Electrical Cardioversion for AF -- The State of the Art

Nicholas P. Gall, M.Sc., M.D., M.R.C.P.; Francis D. Murgatroyd, M.A., F.R.C.P., F.A.C.C.


Pacing Clin Electrophysiol. 2007;30(4):554-567. 

In This Article


Developments in ablation therapy and improved device technology have changed cardiac electrophysiology beyond recognition in the two decades. Atrial fibrillation (AF) is currently attracting particular interest, in part due to its increasing prevalence and thus its impact on healthcare resources,[1,2,3,4,5] in part due to our greater understanding of its pathophysiology and particularly due to the recently realized potential for cure, at least in a proportion of patients.[6] Intuitively, the restoration and maintenance of sinus rhythm would seem to be the ultimate goal of therapy; it had been assumed that this would improve patient symptomatology and prognosis. Recent studies, however, suggest that for many adequate thromboprophylaxis, rate control is at least as good as a rhythm control strategy.[2,7,8,9,10] However, these studies focus on those over the age of 65 or those with thromboembolic risks and therefore are not necessarily applicable to those younger or the highly symptomatic. In these patients, a rhythm control strategy may be preferable; indeed where this strategy was successful in the AFFIRM study it was associated with improved prognosis.[11] AF ablation also appears to be of prognostic benefit in some groups.[12] Furthermore, in some cases, an identified precipitant (e.g., intoxication, thoracotomy) or an acute illness (e.g., thyrotoxicosis, pneumonia) precipitates an episode of sustained AF. In these patients, long-term maintenance of sinus rhythm seems achievable.

For those with persistent AF, the first step in a rhythm control strategy is generally cardioversion. While chemical-induced cardioversion is sometimes possible, particularly with full loading with amiodarone,[2,13] it is generally much less successful than electrical cardioversion, particularly if the arrhythmia has been present for more than 24 hours. Electrical cardioversion, therefore, remains key to the management of these patient groups. While the basic technique of cardioversion has changed little over the years, recent evidence and technological improvements make a review of current practice timely. In this article, we will concentrate on these developments. The focus will be on technical issues and anti-arrhythmic efficacy rather than on thromboembolism and its prevention. It is appropriate initially however to summarize the historical background and the evidence for the best conventional cardioversion technique.

Zoll et al. first described cardioversion[14] in the context of defibrillation of ventricular fibrillation. Subsequently, Lown et al. used this technique in 1962[15] on a small group of patients with either ventricular tachycardia or AF. The 1962 procedure differs very little from that performed today. Paddles were placed in an antero-apical (AA) position with conductive paste between skin and paddle applied with firm pressure. A 2.5 ms pulse of DC energy was given timed to the R-wave with energies between 0 and 400 J. Most patients were undergoing mitral valve surgery -- general anesthesia was used in the small number of patients who were. The same group subsequently published a larger study[16] in 50 patients -- again, most with associated mitral valve disease -- with 65 episodes of AF. An 89% success rate was achieved, after up to five shocks. Only one complication was documented, relating to thromboembolism in a non-anticoagulated patient.

From these and subsequent studies, it became clear that cardioversion was unsuccessful in at least 30% of patients (though at that stage the distinction between absolute failure and clinical failure due to immediate recurrence of AF was not made).[17] Predictors of failure included the age of the patient, the duration of the arrhythmia, the patient's body habitus, and the underlying cardiac condition. A number of investigators have examined the contribution of technical variables to the success of cardioversion and these will be reviewed in this article. However, it would be pertinent first to give an overview of our knowledge of the pathophysiology of AF and the physics of cardioversion.

