Applied Evidence

Atrial fibrillation: Ways to refine your care

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References

Digoxin has a relatively slow onset of action, however, and is less effective than beta-blockers or calcium channel blockers for rate control. What’s more, digoxin is ineffective for slowing the heart rate during exercise or in hyperadrenergic states. Thus, combination therapy will be needed to achieve adequate rate control in many cases.

Agents that predominantly block AV conduction, such as beta-blockers, calcium channel blockers, and digoxin, are contraindicated in patients with WPW syndrome and wide-complex ventricular response related to the preexcitation syndrome. That’s because these drugs can trigger an antegrade conduction along the accessory pathway.18 In this subset of patients, use a Class 1 antiarrhythmic such as flecainide or procainamide, or amiodarone for rate control1 (TABLE 1).

TABLE 1
Rate-control agents: A review of the options

DRUGLOADING DOSE (ONSET)MAINTENANCE DOSEMAJOR ADVERSE EFFECTS
Amiodarone*IV: 150 mg over 10 min (days)Acute care: 0.5-1 mg/min IV
Outpatient: 200 mg/d oral
Hypotension, HB, bradycardia; pulmonary toxicity; skin discoloration, thyroid dysfunction; corneal deposits, optic neuropathy; warfarin interaction
DigoxinIV: 0.25 mg/2h, up to 1.5 mg (≥60 min)Acute care: 0.125-0.375 mg/d IV or oral
Outpatient: 0.125-0.375 mg/d oral
Digitalis toxicity, HB, bradycardia
DiltiazemIV: 0.25 mg/kg over 2 min (2-7 min)Acute care: 5-15 mg/h IV
Outpatient: 120-360 mg/d oral in divided doses (slow release available)
Hypotension, HB, HF
EsmololIV: 500 mcg/kg over 1 min (5 min)Acute care: 60-200 mcg/kg per min IVHypotension, HB, HF, bradycardia; asthma
MetoprololIV: 2.5-5 mg bolus over 2 min; up to 3 doses (5 min)Outpatient: 25-100 mg BID oralHypotension, HB, HF, bradycardia; asthma
PropranololIV: 0.15 mg/kg (5 min)Outpatient: 80-240 mg/d oral in divided dosesHypotension, HB, HF, bradycardia; asthma
VerapamilIV: 0.075-0.15 mg/kg over 2 min (3-5 min)Outpatient: 120-360 mg/d oral in divided doses (slow release available)Hypotension, HB, HF; digoxin interaction
HB, heart block; HF, heart failure; IV, intravenous.
* Recommended for patients with accessory pathway and those with heart failure without accessory pathway; often useful when other measures are unsuccessful or contraindicated.
For patients with heart failure without accessory pathway.
The beta-blockers listed here are representative; other similar agents can also be used to achieve rate control.
Adapted from: Fuster V, et al. Circulation. 2006.1

When should you consider cardioversion?

The NICE guidelines recommend rhythm control as the initial choice for patients who:

  • are symptomatic
  • are <65 years old
  • are presenting for the first time with lone AF or AF secondary to a condition that has been treated or corrected
  • have CHF.16

While the guidelines recommend restoring sinus rhythm in patients with heart failure, a recent study suggests that rhythm control is no more effective for reducing the rate of death from cardiovascular causes compared to a rate-control strategy in this patient population.19 As with other aspects of AF management for which there is no definitive approach, individualized factors—including patient preference—should be your guide.

Electrical vs pharmacological cardioversion. Sinus rhythm can be established with electrical or pharmacological cardioversion. Electrical cardioversion, in which an external defibrillator delivers an electric shock that’s synchronized with the QRS complex, is usually well tolerated; embolization, pulmonary edema, and other arrhythmias are infrequent complications. Cardioversion with biphasic waveform defibrillation typically uses less energy and may have greater efficacy than monophasic waveforms.

The success rate of electrical cardioversion is higher than that of pharmacological cardioversion.8 But the use of electrical cardioversion is limited by the need for general anesthesia or conscious sedation for pain control. Pharmacological cardioversion is more effective for patients who have had AF for <48 hours; after that, the conversion rate drops considerably, and electrical cardioversion is often needed to restore sinus rhythm in a patient whose AF has lasted more than 7 days. A variety of antiarrhythmic drugs (TABLE 2), including propafenone, flecainide, ibutilide, and amiodarone, can be used to restore sinus rhythm. But because of the proarrhythmic potential of most of these agents, patients should be monitored in the hospital while drug therapy is initiated. After sinus rhythm is restored, maintenance therapy may be required.

Whether cardioversion is achieved by electrical or pharmacological means, it is associated with an increased risk of thromboembolism, especially in patients whose AF has persisted for >48 hours. Adequate anticoagulation with warfarin (international normalized rate of 2-3) should be achieved 3 weeks prior to cardioversion and continued for 4 weeks thereafter. Alternatively, excluding atrial thrombus by TEE paves the way for early cardioversion, using IV heparin or low-molecular-weight heparin for anticoagulation.

TABLE 2
Pharmacological cardioversion: Typical drugs and doses

DRUGROUTE OF ADMINISTRATIONTYPICAL DOSAGEPOTENTIAL ADVERSE EFFECTS
AmiodaroneOralInpatient: 1.2-1.8 g/d in divided dose to 10 g total, then 200-400 mg/d or 30 mg/kg as single doseHypotension, bradycardia, QT prolongation, torsades de pointes (rare); GI upset, constipation; phlebitis (IV)
IV5-7 mg/kg over 30-60 min, then 1.2-1.8 g/d continuous
DofetilideOral125-500 mcg BID*QT prolongation, torsades de pointes
FlecainideOral200-300 mgHypotension, atrial flutter with high ventricular rate
IV1.5-3 mg/kg over 10-20 min
IbutilideIV1 mg/10 min; repeat 1 mg PRNQT prolongation, torsades de pointes
PropafenoneOral600 mgHypotension, atrial flutter with high ventricular rate
IV1.5-2 mg/kg over 10-20 min
AF, atrial fibrillation; BID, twice a day; GI, gastrointestinal; IV, intravenous; PRN, as needed.
*Dosage adjusted based on renal function, body size, and age.
Adapted from: Fuster V, et al. Circulation. 2006.1

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