© 2002 by European Society of Cardiology
Copyright © 2002, European Society of Cardiology
Defibrillation and cardioversion
Lown Cardiovascular Center, 21 Longwood Ave., Brookline, MA 02446, USA
Received 18 March 2002; accepted 26 March 2002
Going back to the ‘archaic past and to obsolete ancestors’ [1] provides insight not only where we came from but where we might be heading. Indeed history matters in medicine as it does in everyday life. It is now 40 years since the introduction of DC defibrillation and cardioversion [2,3]. Like the proverbial pebble cast in the water, the ripple effects of these technologies extend beyond the horizon of early prediction. Among the more important consequences were: stimulating the development of coronary care units, facilitating the emergence of coronary bypass and other heart operations, focusing attention on the still formidable out-of-hospital problem of sudden cardiac death, advancing the field of clinical electrophysiology and contributing to implantable devices to protect against death from malignant arrhythmias. Most important are the countless lives saved with this straightforward medical advance.
From time immemorial, drugs, potions and herbs were the mainstay in treating arrhythmias of the heart. This therapeutic approach presented formidable limitations. In the individual patient the effective dose of the drug was unknown. A tedious biological titration was required to avoid serious or even life threatening toxic reactions. When the arrhythmia was ventricular tachycardia, the route for administering drugs was necessarily intravenous, thereby maximizing the likelihood of adverse reactions. When drugs were given orally, the required incremental dosing consumed hours and at times days. Even with the most scrupulous monitoring, toxic reactions were nearly unavoidable.
Looking back it is remarkable how the clinical topography has changed since the introduction of DC defibrillation and cardioversion. One example may be illustrative. Levine, during 33 years of clinical practice, observed only 137 episodes in 107 cases of paroxysmal ventricular tachycardia [4]. This represents approximately three patients annually; it may be far less, since all wide complex tachycardias were designated as ventricular. In contrast during the 3 years after introducing cardioversion, I saw as many patients presenting with a thousand or more episodes. One patient with oft-recurrent drug refractory tachycardia was reverted more than 100 times. Evidently, before the advent of cardioversion, the overwhelming majority of patients with ventricular tachycardia died as a result of their initial episode.
Perhaps the seed of an idea to develop a new approach for controlling all types of tachycardias was planted during the many long night vigils with patients afflicted with these cardiac disorders who did not respond to the few drugs then available. From the wisdom provided by hindsight, it is likely that I would not have resorted to studying electrical discharge unless there was a reasonable basis in the physiology of these disorders to suggest potential effectiveness. What was new, at least in my thinking, was the view that precipitating factors were accidental, namely a combination of impermanent conditions unlikely to reconfigure. It followed that if the tachycardia was terminated, by whatever means, it would not immediately recur. How then was the arrhythmia maintained once initiated? Ample physiological data suggested that the arrhythmia was sustained by recirculation of the wave front of excitation over a fixed or variable pathway or pathways. It followed that if the wave front could be momentarily interrupted, the arrhythmia would cease. Whether it would then promptly recur was uncertain, but seemed unlikely if indeed its initiation was due to an accident.
The above speculations had substantial antecedents in the physiological investigations carried out at the turn of the 20th century. The concept that an arrhythmia was maintained by a recirculating wave front of excitation was demonstrated in the medusa by the American marine biologist A.G. Mayer [5]. The distinguished British physiologist and clinician, Thomas Lewis was among the first to grasp the clinical significance of this observation [6]. Lewis found that most tachyarrhythmias, once initiated, were self-sustaining. He surmised that this was due to the presence of what he designated as a circus movement dependent on an appropriate relation of three factors, namely, the speed of conduction, the refractory period duration and the length of the pathway over which the wave front of depolarization traversed. I was exposed to the ideas of Lewis through my great teacher and unmatched bedside clinician, Dr Samuel A. Levine. He together with Dr Paul D. White were students of Lewis during World War I [7].
