[Effect of carbon monoxide on hemodynamics and oxygen metabolism in inhalation lung injury]

Chemical pneumonitis and carbon monoxide (CO) poisoning may be the etiologic factors in inhalation injury. Since the CO poisoning related with smoke inhalation has a much high mortality we tested the hypothesis that superimposed CO poisoning deteriorates hemodynamics and oxygen metabolism in acid inhalation injury. Ten anesthetized dogs were ventilated in room air to maintain normal PaCO2. Lung injury was produced with 2 ml/kg 0.1 N HCL intratracheally. Five dogs (ACID) were then ventilated with room air, while the others were exposed to 1% CO in air for 10 minutes to produce CO poisoning simultaneously with acid instillation (CO-ACID). Hemodynamic changes, oxygen metabolism and carboxyhemoglobin (COHb) were monitored for 4 hours. Thirty minutes following the challenge PaO2 in ACID and CO-ACID groups fell to 65 +/- 10 and 43 +/- 4 (p less than 0.05), respectively. Acid caused significantly decreased cardiac output and increased pulmonary vascular resistance. CO did not accentuate hemodynamic changes following acid inhalation. However, a significant increase of COHb in CO-ACID group resulted in deterioration of oxygen transportation. Though oxygen extraction increased markedly in both groups the oxygen consumption decreased significantly in CO-ACID group. A constantly depressed mixed venous oxygen tension in CO-ACID group suggests the deterioration of tissue oxygen metabolism.