Chapter 125. Cardioversion

1. What are the indications for cardioversion?

2. What is the difference between cardioversion and defibrillation?

3. What is the difference between monophasic and biphasic cardioverter-defibrillators?

4. How much energy should be used during cardioversion?

5. What are the indications for anticoagulation prior to cardioversion?

Cardioversion is a medical procedure whereby an abnormal heart rhythm (ie, cardiac arrhythmia) is converted back to a normal rhythm using electricity or drugs. Electrical cardioversion, also referred to as direct-current or DC cardioversion, involves the delivery of a synchronized (perfectly timed) electrical shock through the chest wall to the heart to terminate arrhythmias and restore sinus rhythm. Electrical cardioversion is an effective, rapid, and safe technique that has become a routine procedure in the management of patients with cardiac arrhythmias. Pharmacologic cardioversion, also called chemical cardioversion, uses antiarrhythmic medication instead of an electrical shock to restore the heart's normal rhythm.

Investigators at Johns Hopkins Hospital were the first to develop techniques of defibrillation by an electrical shock in the 1930s. The first human defibrillation was performed in the operating room by Claude Beck in 1947, and Paul Zoll introduced defibrillation using alternating current in 1956. Direct-current defibrillation was subsequently pioneered and introduced into clinical practice by Bernard Lown in 1962. Subsequent studies in the early 1960s demonstrated that electrical cardioversion across the closed chest could abolish other cardiac arrhythmias in addition to ventricular fibrillation (VF). Today, atrial fibrillation (AF) is the most frequent arrhythmia encountered in clinical practice and the most commonly cardioverted arrhythmia.

Distinguish Cardioversion and Defibrillation

Electrical cardioversion and defibrillation procedures both use a device (eg, cardioverter-defibrillator) to deliver an electrical shock to the heart to treat abnormal heart rhythms, but they differ in the timing of the shock and energy provided. Electrical cardioversion delivers energy synchronized (ie, perfectly timed) to the QRS complex and is used to treat arrhythmias such as AF, atrial flutter (AFL), or ventricular tachycardia (VT) with a pulse. Cardioversion can be performed electively (ie, nonemergently) in stable patients or emergently in situations to correct a rapid abnormal rhythm associated with faintness, low blood pressure, chest pain, difficulty breathing, or loss of consciousness. Cardioversion is not performed in pulseless patients.

Defibrillation delivers nonsynchronized (ie, occurs at random timing) energy during the cardiac cycle and is used to treat life-threatening arrhythmias such as pulseless VT or VF. Defibrillation is the treatment of choice for the arrhythmias most commonly associated with sudden cardiac arrest. The electrical shock delivered during cardioversion or defibrillation can be delivered externally to the heart using electrodes (external pads or paddles) placed on the chest (most common); directly to the heart using internal paddles during an open chest surgery; or through the electrodes of a permanently implanted cardioverter-defibrillator (ICD).

Mechanism of Cardioversion

Cardioversion disrupts the abnormal electrical circuit(s) in the heart and restores a normal heartbeat. The shock causes all the heart cells to depolarize simultaneously, thereby interrupting and terminating the abnormal electrical rhythm without damaging the heart. This split second interruption of the abnormal beat allows the heart's electrical system to regain control and restore a normal heartbeat. The delivery of energy during the shock is synchronized to the QRS complex, which represents cardiac depolarization, in order to terminate the arrhythmia safely and allow sinus rhythm to resume. The accidental delivery of an electrical shock to the T wave, which represents cardiac repolarization, is unsafe and may result in life-threatening ventricular arrhythmias (Figure 125-1). For this reason, synchronized cardioversion is used, rather than nonsynchronized defibrillation, for the abatement of abnormal rhythms with pulse.

