The effect of smoke inhalation on pulmonary surfactant.

This paper details efforts to define the primary pathophysiology of acute smoke inhalation without the variables of infection, burns, or fluid resuscitation. A standard dose of smoke (wood and kerosene) was delivered at 37 C to mongrel dogs. The parameters studied included blood gases, carboxyhemoglobin, pulmonary and systemic hemodynamics, respiratory mechanics, surface tension area curves as an indication of surfactant activity, and in vivo photomicroscopy. The FiO2 of the smoke was 17 volumes per cent; the carbon monoxide 17,000 ppm. Immediately following smoke exposure, dense, nonsegmental atelectasis developed. Hemodynamic changes were insignificant, but the PaO2 fell to 49 mmHg; the right to left shunt rose from 5 to 41%. Surfactant reduction was significant: enough to cause an increase in the minimum surface tension from 7 to 22 dynes/cm. This surfactant loss may explain the atelectasis seen and the marked instability of subpleural alveolar walls. The data collected are consistent and support the acute inactivation of surfactant as one of the primary pathophysiologic events in smoke inhalation. The clinical correlation is good; surfactant loss may explain why victims of smoke inhalation are so vulnerable to fluid administration if they have thermal burns as well effectiveness of medical devices.