R J Irwin1, M R Lerner, J F Bealer, D J Brackett, D W Tuggle. 1. Department of Surgery, University of Oklahoma Health Sciences Center, and Department of Veterans Affairs Medical Center, Oklahoma City 73126, USA.
Abstract
OBJECTIVE: Bomb blast survivors are occasionally found in profound shock and hypoxic without external signs of injury. We investigated the cardiovascular and pulmonary responses of rats subjected to a blast pressure wave. DESIGN: Prospectively randomized, controlled animal study. MATERIALS AND METHODS: Rats were instrumented and subjected to a blast pressure wave of different intensities from a blast wave generator. Cardiopulmonary parameters were recorded for 3 hours or until death. MEASUREMENTS AND MAIN RESULTS: The cardiovascular response to a blast pressure wave was immediate bradycardia, hypotension, and low cardiac index. Three hours later, the rats developed hypotension, low cardiac index, and low stroke volume. Interestingly, systemic vascular resistance remained unchanged. The pulmonary response was a decreased PaO2 and stable PacO2, suggesting a ventilation-perfusion mismatch from massive pulmonary hemorrhage. CONCLUSIONS: Blast-induced circulatory shock resulted from immediate myocardial depression without a compensatory vasoconstriction. Hypoxia presumably resulted from a ventilation-perfusion mismatch caused by pulmonary hemorrhage.
OBJECTIVE: Bomb blast survivors are occasionally found in profound shock and hypoxic without external signs of injury. We investigated the cardiovascular and pulmonary responses of rats subjected to a blast pressure wave. DESIGN: Prospectively randomized, controlled animal study. MATERIALS AND METHODS:Rats were instrumented and subjected to a blast pressure wave of different intensities from a blast wave generator. Cardiopulmonary parameters were recorded for 3 hours or until death. MEASUREMENTS AND MAIN RESULTS: The cardiovascular response to a blast pressure wave was immediate bradycardia, hypotension, and low cardiac index. Three hours later, the rats developed hypotension, low cardiac index, and low stroke volume. Interestingly, systemic vascular resistance remained unchanged. The pulmonary response was a decreased PaO2 and stable PacO2, suggesting a ventilation-perfusion mismatch from massive pulmonary hemorrhage. CONCLUSIONS: Blast-induced circulatory shock resulted from immediate myocardial depression without a compensatory vasoconstriction. Hypoxia presumably resulted from a ventilation-perfusion mismatch caused by pulmonary hemorrhage.
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