Cardioversion for specific arrhythmias

INTRODUCTION — Electrical cardioversion and defibrillation are commonly used procedures in the management of patients with cardiac arrhythmias.

●Cardioversion is the delivery of energy to the chest that is synchronized to the QRS complex and is used for converting rhythms in patients who are hemodynamically stable and tend to have monomorphic QRS complexes. As an example, elective outpatient cardioversions are routinely performed on patients with persistent atrial fibrillation (AF) to restore sinus rhythm (movie 1).

●Defibrillation is asynchronous delivery of a shock randomly during the cardiac cycle and is typically used during a cardiac arrest caused by ventricular fibrillation.

This topic will review the clinical settings in which electrical cardioversion and defibrillation are used, along with a brief discussion of the complications that can occur independent of the arrhythmia that is being treated. The basic principles and technique of electrical cardioversion and defibrillation, the specific indications for external cardioversion and defibrillation, and the use of the automated external defibrillator are presented separately. (See "Basic principles and technique of external electrical cardioversion and defibrillation" and "Automated external defibrillators".)

EXTERNAL CARDIOVERSION/DEFIBRILLATION

Preparation and personnel — Nonemergency electrical cardioversion should ideally be performed in a controlled environment with monitoring capabilities and the nearby availability of emergency equipment should complications arise. The following are considered part of the routine preparation and monitoring involved in electrical cardioversion:

●Standard cardiorespiratory monitoring, including blood pressure, pulse, oxygen saturation, end-tidal CO₂ monitoring, and cardiac telemetry.

●Intravenous access for administration of sedation and for management of any rhythm-related complications (ie, ventricular fibrillation, sinus bradycardia, etc).

●Available supplemental oxygen, suction device, and intubation equipment for management of respiratory complications (though supplemental oxygen should be removed prior to delivery of the electrical shock) (see 'Supplemental oxygen' below).

●Available code cart with medications used in advanced cardiac life support in the event of life-threatening arrhythmias (see "Advanced cardiac life support (ACLS) in adults").

●There is considerable activation of thoracic skeletal muscles during a transthoracic shock that causes patients and their arms to move during a shock. For this reason, and because these patients are anticoagulated, padding or cushioning should be placed between the patient's extremities and any hard bed railings to avoid injury during cardioversion.

While many cardiologists are trained in the administration of moderate sedation, sedation may also be administered by an anesthesiologist who can immediately assist in the management of respiratory complications should any develop. An advantage of having an anesthesiologist routinely administer sedation for elective cardioversions is that at many hospitals, the use of ultra-short acting sedatives such as propofol is restricted to anesthesiologists. The tradeoff for such involvement is often added costs and scheduling complexity. (See "Procedural sedation in adults in the emergency department: General considerations, preparation, monitoring, and mitigating complications", section on 'Anticipating and mitigating Complications'.)

Elective cardioversions for AF and atrial flutter are usually performed by cardiologists but can also be safely performed autonomously by a midlevel provider. With appropriate training and a protocol that includes a guideline-directed procedural checklist (table 1), physician supervision, and sedation administered by an anesthesiologist, an advanced practice nurse can safely perform cardioversions autonomously with outcomes and patient satisfaction similar to those for cardioversions performed by a physician [1].

Supplemental oxygen — Supplemental oxygen is a fire hazard in the event of electrical arcing during external cardioversion or defibrillation. Because of this, supplemental oxygen flow should be stopped, or the oxygen delivery device (eg, nasal cannula, face mask, etc) removed from the patient, prior to the delivery of an external shock. Oxygen flow can be restarted after the shock has been delivered.

Paddle/pad placement — For electrical cardioversion of atrial tachyarrhythmias, particularly AF, an anterior-posterior pad position is preferred to anterior-lateral placement (figure 1) based on evidence from several randomized trials that have shown higher success rates and lower energy requirements for successful cardioversion with the anterior-posterior configuration [2,3]. The historical rationale for the superiority of the anterior-posterior position is a more favorable shock vector through the atria as well as reduced transthoracic impedance. Moreover, there is some evidence that applying external force to self-adhesive electrodes may decrease transthoracic impedance further [4]. However, pad placement may not significantly affect outcomes of cardioversion with contemporary defibrillator devices that employ impedance compensated biphasic waveforms [5]. For urgent cardioversion/defibrillation of unstable rhythms, an anterior-lateral pad configuration may be preferred for ease of application, and device manufacturer recommendations should be followed in all cases. (See "Basic principles and technique of external electrical cardioversion and defibrillation", section on 'Electrodes'.)

