Drugs are more likely to be effective when used relatively early following the onset of atrial fibrillation. However, when a clear history of recent onset atrial fibrillation has been obtained it is important to establish and treat the likely precipitants. In many instances this will allow spontaneous reversion to sinus rhythm. Important precipitants include hypoxia, dehydration, hypokalaemia, hypertension, thyrotoxicosis and coronary ischaemia. Whilst these precipitants are being treated rate control will usually be required. Short acting oral calcium channel blockers (verapamil or diltiazem) and short acting beta blockers titrated against the patients response are most effective in this setting and likely to facilitate cardioversion. Intravenous verapamil should be avoided. If a patient with new atrial fibrillation is haemodynamically compromised urgent cardioversion is required with full heparinisation. Similarly patients with fast, recent onset atrial fibrillation with broad complexes are probably best treated with early elective DC cardioversion with full heparinisation.

With the above provisos there is a role for chemical cardioversion. Amiodarone (which has class III action and mild beta blocking activity) given through a large peripheral line or centrally can be highly effective, though a rate slowing agent may also be needed. Intravenous flecainide (class I) can also be highly effective. Like other class I agents (quinidine, disopyramide and procainamide), flecainide is best avoided in patients with known or possible coronary artery disease and in conditions known to predispose to torsade de pointes. Digoxin has no role in the cardioversion of atrial fibrillation.

The highest likelihood of successful cardioversion in patients with chronic atrial fibrillation is with DC cardioversion following appropriate investigation and anticoagulation. It should be noted that cardioversion is generally safe during digoxin therapy, so long as potassium and digoxin levels are in the normal range.

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