Electrical cardioversion appears most effective in terminating arrhythmias that arise from a single reentrant circuit such as AFL, atrioventricular nodal reentrant tachycardia (AVNRT), atrioventricular reentrant tachycardia (AVRT), and monomorphic VT. The high-energy shock depolarizes the myocardium and the conduction tissue involved in the reentry circuit of the arrhythmia simultaneously. The depolarization of the myocardium is followed by a period of refractoriness that has the effect of interrupting the reentrant circuit. This interruption breaks the repeating cycle and terminates the arrhythmia. When the reentrant circuit is broken and the arrhythmia stops, the sinus node begins to fire again and a normal heart rhythm is restored. This mechanism of action does not explain how electrical cardioversion terminates AF, which arises from multiple reentrant circuits. As a result of the multiple circuits, successful cardioversion of AF often requires higher energy for termination. The exact mechanism by which electrical cardioversion terminates AF remains unknown. Other arrhythmias, such as junctional tachycardia and multifocal atrial tachycardia, originate from ectopic sites (ie, nonpacemaker) in the heart. Cardioversion is not effective for these types of arrhythmias.

Types of Defibrillators

Cardioverter-defibrillators deliver energy in a variety of waveforms, broadly characterized as monophasic or biphasic. Monophasic devices provide a unidirectional pulse of energy, meaning that electrons flow in a single direction through the heart. Monophasic energy is highly effective, and monophasic cardioverter-defibrillators remain widely used. Alternatively, biphasic devices deliver a sinusoidal biphasic waveform whereby the initial phase of energy is positive followed by a phase of opposite polarity, which means that during the shock the polarity and electron flow reverse. Biphasic cardioverter-defibrillators deliver a more consistent magnitude of current, which terminates arrhythmias more effectively and at lower energies compared to monophasic devices. As a result, biphasic cardioverter-defibrillators are increasing in use and have now become the standard for trans-chest defibrillation. Clinicians must distinguish which type of cardioverter-defibrillator is available for use, as this will dictate how much energy is required for successful cardioversion.

Electrical cardioversion has become a routine procedure in the management of cardiac arrhythmias. Indications include patients in whom the rate of the arrhythmia (eg, AF) cannot be adequately controlled medically or patients who poorly tolerate the arrhythmia (eg, palpitations, angina pectoris, and heart failure). Multiple cardiac rhythms may bear indications for cardioversion or defibrillation (Tables 125-1 and 125-2). The most common reason for the elective cardioversion of atrial arrhythmias is to enhance cardiac performance by restoring sinus rhythm, particularly in patients with mitral stenosis, left ventricular hypertrophy (aortic stenosis, hypertrophic obstructive cardiomyopathy), and diminished myocardial reserve (heart failure, myocardial ischemia, and infarction). Urgent cardioversion may be required for patients with atrial or ventricular arrhythmias who have myocardial ischemia, acute heart failure (pulmonary edema), hypotension, mental status changes, or worsening angina pectoris.

Because electrical cardioversion is a low-risk procedure if properly performed, some authorities believe that every patient deserves one chance to achieve sinus rhythm by cardioversion, even if the short- or long-term prognosis of maintaining sinus rhythm is generally unfavorable. Other experts suggest that not all patients with newly discovered AF warrant an attempt at restoring sinus rhythm since several large, randomized trials have shown that the maintenance of sinus rhythm confers no survival (or other outcome) advantage over rate control. Treatment must be determined based on clinical parameters and patient preferences.

Contraindications to electrical cardioversion include rhythms that do not respond to electrical cardioversion (eg sinus rhythms, multifocal atrial tachycardia), digitalis toxicity, severe electrolyte imbalance (eg, hypokalemia), and known or suspected atrial thrombus. In AF or AFL, suspicion of atrial thrombus should be high if the rhythm onset is unknown or not clearly within the prior 48 hours. Transesophageal echo (TEE) evidence that the left atrium is free of thrombus may permit cardioversion for AF or AFL with unknown or > 48-hour onset.

Cardioversion is routinely performed in most hospitals in a closely monitored setting such as an intensive care unit, an emergency department, or a specially equipped procedure room. Although patients with atrial arrhythmias are often admitted to the hospital electively for cardioversion, outpatient cardioversion is a low-risk, effective, and economical procedure. If performed on an outpatient basis, patients are observed until most of the effects of sedation have abated (1–2 hours) and require transport home safely after the procedure due to the residual effects of anesthesia. Overnight hospitalization is seldom required.

Preprocedure Checklist

Prior to performing electrical cardioversion, structured measures should be integrated for all patients (Figure 125-2) as follows:

1. Informed consent (patient or decision maker)

2. Fasting (nothing oral) 6–8 hours prior to cardioversion (if elective)

3. History and physical examination

   1. History should include current medications, allergies, previous adverse drug reactions or contraindications to sedation, diseases/disorders, prior hospitalizations, pregnancy status, nothing oral status, and anticoagulation status (if presenting arrhythmia is AF/AFL).

