Alveolar Dead Space and Arterial to End-Tidal Carbon Dioxide Differences During Hypothermia in Dog and Man

J. W. Severinghaus, M. A. Stupfel, A. F. Bradley


Hyperventilation is widely used during hypothermia because it seems to protect dogs from ventricular fibrillation. Some workers have suggested that pulmonary carbon dioxide elimination may be hindered by hypothermia. We therefore determined the physiological dead space and the arterial to alveolar (end-tidal) carbon dioxide difference (a-A Pco2) in dogs and patients. Hypothermia did not result in a block of carbon dioxide elimination. Metabolic acidosis occurred with both anesthesia and hypothermia in dogs, but in man only after cardiac inflow occlusion. In five men, but not in dogs, the a-A Pco2 increased as a result of induction of anesthesia and artificial respiration, rising from 2 to 4 mm Hg. In man, subsequent mean values were: after cooling to 30°C, 4 mm; after opening the chest and retracting a lung, 6 mm; following release of occluded circulation, 15 mm, which was 55% of arterial Pco2. This indicates stoppage of the pulmonary capillary blood flow in over half the lung. Normal or euventilation during hypothermia is defined such that carbon dioxide elimination equals its rate of metabolic production. The associated Pco2 is the same as for normal blood cooled in vitro, e.g. 40 mm Hg at 37°, 30.5 mm Hg, at 31°, 22.9 mm Hg at 25° and 13.3 mm Hg at 15°C. Fortuituously, this ‘normal’ ventilation was found to be approximated by maintenance of the control normal rate and depth as cooling progressed. An incidental observation in seven normal men is that oxygen administration resulted in slight (4–8%) impairment in pulmonary capillary blood flow distribution.

Submitted on January 22, 1957