Acute Rate Control in AF

Verapamil and diltiazem are generally well-tolerated nondihydropyridine calcium-channel blockers used for rate control in AF. The oral forms of these medications can depress left ventricular function. Intravenous verapamil and diltiazem are generally equally effective (24) for acute heart-rate control, but iv diltiazem has been demonstrated to be safe to use in patients with moderate to severe CHF (25-27). Intravenous diltiazem or digoxin are the preferred agents in patients with severe left ventricular dysfunction. Intravenous diltiazem has the additional benefit of more rapid heart rate control than digoxin in the setting of CHF.

Often, the dose of iv calcium-channel blockers or beta-blockers is limited by hypotension. In this circumstance, digoxin can be used to control heart rates. If this is not adequate, vasoconstrictors such as neosynephrine may need to be combined with calcium-blockers or beta-blockers to maintain hemodynamic stability if electrical cardioversion cannot be performed. Amiodarone can also be used to control rate in AF in critically ill patients. In one study (28) of 8 patients with ejection fractions <15%, iv amiodarone decreased the mean ventricular response by 28%. In another study (29) comparing amiodarone to digoxin, amiodarone was more effective in decreasing heart rates at 1 h and at 6 h from onset on infusion compared to digoxin. Amiodarone decreased the mean heart rates from 157 to 92 bpm over 6 h. In this study, over one-half of the patients had class 3 or 4 CHF, again demonstrating that iv amiodarone can be used with caution in critically ill patients.

Clonidine, a central-acting sympatholytic medication has been shown in small series to aid in slowing ventricular response to AF both acutely and chronically (30-31). Intravenous procainamide is used to reduce the ventricular response in patients with hemodynamically stable pre-excited AF (i.e., AF with rapid conduction of atrial impulses to the ventricle over an accessory pathway) by increasing the refractory period of the accessory pathway.

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