The Effects of Halotthane on Respiratory and Cardiovascular Responses to Hypoxia in Dogs

The effects of 0.75 to 2 per cent end-tidal halothane on cardiovascular and respiratory responses to hypoxia were quantitated. Moderate hypoxia (Pa02. 45 torr) caused stimulation of ventilation and cardiac output at all levels of halothane anesthesia. Although severe hypoxia (Pa02 30 torr) further stimulated ventilation and cardiac output at 0.75 to 1.25 per cent halothane, increasing the halothane concentration to 1.0–1.5 per cent rapidly converted hyperventilation and elevated cardiac output to respiratory or cardiac arrest. Oxygen transport did not meet oxygen consumption requirements; hence, severe metabolic acidosis developed during severe hypoxia. Within narrow limits, the dose of halothane is most important in determining the physiologic response to severe hypoxia.