Energy selection — The amount of energy selected for initial attempts of cardioversion or defibrillation has been controversial. The energy selected should be sufficient to accomplish prompt cardioversion or defibrillation because repeated failures expose the heart to damage from prolonged ischemia and multiple shocks. On the other hand, excessive energy should be avoided, since myocardial damage from high-energy shocks has been demonstrated in experimental studies, although the frequency with which this occurs in humans is not known [6,7].

Early defibrillators delivered energy in a monophasic waveform, meaning that electrons flowed in a single direction. The newer defibrillators deliver a biphasic waveform, meaning that during the shock, polarity and electron flow reverse. In addition to reversing polarity, biphasic defibrillators also deliver a more consistent magnitude of current (figure 2). In general, biphasic defibrillators successfully terminate arrhythmias at lower energies than monophasic defibrillators. The relative efficacy of biphasic and monophasic defibrillators has been compared in a number of settings and is discussed in detail separately. (See "Basic principles and technique of external electrical cardioversion and defibrillation", section on 'Monophasic versus biphasic waveforms'.)

While nearly all available external defibrillators now use a biphasic waveform, it is still important to fully understand the type of waveform that is delivered when using an external defibrillator. For example, the Zoll brand of external defibrillators uses a truncated waveform that results in the delivery of more current to the heart compared to defibrillators made by other manufacturers that use a standard biphasic waveform, when set to deliver the same amount of energy in joules. Unlike most defibrillators that deliver a maximum energy of 360 joules, the Zoll defibrillators have a maximum energy setting of 200 joules but deliver similar current to the heart with comparable defibrillation efficacy. The energy selection recommendations in this topic are in joules and are for defibrillators that use a standard biphasic waveform. Lower energies can be used with defibrillators that use a truncated biphasic waveform.

In 2010, the American Heart Association issued guidelines for cardiopulmonary resuscitation and emergency cardiovascular care that discussed detailed starting energy levels for treatment of various types of arrhythmias [8]. In the 2014 AHA/ACC/HRS guidelines on the management of AF, no specific energy levels for cardioversion or defibrillation are discussed, but some broad concepts are presented. We agree with the suggested initial energy selection for specific arrhythmias as addressed in the society guidelines, with the following suggested initial energy requirements for monophasic and biphasic waveforms [8]:

●When available, a biphasic defibrillator is preferred due to greater efficacy.

●For AF, 120 to 200 joules (algorithm 1).

●For atrial flutter, 50 to 100 joules.

●For ventricular tachycardia with a pulse, 100 joules.

●For ventricular fibrillation or pulseless ventricular tachycardia, 200 to 360 joules (algorithm 2).

●To increase the likelihood of initial shock success and reduce the duration of sedation, a higher initial energy may be considered, particularly in obese patients or in patients known to be difficult to cardiovert.

When an external defibrillator is being prepared to deliver a rescue shock in the event that an implantable defibrillator fails to convert a patient during defibrillation threshold testing, the energy should be set to the maximum output and in the asynchronous mode.

Cardioversion with higher energy levels may be effective when prior cardioversion attempts using a maximal energy of 360 joules have failed to restore sinus rhythm. In one study, 55 patients who did not have sinus rhythm restored after at least two attempts of external cardioversion with 360 joules underwent cardioversion with 720 joules, which was performed by using two external cardioverters, each connected to its own pair of patches [9]. Sinus rhythm was restored in 84 percent of these patients with no major complications, hemodynamic compromise, or strokes occurring after the procedure.

As another option besides high-energy cardioversion, pretreatment with an antiarrhythmic drug can facilitate cardioversion at lower energy levels. Pretreatment with ibutilide prior to electrical cardioversion has been shown to significantly improve the rate of successful cardioversion to sinus rhythm and was also associated with the use of significantly lower energy levels to achieve cardioversion [10]. Amiodarone, sotalol, quinidine, and procainamide have also been shown to increase the likelihood of successful cardioversion or lower the energy threshold required for cardioversion [11]. When an antiarrhythmic drug is chosen, however, the potential side effects must be carefully considered. (See "Amiodarone: Adverse effects, potential toxicities, and approach to monitoring" and "Clinical uses of sotalol".)

Synchronization — When delivering energy to the chest to defibrillate a patient who is experiencing ventricular fibrillation, the energy is delivered promptly as soon as the shock button is pressed on the defibrillator.

In contrast, when cardioverting a patient who is hemodynamically stable, it is critical that the energy is not delivered during the electrically vulnerable period during the QT interval as this could inadvertently induce ventricular fibrillation. Synchronized cardioversion prevents induction of ventricular fibrillation by delivering the energy synchronous with the QRS complex.

●To perform synchronous cardioversion, the external defibrillator must be set to synchronous mode by pressing the "synchronize" button. This should result in markers displayed on what the device has determined are the QRS complexes during the arrhythmia.