Data from numerous reported animal studies persuaded me that momentary electrical depolarization of the heart could extinguish the disordered rhythm by erasing abnormal reentry circuit or circuits. The sinus node, possessing the highest cardiac automaticity, would then resume its role as the dominant pacemaker. While the concept was straightforward, its implementation was extraordinarily complex. Despite the seeming soundness of the theory, a transthoracic electrical method did not emerge until the mid 1950s when Zoll introduced alternating current (AC) for defibrillating the heart [8].
Since AC was exclusively used on patients being resuscitated from sudden death, the safety and efficacy of the device did not seem critical and had not been tested. When I wished to extend the uses of electrical discharge to other tachyarrhythmias, these issues became paramount. It turned out that AC was not consistently effective, worse still, it was enormously hazardous [9]. It burned underlying muscle, provoked a spate of cardiac arrhythmias, ventricular as well as atrial fibrillation, and injured the myocardium. These adverse consequences precluded its clinical use.
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1 Direct current (DC) defibrillation |
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 Top 1 Direct current (DC)... 2 Cardioversion3 Ventricular tachycardia4 Atrial fibrillation (AF)5 Final commentsReferences |
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The question therefore was not only whether instant depolarization of the heart by electric discharge would abolish a sustained tachyarrhythmia but how to make electricity safe for human use. We turned to capacitor discharge. This had ancient antecedents. Indeed the history of electrical applications to the heart begins in the 18th century with direct current derived from a Leyden jar. Priority belongs to Abildgard who in 1775 relates to having shocked a single chicken into lifelessness and upon repeating the shock, the bird took off and eluded further experimentation [10]. Benjamin Franklin, was a pioneer in experimentation with electricity as in much else. At about the same time as Abildgard, he shocked a host of animals with static electricity. During his kite flying experiments, he was knocked senseless several times by lightning. Medical history does not recount whether any arrhythmias were induced. These brave experiments led Franklin to the observation, "If there is no other use discovered for electricity, this however is something considerable that it may help make a vain man humble." [7]
We set ourselves two preconditions: that the electrical discharge during transthoracic application should depolarize the entire myocardium and equally important that the discharge not injure heart or subjacent tissues. The problem we faced is the endless variety of wave forms obtained by modifying the parameters of the DC discharge circuit. There was no a priori physiological basis for selecting any particular wave form as suitable for human use. This could only be derived from extensive modification of the capacitor and inductor in the discharge circuit, while determining both its safety as well as effectiveness to defibrillate the canine heart.
After a year of extensive animal experimentations, we found that an under-damped sine wave discharge consistently terminated ventricular tachycardia and ventricular fibrillation. This was true as well in the markedly hypoxic, acidotic and ischemic heart and was not associated with detectable heart or skeletal muscle damage. Only multiple oft-repeated discharges of 400 J resulted in intraventricular block and currents of injury sometimes associated with ventricular arrhythmias. The DC defibrillator we had developed was rapidly adopted world-wide and became the standard of care for cardiac resuscitation [2].
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2 Cardioversion |
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Top1 Direct current (DC)...2 Cardioversion3 Ventricular tachycardia4 Atrial fibrillation (AF)5 Final commentsReferences |
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The intent was to develop an electrical instrument that was safe for elective termination of a host of tachyarrhythmias. One vexing problem surfaced early limiting the use of DC discharge in humans. This related to the infrequent yet consistent provocation of ventricular fibrillation (VF) after some transthoracic DC discharges. The phenomenon was totally random and noted in less than 2% of normal dogs. One could not be certain that the incidence would not be much higher in patients with organic heart disease who are the very patients presenting with arrhythmias requiring electrical reversion.
