Effect of nisoldipine on hemodynamic responses to defibrillation.
Sequences of ventricular fibrillation-defibrillation cause transient hypertension; we hypothesized that this "adrenergic overshoot" might be blunted by the functional antiadrenergic effect of the calcium channel blocking drug nisoldipine, with a potentially beneficial reduction in myocardial oxygen requirements. However, other calcium channel blocking drugs have been shown to reduce shock success for defibrillation, a deleterious effect. Thus the purposes of this study were to assess the effect of nisoldipine on the hemodynamic responses to the sequences of ventricular fibrillation-defibrillation, and its effect on the energy requirements for defibrillation. In 16 dogs we administered intravenous nisoldipine (1 microgram/kg bolus followed by an infusion of 0.075 to 0.50 microgram/kg/min) to lower mean blood pressure 10% and 20% below baseline. Ventricular fibrillation was induced electrically, and shocks of varying energy levels (30, 50, and 100 joules) were administered to determine defibrillation energy requirements. Heart rates and blood pressures were recorded up to 3 minutes after each shock to determine hemodynamic responses. Measurements were made before nisoldipine administration and again at the two levels of drug-induced blood pressure decline. We found that the usual systolic blood pressure "overshoot" after defibrillation (typically maximum at 15 to 30 seconds after shocks) was significantly blunted after nisoldipine administration (p less than 0.05). Heart rate slowing after defibrillation (a cholinergic response) was not affected. Nisoldipine did not alter shock success rates, which varied from 12 +/- 7%SE at 30 joules to 68 +/- 12% at 100 joules. Thus nisoldipine blunted the "adrenergic overshoot" of systolic blood pressure following defibrillation, a potentially beneficial effect, without altering the energy requirements for transthoracic defibrillation.