Hemodynamic effects of barbiturates and benzodiazepines
Intravenous administration of a short-acting barbiturate is the most common method for the rapid and pleasant induction of anesthesia. Recently, benzodiazepine derivatives such as diazepam have achieved popularity as an alternative for induction and maintenance of anesthesia. Often the reason for selecting a specific barbiturate or benzodiazepine is the likely hemodynamic changes that will follow intravenous administration of that drug. This review summarizes hemodynamic changes that occur after intravenous administration of barbiturates or benzodiazepines to patients with and without underlying heart disease.
Hemodynamic effects of short-acting barbiturates (thiopental, thiamylal, methohexital) used for induction of anesthesia may be due to (1) direct myocardial depression, (2) peripheral venous pooling with decreased left ventricular diastolic filling and stroke volume, and (3) decreased sympathetic nervous system outflow from the central nervous system.1
Direct myocardial depression reflected by reduced myocardial contractility is readily demonstrated with the use of isolated heart preparations after even moderate doses of barbiturates.1 In man negative inotropic effects may be obscured by baroreceptor-mediated reflex responses. Decreased tone of systemic capacitance vessels leading to peripheral venous pooling, decreased venous return, left ventricular diastolic filling, and stroke volume is implied by the demonstration of increased venous forearm distensibility following thiopental administration to human subjects.2 This peripheral venous dilatation might also obscure any tendency for the central venous pressure to increase secondary to direct myocardial depression. The impact of reduced central nervous system sympathetic outflow is likely to be transient due to reflexly mediated increases in peripheral sympathetic nervous system activity.
Filner and . . .