Ignorance of the history of cardiovascular physiology caused me to waste enormous time in attempting to understand a phenomenon long familiar to physiologists. In 1914, the brilliant British physiologist, George R. Mines, studied this very problem. He observed the onset of VF after applying directly to the rabbit heart a single brief duration electrical shock from an induction coil. He timed the discharge to occur in various periods of the cardiac cycle. Mines discovered that if a shock was delivered during early electrical diastole, fibrillation could be induced [11]. For the first time, he identified a narrow zone in electrical diastole during which the heart was extremely vulnerable to ventricular fibrillation [12].
If the heart was susceptible to VF only during a brief, fixed interval in the cardiac cycle, this period could be readily avoided. We found that the vulnerable period for VF coincided with inscription of the apex of the T wave in the surface electrocardiogram, representing the terminal portion of the refractory state when adjacent heart fibers were in differing states of repolarization. There was ample evidence that such a vulnerable state exists in man. The solution was straightforward namely to synchronize the electrical discharge to fall outside the vulnerable period. I named the process of reverting tachyarrhythmias transthoracically with a carefully timed DC discharge ‘cardioversion,’ the instrument a ‘cardioverter’ and to ‘cardiovert’ the act of restoring sinus rhythm electrically.
The first generation instruments had a timing pod permitting the operator to set manually the discharge anywhere in the cardiac cycle. While the instructions to avoid the vulnerable period seemed clear, nonetheless, much confusion ensued and many inadvertent cases of VF were reported induced by discharging the shock to fall at the apex of the T wave. Though in several articles and numerous lectures the danger of the T wave for triggering a discharge was emphasized, apparently this was forgotten and all that was recalled was the apex of the T wave as target rather than to be scrupulously avoided. We thereupon removed from cardioverters all self-actuated timing devices and automatically triggered the discharge from the QRS complex.
Cardioversion, is by definition, synchronized direct current discharge, and thus this term does not apply to ventricular defibrillation or to the pharmacologic reversion of arrhythmias. By employing a capacitor discharge with a specific under-damped pulse and timing release of the pulse within a safe part of the cardiac cycle, the twin dangers of electricity, namely ventricular standstill and fibrillation were avoided.
Cardioversion was first employed in 1961, at the Peter Bent Brigham Hospital in Boston, in a woman in the throes of an acute myocardial infarction with frothing pulmonary edema due to drug refractory ventricular tachycardia. A single 100 J discharge restored sinus rhythm. Remarkably within 3 min, she was entirely free of pulmonary congestion. The event seemed miraculous. Even more so since the dazed patient thought that she was in the ‘hereafter.’ We had a difficult job persuading her that she was in a hospital not in heaven.
As a historic footnote—it needs be noted that research funds for the early stages of this endeavor were refused by the National Institute of Health and publication of the first manuscript was rejected, the reviewer opined that the technology had ‘little clinical relevance.’ It was press and radio that acquainted doctors with these new methodologies and promoted the rapid acceptance of cardioversion thus heralding the modern age of media dominance in medical communication. Within a year, cardioversion became the standard of care.
In this brief communication, only two most common arrhythmias will be addressed, namely, ventricular tachycardia and atrial fibrillation.
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3 Ventricular tachycardia |
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Top1 Direct current (DC)...2 Cardioversion3 Ventricular tachycardia4 Atrial fibrillation (AF)5 Final commentsReferences |
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The most dramatic effects of cardioversion are observed in patients with ventricular tachycardia. Unlike the response when using antiarrhythmic drugs, the outcome is nearly instantaneous. There is no negative inotropic effect, blood pressure does not plummet and the sinus node is not depressed with threatening bradycardia requiring pacemaker insertion. In fact the opposite occurs, blood pressure and ventricular contractility are improved immediately upon resumption of sinus rhythm. Patients with recurrent ventricular tachycardia who previously required long hospitalizations now could be managed on an outpatient basis.