●It is important to ensure that the markers are accurately placed on the QRS complexes before shocking the patient. When the QRS voltage is small, the markers may be inaccurate. At times, it may be necessary to select a different ECG lead that shows a prominent QRS complex to improve synchronization.

●When the defibrillator is set to synchronous mode, the shock button must be depressed and held until a QRS is detected and the shock is delivered.

●If the first shock fails to convert the arrhythmia and a second shock is being planned, it is critical to resynchronize the defibrillator. Most external defibrillators will default back to asynchronous mode after a shock is delivered. Failure to resynchronize the defibrillator can lead to induction of ventricular fibrillation in a patient intended to undergo cardioversion.

Efficacy — External cardioversion and defibrillation have been used in the treatment of a variety of arrhythmias, with variable results depending on the chronicity of the arrhythmia, triggers for the arrhythmia, and the patient’s overall clinical condition. For example, electrical cardioversion success rates approach 100 percent in patients with atrial flutter or AF of short duration and no structural heart disease, while the success rates are much lower in patients with chronic AF and concomitant mitral valve disease. The term "failed cardioversion" can indicate failure to restore sinus rhythm at all, or an immediate recurrence of the arrhythmia. It is important to differentiate these two failure mechanisms because different approaches can be used to address each type of failure.

While antiarrhythmic medications can sometimes result in restoration of sinus rhythm without electrical cardioversion, they are primarily used in an effort to maintain sinus rhythm following successful electrical cardioversion. However, many antiarrhythmic drugs can alter the defibrillation threshold, ie, the minimal amount of energy necessary for reversion of an arrhythmia (table 2). Amiodarone, quinidine, flecainide, and phenytoin may cause a significant rise in defibrillation thresholds [12-15]. (See "Amiodarone: Clinical uses" and "Amiodarone: Adverse effects, potential toxicities, and approach to monitoring".)

Atrial fibrillation — AF is the most frequent arrhythmia treated with electrical cardioversion (movie 1). Cardioversion is part of the overall treatment approach to AF, which also includes rate control and anticoagulation.

To reduce the risk of thromboembolism following cardioversion, therapeutic anticoagulation is generally recommended for at least three to four weeks before and after cardioversion. Alternatively, the presence of existing intracardiac thrombus should be excluded using transesophageal echocardiography prior to cardioversion if therapeutic anticoagulation has not been achieved for an adequate duration. However, a negative TEE does not preclude the need for anticoagulation at the time of the cardioversion or afterwards. Detailed discussions regarding the decision to perform cardioversion versus rate control, as well as the optimal approach to anticoagulation, are provided elsewhere. (See "Atrial fibrillation: Cardioversion" and "Management of atrial fibrillation: Rhythm control versus rate control" and "Prevention of embolization prior to and after restoration of sinus rhythm in atrial fibrillation" and "Atrial fibrillation in adults: Use of oral anticoagulants" and "Role of echocardiography in atrial fibrillation", section on 'Transesophageal echocardiography'.)

The energy requirement for successful cardioversion of AF varies according to the type of electrical waveform and chronicity of AF (algorithm 1) [8]. (See "Basic principles and technique of external electrical cardioversion and defibrillation", section on 'Energy selection for cardioversion and defibrillation'.)

Most currently available defibrillators deliver biphasic waveforms. When biphasic waveforms are used, the efficacy is higher [16,17]. In a study of 912 patients with AF or atrial flutter, restoration of sinus rhythm was higher with the use of biphasic waveforms (94 versus 84 percent for monophasic waveforms) and the cumulative energy was lower (199 J versus 554 J) [16]. The use of biphasic waveforms may be of particular benefit in patients who fail to revert with the use of monophasic waveforms [18].

Although it had been hoped that cardioversion to and maintenance of sinus rhythm would improve the prognosis of and reduce embolic risk in patients with AF, this concept was not confirmed in the two largest randomized trials comparing rate control plus anticoagulation versus rhythm control for AF (the AFFIRM and RACE trials) [19,20]. Both studies showed a trend toward a lower incidence of the primary endpoint with rate control and anticoagulation (hazard ratio 0.87 for mortality in AFFIRM and 0.73 for a composite endpoint in RACE). In addition, embolization occurred with equal frequency regardless of whether a rhythm control or a rate control strategy was adopted. In both groups, embolization primarily occurred after warfarin had been stopped or when the INR was subtherapeutic. (See "Management of atrial fibrillation: Rhythm control versus rate control".)

