Blunt Pulmonary Injury Induces Profound Pulmonary Hypertension in a Porcine Polytrauma Model

Abstract

Traumatic blunt pulmonary injuries, while typically appearing mild on initial exam, notoriously progress into cases of pulmonary hypertension (PHT) and pulmonary edema often worsened with the fluid resuscitation necessitated by such injuries. Increased hypoxemia in acute lung injury is believed to cause pulmonary vasoconstriction which further increases pulmonary arterial pressure, and worsens hypoxemia in a vicious cycle of persistent PHT. The relationship between pulmonary hemodynamics and pulmonary edema, however is not well understood. We hypothesize that the initial increase in pulmonary vasoconstriction occurs to isolate damaged lung tissue and prevent pulmonary infiltration due to traumatic disruption of the alveolar air-liquid interface. In this study, we tested this hypothesis by examining the development of extravascular lung water in relation to pulmonary vasoconstriction in a porcine polytrauma model of acute lung injury. Pulmonary function and hemodynamics were examined before and after localized blunt right chest injury trauma in anesthetized, mechanically ventilated Yorkshire cross pigs (26+/- 1 kg, n=9). Acute grade II-III lung injury was verified at the end of the experiment. Cardiac output was measured via thermodilution with a SwanGanz catheter and extravascular lung water index (ELWI) and pulmonary capillary permeability were assessed in real time using the Pulse Ion Contour Cardiac Output (PiCCO) method (Getinge). Pulmonary arterial pressure increased within 60 minutes of initial lung injury (19 +/- 1 mm Hg at baseline vs 23 +/- 2 mm Hg) despite a drop in mean arterial pressure (60 +/- 1 mm Hg at baseline to 48 +/- 4 mm Hg after trauma). The ratio of pulmonary vascular resistance to systemic vascular resistance (PVR/SVR), indicated a selective pulmonary vasoconstriction(0.23 +/- 0.01 to 0.41 +/- 0.05, p = 0.054). ELWI was negatively correlated with the PVR/SVR ratio (r=0.44, p=0.010). Central venous pressure was lowest (6 +/- 0.6 mm Hg) right after trauma and increased (8 +/- 0.4 mm Hg) 2 hours after trauma along with the increase in PVR/SVR post trauma. Results suggests that traumatic pulmonary edema was limited via autoregulatory vasoconstriction. While effective in preventing pulmonary fluid extravasation, pulmonary hypertension resulted in a marked increase in heart afterload and accumulation of fluid in the right heart. The magnitude of this effect was such that even a moderate degree of fluid resuscitation risked precipitating florid congestive heart failure. Our data suggest that great caution must be exercised during fluid resuscitation of the blunt pulmonary trauma patient. The views expressed are those of the authors and do not reflect the official policy or position of the Department of the Army, Department of Defense, or the U.S. Government.