   2. Use history to estimate duration of AF/AFL duration and determine need for anticoagulation and/or TEE evaluation.

   3. Physical examination should include vital signs, oxygen saturation, pulmonary and cardiovascular examination, and oral cavity and airway examination. Patients who have an abnormal airway exam should be considered to be at increased risk for airway obstruction during sedation and may potentially have a difficult airway to manage if mask ventilation or intubation becomes necessary. Patients who present with any high-risk features (Table 125-3) should be considered for anesthesiology consultation prior to the initiation of the procedure.

4. A 12-lead electrocardiogram (ECG) is used to confirm rhythm.

5. If any electrolyte abnormality (hypokalemia, hyperkalemia) or drug toxicity (digitalis) is suspected, appropriate blood levels should be checked.

6. Peripheral venous access (for preprocedure sedation and postprocedure medications or fluids if needed) is obtained.

7. Skin preparation includes shaving of the chest hair, if present (with electric clippers rather than a blade) to ensure good contact of the skin and electrode pads. High-quality continuous ECG from the cardioverter-defibrillator will confirm proper contact of electrode pads to the skin.

8. Emergency resuscitation equipment available (Figure 125-2).

Anticoagulation

Cardioversion may be associated with pulmonary or systemic embolization. This complication is more likely to occur in patients with AF/AFL > 48 hours (ie, high-risk group) who have not been anticoagulated prior to cardioversion. In case-control series, the estimated risk of thromboembolism is between 1% and 5% in (nonanticoagulated patients) with AF/AFL > 48 hours undergoing cardioversion.

In patients with AF/AFL >48 hours, oral anticoagulation with warfarin (International Normalized Ratio (INR) 2.0 to 3.0) for 3–4 weeks prior to cardioversion reduces the thromboembolic risk to 0.5–0.8%. Anticoagulation before cardioversion allows time for adherence of any preexisting atrial thrombus and for prevention of new thrombus formation. Alternatively, anticoagulation with intravenous unfractionated heparin can be initiated and a TEE performed to evaluate the left atrium and left atrial appendage for evidence of thrombus. If there is no evidence of thrombus, cardioversion can safely be performed (thromboembolic risk 0.8%). The 2008 American College of Chest Physicians (ACCP) guidelines recommend that patients undergoing urgent cardioversion be heparinized as soon as possible to prevent thrombi from forming due to atrial appendage dysfunction after cardioversion. Cardioversion in patients who present with acute AF/AFL < 48 hours (ie, low-risk group) is associated with a low clinical rate of thrombembolism (0.8%).

Late thromboembolic events after cardioversion are probably due to both the development of thrombus as a consequence of atrial stunning and the delayed recovery of atrial contraction after cardioversion. Pooled data from 32 studies of cardioversioon of AF/AFL suggest that 98% of clinical thromboembolic events occur within 10 days of cardioversion. Anticoagulation after the procedure prevents thrombus formation from occurring before normal atrial mechanical activity has resumed, a process that may be delayed for several weeks due to atrial stunning. The American College of Chest Physicians (ACCP) and American College of Cardiology/American Heart Association, and the European Society of Cardiology (ACC/AHA/ESC) guidelines therefore recommend continuation of warfarin therapy for at least 4 weeks after cardioversion. This recommendation only addresses protection from embolic events related to the cardioversion period. Patients with AF at high risk from thromboembolic events based on CHADS2 score (an acronym for Congestive heart failure, Hypertension, Age > 75, Diabetes mellitus and prior Stroke or transient ischemic attack) may require long-term anticoagulation (see Chapter 126).

Care standards require administration of anticoagulant medications when preparing patients with AF/AFL of > 48 hours for cardioversion. The ACC/AHA/ESC guidelines for the management of anticoagulation in patients with AF/AFL undergoing cardioversion recommend anticoagulation for at least 3 weeks prior and 4 weeks following cardioversion if the abnormal rhythm has been present for > 48 hours, with exceptions based on TEE evaluation (Table 125-4).

