The first implantable cardioverter–defibrillator (ICD) was placed in 1982. Since that time, their use has ex-panded exponentially. Several large clinical trials have demonstrated the superiority of ICDs compared with pharmacological therapy for the secondary prevention of arrhythmic death and possibly as primary therapy for patients at risk for ventricular arrhythmias.
Combination therapy employing both antiarrhyth-mic drugs and ICDs is becoming more common. While the antiarrhythmic drugs have multiple positive effects on the overall therapy, they may alter the frequency of ICD discharge and the ability of the device to detect ventricular tachycardia. A serious concern is the poten-tial for a given drug to increase the defibrillation threshold, thereby rendering the device ineffective.
In general, drugs that block the sodium channel and shorten the action potential tend to increase the defib-rillation threshold. Drugs that prolong repolarization also tend to decrease this threshold. These changes have obvious important ramifications for patients with ICDs.
Effects of antiarrhythmic drugs on defibrillation thresholds
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