The Cardiovascular and Metabolic Effects of Halothane in Normoxic and Hypoxic Newborn Lambs

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Abstract
O2 consumption, cardiac output and tissue O2 delivery were measured in normoxic and hypoxic 1-3-day old lambs during the following 6 conditions: (control) paralysis with pancuronium and controlled ventilation with room air; paralysis, controlled ventilation and hypoxia (PaO2 [arterial O2 partial pressure] = 30 .+-. 3 mm Hg, [SD]; paralysis, controlled ventilation with room air and 0.5 MAC [maximum alveolar concentration], halothane; paralysis, controlled ventilation, hypoxia, and 0.5 MAC halothane; paralysis, controlled ventilation with room air and 1 MAC halothane; and paralysis, controlled ventilation, hypoxia and 1 MAC halothane. During normoxia, 0.5 and 1 MAC halothane decreased total body O2 consumption, cardiac output and arterial blood pressure. One-half MAC halothane had no effect on blood flow to any organ except muscle, whose flow decreased 64%. One MAC halothane decreased blood flow to the brain, heart, kidney, muscle and gut. Both concentrations of halothane decreased serum catecholamine levels below control values and prevented hypoxia from increasing catecholamine levels. Hypoxia decreased the O2 consumption about 40% from the immediately previous normoxic value, whether the animals were anesthetized or not. Tissue O2 recovery followed changes in blood flow. The cardiac output, arterial blood pressure, and heart rate of anesthetized, hypoxic animals were not different from those in the previous normoxic condition. Halothane did not prevent redistribution of blood flow to the heart and brain of hypoxic animals, nor did halothane prevent hypoxic pulmonary vasoconstriction. Halothane did prevent the increase in serum catecholamine levels that occurs in unanesthetized, hypoxic animals. If halothane has similar effects in humans, it may be useful in treating hypoxic infants in the operating room and intensive care unit.