As with other arrhythmias, information from the interventional electrophysiology laboratory and experimental observations have led to the rapid evolution of our understanding of the pathogenesis of AF.[18,19] It is now clear that AF requires triggers for its initiation and a substrate for its maintenance. Since the seminal paper of Haissaguerre et al.,[6] highlights the importance of rapidly firing ectopic foci in and around pulmonary veins, it is now clear that these foci (and ectopic activity arising largely from other venous-atrial interfaces) are critical in AF induction. This is the basis for the pulmonary vein isolation procedure. Current theories suggest that areas of both fixed and functional block in the atria interact with these foci setting up multiple wavelets of re-entry, anisotropic re-entry. In addition, parts of the myocardium may not be able to conduct one-to-one with these rapidly firing foci leading to so-called fibrillatory conduction. These foci may also perpetuate the arrhythmia and have become known as drivers. Single re-entrant circuits, mother rotors, can also act as drivers. More recent evidence suggests that rapidly firing extravenous foci[20] perhaps related to local parasympathetic ganglia may also play a significant role.[21] With time, due to the rapid and repeated activation of atrial myocytes, remodeling occurs, both structural and electrophysiological. Intracellular calcium overload leads to activation of an immediate early gene response. Ion channel changes alter myocyte electrophysiology. Conduction velocity decreases, the action potential shortens as does the atrial refractory period. There is also loss of the normal variation in the refractory period with changes in heart rate. Activation of the renin-angiotensin and redox signaling systems is also important in this process,[22] at least in the short-term.[23] These electrophysiological changes are progressive and lead to the perpetuation of fibrillation.[24] With the return of sinus rhythm, by whatever means, these short-term electrophysiological changes are reversible, at least in experimental preparations. Cardioversion at this stage, therefore, may halt or reverse this electrical "remodeling" (see later). As AF persists, however, irreversible structural changes occur including fibrosis and cell death, both necrotic and apoptotic, contributing to the AF substrate, thus increasing the risk of recurrence.

Much of what is known about the physics of defibrillation is derived from studies of ventricular fibrillation.[25] As discussed, AF is an arrhythmia characterized by multiple, random re-entrant wavelets circulating in both atria. Cardioversion aims to induce a co-ordinated change in the action potential in a significant proportion of the atrial myocardium -- a critical mass -- such that the wavelets terminate and normal electrical activity can resume. If too little energy is used, sufficient wavelets may persist to reinitiate the arrhythmia. The shock produces a current gradient across the myocardium which affects the myocytes according to their state of activation; depolarization or hyperpolarization may occur depending on their location with respect to each individual electrode. If the shock occurs during the action potential little effect may be seen, although if it is of large enough magnitude and early enough the action potential may be prolonged. Later in the action potential, further depolarization may be induced. The precise mechanisms of defibrillation at a microscopic level remain poorly understood, however.

The major determinant of shock success is the current density. This depends upon the energy used, the current path, and the transthoracic impedance (TTI) between the shock electrodes. Too little energy will not terminate the arrhythmia; for external shocks perhaps as little as 4% of the energy given affects the myocardium. There are a number of determinants of TTI[26] including paddle characteristics (size, constitution, and positioning), the couplant used to conduct the charge from the electrode to the skin, the number of shocks, the timing between shocks, and the electrical conductivity of the tissues between the electrodes and the heart.

Complications of cardioversion are fortunately very rare particularly if care is taken as to technique and pre-procedural preparation. Potential complications relate to the general anesthetic, the induction of ventricular arrhythmia with non-QRS synchronized shocks, thromboembolic events if there has been inadequate anti-coagulation, and skin burns from the external paddles. In patients with pacemakers or defibrillators care is needed to ensure that the cardioversion current is not conducted along the leads damaging the lead-myocardial interface. The most frequent complications relate to a failure to cardiovert or to the reappearance of AF soon after the procedure. The latter has been divided into the immediate reinitiation of AF (IRAF), where reinitiation occurs within a very short time period, perhaps a minute or two; early reinitiation where AF recurs within a week or two; and late recurrences.[27] The differentiation of the "failure mode" is clearly important as the management of the complete failure to cardiovert (see Section 2) differs markedly from the management of an immediate or early recurrence (see Section 3).

As expected, inadequate patient preparation, particularly with regard to anti-coagulation, and anesthetic are the major contraindications to cardioversion other than in the hemodynamically unstable patient.


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