BACKGROUND: Pneumothoraces are relatively common among trauma patients and can rapidly progress to tension physiology and death if not identified and treated. We sought to develop a reliable and reproducible large animal model of tension pneumothorax and to examine the cardiovascular effects during progression from simple pneumothorax to tension pneumothorax. MATERIALS AND METHODS: Ten swine were intubated, sedated, and placed on mechanical ventilation. After a midline celiotomy, a 10-mm balloon-tipped laparoscopic trocar was placed through the diaphragm, and a 28F chest tube was placed in the standard position and clamped. Thoracic insufflation was performed in 5-mm increments, and continuous cardiovascular measurements were obtained. RESULTS: Mean insufflation pressures of 10 mm Hg were associated with a 67% decrease in cardiac output (6.6 L/min versus 2.2 l/min; P = 0.04). An additional increase in the insufflation pressure (mean 15 mm Hg) was associated with an 82% decrease in cardiac output from baseline (6.8 versus 1.2 L/min; P < 0.01). Increasing insufflation pressures were associated with a corresponding increase in central venous pressure (from 7.6 mm Hg to 15.2 mm Hg; P < 0.01) and a simultaneous decrease in the pulmonary artery diastolic pressure (from 15 mm Hg to 12 mm Hg; P = 0.06), with the central venous pressure and pulmonary artery diastolic pressure approaching equalization immediately before the development of major hemodynamic decline. Pulseless electrical activity arrest was induced at an average of 20 mm Hg. Tension physiology was immediately reversible with adequate decompression, allowing for multiple repeated trials. CONCLUSIONS: A reliable and highly reproducible model was created for severe tension pneumothorax in a large animal. Major cardiovascular instability proceeding to pulseless electrical activity arrest with stepwise insufflation was noted. This model could be highly useful for studying new diagnostic and treatment modalities for tension pneumothorax. Published by Elsevier Inc.
BACKGROUND: Pneumothoraces are relatively common among traumapatients and can rapidly progress to tension physiology and death if not identified and treated. We sought to develop a reliable and reproducible large animal model of tension pneumothorax and to examine the cardiovascular effects during progression from simple pneumothorax to tension pneumothorax. MATERIALS AND METHODS: Ten swine were intubated, sedated, and placed on mechanical ventilation. After a midline celiotomy, a 10-mm balloon-tipped laparoscopic trocar was placed through the diaphragm, and a 28F chest tube was placed in the standard position and clamped. Thoracic insufflation was performed in 5-mm increments, and continuous cardiovascular measurements were obtained. RESULTS: Mean insufflation pressures of 10 mm Hg were associated with a 67% decrease in cardiac output (6.6 L/min versus 2.2 l/min; P = 0.04). An additional increase in the insufflation pressure (mean 15 mm Hg) was associated with an 82% decrease in cardiac output from baseline (6.8 versus 1.2 L/min; P < 0.01). Increasing insufflation pressures were associated with a corresponding increase in central venous pressure (from 7.6 mm Hg to 15.2 mm Hg; P < 0.01) and a simultaneous decrease in the pulmonary artery diastolic pressure (from 15 mm Hg to 12 mm Hg; P = 0.06), with the central venous pressure and pulmonary artery diastolic pressure approaching equalization immediately before the development of major hemodynamic decline. Pulseless electrical activity arrest was induced at an average of 20 mm Hg. Tension physiology was immediately reversible with adequate decompression, allowing for multiple repeated trials. CONCLUSIONS: A reliable and highly reproducible model was created for severe tension pneumothorax in a large animal. Major cardiovascular instability proceeding to pulseless electrical activity arrest with stepwise insufflation was noted. This model could be highly useful for studying new diagnostic and treatment modalities for tension pneumothorax. Published by Elsevier Inc.