Atrial flutter — Electrical cardioversion is highly successful in the treatment of typical (type I) atrial flutter, which arises from a single reentrant circuit in the right atrium (waveform 1 and figure 3). The energy requirement for successful cardioversion of typical (type I) atrial flutter is usually lower than that required for AF (algorithm 1) [8]. Many patients with type I atrial flutter can be cardioverted with 50 to 100 joules or less [21-24]. In a review including 985 cardioversions in 840 patients with atrial flutter, the median energy level for successful cardioversion was 50 joules with a biphasic defibrillator [22]. (See "Restoration of sinus rhythm in atrial flutter" and "Electrocardiographic and electrophysiologic features of atrial flutter" and "Basic principles and technique of external electrical cardioversion and defibrillation", section on 'Energy selection for cardioversion and defibrillation'.)

In contrast to typical (type I) atrial flutter, atypical (type II) atrial flutter may result from reentrant circuits in various locations and tends to require higher energy levels for cardioversion, but in most cases sinus rhythm can be successfully restored. While starting at 50 to 100 joules may be effective for cardioversion of atypical (type II) atrial flutter, particularly with biphasic defibrillators, this approach has the potential adverse effect of requiring additional shocks [21]. (See "Electrocardiographic and electrophysiologic features of atrial flutter".)

The role of anticoagulation during and after cardioversion is similar to that with AF and is discussed in detail elsewhere. (See "Embolic risk and the role of anticoagulation in atrial flutter".)

Supraventricular tachycardia — The most common mechanisms for supraventricular tachycardia are atrioventricular (AV) nodal reentry, AV reentrant tachycardia, and atrial tachycardia. These arrhythmias often terminate with vagal maneuvers or intravenous antiarrhythmic therapy with adenosine or verapamil when they are AV nodal dependent; as such, electrical cardioversion is usually not required. However, if these arrhythmias persist and electrical cardioversion is attempted, cardioversion is usually successful but may require relatively high energy levels, probably due to the deep location of the reentrant pathway. If sinus rhythm is not restored following an initial 50 to 100 joule shock, subsequent shocks should be at higher energy levels (algorithm 1). (See "Atrioventricular nodal reentrant tachycardia".)

Ventricular tachycardia — Electrical cardioversion is usually successful in the acute treatment of ventricular tachycardia (VT), which typically arises from a reentrant circuit in the ventricle. If a distinct QRS and T wave are identified, allowing the delivery of energy to be synchronized to the QRS complex, monomorphic VT can often be terminated with a low-energy shock. Despite the potential for terminating VT with very low-energy shocks, one must consider the seriousness of the arrhythmia and the desire to avoid repeated shocks. As a result, the initial synchronized shock in these circumstances is recommended to be 100 joules (algorithm 1) [8]. (See "Sustained monomorphic ventricular tachycardia in patients with structural heart disease: Treatment and prognosis" and "Basic principles and technique of external electrical cardioversion and defibrillation", section on 'Energy selection for cardioversion and defibrillation'.)

In contrast, synchronized cardioversion may be impossible or hazardous if the VT is rapid and distinct QRS complexes are not identified, if the QRS complexes are wide and bizarre, or if the VT is polymorphic. In these settings, there is a potential for delivery of a discharge on the T wave, possibly provoking ventricular fibrillation. Under these circumstances, nonsynchronized defibrillation should be performed starting with 200 joules for a biphasic device. (See "Catecholaminergic polymorphic ventricular tachycardia".)

Ventricular fibrillation — The only definitive treatment for ventricular fibrillation (VF) is defibrillation. When defibrillation is performed promptly, the success rate for terminating ventricular fibrillation can be as high as 95 percent [25-28]. However, the success rate falls substantially as the duration of ventricular fibrillation increases, probably due to myocardial ischemia, acidosis, and other metabolic changes. These cellular changes are associated with an electrophysiologic deterioration of ventricular fibrillation, leading to an increase in fibrillation cycle length and prolonged diastolic duration between fibrillation action potentials [29].

For these reasons, defibrillation as soon as possible has been considered to be the standard of care for VF (algorithm 2). Some studies suggest that when VF has been present for longer than four to five minutes, outcomes are better if cardiopulmonary resuscitation is performed prior to defibrillation [30,31]. The recommended starting energy to effectively defibrillate VF is 200 joules with biphasic waveforms (algorithm 1) [8]. There is no reported benefit to using more than 360 joules, and there may be harm since high-energy shocks may be associated with myocardial damage and the risk for developing new arrhythmias. (See "Supportive data for advanced cardiac life support in adults with sudden cardiac arrest", section on 'Defibrillation' and "Advanced cardiac life support (ACLS) in adults", section on 'Pulseless ventricular tachycardia and ventricular fibrillation' and "Basic principles and technique of external electrical cardioversion and defibrillation", section on 'Energy selection for cardioversion and defibrillation' and 'Complications' below.)

