CHANGES IN BLOOD ACID-BASE BALANCE DURING ASPHYXIA AND RESUSCITATION

Abstract

Acid-base changes in the arterial blood of dogs during fatal asphyxia and during successful resuscitation were studied. Asphyxia was produced by tracheal obstruction or by N inhalation. During fatal obstructive asphyxia, an early respiratory acidosis occurred followed by an uncompen-sated metabolic acidosis. By the time circulation failed, arterial pCO2 reached an avg. value of 64.9 mm. Hg and the pH fell to 7.2 (7 dogs). In fatal N asphyxia, an early profound respiratory alkalosis was overcome by a late uncom-pensated metabolic acidosis, so that both arterial pCo2 and [H+] were slightly above normal when the circulation failed. During artificial respiration with air at the animal''s control rate and tidal volume, arterial pCO2 and [H+] continued to rise in most cases. In all cases, both of these values remained above normal until spontaneous respiration was resumed. On restoration of spontaneous breathing, hyperventilation occurred in an attempt to compensate the acidosis. These results indicate that there is no deficiency in the arterial levels of pCO or [H+] during the entire course of obstructive asphyxia or in the later stages of N asphyxia. They further indicate that artificial respiration with air at a normal minute vol. does not produce a deficiency in the levels of these agents in the arterial blood. Thus, it would appear to be unnecessary to include CO2 in the resuscitative mixture in order to maintain normal arterial levels of pCO during artificial respiration in the 2 types of asphyxia studied in this investigation.