Why the study?
Does the maintenance of beta-blockers interact adversely with specific anesthetic agents in patients with ischemic heart disease and hypertension?
Does the maintenance of beta-blockers interact adversely with specific anesthetic agents in patients with ischemic heart disease and hypertension?
Maintenance of beta-blockers during anesthesia is generally safe and protective for ischemic myocardium, but specific anesthetic agents like methoxyflurane, trichloroethylene, and enflurane (with propranolol) should be avoided due to adverse cardiac interactions.
The possibility of interactions between beta-adrenoceptor antagonists and anaesthetic drugs is particularly relevant to the anaesthetic management of patients suffering from arterial hypertension and ischaemic heart disease. Maintenance of adrenergic beta-receptor blockade in patients with ischaemic heart disease and arterial hypertension is now widely accepted in order to avoid the cardiac risks of its sudden withdrawal and also to minimize the effects of sympathetic overactivity on the cardiovascular system. However, maintenance of adrenergic beta-receptor blockade may impose some constraints on the choice of the anaesthetic agent. While no adverse interaction has been found between beta blockade and anaesthesia with halothane, halothane supplementing nitrous oxide, or isoflurane, substantial reductions of cardiac performance have been observed in the case of the association of beta blockade and anaesthesia using methoxyflurane or trichloroethylene. An adverse interaction has also been observed between propranolol and enflurane anaesthesia but not between oxprenolol and enflurane anaesthesia. Recent studies of the effects of anaesthesia in the presence of critically narrowed coronary arteries have shown that both halothane and enflurane may cause regional myocardial dysfunction. This dysfunction is minimized by oxprenolol and it appears that adrenergic beta-receptor blockade, besides improving cardiovascular stability, protects the myocardium supplied by narrowed coronary arteries.
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Foëx et al. (1982) studied this question.
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