Special populations

Cardioversion during pregnancy — Cardioversion can be performed during pregnancy without affecting the rhythm of the fetus [32,33]. It is recommended, however, that the fetal heart rate be monitored during the procedure using standard fetal monitoring techniques. (See "Nonstress test and contraction stress test".)

Cardioversion in patients with permanent pacemakers/ICDs — Several precautions are necessary when attempting external electrical cardioversion or defibrillation in a patient with a permanent pacemaker or an implantable cardioverter-defibrillator (ICD). Defibrillation in these patients can damage the pulse generator, the lead system, or the myocardial tissue, resulting in device dysfunction [34]. The electrode paddle (or patch) should be at least 12 cm from the pulse generator and an anteroposterior paddle position is recommended [35,36]. Elective cardioversion should be initiated with the lowest indicated energy (which will vary depending on the arrhythmia) in order to avoid damage to the device circuitry and the electrode-myocardial interface. After cardioversion, the pacemaker should be interrogated and evaluated to ensure normal pacemaker function. When these precautions have been used, cardioversion with either monophasic or biphasic shocks is safe and effective in patients with an implantable device [37].

Alternatively, in patients with an ICD, internal cardioversion can be attempted by an electrophysiologist using the device programmer to deliver the shock. (See 'Internal cardioversion/defibrillation' below.)

Cardioversion in patients with digitalis toxicity — Patients with digitalis overdose or intoxication can present with almost any type of arrhythmia, including tachyarrhythmias and bradyarrhythmias. In particular, ventricular arrhythmias (including VF) are more likely to occur in patients who have digitalis toxicity, especially if the patient is also hypokalemic. There is a relative contraindication to cardioversion in the setting of digitalis toxicity since digitalis sensitizes the heart to the electrical stimulus and, hence, cardioversion could trigger additional arrhythmias, most importantly ventricular fibrillation.

●Supraventricular arrhythmias – Cardioversion should be deferred until digitalis levels have returned to a normal range and clinical toxicity has resolved. If urgent restoration of sinus rhythm is necessary for a hemodynamically unstable supraventricular arrhythmia, the lowest energy that is likely to be successful should be used. In addition, rapid atrial pacing may be successful for certain arrhythmias (eg, atrial flutter) and is probably the safest method. (See "Atrial fibrillation: Cardioversion", section on 'Electrical cardioversion' and "Restoration of sinus rhythm in atrial flutter", section on 'Atrial overdrive pacing'.)

●Ventricular arrhythmias – If cardioversion must be performed for a life-threatening ventricular arrhythmia, prophylactic lidocaine (1 mg/kg up to a maximum dose of 100 mg IV push) should be given and the lowest indicated energy levels used.

When time permits, hypokalemia should be corrected prior to cardioversion. (See "Digitalis (cardiac glycoside) poisoning".)

Complications — While electrical cardioversion and defibrillation are generally well tolerated, complications may occur. Most complications are self-limiting (eg, changes in the electrocardiogram, hypotension related to sedation and/or vasodilation) or relatively benign (eg, skin irritation). However, providers should be aware of potential life-threatening complications such as postcardioversion arrhythmias and the possibility of thromboembolism.

ST segment and T wave changes — Electrocardiographic (ECG) changes can occur immediately after cardioversion, usually consisting of ST segment and T wave changes [38-42]. ECG changes, including ST segment elevation, are nonspecific findings and should not be used as the sole criteria for identifying an acute ischemic event as the cause for the ventricular tachyarrhythmia [42].

In one study of 56 patients with ventricular arrhythmias treated with monophasic shocks, ST segment and T wave changes were common immediately after cardioversion but usually resolved within five minutes [38]. The ECG changes included ST segment elevation in 15 percent, ST segment depression in 35 percent, or an increase in T wave amplitude.

Transient ST elevation has also been reported in a series of patients undergoing cardioversion with monophasic waveforms for atrial arrhythmias [39]. These changes were noted primarily in the precordial leads, and normalized within 1.5 minutes. The occurrence of ST segment elevation was associated with a lower conversion rate and lower rate of long-term maintenance of sinus rhythm.

The pathogenesis of ST elevation is uncertain, since elevations in cardiac enzymes (ie, CK-MB and troponin) are uncommon and, when they occur, are usually minimal [43-45]. However, both the incidence and the extent of ST segment changes appear to be lower with the use of biphasic waveforms [46,47].

Arrhythmia and conduction abnormalities — Arrhythmias are frequently observed after cardioversion [38,48-51]. In many cases these arrhythmias are benign (eg, sinus tachycardia, nonsustained ventricular tachycardia [VT]), but in other cases the arrhythmias can be clinically and/or hemodynamically significant (eg, ventricular fibrillation [VF], sustained VT).