Following preprocedure preparation, a standardized procedure algorithm for performing electrical cardioversion should be followed (see Figure 125-2), including ECG lead and electrode pad placement, sedation, energy selection, synchronization, shock delivery, postshock patient and ECG assessment, and postprocedure monitoring.

ECG Lead Placement

Cardioverter-defibrillators provide the option of continuously monitoring the patient's ECG using either external electrode pads or ECG leads. As a result, the ECG leads (typically three leads) are not required for cardioversion, but it is recommended that the leads be attached to the patient in nonemergent situations. Attaching the ECG leads provides additional information about the patient's heart rhythm and allows the operator to switch the lead used for monitoring and synchronization by the cardioverter-defibrillator. Using a standard three-lead (color-coded) ECG cable, the white lead is placed on the right side of the chest just below the right clavicle, the black lead is placed on the left chest just below the left clavicle, and the red lead is placed in the left midaxillary line near the apex of the heart.

Electrode Positioning

Two electrodes (self-adhesive pads or hand-held paddles) are placed on the thorax for external cardioversion and determine the trans-thoracic current pathway. Electrode positioning on the chest is important to maximize current flow through the heart. The most commonly used electrodes for external cardioversion are self-adhesive (ie, hands-free), pre-gelled, low-impedance, disposable-pad electrodes. A variety of anatomic pad placements can be used. Common electrode positions for transthoracic cardioversion/defibrillation include apex-anterior, apex-posterior, and anterior-posterior positions (Figure 125-3). Though all positions are effective, several studies have suggested that less energy is required, and the success rate is higher with the anterior-posterior electrode position in patients cardioverted for AF. More of the atrial mass is placed in the shock vector with anterior-posterior pads compared with apical-anterior pads. Some patients who do not respond to one method occasionally respond to another method. Therefore, if initial shocks are unsuccessful in terminating the arrhythmia, the pads should be repositioned and cardioversion repeated. Electrode pad size is an important determinant of transthoracic current flow during cardioversion, and the optimal electrode size for humans is approximately 8–12 cm in diameter.

While self-adhesive pads are convenient and safe, hand-held paddles with manual pressure may be more effective than self-adhesive pads. This was illustrated in a randomized trial of patients referred for cardioversion for persistent AF, in which success rates were slightly higher for patients assigned to paddle electrodes (96% vs 88%). Improved electrode-to-skin contact and reduced transthoracic impedance with handheld electrodes may explain the benefit. Handheld paddles require the use of conducting gel to ensure good contact between the paddles and skin.

Sedation

External cardioversion under conscious sedation or general anesthesia reduces pain and anxiety related to the procedure, since electrical cardioversion is an uncomfortable procedure. Prior to the initiation of sedation, the staff must determine and document the availability of a responsible adult to accompany the patient home at discharge postprocedure. Patent intravenous access must be secured in all patients. All equipment necessary for emergency resuscitation including oxygen, oxygen equipment/supplies, resuscitation bag and mask, monitoring equipment (ECG, pulse oximeter, blood pressure), functioning suction apparatus/catheters, and agents to reverse the effects of drugs administered to produce the moderate sedation (eg naloxone, flumazenil) must be readily available. Crash cart/defibrillator and emergency airway equipment should be immediately accessible. Additionally, a physician skilled in airway management (eg, anesthesiologist) should be present or immediately available. Short-acting intravenous sedatives and short-acting analgesic agents that produce conscious sedation enable rapid recovery after the procedure (Table 125-5). As a result, overnight hospitalization is seldom required. A typical medication combination for conscious sedation would include intravenous midazolam plus fentanyl.

Conscious sedation is assessed by lack of response to tactile and verbal stimuli. The patient's ability to communicate should be preserved. Heart rate and rhythm, blood pressure, oxygen saturation, respiratory rate, and response to verbal stimuli (level of consciousness) should be continuously monitored until the patient regains consciousness and makes a full recovery. The patient usually awakens 5–10 minutes after the cardioversion. The patient should be monitored until full consciousness is restored and at least 1 hour (preferably several hours) after the last dosing of a sedative or an analgesic.

