Ventilation and perfusion alterations after smoke inhalation injury

Previous studies of human victims of smoke inhalation injury have demonstrated retention of intravenously infused 133xenon2, 6 suggesting either: (1) true intrapulmonary shunting (Qs) secondary to alveolar collapse, flooding, or obliteration, or (2) perfusion of low ventilation/perfusion compartments (low VA/Q) secondary to bronchospasm, bronchial constriction, or partial bronchial occlusion by cellular debris. To differentiate between and quantitate the relative contribution of intrapulmonary shunt versus low VA/Q compartments, multiple inert gas analysis, as described by Wagner et al.,12 was applied to human victims of smoke inhalation. Studies of an animal model of injury were subsequently performed to confirm these observations. These experiments suggest that early alterations of ventilation and perfusion resulted from increased high VA/Q and dead-space ventilation. Late alterations included significantly increased perfusion of low VA/Q compartments and return of high VA/Q ventilation to baseline levels. True intrapulmonary shunting was notably absent. This physiologic sequence may represent early regional pulmonary vasospasm followed by regional bronchial obstruction and gradual alveolar secondary to bronchospasm, bronchial edema, or partial occlusion by cellular debris.