The success rate with cardioversion of ventricular tachycardia is generally around 95%. This is independent of the pathogenesis of the arrhythmia whether provoked by acute myocardial infarction or by other factors. The energy required to restore sinus rhythm proved to be very low unlike the case with ventricular fibrillation. In a large experience we found that 10 J would revert about 50% of the episodes. It was rare that one failed with 100 J. This was also true with atrial flutter, even lesser energies sufficed in the order of 0.5–5 J, but with atrial as well as with ventricular fibrillation 100 J or higher settings were required. Why a single reentry path can be so readily subdued, while the presence of multiple more chaotic circulating wavelets are resistant awaits explanation.
The availability and ease of use of cardioversion as well as the almost simultaneous introduction of Lidocaine [13], removed the challenge of terminating ventricular tachycardia. The far bigger problem was how to prevent recurrences of this potentially malignant arrhythmias in the numerous patients surviving a first episode.
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4 Atrial fibrillation (AF) |
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Top1 Direct current (DC)...2 Cardioversion3 Ventricular tachycardia4 Atrial fibrillation (AF)5 Final commentsReferences |
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While cardioversion was introduced for drug refractory ventricular tachycardia, by far the commonest arrhythmia treated was atrial fibrillation. It is the most frequent sustained cardiac rhythm disorder and will continue to increase in frequency as the population ages. AF is estimated to have an incidence of over 5% among individuals 65 and older [14].
Being initially clueless which patients with AF to cardiovert, we treated all comers. We even attempted to revert someone for 23 years in continuous fibrillation. With experience, clinical guidelines began to emerge. A flood of patients from all over the world, permitted prompt insight of the factors conducing to success and those leading to complications. The duration of AF was key determinant of the ease of restoring NSR. Among the first 350 patients involving 456 episodes of AF, 94% were successfully reverted. Only 2% failures were encountered when the arrhythmia was present for 3 months and the mean effective energy was 87 J. When the arrhythmia had been present for as long as 10 years, the failure rate was 39% and the mean energy required was 240 J. The longer the persistence of the AF, the higher the complication rate [7]. On the basis of a far larger experience, we concluded that reversion should not be attempted when AF had been continuously present for a year or longer.
The problem dogging at the heels of successful reversion was the prompt recurrence of AF. A number of electrocardiographic features immediately after cardioversion predicted failure to maintain a normal mechanism. The importance of such findings after the fact would seem of scant clinical importance. On the contrary, these observations precluded repeat attempts of cardioversion and furthermore enabled prediction of outcome from electrocardiographic features present before the onset of AF.
The speed of restoration of sinus rhythm was found to be a powerful predictor of whether a normal rhythm would persist. We observed three types of transitions to a normal mechanism following cardioversion. In the majority, sinus rhythm was restored instantly with regularly discharging well formed slow P waves which accelerated within less than a minute to the patient's usual heart rate. Such robust sinus mechanisms when unaccompanied by frequent atrial ectopic activity indicated the long sustenance of a normal mechanism. In the second category, designated ‘somnolent sinus,’ a regular junctional rhythm emerged with atrial ectopic activity before a slow sinus mechanism assumed dominance. Such a transition augured a higher recurrence rate of AF. The third mechanism which I named the ‘sick sinus’ was associated with a slow junctional rhythm interrupted by flurries of ectopic tachycardia with varying rates accompanied by brief paroxysms of atrial flutter of AF. Characteristic was the changing morphology of the P wave frequently diminutive and barely recognizable. The striking ever changing configuration of the P wave was specially noteworthy in intratrial electrograms. Invariably and happily, atrial fibrillation resumed within minutes. In those patients in whom a chaotic rhythm persevered, a temporary pacemaker was required until AF returned.
