Effect of anesthesia and positive pressure ventilation on early postburn hemodynamic instability.

Our purpose was to determine the effect of anesthesia and positive pressure ventilation, PPV, on early postburn (1-12 hr) cardiopulmonary changes. Adult sheep were given a 40% full-thickness TBS burn not involving chest wall. Halothane anesthesia and PPV alone decreased cardiac output by 20% but also decreased oxygen demands by 30% from the awake state. Systemic vascular resistance, SVR, was increased by 40% over the awake state in the first several hours postburn: cardiac output was decreased despite baseline filling pressures. Low molecular weight dextran, LMWD, prevented the increased SVR by decreasing resistance to flow. A continued decrease in cardiac output was evident during the next 6-12 hr postburn with anesthesia while awake sheep values returned to baseline. Fluid requirements to maintain filling pressures also increased by 30% over the awake state. Static lung compliance, CSTAT, decreased from a baseline of 43 +/- 5 to 32 +/- 4 ml/cm H2O with anesthesia and ventilation. This was due to nonburn chest wall edema: lung water was normal. The 7-cm H2O increase in inspiratory pressure necessary to maintain constant volume was the cause of the decreased cardiac output, because maintaining pressure constant resulted in no decrease in cardiac output. VO2 remained relatively constant due to increased O2 extraction. LMWD prevented the CSTAT changes and, in turn, the decreased output. We conclude that both the increase in SVR and decrease in CSTAT postburn resulted in a significant decrease in cardiac output with anesthesia not seen in the awake burn state. The decreased output was, however, in large part compensated for by decreased O2 demands and increased O2 extraction.