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Effect of calcium channel blockers on hemodynamic responses to defibrillation
P R Hite1, E Schröder, R A Kieso
1Cardiovascular Center, University of Iowa, Iowa City.
Insights
Calcium channel blockers like diltiazem and verapamil blunt the blood pressure rise after defibrillation. Nifedipine did not affect blood pressure, but slowed heart rate in this canine study.
Area of Science:
- Cardiology
- Pharmacology
- Physiology
Background:
- The hemodynamic response to defibrillation involves an adrenergic component crucial for blood pressure maintenance.
- Calcium channel blockers possess antiadrenergic effects, suggesting potential interference with this response.
Purpose of the Study:
- To investigate the hypothesis that calcium channel blockers blunt the adrenergic response to defibrillation.
- To evaluate the effects of diltiazem, verapamil, and nifedipine on hemodynamic parameters following defibrillation in a canine model.
Main Methods:
- Ventricular fibrillation was induced in 35 closed-chest dogs, followed by transthoracic shocks to determine defibrillation energy requirements.
- Hemodynamic parameters (heart rate, blood pressure) were recorded during sequences of defibrillation.
- Drug interventions included infusions of diltiazem, verapamil, or nifedipine, with a control group receiving no intervention.
Main Results:
- Diltiazem and verapamil significantly blunted the post-shock rise in mean arterial pressure compared to baseline and control.
- Nifedipine treatment did not alter blood pressure responses post-defibrillation.
- Heart rate remained unaffected by diltiazem and verapamil, but was slowed by nifedipine.
Conclusions:
- Diltiazem and verapamil attenuate the adrenergic-mediated blood pressure recovery after defibrillation.
- Nifedipine's effects on hemodynamics post-defibrillation differ from diltiazem and verapamil.
- These findings highlight the differential impact of calcium channel blockers on the cardiovascular response to defibrillation.
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 received 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 micrograms/min for 3 minutes plus 2 to 20 micrograms/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 less than 0.05) and verapamil (108 +/- 9 versus 78 +/- 12 mm Hg and 113 +/- 7 versus 90 +/- 10 mm Hg, p less than 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.(ABSTRACT TRUNCATED AT 250 WORDS)