AV conduction duration was another predictor of outcome [7]. Consistently the P–R interval is prolonged in those who develop AF. In fact rarely does one encounter a short P–R interval other than in the very minuscule subset with WPW or LGL syndromes. When this interval is greater than 0.32 s, AF is more likely to recur. It appears that prolonged AV conduction is a precondition for the emergence of AF. Perhaps for AF to occur requires a reentry pathway with an intrinsically long refractory period. This electrocardiographic observation helps predict when AF is likely to emerge. For example in patients with mitral valvular disease, a lengthening P–R interval augurs onset of AF. If monitoring patients with first degree heart block, reveals the presence of frequent extrasystoles and specially nocturnal mini bursts of AF, small doses of prophylactic antiarrhythmic drugs may delay for many years the onset of the sustained arrhythmia.
An unexpected finding was the observation that the size of fibrillatory ‘f’ waves was a prognostic factor. The larger ‘f’ wave amplitude (best measured in lead V1), the less energy required to restore sinus rhythm and the more enduring will be the normal mechanism. The explanation is straightforward: atrial size is a key predictor of the ease of reversion and of maintenance of sinus rhythm. Furthermore, the larger the atrium the smaller the ‘f’ waves [15]. If f waves are barely detectable, large energies will be required and a sick sinus syndrome may be the consequence of cardioversion. Recent data are confirmatory of this observation and suggest that recurrence of arrhythmia is predicted by a left atrial size of 45 mm or greater and a less than 10% increase in the ‘a’ wave on Doppler echocardiography following cardioversion [16]. Doppler echocardiography is useful in documenting the presence of atrial contraction, as the absence of an atrial ‘a’ wave suggests electromechanical dissociation.
We learned that higher energy levels were required to terminate AF in congestive heart failure. Restoration of cardiac compensation and achievement of a dry weight before cardioversion increased the success rate. The polycythemic individual may be difficult or impossible to revert until adequate phlebotomy lowers the hematocrit to less than 50. We also observed that patients with severe mitral valve disease having giant scarred atria who have had valve repair or replacement are recalcitrant to cardioversion and do not persist in sinus rhythm.
In summary, the maintenance of NSR following cardioversion of AF is dependent on factors such as the duration of arrhythmia, size of the left atrium, the state A-V conduction, presence of valvular heart disease, the patient's age, and a host of lesser variables. We rapidly discovered that while the heart can be readily depolarized transthoracically, resumption and most especially maintenance of sinus rhythm are not thereby assured.
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5 Final comments |
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Top1 Direct current (DC)...2 Cardioversion3 Ventricular tachycardia4 Atrial fibrillation (AF)5 Final commentsReferences |
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DC defibrillation and cardioversion, though developed through long and arduous animal experimentation and human studies, are now taken for granted akin to the sphygmomanometer or the electrocardiogram. Substantial medical advances followed the introduction of a simple and safe defibrillator and the cardioverter. The research agenda now addresses a problem that cardioversion could not resolve, that of preventing arrhythmia recurrence. Effective approaches are now being introduced permitting radio ablation of the pathologic nidus of ventricular tachycardia. Progress in dealing with atrial fibrillation has been slower. Promising is that in a number of patients with AF, the initiating zone for the ectopic activity is lodged in the pulmonary veins and therefore lends itself to eradication [17]. No doubt newer discoveries totally unimagined at the moment will be entering the proscenium to prevent tachyarrhythmias. The ultimate in prevention will be to identify and protect the susceptible individual. Until such a time, defibrillation and cardioversion will remain indispensable technologies.
In ending, a small footnote to history is appropriate. I desisted patenting either the DC defibrillator or the cardioverter. I reflect without regret on the material riches denied me as a consequence. Yet at this final stage of life there is a sense of deep fulfillment for returning the discoveries to those who ultimately made the investigations possible.
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Notes |
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1 Professor of Cardiology Emeritus Harvard School of Public Health. Physician Brigham and Women's Hospital, Boston, MA, USA. Co-founder International Physicians for the Prevention of Nuclear War. Founder and Chairman SatelLife.
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Top1 Direct current (DC)...2 Cardioversion3 Ventricular tachycardia4 Atrial fibrillation (AF)5 Final commentsReferences |
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