduction at the A-V junction. Pacing in special circumstances Postcardiac surgery. Sinus bradycardia and a variety of atrial or ventricular arrhythmias occur frequently following open heart surgery and fleeting or even permanent complete heart block occurs following complex intracardiac repair and especially t hat of the tricuspid valve in Ebstein's malformation. ~'~ Even in the absence of such arrhythmias, a sinus bradycardia relative to postoperative requirement frequently exists. ~1 As the cardiac o u t p u t is markedly rate-dependent postoperatively, rate control by atrial or, if necessary, ventricular pacing is indicated. Temporary myocardial wires in the atrium and ventricles which can be extracted postoperatively should be left routinely. 5~ Should the patient have an indication for permanent postoperative pacing or develop one intraoperatively, a permanent left ventricular myocardial lead should be left 53 and attached to a non-invasively rate-variable pulse generator2 ~ Rate can be controlled by the implanted unit. If a single rate unit is implanted, the temporary leads should be used as well, and rates above t h a t of the implant will inhibit it. If permanent pacemaker implant is considered, a permanent left ventricular electrode can be left in place and insulated in the subcutaneous tissue. Should permanent pacing be required it can be established by connecting a generator to t h a t electrode. Acute myocardial infarction. Indications for pacing in acute myocardial infarction have undergone profound change from recommendation t h a t many patients ~'~should be paced to a therapeutic nihilism which held that mortality rates are unchanged with or without pacing2 ~ The recognition that prognosis of block varies whether the infarct is anterior or inferior has caused a teassessrnent of the indications. ~ Anterior infarction with complete heart block implies massive myocardial damage, and cardiogenic shock and/ or congestive heart failure cause death in over 50 per cent of patients2 ~, ~ For the inferior infarct the collected mortality rate is about 25 to 40 per cent/~,. ~1 In the former, death may occur despite successful pacing; in the latter, survival is usual without need for pacing. Nevertheless, some patients persist in heart block, survive, and
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depend on p e r m a n e n t pacing for prolonged survival. Aside from the d e v e l o p m e n t of secondor third-degree A-V block, those with a c u t e m y o c a r d i a l infarction develop b r a d y a r r h y t h m i a s , sinus b r a d y c a r d i a S-A block in 5-20 per c e n t : "~. ~3 and t a c h y a r r h y t h m i a in a b o u t o n e - q u a r t e r of patients. ~- ~5 B o t h can be m a n a g e d with pacing a n d / o r medications as necessary and frequently better in a c o m b i n a t i o n of both. T h e indications for pacing during a c u t e m y o c a r d i a l infarction at present are: 1. S y m p t o m a t i c bradycardias, including sinus bradycardia, S-A block, and sick sinus syndrome. 2. Drug-resistant t a c h y a r r h y t h m i a s . 3. A c u t e onset of right or left bundle or bifascicular block. 4. A c u t e onset of Mobitz I I or complete A-V block with anterior infarction. 5. R h y t h m s p r o b a b l y n o t requiring pacing are Mobitz ! (Wenckebach) block or complete A-V block during inferior infarction and a rate of 40 to 50 or above w i t h o u t periods of greater b r a d y c a r dia, asystole, or escape ventricular p r e m a t u r e c o n t r a c t i o n s which are readily controlled with drugs. Of perhaps greater i m p o r t a n c e is the prognosis of the patient who develops new bundle b r a n c h block during the course of acute m y o c a r d i a l infarction b u t never develops second degree or third degree A-V block. ~r '~ Such a patient is likely to go u n p a c e d b u t early post-recovery m o r t a l i t y m a y be high. T h o s e with new right bundle b r a n c h block and left axis deviation or right axis deviation, i.e., left anterior or posterior hemiblock, carry an especially high m o r t a l i t y rate with 25 per cent of such patients dying suddenly during the first post-infarction year. T h e p r o p h y lactic m a n a g e m e n t of such patients is still in dispute, most likely because neither the techniques for detecting the severity of the persistent block nor those provocative tests now available have a d e q u a t e diagnostic specificity. Newly developed approaches to bundle of His recording with the electrode for t e m p o r a r y pacing during its removal. "pull-out His recording" have already begun ~o add to t h a t specificity. Over 80 per cent of patients can have a simple His potential recording performed during removal of a conventional ~emporary pacing electrode. ~ In these patients o m i n o u s findings such as a split His potential ~ or m a r k e d l y prolonged H-V time.