Energy Selection and Transthoracic Impedance

Successful cardioversion depends on the adequate delivery of energy to the heart, determined by the amount of energy provided by the cardioverter-defibrillator and the patient's transthoracic impedance. The amount of energy provided by the cardioverter-defibrillator is adjustable and selected at the time of cardioversion. The amount of energy selected for initial attempts of cardioversion-defibrillation has been controversial. More organized arrhythmias, such as AFL and VT, terminate with lower energy compared to AF and VF. In urgent settings, such as hemodynamic collapse associated with VT or VF, high-energy defibrillation (ie, 200 J max with a biphasic defibrillator; 360 J max with a monophasic defibrillator) may be used, but lower energy may be considered in this situation, with monophasic defibrillators based on manufacturer recommendation (starting dose of 120 J is acceptable). There is no benefit to using greater than 360 joules. For cardioversion, lower energies effectively convert to sinus rhythm in most hemodynamically stable patients. In cardioversion, the minimum effective energy dose for shocks should be administered initially, and energy dose can be titrated up for additional shocks when the clinical situation permits (Table 125-6).

High transthoracic impedance, defined as the resistance of the chest to the flow of electrical current, degrades current flow through the heart. During transthoracic cardioversion, a considerably larger current must be delivered to compensate for transthoracic impedance. In animal studies, 82% of the transthoracic current was shunted to the thoracic cage, 14% to the lungs, and only 4% passed through to the heart during cardioversion. Obesity and severe obstructive lung disease increase impedance, which reduces the efficacy of cardioversion. Measures to reduce impedance should be undertaken, which include applying pressure to the pads, shocking during end-expiration, improving skin–electrode interface, and the use of conducting gels. The repeat administration of shocks also lowers impedance and improves efficacy of cardioversion. Conversely, increasing the distance between electrodes or increasing the amount of tissue or lung parenchyma between the electrodes increases impedance.

Synchronization

Once the ECG leads and electrode pads are attached to the patient and the cardioverter-defibrillator is powered on, a good quality rhythm strip should be obtained to confirm the rhythm. The synchronize mode should be switched on, and confirmation of synchronization with the QRS complex should be confirmed on the monitor and on a telemetry printout. If the QRS is low amplitude or synchronization occurs with the T wave, the lead used for monitoring and synchronization on the cardioverter-defibrillator should be switched until a satisfactory QRS is seen and appropriate synchronization with each QRS complex is confirmed. Synchronization is essential to avoid delivery of a shock during the vulnerable repolarization period, which can result in VF (see Figure 125-1). If defibrillation is intended, the mode must be switched to asynchronous as the lack of an identifiable QRS complex will prevent the cardioverter-defibrillator from discharging in the synchronous mode.

Shock Delivery

A continuous rhythm strip should be obtained during the electroshock. Once the electrode pads are positioned and the appropriate energy and mode (synchronized or nonsynchronized) are selected, the adequacy of patient sedation should be confirmed. Next, the cardioverter-defibrillator capacitors are charged, the staff is warned to stay clear of the patient, and the shock is delivered to the patient. The patient is subsequently examined for adequacy of airway, breathing, and circulation, and the rhythm is confirmed by ECG. If the first attempt is unsuccessful, the procedure can be repeated as necessary with higher-energy shocks and/or changing the electrode pad position. This can be repeated until the arrhythmia terminates or a decision is made to abandon electrical cardioversion.

Efficacy of Cardioversion

The overall immediate success rate of electrical cardioversion with AF is 75–94% and is inversely proportional to the duration of AF and size of the left atrium (Table 125-6). Although sinus rhythm can be restored in a substantial proportion of patients, the rate of relapse is high without concomitant antiarrhythmic drug therapy. After electrical cardioversion only 20–40% of patients maintain sinus rhythm for the first year compared to 29–53% in patients treated with antiarrhythmic drugs before electrical cardioversion and throughout follow-up. Most recurrences of AF occur within the first month after electrical cardioversion. Pretreatment with antiarrhythmic drugs (eg, amiodarone, flecanide, ibutilide, propafenone, or sotalol), recommended by the ACC/AHA/ESC, can enhance the success of electrical cardioversion and prevent recurrent AF. Pretreatment with pharmacological agents may have the greatest efficacy in patients who fail to respond to cardioversion and in those who develop acute or subacute recurrence of AF. In addition, prophylactic antiarrhythmic drug therapy may obviate the need for electrical cardioversion or reduce the energy required for the procedure by lowering the cardioversion threshold. In randomized trials of electrical cardioversion, patients pretreated with intravenous ibutilide were more often converted to sinus rhythm compared to untreated controls, and patients in whom cardioversion initially failed could more often be converted when the procedure was repeated after treatment with ibutilide.

