RESPIRATORY ALKALOSIS DURING ANESTHESIA I. EFFECTS ON CIRCULATORY, RESPIRATORY, AND MUSCULAR ACTIVITY

¹ From the Departments of Pharmacology and Anesthesia, University of Wisconsin School of Medicine, Madison

Dogs anesthetized with cyclopropane, morphine-ether, morphine-chloretone, barbital, pentobarbital or pentothal were hyperventilated mechanically for periods ranging from one to fifteen hours. The percentage reduction in arterial CO₂ content averaged 66 per cent in 57 experiments, the range being 40 to 87 per cent. The following sequence of changes in arterial pressure was observed: (a) an immediate and pronounced arterial hypotension, (b) a gradual recovery of arterial pressure during hyperventilation to the original or to a higher level if sufficient time is allowed, (c) an immediate further increase when hyperventilation is discontinued, (d) the final stabilization at or near the initial pressure. Fatal circulatory failure was not observed except in one animal with chronic cardiac lesions.

The arterial hypotension which results from hyperventilation during anesthesia is not related primarily to heat or water loss or to mechanical interference with the pulmonary circulation by changes in intrapulmonic pressure.

The arterial hypotension during anesthesia results from the combined effects of loss of CO₂ and narcosis. The fall in arterial pressure is proportional to the depth of anesthesia rather than to the extent of loss of CO₂. No significant fall in pressure occurs in the "unanesthetized" dog hyperventilated during recovery from cyclopropane or pentothal anesthesia or in the dog in which local anesthesia alone is used.

The duration of apnea is inversely proportional to the duration of hyperventilation, indicating a gradual recovery of central irritability. It was not possible to induce fatal respiratory paralysis in this series of animals by hyperventilation during ordinary anesthesia. When large doses of any depressant drug are administered just prior to discontinuance of hyperventilation, paralysis occurs as a summation effect.

The tetany characteristic of alkalosis was not observed during anesthesia but occurred in the decerebrate preparation and in the unanesthetized dog. The relation of these findings to the theory of acapnial "shock" is briefly discussed.