●Ventricular arrhythmias – Runs of nonsustained ventricular tachycardia (VT) are seen in up to five percent of patients, and can occur in patients with or without structural heart disease [38]. On the other hand, a sustained ventricular arrhythmia generally occurs only in patients with clinically documented VT or long-lasting VF [38,49]. Cardioversion can also induce VF, usually but not always after the administration of an asynchronous shock [49]. The occurrence of ventricular arrhythmias does not appear to be related to the number of shocks and cannot be prevented by antiarrhythmic therapy. Conversely, antiarrhythmic drugs may contribute to the development of new arrhythmias [52].

●Atrial arrhythmias – Atrial arrhythmias can also occur following cardioversion. Approximately 30 percent of patients have a supraventricular tachycardia, primarily sinus tachycardia. However, AV nodal reentrant tachycardia and atrial flutter have been observed following cardioversion attempts for chronic AF [50].

●Bradyarrhythmias and conduction abnormalities – Bradyarrhythmias following electrical cardioversion are relatively rare. In a retrospective multicenter cohort study of 6906 electrical cardioversions in 2868 patients with AF and less than 48 hours of symptoms, bradyarrhythmias were identified following 63 cardioversions (0.9 percent) in 54 patients [53]. Pre-procedure use of digoxin, beta blocker, or antiarrhythmic drug did not impact the development of bradyarrhythmias post-cardioversion. Nevertheless, it is reasonable to anticipate clinically significant bradycardia in patients undergoing cardioversion who have been in AF for over a year, have very slow ventricular rates during AF, or in whom amiodarone loading was recently administered.

A transient left bundle branch block is occasionally seen after cardioversion, but high-degree atrioventricular block is more common. In one study of 75 patients who underwent 112 shocks, sinus bradycardia occurred in 18 patients and high-degree AV block in 11 [48]. Temporary pacing was necessary in 10 patients. The likelihood of requiring either external or transvenous cardiac pacing immediately after a cardioversion is much lower in clinical practice than this study suggests. The incidence appears to be less than 1 percent. Patients receiving antiarrhythmic drugs are more prone to develop bradycardia and asystole and an external pacemaker should be readily available in such patients [48,49]. (See "Temporary cardiac pacing".)

Thromboembolism — Cardioversion may be associated with pulmonary or systemic thromboembolism. Thromboembolism after the return of synchronous atrial contraction can occur because of dislodgement of left atrial thrombi present at the time of cardioversion or a thrombus that forms after cardioversion due to transient post conversion left atrial mechanical dysfunction. This complication is more likely to occur in patients with AF who have not been anticoagulated prior to cardioversion. Patients with a previous embolism do not have an increased risk of embolization if anticoagulation of adequate intensity and length are administered [54]. The estimated incidence of thromboembolism varies, but in a large nonrandomized series that included 437 patients, thromboembolism occurred in 5.3 percent of patients who were not anticoagulated compared with 0.8 percent of those who were receiving anticoagulation [55]. For patients with AF of at least 48 hours duration, the current recommendation is to anticoagulate patients for several weeks prior to and following cardioversion. (See "Prevention of embolization prior to and after restoration of sinus rhythm in atrial fibrillation".)

Myocardial necrosis — Minimal myocardial necrosis, particularly of the epicardium, may occur as a result of high-energy shocks. This is typically asymptomatic and is manifested by small rises in serum CK-MB and troponin levels. In contrast, substantial elevations of either CK-MB or troponin following electrical cardioversion, or the development of chest pain suggestive of angina, suggests the presence of myocardial injury from causes unrelated to the procedure. As such, we do not routinely monitor cardiac enzymes following electrical cardioversion in asymptomatic patients.

Although the cause is unknown, it has been suggested that myocardial necrosis may be due to the sustained depolarization of a critical mass of myocardial cells [40]. The risk of myocardial necrosis appears related to the amount of energy delivered with each shock rather than to the number of shocks, although many repeated shocks may lead to myocardial damage and scarring.

●In one study of 30 patients who underwent cardioversion, an increase in serum CK-MB was seen in only two patients, despite substantial release of CK from skeletal muscle [56]. Furthermore, the small release of CK-MB in this report cannot be considered diagnostic for myocardial damage since the total CK from skeletal muscle includes approximately 1 percent CK-MB [57]. (See "Troponin testing: Clinical use".)

●The desire for improved specificity in the diagnosis of myocardial injury has led to measurement of the serum troponin levels. Among 38 patients undergoing elective cardioversion, only three patients had minimal elevations of troponin I (0.8 to 1.5 mcg/L), suggesting subtle myocardial injury [44]. Two other studies, however, reported no elevations in troponin T following cardioversion [45,58].

