Atrial fibrillation is the most common dysrhythmia in the general population and is highly prevalent in the critically ill.4 Affected patients are at increased risk of cardiovascular morbidity and mortality.5 It is characterized by disorganized atrial electrical activity probably owing to multiple reentry circuits within the atria that results in loss of atrial contraction and irregular and often times rapid ventricular rates. It is easily recognized on the surface EKG as a narrow complex, irregularly irregular, supraventricular rhythm with a loss of clear P waves, and/or the presence of fibrillatory waves (Figure 23–6). This feature distinguishes atrial fibrillation from the other organized atrial arrhythmias.
A 12-lead electrocardiogram showing atrial fibrillation with a rapid ventricular rate of 179 beats/min. Note the absence of clear P waves and an irregularly irregular rhythm.
Atrial fibrillation increases with age and is greater in men compared to women. Most forms of structural heart disease are associated with atrial fibrillation; most commonly hypertensive heart disease, underlying coronary artery disease, and rheumatic heart disease. Other cardiopulmonary and systemic diseases including obstructive sleep apnea, diabetes, obesity, metabolic syndrome, hyperthyroidism, chronic kidney disease, and postsurgical states have also been associated with atrial fibrillation. Premature atrial contractions are a trigger for atrial fibrillation. In addition, transition between atrial fibrillation and other supraventricular arrhythmias, especially typical atrial flutter is noted frequently. Initial diagnostic workup should include a careful history and physical examination(focusing on the duration and symptoms associated with the arrhythmia, identifiable exacerbating factors, and underlying cardiopulmonary or systemic disease processes), pertinent labs (including serum electrolytes and thyroid function tests), and specific cardiovascular workup (transthoracic and in select cases transesophageal echocardiogram).
As with other arrhythmias, initial assessment should focus on hemodynamic stability as well as identification and correction of underlying causes. Therapeutic considerations in atrial fibrillation include the three nonmutually exclusive strategies of rate control, rhythm control, and systemic thromboembolism prevention.6,7,8,9 Recent clinical trials have demonstrated similar outcomes with rate and rhythm control strategies; however, there may be crossover from one to another strategy due to the natural history of the disease, failure of the initial strategy, or patient preference.10
Rhythm control strategies include synchronized DC cardioversion, pharmacologic conversion using antiarrhythmic drugs, radiofrequency catheter ablation, and/or surgical procedures (eg, Maze procedure). Urgent cardioversion should be considered for hemodynamically unstable, severely symptomatic patients, and in the presence of underlying preexcitation. Indications have been summarized in Table 23–1. Several antiarrhythmic agents can be used for pharmacologic rhythm control; however, careful attention should be paid to appropriate patient selection and the side-effect profile and proarrhythmic potential of these medications.
Table 23–1Indications for urgent cardioversion in atrial fibrillation. |Favorite Table|Download (.pdf) Table 23–1 Indications for urgent cardioversion in atrial fibrillation.
|Acute or ongoing myocardial ischemia |
|Congestive heart failure and/or acute pulmonary edema |
|Underlying preexcitation with rapid ventricular rates and/or hemodynamic instability |
For patients without evidence of structural heart disease or coronary artery disease, class Ic agents like propafenone or flecainide can be considered. Patients should be monitored for QRS widening after initiation of these drugs. For patients with evidence of structural heart disease, amiodarone, sotalol, dronedarone, ibutilide, and dofetilide are the most commonly recommended antiarrhythmic agents. In patients with coronary artery disease without left ventricular dysfunction sotalol, dofetilide, amiodarone, and dronedarone are reasonable choices. In patients with left ventricular (LV) dysfunction and clinical heart failure, antiarrhythmic choices include amiodarone and dofetilide. QT interval should be monitored with class III antiarrhythmics. Sotalol and dofetilide are both affected by renal insufficiency and may require dose adjustment or discontinuation. Amiodarone requires dose adjustment in hepatic dysfunction and has significant systemic side effects with a propensity to cause pulmonary, cardiac, thyroid, ocular, dermatologic, hepatic, and gastrointestinal side effects which must be carefully considered prior to initiating treatment.
Most patients will require slowing of the ventricular rate associated with atrial fibrillation. Pharmacologic approach includes AV nodal blocking agents, namely, nondihydropyridine calcium channel blockers and beta-blockers. In patients with congestive heart failure or hypotension, digoxin can be considered. In select patients, combination therapy may be necessary, but excessive AV nodal blockade should be avoided. A-V node ablation with ventricular pacing is an alternative nonpharmacologic rate control approach, but rarely an acute treatment.
An important aspect of atrial fibrillation management includes prevention of thromboembolism. Patients with atrial fibrillation are at risk for systemic embolization and stroke. The noncontracting atria are a potential nidus for thrombus formation, which usually occurs in the left atrium and left atrial appendage. Multivariate risk models are available to aid in estimation of the thromboembolic risk in patients with nonvalvular atrial fibrillation so that appropriate antithrombotic prevention strategies can be recommended. The most commonly used and well validated being the CHADS2 point score (Congestive heart failure, Hypertension, Age ≥ 75 years, Diabetes mellitus, and prior Stroke or transient ischemic attack) index.11 Patients without any of these risk factors have a CHADS2 score of 0 are at low risk of thromboembolic events and do not require long-term antithrombotic therapy. Patients with a score of 1 are at intermediate risk and can be treated with oral anticoagulant therapy or aspirin. Patients with a score of 2 or higher on the CHADS2 index are considered to be at high risk for thromboembolic events and anticoagulant therapy is recommended unless there are contraindications. Choices include the conventionally used vitamin K antagonist warfarin or newer direct thrombin inhibitor such as dabigatran and factor Xa inhibitors, such as rivaroxaban or apixaban. The new agents should not be used in the presence of severe renal insufficiency, prosthetic heart valves, and in cases of valvular atrial fibrillation. Initial therapy in critically ill patients may be unfractionated or fractionated heparin in the acute period of care prior to conversion to one of these agents.
Hemodynamically stable patients with atrial fibrillation of unknown duration or those with atrial fibrillation for more than 48 hours should be therapeutically anticoagulated for 3 to 4 weeks before elective conversion is attempted. Alternatively, the patient can be started on anticoagulation and if a transesophageal echocardiogram rules out existing thrombi, elective cardioversion can be performed safely. Anticoagulation should be continued for 4 weeks after cardioversion.
The differences in the pathophysiology and management of patients that present with atrial fibrillation with an underlying accessory pathway are noteworthy. A rapid ventricular rate (usually greater than 200 beats/min) and evidence of preexcitation are clues to this diagnosis. For hemodynamically unstable patients urgent cardioversion should be considered. AV nodal blockers should be avoided as they can promote conduction down the accessory pathway resulting in rapid ventricular rates and ventricular fibrillation. Digoxin and adenosine should also be avoided. Antiarrhythmic choices for rhythm control include procainamide, amiodarone, ibutilide, flecainide, and propafenone. Transvenous radiofrequency catheter ablation of bypass tracts obviates the need for long-term pharmacologic therapy and has largely replaced surgical ablation due to its high curative success rates in patients with bypass tracts.