Pharmacologic Cardioversion

The development of new drugs has increased the popularity of pharmacologic cardioversion. Although pharmacologic and electrical cardioversion have not been directly compared, pharmacologic approaches appear simpler but are less effective. Unlike electrical cardioversion, pharmacologic cardioversion does not require conscious sedation or anesthesia. The major risk is related to the toxicity of antiarrhythmic drugs such as drug-induced torsades de pointes. Medications indicated for the pharmacologic cardioversion of AF less than or equal to 7 days’ duration include flecanide, dofetilide, propafenone, ibutilide, or amiodarone. Pharmacologic cardioversion of AF present for more than 7 days includes dofetilide, amiodarone, or ibutilide.

Ibutilide is a class III antiarrhythmic drug (potassium-channel blocker) that prolongs the time for repolarization in atrial and ventricular myocardium. It is only available for intravenous use and is approved for the acute termination of AF/AFL of recent onset, but more effective for conversion of AFL. The 2006 practice guidelines from ACC/AHA/ESC recommend intravenous ibutilide for the pharmacologic cardioversion of AF/AFL ≤ 7 days’ duration (class I recommendation) and for cardioversion of AF/AFL of more than 7 days duration (class IIA recommendation). In most patients who respond to ibutilide, arrhythmia termination is seen within 40 to 60 minutes after initiating the infusion. Ibutilide has a conversion rate of up to 75% to 80% in recent-onset atrial fibrillation and flutter; the conversion rate is higher for atrial flutter than for atrial fibrillation. Ibutilide has a 4% risk of torsades de pointes and should be avoided in patients with heart failure or prolonged QT interval.

Serum potassium and magnesium should be measured and electrolyte disturbances, especially hypokalemia or hypomagnesemia, corrected prior to use and throughout therapy with ibutilide. Ibutilide should be administered with continuous ECG monitoring at a dose of 0.01 mg/kg infused over 10 minutes for patients weighing less than 60 kg and at a dose of 1 mg over 10 minutes for patients weighing more than 60 kg. If the arrhythmia does not terminate 10 minutes after the end of the infusion, a second bolus (same dose over 10 minutes) can be given. The infusion should be stopped when the presenting arrhythmia is terminated or the patient develops sustained or nonsustained VT or marked prolongation of the QT interval. Because of the risk of QT prolongation and arrhythmias, patients treated with ibutilide should be observed with continuous ECG monitoring for at least 4 hours after the infusion or until the QTC interval has returned to baseline. There is no evidence that the risk of thromboembolism with pharmacologic cardioversion differs from electrical cardioversion. Recommendations for anticoagulation are therefore the same for both methods.

Complications after electrical cardioversion are uncommon but can be serious and are mainly related to thromboembolism and arrhythmias (Table 125-7).

Thromboembolism

Thrombi can form within the atria (especially the left atrial appendage) due to stagnant blood flow that exists with AF/AFL. As a result, pulmonary and systemic embolization can occur after cardioversion (spontaneous, pharmacologic, or electrical) if an embolus becomes dislodged from the atria as the heart begins to contract normally. Such emboli in the systemic circulation could lead to stroke, myocardial infarction, bowel ischemia or infarction, or limb ischemia. Emboli occur less frequently in patients who have had AF/AFL < 48 hours (thromboembolic risk 0.8%). If patients with AF/AFL are appropriately anticoagulated for 3–4 weeks before cardioversion, the incidence of thromboembolism is 0.5–0.8%. The incidence is approximately 0.8% in TEE-guided cardioversion. The incidence of embolism in AF/AFL without precardioversion anticoagulation ranges from 1 to 5%. Patients with a previous embolism do not have an increased risk of embolization if anticoagulation is adequate. The risk of thromboembolism is highest in patients with rheumatic (or other) mitral stenosis, large left atrium, chronic AF, diabetes, hypertension, and prior cardiac embolic stroke.