Myocardial dysfunction — Global left ventricular dysfunction due to myocardial stunning may be seen in patients with cardiac arrest who have undergone successful cardiopulmonary resuscitation. This is related in part to defibrillation, but is also a result of the arrhythmia itself and due to the absence of cardiac output and coronary blood flow during the period of arrest with resultant ischemia. Myocardial dysfunction due to stunning may reverse within the first 24 to 48 hours after cardiac arrest. It is routine to image the heart and evaluate ventricular function shortly after a patient suffers a cardiac arrest to determine if there is evidence of structural heart disease. This evaluation should not be delayed. However, it is important to recognize that ventricular dysfunction may be transient and that imaging should be repeated within a few days if ventricular dysfunction is present immediately after the arrest [59].

In animals, the severity of postresuscitation myocardial dysfunction is related, in part, to the energy used for defibrillation [60]. Further support for this observation comes from another animal study comparing biphasic and monophasic waveforms for reversion of ventricular fibrillation [61]. Although lower-energy biphasic waveforms were as effective as higher-energy monophasic waveforms for restoration of sinus rhythm, there was less myocardial dysfunction after defibrillation with the use of biphasic waveforms.

The process of electrical cardioversion may transiently injure or "stun" the atria as well [62,63].

Pulmonary edema — Pulmonary edema is a rare complication of cardioversion, which is probably due to transient left atrial standstill or left ventricular dysfunction. It is unrelated to the amount of energy used. Pulmonary edema may be more common in patients with AF associated with valvular heart disease or left ventricular dysfunction. In this setting, the return of atrial systole after cardioversion can result in a significant elevation in left atrial pressure and pulmonary edema [64].

Transient hypotension — Transient hypotension can occur for several hours after cardioversion. Most patients require no therapy; if necessary, the fall in blood pressure usually responds to fluid replacement [65]. Although the mechanism is not certain, the hypotension may be related to vasodilation or the use of sedation during the procedure.

Cutaneous burns — Following cardioversion or defibrillation, skin burns occur in 20 to 25 percent of patients and are more likely with improper technique and placement of electrodes [66]. The risk of burns is less with the use of biphasic waveforms and the use of gel-based pads [67]. The use of steroid cream, silver sulfadiazine cream, or topical ibuprofen reduces the pain and inflammation [68,69].

INTERNAL CARDIOVERSION/DEFIBRILLATION

Technique and efficacy — Internal or intracardiac cardioversion is an effective technique for patients in whom external cardioversion has failed to restore sinus rhythm. However, the need for internal cardioversion has been greatly diminished due to the efficacy of biphasic waveform defibrillators and the availability of ibutilide in restoring sinus rhythm. In addition, given the invasive nature of the procedure, specialized training is required to perform internal cardioversion. An ACC/AHA task force on clinical competency has published recommendations for technical and cognitive skills needed to perform internal direct current cardioversion (table 3A-B) [70].

Internal cardioversion can be performed in various ways:

●Using a preexisting ICD to deliver a clinician-directed shock.

●Using epicardial wires placed during surgery or internal paddles applied directly to the epicardium in a patient with a sternotomy [71].

●Two defibrillation electrodes are placed in the right atrium and coronary sinus or in the right atrium and left pulmonary artery, respectively, and then intracardiac shocks are delivered by an external defibrillator.

Internal cardioversion complications — Although internal cardioversion is an effective approach for restoring sinus rhythms in patients with AF refractory to pharmacologic or external electrical cardioversion, one study reported that complications occurred in 19 percent of patients, including low cardiac output from ventricular stunning, pericardial effusion, and a brief period of ventricular asystole requiring ventricular pacing [72]. Another report of 25 patients found that 36 percent developed transient bradycardia, related to sinus and atrioventricular nodal depression, requiring temporary ventricular pacing [73]. Shocks of up to 20 joules did not affect the function of permanent pacemakers.

Implantable cardioverter-defibrillators — ICDs are in widespread use in patients with a history of sustained ventricular tachycardia or ventricular fibrillation and also for primary prevention in selected patients. In patients with an ICD, internal cardioversion can be attempted by a cardiologist using the device programmer to deliver the shock. The advantage of using the ICD is that it avoids the risk of a skin irritation from an external shock and the small chance of damage to the ICD system from the shock. The disadvantage of using the ICD is that it consumes some of the battery in the device and does not always work for cardioversion of atrial arrhythmias. Indications for and efficacy of ICDs are discussed in detail elsewhere. (See "Implantable cardioverter-defibrillators: Overview of indications, components, and functions" and "Primary prevention of sudden cardiac death in patients with cardiomyopathy and heart failure with reduced LVEF".)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Atrial fibrillation" and "Society guideline links: Arrhythmias in adults" and "Society guideline links: Ventricular arrhythmias" and "Society guideline links: Supraventricular arrhythmias".)