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alone or during lidocaine administration, have distinct prognostic value. 7~ Further, s y m p t o m a t ic, u n p a c e d post-infarct patients with H-V time longer t h a n 65 msec. b u t no o t h e r evidence of h e a r t block, have a m o r t a l i t y rate of 69 per cent c o m p a r e d to 20 per cent for similar patients subjected to p e r m a n e n t pacingY 1 S u c h specificity m a y well reduce the t o t a l n u m b e r of patients who, having seemingly recovered from acute m y o c a r d i a l infarction, die suddenly. Finally a c a u t i o n a r y word concerning temporary pacing during a c u t e m y o c a r d i a l infarction. T h o s e with ischemic h e a r t disease and acute m y o c a r d i a l infarction are maximally sensitive to ventricular fibrillation 72 and especially to the a n o d a l stimulus from the almost universally used bipolar t e m p o r a r y electrode falling in the vulnerable period of the cardiac cycle. ~:~ Loss of pacer sensing because of decrease in Q R S amplitude can be as high as 15 per cent TM during acute infarction. U n d e r those circumstances pacer stimuli m a y become competitive and 14 of the 30 reported and d o c u m e n t e d cases of pacemakercaused ventricular fibrillation have been from a competitive pacer during a c u t e myocardial infarction, so t h a t caution m u s t be exercised, Pacer function m u s t be frequently assessed, and the use of the unipolar c a t h o d a l stimulation with the anode out of the ventricle m u s t be consideredY 5 REFERENCES
1. Zoll, P. M.: Resuscitation of the heart in ventricular standstill by external electrical stimulation, N. EngL J. Med. 247:768, 1952. 2. Weirich, W. L., Gott, V~ L., and Lillehei, C. W.: The treatment of complete heart block by the combined use of a myocardial electrode and an artificial pacemaker, Surg. Forum 8:360, 1957. 3. Lagergren, H., and Johansson, L.: Intracardiac stimulation for complete heart block, Acta Chir. Scand. 125:562, 1963. 4. Chardack, W. M., Gage, A. A., Federico, A. J, Schimert, G., and Greatbatch, W.: Five years' clinical experience with an implanted pacemaker; an appraisal, Surgery 58:915, 1965. 5. Chardack, W, Gage, A. A., and Greatbatch, W.: A transistorized self-contained implantable pacemaker for the long term correction of complete heart block, Surgery 48:643, 1960. 6. Friedberg, C. K., Donoso, E., and Stein, W. G.: Nonsurgical acquired heart block, Ann. N. Y. Acad. Sci. 111:835, 1964. 7. Lemberg, L., Castellanos, A., and Berkovits, B.: Pacing on demand in A-V block, J.A.M.A. 191:12, 1965. 8. Parsonnet, V., Zucker, I: R., Gilbert L., and Myers, G. H.: Clinical use of an implantable standby pacemaker, J.A.M.A. 196:784, 1966.
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operative cardiac surgical patients, J. Thorac. Cardiovasc. Surg. 55:271, 1968. Litwak, R. S., Kuhn, L. A., Gadboys, H. L., Lukban, S. B., and Sukurai, H.: Support of myocardial performance after open cardiac operations by rate augmentation, J. Thorac. Cardiovasc. Surg. 56:484, 1968. Lajos, T. Z.: Pacemaker wire extension for permanent and temporary pacing, Ann. Thorac. Surg. 15:207, 1973. Parsonnet, V., Cuddy, T. E., Escher, D. J. W., Furman, S., Morse, D., Gilbert, L., and Zucker, I. R.: A permanent pacemaker capable of external non-invasive programming, Trans. Am. Soc. Artif. Intern. Organs 29:224, 1973. Bruce, R. A., Blackmon, J. R., Cobb, L. A., and Dodge, H. T.: T r e a t m e n t of asystole or heart block during acute myocardial infarction with electrode catheter pacing, AM. HEART J. 69:460, 1965. Chatterjee, K., Harris, A., a n d Leatham, A.: The risk of pacing after infarction, and current recommendations, Lancet 2:1061, 1969. Godman, M. J,, Lassers, B. W., and Julian, D. G.: Complete bundle-branch block complicating acute myocardial infarction, N. Engl. J. Med. 282:237, 1970. Norris, R. M.: Heart block in posterior and anterior myocardial infarction, Br. Heart J. 31:352, 1969. Resnekov, L., and Lipp, H.: Pacemaking and acute myocardial infarction, Progr. Cardiovasc. Dis. 14:475, 1972. Christiansen, I., Haghfelt, T., and Amtorp, O.: Complete heart block in acute myocardial infarction: drug therapy, AM. HEART J. 85:162, 1973. Hatee, L., and Rokseth, R.: Conservative t r e a t m e n t of AV block in acute myocardial infarction, Br. Heart J. 33:595, 1971. Imperial, E. S., Carballo, R., and Zimmerman, H. A.: Disturbances of rate, rhythm, and conduction in acute myocardial infarction, Am. J. Cardiol. 5:24, 1960. Lown, B., Hood, W. B., Fakhro, A. M., Kaplinsky, E., and
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Roberge, G.: Unresolved problems in coronary care, Am. J. Cardiol. 20:494, 1967. E1-Sherif, N.: Tachycardia and bradycardia dependent bundle branch block after acute myocardial ischemia, Br. Heart J. 36:291, 1974. Hass, J.: Mechanisms of ventricular arrhythmias associated with myocardial infarction, Am. J. Cardiol. 24:800, 1969. Atkins, J. M., Leshin, S. J., Blomquist, G., and Mullins, C. B.: Ventricular conduction blocks and sudden death in acute myocardial infarction, N. Engl. J. Med. 288:281, 1973. Gould, L., Venkataraman, K., Mohammad, N., and Gomprecht, R. F.: Prognosis of right bundle branch block in acute myocardial infarction, J.A.M.A. 219:502, 1972. Fisher, J.: Unpublished data. Narula, O. S., Scherlag, B. J., Samet, P., and Javier, R. P.: Atrioventricular block: localization and classification by His bundle recordings, Am. J. Med. 50:146, 1971. Vera, Z., Mason, D. T., Fletcher, R. D., Awan, N. A., and Massumi, R. A.: Prolonged His-Q interval in chronic bifascicular block. Relation to impending complete heart block, Circulation 53:46, 1976. Altschuler, H., Fisher, J., and Furman, S.: Unpublished data. Bilitch, M., Cosby, R. S., and Cafferky, E. A.: Ventricular fibrillation and competitive pacing, N. Engl. J. Med. 276:598, 1967. Preston, T. A.: Anodal stimulation as a cause of pacemaker induced ventricular fibrillation, AM. HEART J. 86:366, 1973. Chatterjee, K., Sutton, R., and Davies, J. G.: Low intracardiac potentials in myocardial infarction as a cause of failure of inhibition of demand pacemakers, Lancet 1:511, 1968. Preston, T. A.: Temporary unipolar pacing using a dual cathode, J. Electrocardiol. 9:193, 1976.
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