Arrhythmias

Arrhythmias are occasionally observed after cardioversion. Premature atrial or ventricular beats are not uncommon after cardioversion, and atrial arrhythmias, primarily sinus tachycardia, are seen in up to 30% of patients. Alternatively, bradycardia is seen in up to 25% of patients immediately after cardioversion since cardioversion increases vagal tone. In one study of 75 patients undergoing cardioversion, sinus bradycardia occurred in 18 patients (24%), high-degree atrioventricular block occurred in 11 (15%), and temporary pacing was required in 10 (13%). Nonsustained VT is seen in up to 5% of patients and can occur in patients without structural heart disease. Patients receiving antiarrhythmic drugs are more prone to develop bradycardia and asystole postcardioversion. Temporary transthoracic pacing should be readily available at the time of cardioversion. Life-threatening arrhythmias are infrequent and may occur if the device is not properly synchronized. The occurrence of ventricular arrhythmias does not appear to be related to the number of shocks and cannot be prevented by antiarrhythmic therapy. Electrolyte imbalances, such as hypokalemia, and digitalis toxicity increase the risk of ventricular tachyarrhythmias.

Airway Compromise

Oversedation occurs most frequently in the elderly and in patients with renal and hepatic impairment and can cause respiratory depression. Dose adjustment should be considered in those populations. The patient's airway and oxygenation should be monitored carefully until complete recovery. Reversal agents for opiates and benzodiazepines (naloxone and flumazenil, respectively) should be readily available during the procedure. If the patient has identifiable high-risk airway features (described earlier) consultation with an anesthesiologist may be valuable.

Chest Wall Injury and Skin Burns

First-degree skin burns of the chest wall, which can be painful, have been described with electrical cardioversion. These burns can be moderate to severe in up to 20–25% of patients undergoing cardioversion. In order to reduce the frequency and severity of burns, good skin–electrode interface should be confirmed, liberal conductive gel utilized (when using handheld paddles), and the lowest effective amount of energy should be used. Skin burns are more likely with improper technique and placement of electrodes. Though not performed routinely, the pretreatment of the skin with topical ibuprofen or steroid cream can reduce the pain and inflammation. The incidence of skin burns has been substantially reduced with the use of pre-gelled pads and biphasic defibrillators.

Electrocardiographic Changes and Myocardial Injury

Electrocardiographic changes, including ST segment and T wave changes, can occur immediately after cardioversion. The frequency and extent of ST segment changes are lower with biphasic defibrillators. The QRS and QT intervals are not altered. Electrocardiogram findings are nonspecific, typically resolve within 5 minutes, and should not be used as the sole criteria for identifying an acute ischemic event. The pathogenesis of ST elevation is uncertain since elevations in creatine kinase MB isoenzyme or troponin are uncommon and are usually minimal when they occur. Some myocardial tissue damage or stunning may occur as a result of high-energy shocks or repeated shocks. Significant damage is uncommon, and there are generally no short- or long-term complications. Any decline in cardiac function after cardioversion is typically temporary and does not produce symptoms.

Injuries to the Operator

Operator injuries during cardioversion occur very rarely, with an incidence of less than 1 in 1700. Cases of major electrocution have been described in extremely rare instances and have all been associated with equipment failure.

Physical Trauma to the Patient

Physical trauma to the patient is a rare complication and results from vigorous body movements during the delivery of the electric shock.

Troubleshooting

Failure of the monitor to work properly typically reflects a mechanical problem. The power source, lead connections, ECG leads, and electrode pads should be checked and confirmed. If the timing artifact during synchronization mode falls on the T wave, the monitoring lead should be changed until the correct position of the timing artifact is confirmed on the QRS complex. If the capacitor fails to discharge, this probably represents a failure to identify a QRS complex while in synchronized mode. The monitoring lead should be switched, synchronization on the QRS complex confirmed, and cardioversion reattempted.

