Intoxication with beta-sympathicolytics

Abstract

Based on the review of available literature, this article states the possible clinical problems with beta-blocker intoxication. Some 26% of severe cases of intoxication will die. This fact stimulated the attempt, using animal experiments, to gain an insight into the pathophysiological profile of this intoxication. The results of these animal experiments led to the following conclusion: toxic doses of beta-blockers result in a dose-dependent decrease of myocardial contractility. This negative inotropic effect is not related to the antagonizing effects of the beta-blocker at the beta-adrenergic receptor level, nor to the additional properties of this group of drugs, but is influenced by a combination of other factors. These include (1) a direct negative inotropic effect on the myocardium, probably caused by a calcium dependent mechanism; (2) a decrease in serum calcium concentration, probably caused by a decreased parathormone production; (3) a centrally mediated hypotensive action. Toxic doses of beta-blockers do not only affect the myocardium and the haemodynamic system, they can also lead to respiratory arrest. This arrest is caused by the direct effect of these drugs on the central nervous system and can, in itself, be the cause of death. Such results lead to the following therapeutic advice: patients with severe beta-blocker intoxication must be admitted to an Intensive Care Unit, as early initiation of ventilation, as well as administration of beta-antagonist can be essential; the drop in serum calcium concentration must be corrected; drugs which can improve myocardial contractility, other than via the beta-adrenergic receptor, such as phosphodiesterase inhibitors and glucagon, should be administered.