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Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

●Basics topics (see "Patient education: Heart failure and atrial fibrillation (The Basics)")

●Beyond the Basics topics (see "Patient education: Cardioversion (Beyond the Basics)" and "Patient education: Implantable cardioverter-defibrillators (Beyond the Basics)")

SUMMARY AND RECOMMENDATIONS

●Definitions – Electrical cardioversion and defibrillation are commonly performed procedures in the management of patients with cardiac arrhythmias. (See 'Introduction' above.)

•Cardioversion is the delivery of energy to the chest that is synchronized to the QRS complex; it is used for converting rhythms with monomorphic QRS complexes in patients who are hemodynamically stable (movie 1).

•Defibrillation is asynchronous delivery of a shock randomly during the cardiac cycle and is typically used during a cardiac arrest caused by ventricular fibrillation.

●Energy selection – When available, a biphasic defibrillator is preferred due to greater efficacy. Nearly all available external defibrillators now use a biphasic waveform. However, it is still important to fully understand the type of waveform that is delivered when using an external defibrillator. The energy selection recommendations in this topic are in joules and are for defibrillators that use a standard biphasic waveform. Lower energies can be used with defibrillators that use a truncated biphasic waveform. (See 'Energy selection' above.)

Once an arrhythmia has been identified, the most important factor in the likelihood of a successful cardioversion or defibrillation is the choice of the initial energy level to be delivered to the patient. To increase the likelihood of initial shock success and reduce the duration of sedation, a higher initial energy may be considered. The following are suggested initial energy requirements for monophasic and biphasic waveforms (see "Basic principles and technique of external electrical cardioversion and defibrillation", section on 'Energy selection for cardioversion and defibrillation'):

•For AF, 120 to 200 joules (algorithm 1)

•For atrial flutter, 50 to 100 joules

•For ventricular tachycardia with a pulse, 100 joules

•For ventricular fibrillation or pulseless ventricular tachycardia, 200 to 360 joules (algorithm 2)

●Efficacy – External cardioversion and defibrillation have been used in the treatment of a variety of arrhythmias, with variable results depending on the chronicity of the arrhythmia, triggers for the arrhythmia, and the patient’s overall clinical condition. The term "failed cardioversion" can indicate failure to restore sinus rhythm at all, or an immediate recurrence of the arrhythmia. It is important to differentiate these two failure mechanisms because different approaches can be used to address each type of failure. (See 'Efficacy' above.)

•Atrial fibrillation or atrial flutter – Electrical cardioversion success rates approach 100 percent in patients with atrial flutter or atrial fibrillation (AF) of short duration and no structural heart disease, while the success rates are much lower in patients with chronic AF and concomitant mitral valve disease. (See 'Atrial fibrillation' above and 'Atrial flutter' above.)

•Ventricular tachycardia – Electrical cardioversion is usually successful in the acute treatment of ventricular tachycardia. If a distinct QRS and T wave are identified, synchronized cardioversion can be attempted. In contrast, synchronized cardioversion may be impossible or hazardous if distinct QRS complexes are not identified. As such, under these circumstances, asynchronous defibrillation should be used. (See 'Ventricular tachycardia' above.)

•Ventricular fibrillation – Defibrillation is the only definitive treatment for ventricular fibrillation (VF), with high success rates when performed promptly. However, the success rate falls substantially as the duration of ventricular fibrillation increases, probably due to myocardial ischemia, acidosis, and other metabolic changes. For these reasons, defibrillation as soon as possible has been considered to be the standard of care for VF (algorithm 2). (See 'Ventricular fibrillation' above.)

●Complications – While electrical cardioversion and defibrillation are generally well tolerated, complications may occur. Most complications are self-limited (eg, changes in the electrocardiogram, hypotension related to sedation and/or vasodilation) or relatively benign (eg, skin irritation). However, providers should be aware of potential life-threatening complications such as post-cardioversion arrhythmias and thromboembolism. (See 'Complications' above.)

●Internal cardioversion – Internal or intracardiac cardioversion is an effective technique for patients in whom external cardioversion has failed to restore sinus rhythm. The need for internal cardioversion has been greatly diminished due to the efficacy of biphasic waveform defibrillators in restoring sinus rhythm. Given the invasive nature of the procedure, specialized training is required to perform internal cardioversion. (See 'Internal cardioversion/defibrillation' above.)

ACKNOWLEDGMENT — The UpToDate editorial staff acknowledges Ramsey Wehbe, MD, who contributed to earlier versions of this topic review.