CHAPTER 4 Shameer Ahmed, MD, and Gerald V. Naccarelli, MD Atrial fibrillation (AF) is the most common sustained cardiac tachyarrhythmia requiring hospital admission. AF is associated with significant morbidity, including 5-fold increased risk of embolic strokes,1–3 3-fold increase of congestive heart failure, and decreased exercise tolerance. AF is also associated with a 2-fold increase in mortality.4 The restoration of sinus rhythm (SR) from AF is performed primarily to improve symptoms and cardiovascular outcomes. This can be achieved by various options such as cardioversion (electrical or pharmacological), surgical ablation, catheter ablation either by radiofrequency or cryoballoon-assisted pulmonary vein isolation. In this chapter, we will discuss the rhythm-control strategy with two most widely used approaches for converting AF to SR: direct-current (DC) cardioversion and pharmacological cardioversion (antiarrhythmic agents). When a patient has had 2 or more episodes, AF is considered recurrent. If the arrhythmia terminates spontaneously (in less than 7 days), recurrent AF is designated paroxysmal. When AF is sustained beyond 7 days, AF is designated persistent. The category of persistent AF also includes cases of long-standing AF (e.g., greater than 1 year), usually leading to permanent AF, in which cardioversion has failed or has not been attempted.3 The term “lone AF” applies to young individuals (under 60 years of age) without clinical or echocardiographic evidence of cardiopulmonary disease, including hypertension.5 Cardioversion can be achieved through the use of antiarrhythmic drug (medical conversion) or electric shock (DC) or both. Hemodynamically stable patients with a rapid ventricular response usually need acute control of their ventricular rate to improve symptoms. β-blockers and calcium channel blockers (nondihydropyridine) are used for adequate ventricular rate control in hemodynamically stable patients. Digoxin and amiodarone may be appropriate for rate control in hemodynamically decompensated patients.6 After ventricular rate control has been achieved, many patients convert to SR spontaneously.7 Spontaneous conversion is most likely to occur in patients with a duration of AF less than 48 hours.8 The rate of spontaneous conversion with recent onset AF has been reported to be around 50% at 24 hours. The first reported case of DC cardioversion for AF was by Vishnevskii and Tsukerman in 1959.9 Because of the inception of this method and development in technology, little has changed in the technique of cardioversion. DC cardioversion under sedation is a very well recognized, tolerated, and widely accepted method for prompt cardioversion of AF. Emergency DC cardioversion is considered if the patient is decompensated hemodynamically owing to a rapid ventricular rate.10 These patients may have severe acute congestive heart failure, ongoing myocardial ischemia, or hypotension and restoration of atrial contribution in cardiac output is often helpful in the management of these patients. Immediate DC cardioversion is recommended for patients with AF involving preexcitation when very rapid tachycardia or hemodynamic instability occurs. Unfractionated heparin or low molecular weight heparin should be administered before cardioversion, if AF > 48 hours duration and if the patient is not on therapeutic doses of an oral anticoagulant. After cardioversion, heparin should be continued until the INR is therapeutic (2.0–3.0) if warfarin therapy is initiated. The use of the novel anticoagulants (dabigatran, rivaroxaban, apixaban), all have shown no increased thromboembolic events compared with warfarin in AF patients undergoing cardioversion; and can minimize the use of heparin as therapeutic levels are achieved quickly. In patients with AF duration of < 48 hours, acute therapeutic anticoagulation is not warranted. Hemodynamically stable patients with new onset or newly recognized AF, patients with infrequent symptomatic episodes, and patients with persistent AF who are limited symptomatically by AF are candidates for DC cardioversion therapy. Cardioversion with maintenance of SR is likely to be unsuccessful if the cause (thyrotoxicosis, pericarditis, and mitral valve disease) for the AF has not been corrected prior to attempted cardioversion. DC cardioversion should be performed under proper sedation (etomidate, propofol) with monitoring of the patient’s vital signs (blood pressure, heart rate, and oxygen saturation). If an elective DC cardioversion is planned, the patient should be fasting for 6 to 8 hours, and oxygen saturation and electrolytes should be normal. Unless adequate anticoagulation has been documented for 3 weeks or AF is less than 48 hours from a definite onset, a transesophageal echocardiogram (TEE) approach can be used to rule out atrial thrombi. After cardioversion, the patient should have 2 to 3 hours of electrocardiographic and hemodynamic monitoring before discharge. For nonvalvular AF, there is a very low risk of systemic embolization if the duration of the arrhythmia is less than 48 hours and there are no cardiac abnormalities (e.g., significant left ventricular systolic dysfunction, mitral stenosis) on transthoracic echocardiography, and no prior history of thromboembolism. Patients with new-onset AF of longer than 48 hours or of unknown duration should be anticoagulated for at least 3 weeks before cardioversion, if a TEE approach is not used. The success of traditionally external, monophasic DC cardioversion by applying electric current through paddles or patches to the chest wall is greater than 80%, and the rate of conversion varies with energy input method. The superiority of biphasic over monophasic waveform was first demonstrated in canine models in 19679 and since has been verified in clinical studies. Internal cardioversion with intracardiac catheter can be performed but has been largely abandoned because of the higher success of biphasic shock cardioversion. The current recommendation is to start with 150 to 200 J biphasic waveforms, particularly when cardioverting patients with AF of long duration. The