Event-related potentials elicited by neutral stimuli and emotion-expressing human faces

Abstract

The hemodynamic response to sequences of ventricular fibrillation and defibrillation includes an adrenergic component that is important for the maintenance of blood pressure after successful defibrillation. Because calcium channel blocking drugs have antiadrenergic effects, we hypothesized that they might blunt the adrenergic response to defibrillation. Ventricular fibrillation was induced in 35 closed-chest dogs. Each recaived 4 to 7 direct current transthoracic shocks at three energy levels to determine defibrillation energy requirements. Heart rate and blood pressure were recorded. Energy sequences were repeated after 45 minutes of no intervention (control, n = 5) or after 45-minute infusions of diltiazem (0.1 mg/kg/min, n = 10), verapamil (0.1 mg/kg bolus plus 0.01 mg/kg/min, n = 10), or nifedipine (40 μg/min for 3 minutes plus 2 to 20 μg/min adjusted to maintain a 10 mm Hg drop in mean arterial pressure, n = 10). Our results show that the normal post-shock rise in mean arterial pressure was blunted by the calcium channel blockers diltiazem (systolic arterial pressure at 15 and 60 seconds post-shock, pre-drug versus post-drug: 102 ± 9 versus 64 ± 9 mm Hg and 113 ± 10 versus 87 ± 6 mm Hg; p < 0.05) and verapamil (108 ± 9 versus 78 ± 12 mm Hg and 113 ± 7 versus 90 ± 10 mm Hg, p < 0.05). There were no differences in blood pressure responses after nifedipine treatment or no drug. Heart rate responses were not altered by diltiazem or verapamil; after nifedipine administration, post-shock heart rates were slower. After treatment with diltiazem and verapamil there was a modest reduction in percent shock success across all energy levels (diltiazem: 28% ± 7% versus 17% ± 6%, 71% ± 9% versus 52% ± 14%, and 87% ± 13% versus 82% ± 11% at 25 J, 50 J, and 100 J, respectively [ p < 0.05 ]; verapamil: 50% ± 14% versus 15% ± 2%, 64% ± 11% versus 44% ± 14%, and 82% ± 9% versus 72% ± 13%, respectively [ p < 0.05 ]). Nifedipine did not alter shock success rates. This study suggests that calcium channel blocking drugs blunt the adrenergic response to defibrillation.