Cardioversion Unsuccessful

Important factors that determine the immediate and long-term success of cardioversion of atrial arrhythmias include the duration of the arrhythmia, the extent of atrial fibrosis, the size of the left atrium, and underlying structural heart disease (Table 125-8). If cardioversion is unsuccessful, a repeat ECG should be obtained to confirm the underlying rhythm. Next, the cardioversion telemetry strips should be carefully examined to distinguish between true failure to cardiovert and successful cardioversion that is followed by recurrence of arrhythmia. Patients with recurrence of arrhythmia might benefit from antiarrhythmic therapy before repeat attempts at cardioversion. For patients who truly fail to cardiovert, a higher level of energy, an alternate electrode pad configuration, or a biphasic device can be used on repeat attempts. In patients in whom AF recurs acutely or cardioversion fails, the combination of AV nodal blocker plus intravenous loading with amiodarone, procainamide, or ibutilide may pharmacologically restore sinus rhythm. If the AF persists, repeat cardioversion can be performed, and if successful the patient may be placed on long-term antiarrhythmic therapy. Electrolyte disturbances, digitalis toxicity, and thyrotoxicosis may result in failure to cardiovert and should be corrected prior to cardioversion.

Pregnancy

Successful cardioversion has been performed in all three trimesters of pregnancy without adverse consequences to the mother or fetus. Cardioversion does not affect the rhythm of the fetus though it is recommended that the fetal heart rhythm be monitored during the procedure.

Implantable Pacemakers and Cardioverter-Defibrillators

Several precautions are necessary when performing cardioversion in a patient with a permanent implanted device (pacemaker or ICD). Electrical cardioversion can change the settings of the device and may damage the pulse generator, the lead system, or myocardial tissue resulting in device dysfunction. To prevent this, the electrode pads should be placed at least 12 cm from the implanted device, preferably in the anterior-posterior position. Elective cardioversion should be initiated at low energies to reduce the risk of damage. The implantable device should be interrogated before and after cardioversion to ensure normal device function. When these precautions are employed, cardioversion with either monophasic or biphasic shocks is safe and effective in patients with implantable devices.

In 2000, an ACC/AHA task force on clinical competency published recommendations for technical and cognitive skills needed to perform external electrical cardioversion. The ACC/AHA also recommends that the minimum training necessary for competence to perform external electrical cardioversion should include competence in the interpretation of 12-lead ECGs. Previous ACC/AHA task forces recommended a minimum of eight supervised electrical cardioversions as a minimum requirement. The competence in electrical cardioversion may be achievable without formal training in cardiovascular disease. For physicians without adequate experience with electrical cardioversion, a cardiologist should be enlisted to assist with or perform the procedure. There are no published clinical competency recommendations for the use of pharmacologic cardioversion with antiarrhythmic drugs. For physicians without adequate experience with antiarrhythmic drugs, a cardiologist may be enlisted to assist with pharmacologic cardioversion as well.

Secondary Prevention

Maintenance therapy with antiarrhythmic drugs is not typically recommended after electrical cardioverson in patients with a first episode of AF, particularly those at low risk for recurrence (eg, short duration and normal left atrial size) or those with a reversible cause (eg, cardiac surgery, pulmonary embolus, or hyperthyroidism). In other patients with recurrent paroxysmal or persistent AF, maintenance antiarrhythmic drug therapy may be administered to reduce the risk of recurrence if a rhythm control strategy is chosen. Because of the adverse effects associated with antiarrhythmic drugs and no difference in outcomes between rhythm and rate control strategies, many authorities reserve the use of long-term antiarrhythmic drug therapy to patients that remain symptomatic with rate control (Table 125-9).

Transitions of Care

After cardioversion, all patients should receive warfarin therapy for at least 4 weeks. A plan for anticoagulation and follow-up with INR monitoring with a primary physician, cardiologist, or specialized Coumadin clinic should be established. Patients with AF at high risk from thromboembolic events based on CHADS2 score may require long-term anticoagulation. Patients with new-onset AF should undergo thyroid function testing and receive an echocardiogram. Patients with no recurrence can follow up with their primary care physicians as outpatients and do not require any additional testing. Patients with either recurrent, symptomatic AF (despite attempts at rate control) or patients who prefer a rhythm control strategy should be referred to a cardiologist. Cardiology referral for initiation of an antiarrhythmic drug, if required, may also be indicated unless the physician is experienced with and knowledgeable of administration of these drugs. Because most antiarrhythmic agents can also be proarrhythmic, and because many have dangerous side effects to monitor, their initiation and maintenance should be performed by a clinician experienced in their use.