energy is delivered in a “synchronous” fashion to ensure delivery during the QRS complex. Asynchronous delivery into the T wave could result in ventricular fibrillation. It should be noted that the default setting for defibrillators is the “asynchronous” mode. When a “synchronous” shock is delivered, the defibrillator defaults to the “asynchronous” mode. Conventionally electrodes are placed either anteroposteriorly or anterolaterally. There is some evidence that anteroposterior position is superior to anterolateral position.11 If initial shocks are unsuccessful for terminating the arrhythmia, the electrodes should be repositioned and cardioversion repeated. Only 4% to 5% of the shocking energy actually reaches the heart and the majority of gets dissipated to surrounding tissue between skin and heart interface.12 One major technical variable that influences the results of DC therapy is transthoracic resistance. The size of the electrode, skin to electrode contact and nonsalt containing gels all effect the transthoracic impedance.13 Successful DC is usually defined as termination of AF, documented as the presence of two or more consecutive P waves after shock delivery. The various hemodynamic changes post-DC cardioversion include improvement of atrial contractions and left ventricular systolic function. At times, improvement may happen more slowly due to atrial and ventricular “stunning” especially when the duration of AF prior to cardioversion is prolonged.14 The risks and complications of cardioversion are associated with thrombo-embolic events, postcardioversion arrhythmias, and the risks of sedation. The procedure is associated with 1% to 2% risk of thromboembolism. The risk of thromboembolic events is minimized by the use of therapeutic anticoagulation as noted previously. Skin burns are a common complication and can be treated postprocedure with 1% hydrocortisone cream. The patient may become hypoxic or hypoventilate from sedation, so careful oxygen saturation monitoring and airway protection are mandatory. Hypotension and pulmonary edema are rare. Ventricular tachycardia and fibrillation may arise in the presence of hypokalemia, digitalis intoxication, improper synchronization, or lack of synchronization. In patients with sinus node dysfunction, especially in elderly patients with structural heart disease or sick sinus syndrome, prolonged sinus arrest without an adequate escape rhythm may occur. Physiologic pacing in patients with sick sinus syndrome and SR appears to decrease the likelihood of developing AF, especially if the initiation of AF episodes is bradycardia-dependent.15 If DC cardioversion in planned in patients with implanted pacemakers and implantable cardioverter-defibrillators (ICDs), the electrodes should be placed at least 8 cm from the pacemaker battery, and the anteroposterior positioning and biphasic shock waveform is recommended. These patients should be monitored carefully. After cardioversion, the device should be interrogated and evaluated to ensure normal function. Although DC cardioversion is an effective technique for converting AF to SR, the postprocedure recurrence rate is high. Recurrences after cardioversion can be divided into three phases: immediate (within the first few minutes); early (during the first 5 days); and late.16 Factors that predispose to AF recurrence are age, AF duration before cardioversion, the number of previous recurrences, an increased LA size or reduced LA function, and the presence of coronary heart disease or pulmonary or mitral valve disease. Atrial ectopic beats with a long–short sequence, faster heart rates, and variations in atrial conduction increase the risk of AF recurrence. Pretreatment with antiarrhythmic drugs increases the likelihood of restoration and postcardioversion maintenance of SR.17,18 DC cardioversion may be repeated if AF recurs acutely in patients who have not been pretreated with antiarrhythmic therapy. Repeated cardioversion may be a reasonable approach for patients with AF that recurs after a longer duration of SR. Repeat cardioversion or catheter ablation of AF may be necessary in patients who remain symptomatic when in recurrent AF. It is reasonable to avoid cardioversion attempts in patients with new onset AF patients who are minimally symptomatic, particularly those with multiple comorbidities or poor overall prognosis. Patients who had recurrence while taking adequate doses of appropriate antiarrhythmic drug therapy are also suboptimal candidates for DC cardioversion. Drug-refractory patients may be able to be converted to SR but are less likely to maintain SR long-term. Despite the inception of invasive methods for AF management with catheter ablation, pharmacological therapy remains a cornerstone in the rhythm control of AF. These pharmacological agents can be initiated prior to DC cardioversion to increase the likelihood of a successful electrical cardioversion, to maintain SR after cardioversion, or for long-term antiarrhythmic therapy. Pharmacological conversion is preferred in those for whom the risk of DC cardioversion procedural sedation is high. The evidence from available literature suggests significantly lower rates of successful conversion using pharmacological agents compared to electrical cardioversion.10,19 Besides low success rate the other significant disadvantages include the need for prolonged telemetric monitoring to detect sinus node dysfunction, atrioventricular (AV) block, proarrhythmic response, and conversion of AF to atrial flutter. The various antiarrhythmic agents used for rhythm control of AF include: quinidine, disopyramide, procainamide (class IA); flecainide, propafenone (class IC); amiodarone, ibutilide, dofetilide, sotalol, dronedarone (class III and multichannel blockers). If the duration of AF is a week or less, class IC or class III agents are effective for pharmacological conversion of AF. If the AF is persistent, class III agents especially amiodarone, ibutilide, or dofetilide have some role for conversion. A summary of the efficacy and adverse events of pharmacological agents is shown in Table 4.1.
