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The effects of verapamil on left ventricular function in the presence of beta-adrenergic blockade
T P Barragry1, J W Blatchford, I C Tuna
1Department of Surgery, University of Minnesota, Minneapolis.
Insights
Verapamil can cause negative effects on heart function, especially when combined with beta-blockers. Caution is advised when using verapamil for supraventricular tachyarrhythmias in patients on beta-adrenergic blocking agents.
Area of Science:
- Cardiology
- Pharmacology
Background:
- Supraventricular tachyarrhythmias are common after myocardial revascularization.
- Intravenous verapamil effectively terminates these arrhythmias.
Purpose of the Study:
- To assess the impact of verapamil on left ventricular systolic function.
Main Methods:
- Ultrasonic dimension transducers were implanted in dogs.
- Verapamil's effects on cardiac output and contractility were studied in awake, unsedated animals.
- Experiments included assessments with and without beta-adrenergic blockade (atropine and propranolol).
Main Results:
- In intact animals, verapamil caused reflex tachycardia, increasing cardiac output without altering contractility.
- When beta-adrenergic blockade was present, verapamil decreased both cardiac output and contractility.
- The body's compensatory catecholamine release counteracted verapamil's negative effects in the absence of beta-blockade.
Conclusions:
- Verapamil's negative inotropic and chronotropic effects are unmasked when compensatory mechanisms are blocked by beta-adrenergic blockers.
- Clinical use of verapamil in patients on beta-adrenergic blocking agents requires caution.
- This is particularly relevant as more patients receive beta-blockers perioperatively.
Abstract:
Supraventricular tachyarrhythmias frequently complicate myocardial revascularization. Intravenous administration of verapamil has been effective in terminating these arrhythmias. To determine the effects of verapamil on left ventricular systolic function, we implanted ultrasonic dimension transducers in dogs and, after they had recovered from the operation, studied them while they were awake and unsedated. Intravenous administration of verapamil (0.2 mg/kg) resulted in an elevation of cardiac output above baseline because of reflex-induced tachycardia. Contractility, as measured by the load-independent end-systolic pressure-volume relationship, remained unchanged. When the animals were pretreated with atropine and propranolol, verapamil resulted in a fall in cardiac output and contractility. The intact animal responded to the vasodilatory effect of verapamil by releasing catecholamines to maintain cardiac output and hemodynamic stability. Only when this compensatory mechanism was blocked by a beta-adrenergic blocker do the inherently negative inotropic and chronotropic effects of verapamil become apparent. The clinical ramifications of this finding are of greater importance to the surgeon as more patients receive beta-adrenergic blocking agents up to the time of the immediate preoperative period. We conclude that verapamil should be administered with caution to patients with supraventricular tachyarrhythmias who have been receiving beta-adrenergic blocking agents.