We examined the cardiovascular and respiratory responses to enflurane-oxygen anesthesia in 12 unpremedicated volunteers during the 2nd and 7th hours of continuous anesthesia without surgery: During the 2nd hour, spontaneous ventilation at 1 MAC (1.86% end-tidal) enflurane produced a marked reduction of tidal volume with a mean Paco2 of 61 torr. Hypercapnia produced cardiovascular stimulation. Cardiac output (CO) increased 31% above the awake control value due to a 41% increase in heart rate (HR). Stroke volume and central venous pressure were unchanged. Systemic vascular resistance fell 52% and mean arterial pressure decreased 38%. Increasing the enflurane concentration to 1.5 MAC accentuated the respiratory depression as the mean Paco2 rose to 76 torr with further increases in CO and HR. Attempts to study cardiovascular responses at 2 MAC were thwarted by apnea.
These results differ from results obtained during controlled ventilation and normal Paco2 in the same subjects. When ventilation is controlled, all cardiovascular variables show a concentration-related depression.
Seven hours of continuous anesthesia produced a significant reversal of the depression of tidal volume. Paco2 was 46, 56, and 67 torr at 1, 1.5, and, for the first time, 2 MAC. The only significant changes in cardiovascular function from the 2nd hour at 1 MAC were increases in HR and left ventricular work. Deepening anesthesia did not produce further significant changes except for greater depression of the Bcg IJ wave and aortic dP/dt at 1.5 MAC.
We conclude that adaptation to the respiratory depression of enflurane occurs over time, although the circulatory adaptation is apparently masked during spontaneous ventilation. With most inhalation anesthetics, including enflurane during controlied ventilation, the circulatory system gradually shows reversal of the initial depressant effects, or even an increase above control values. The fact that this phenomenon is not seen during spontaneous ventilation with enflurane may be due to the decreased sympathetic stimulation caused by the drop in Paco2 which occurs as a function of time during enflurane anesthesia.