Rhythm Control: Cardioversion and Antiarrhythmic Agents
INTRODUCTION
CARDIOVERSION
ELECTRICAL CARDIOVERSION
Cardioversion Method
Complications from DC Cardioversion
DC Cardioversion in Patients with Cardiac Implantable Electrical Devices
AF Recurrence after DC Cardioversion
PHARMACOLOGICAL CARDIOVERSION
Drug (Class) | Efficacy | Adverse Effects (Cardiac) | Adverse Effects (Noncardiac) |
Disopyramide, procainamide and quinidine (IA) | Primary cardioversion rate—low; (8%–37%) at 24 months for maintenance of SR post-DC20,64 | Disopyramide: negative inotropic Procainamide and Quinidine: torsades de pointes | Disopyramide: urinary retention, hypoglycemia Procainamide: drug-induced lupus Quinidine: low platelets, rash |
Flecainide (IC) | Conversion rate 64% to 75% postoral and IV administration for AF < 7days21 | Atrial flutter with 1:1 conduction, increase in QRS duration: CONTRAINDICATED in coronary artery disease and LV dysfunction | Dizziness, headaches, visual disturbance (5%–10%) |
Propafenone (IC) | Atrial flutter with 1:1 conduction, increase in QRS duration: CONTRAINDICATED in coronary artery disease and LV dysfunction | Metallic taste, dizziness, visual disturbance (5%–10%) | |
Dofetilide (III) | Conversion rates: 6% to 30%31 | QT prolongation and torsades de pointes (0.3%–4.7%) | Headache, gastrointestinal disturbances, “flulike” symptoms |
Sotalol (III) | Conversion rate: ~20% for recent onset AF33 | Bradycardia, torsades de pointes (~4.1%), exacerbation of heart failure65 | Bronchospasm, fatigue |
Amiodarone (III) | Conversion rates: 64% to 84% (IV),35,37,38 27% to 87% (oral)39–41 Maintenance in SR; oral ~60%35 | Bradycardia, QT prolongation, torsades de pointes—low incidence | Acute hypersensitivity pneumonitis or chronic interstitial infiltrates (pulmonary); transaminitis, cirrhosis (hepatic); hypothyroidism or hyperthyroidism (thyroid); photosensitivity; optic neuritis; blue-gray skin discoloration; tremor; alopecia (other) |
Only as IV administration; conversion rate: 28% to 31% and 40% to 45% for atrial flutter49 | Torsades de pointes, monomorphic ventricular tachycardia (3.6% < 8.3%) | Nausea | |
Dronedarone (III) | Conversion rate: 5.8% to 14.8%46 | Bradycardia, CONTRAINDICATED in permanent AF and advanced heart failure | Gastrointestinal: nausea and diarrhea (10%), anorexia, liver toxicity |
Vernakalent (III) | Conversion rate: ~50% | Ventricular arrhythmia, complete AV block, cardiogenic shock | Altered taste, sneezing, paresthesias |
Disopyramide, Quinidine, Procainamide
Class IA sodium channel-blocking drugs have been used in the past for the medical conversion of AF and maintenance of SR. These drugs are now uncommonly used because other agents have greater efficacy and fewer side effects. Quinidine is predominantly eliminated by hepatic metabolism, whereas disopyramide is excreted 60% by renal route. Disopyramide has negative inotropic effects. The other major adverse effects are related to anticholinergic side effects including dry mouth, eyes, nose, and throat, urinary difficulty or urinary retention, precipitation of closed-angle glaucoma, and hypoglycemia. Procainamide is metabolized to the active metabolite 3-n-acetyl-procainamide in the liver.
The use of quinidine, procainamide, and disopyramide for pharmacological cardioversion of AF or maintenance after electrical cardioversion is effective, but all are associated with a small incidence of torsades de pointes.20
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