Ps. Barie et al., ALTERATIONS OF PULMONARY GAS-EXCHANGE AFTER SUPERIMPOSED CARBON-MONOXIDE POISONING IN ACUTE LUNG INJURY, Surgery, 115(6), 1994, pp. 678-686
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.