ALTERATIONS OF PULMONARY GAS-EXCHANGE AFTER SUPERIMPOSED CARBON-MONOXIDE POISONING IN ACUTE LUNG INJURY

Background. Smoke inhalation injury produces substantial morbidity and mortality caused both by immediate catastrophic pulmonary failure and by the subsequent development of pneumonia. Although carbon monoxide (CO) poisoning is present to a degree in nearly all instances of smoke inhalation, the importance of CO in the pathogenesis of smoke inhalat ion injury remains controversial because smoke contains numerous other potential pulmonary toxins such as aldehydes, chlorine gas, and hydro chloric acid. This study was performed to determine whether CO poisoni ng acts as a cofactor in the evolution of inhalation injury. Methods. Four groups of anesthetized dogs received ventilation with 1% CO in ro om air alone, intratracheal instillation of 2.0 ml/kg 0.1 N hydrochlor ic acid (HCl) alone, or acid either immediately or 30 minutes before C O. Ventilation/perfusion relationships were measured for 4 hours there after with the multiple inert gas elimination technique. Results. Acid instillation established 30 minutes before CO poisoning resulted in s ignificantly decreased carboxyhemoglobin concentrations after ventilat ion with 1% CO in air for 10 minutes. However, CO elimination was mark edly delayed in both acid-challenged groups ventilated with CO. Moreov er, acid instillation immediately before CO poisoning significantly ex acerbated the development of ventilation/perfusion inequality caused b y the acid, because the development of shunt was accelerated. Conclusi ons. CO poisoning is an important cofactor in the development of inhal ation injury by acceleration of the development of ventilation/perfusi on inequality after inhalation.