Effects of a ‘CO₂ buffer’ on hypercapnia of apneic oxygenation

¹ Department of Cardio-Respiratory Diseases and Department of Anesthesia, Walter Reed Army Institute of Research and Walter Reed Army Hospital, Washington, D. C.

Eight dogs maintained in ‘apneic oxygenation’ for 60 minutes were given a .3 M intravenous infusion of 2-amino-2-(hydroxymethyl)-1, 3-propanediol (THAM) in a .3% NaCl solution at the rate of 1.1 ml/ kg/min. After 1 hour of apnea, arterial O₂ saturation was 100%, plasma CO₂ 53.2 mm/l., plasma HCO^–₃ 50.6 mm/l., arterial blood pH 7.37 and PaCO₂ 98 mm Hg. Blood pressure remained close to the preapneic control period and intracranial pressure did not change significantly. Plasma catecholamines levels did not change. There was a fall in hematocrit, in Na⁺ and Cl^– plasma concentration while K⁺ did not change. After a 20-minute lag, urine output equaled fluid input. Urinary pH was 7.54, HCO^–₃ concentration 89 mm/l., THAM 85 mm/l. and 18–28% of the total CO₂ produced by the animal during apnea was recovered in the urine excreted during that time. All the animals survived, indicating that the dog will tolerate well a plasma concentration of CO₂ over twice its normal level when its two fractions HCO^–₃ and H₂CO₃ are in suitable proportion to maintain the biological neutrality of the internal environment (e.g. 7.40). In the presence of a normal pH and an elevated pCO₂ there is no measurable stimulation of the sympathoadrenal system and the circulation is not altered.