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Effects of intravenous verapamil on hemodynamics in patients with heart disease
Insights
Intravenous verapamil significantly reduced mean arterial pressure and systemic vascular resistance in cardiac patients. However, its negative inotropic effects were offset by afterload reduction, maintaining cardiac index.
Area of Science:
- Cardiology
- Pharmacology
Background:
- Coronary artery disease and rheumatic valvular disease are significant cardiac conditions.
- Verapamil is a calcium channel blocker with known hemodynamic effects.
Purpose of the Study:
- To evaluate the hemodynamic effects of intravenous verapamil in patients with coronary artery disease and rheumatic valvular disease.
Main Methods:
- Cardiac catheterization was performed on 13 patients with coronary artery disease and seven with rheumatic valvular disease.
- Hemodynamic parameters were measured before and after a 10 mg intravenous injection of verapamil.
Main Results:
- Verapamil caused a significant decrease in mean arterial pressure (-12%) and systemic vascular resistance (-21%).
- Left ventricular end-diastolic pressure increased (+36%), and LV dp/dt max decreased (-25%).
- Heart rate, cardiac index, left ventricular minute work, and pulmonary artery pressures showed no statistically significant changes.
Conclusions:
- Verapamil's negative inotropic effect is counterbalanced by its afterload-reducing properties.
- Cardiac index is not compromised by verapamil in patients with cardiac disease due to this balance.
Abstract:
The hemodynamic effects of intravenous verapamil (10 mg.) were evaluated in 13 patients with coronary artery disease and in seven patients with rheumatic valvular disease during cardiac catheterization. The peak effects were apparent at 3 to 5 minutes after injection and lasted about 10 minutes. The mean arterial pressure fell from 97.8 +/- 3.4 to 85.9 +/- 2.7 mm. Hg (-12%; p less than 0.01) accompanied by a significant decrease (-21%, p less than 0.001) in systemic vascular resistance (from 1435 +/- 80 to 1131 +/- 82 dynes-sex.-cm.-5) with an increase in left ventricular end-diastolic pressure (from 11.0 +/- 0.9 to 15.0 +/- 1.0 mm. Hg; +36%, p less than 0.01) and a reduction in LV dp/dt max (from 1343 +/- 152 to 1007 +/- 102 mm. Hg/sex.; -25%, p less than 0.05). The changes in heart rate (from 75.7 +/- 3.0 to 80.2 +/- 2.8 beats/min.), cardiac index (from 3.17 +/- 0.15 to 3.61 +/- 0.17 L./min./M.2), left ventricular minute work (from 3.63 +/- 0.28 to 3.31 +/- 0.23 Kg.-m./min./M.2) and mean pulmonary artery pressures (from 15.7 +/- 1.0 to 18.1 +/- 0.8 mm. Hg) were not statistically significant. The intrinsic negative inotropic action of verapamil is, therefore, minimized by its effect on afterload so that cardiac index is not reduced by the drug in patients with cardiac disease.