Hemodynamic changes in dogs caused by sodium pentobarbital anesthesia

Abstract

By the use of implanted flow probes and catheters, hemodynamic changes resulting from sodium pentobarbital anesthesia were recorded in unrestrained dogs. Training caused the average mean arterial pressure to fall from about 120 to near 85 mm Hg, and cardiac output to decrease about 25% to 100 ml/kg per min or less. Pentobarbital (30 mgAg) caused an immediate large increase in heart rate, decrease in stroke volume, and a transient moderate fall in cardiac output and arterial pressure; there was little change in peripheral resistance. When values stabilized about 5 min after induction of anesthesia, increased heart rate and decreased stroke volume were maintained, but mean arterial pressure, cardiac output and peripheral resistance were not significantly different from control values. Changes recorded up to 4 hr were gradual elevation of arterial pressure of about 40 mm Hg, and increase in either peripheral resistance up to 74%, or cardiac output up to 28%. The high heart rate and diminished stroke volume persisted. There was always a pronounced reduction in pulse pressure. The change in heart rate was attributed to vagal blocking effect of pentobarbital. The elevation of arterial pressure was due to rise in either peripheral resistance or cardiac output.