Fentanyl-diazepam anesthesia with or without N2O does not attenuate cardiopulmonary baroreflex-mediated vasoconstrictor responses to controlled hypovolemia in humans.

Cardiopulmonary baroreceptors located primarily on the low-pressure side of the circulation sense slight reductions in cardiac filling pressures and elicit sustained peripheral vasoconstriction. Because most inhalation and many intravenous anesthetics attenuate arterial baroreflex function, the low-pressure baroreflex may serve a major role in maintaining blood pressure during intraoperative hypovolemia. To activate the low-pressure baroreflex, progressive nonhypotensive reductions in central venous pressure were produced with graded applications of lower body negative pressure (LBNP, -5, -10, -15 mm Hg) in 18 ASA class I patients before elective surgery. This produced linear reductions in stroke volume as determined by impedance cardiography and cardiac output. Cardiopulmonary baroreflex-mediated increases in total and forearm vascular resistance assisted in maintaining stable blood pressure. After ten patients were anesthetized with fentanyl (12.5 micrograms/kg) and diazepam (0.25 mg/kg) and an additional eight received these agents plus supplemental N2O (70%), reflex vasoconstrictor responses to LBNP were not attenuated and, therefore, blood pressure continued to be well maintained despite substantial reductions in cardiac filling pressures. Thus, these anesthetic regimens preserved vasoconstrictor responses mediated by cardiopulmonary baroreflexes. This promoted cardiovascular stability that may be particularly beneficial in patients with cerebral, cardiovascular, or renal disease undergoing surgical procedures with potential for rapid blood loss.