title: The pathophysiology of tension pneumothorax in ventilated swine.
abstract: It remains unclear as to whether the cardiovascular collapse observed in tension pneumothorax (TP) is strictly a mechanical pressure-related phenomenon or secondary to hypoxemia. This study describes the pathophysiologic changes associated with a surgically induced progressive TP in a ventilated swine model. With a balloon occlusion catheter surgically placed into the pleural space, progressive volumes of pneumothorax were created in six anesthetized pigs on positive-pressure ventilation. Air was introduced into the right hemithorax in 100-mL increments every 4-5 min, with measurements of heart rate (HR), mean arterial pressure (MAP), central venous pressure (CVP), mean intrapleural pressure (MIP), oxygen saturation (O2%), arterial blood gas (ABG), and cardiac output (C.O.). With the induced progressive TP, results showed that O2% measures decreased immediately and continued to decline throughout the experiment to levels below 50% prior to cardiovascular collapse. The MAP and HR remained relatively stable until approximately 57% total lung capacity progressive TP (600 mL) was reached. At this point, a significant decline in MAP and increase in HR was noted, indicating tension physiology. The C.O. showed a small but significant decrease after 200 mL of air was injected, with a progressive decline after this point. At > 97% total lung capacity TP, lethal cardiovascular collapse occurred in all animals and was associated with an abrupt drop in C.O., HR, and MAP. There was a concurrent equalization of MIP with CVP at the point of collapse. Arterial blood gas measures correlated with O2% trends during the trials. We conclude that the findings of this study support the alternative hypothesis that significant hypoxemia occurs early and precedes hypotension in ventilated animals with TP. Occlusive mechanical compression, suggested by equalization of MIP and CVP, is probably a late event.
authors.affiliation: Department of Emergency Medicine, University of California, San Diego Medical Center, USA.
authors.forename: E D
authors.initials: ED
authors.lastname: Barton
authors.forename: P
authors.initials: P
authors.lastname: Rhee
authors.forename: K C
authors.initials: KC
authors.lastname: Hutton
authors.forename: P
authors.initials: P
authors.lastname: Rosen
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D004195:Disease Models, Animal; D005260:Female; D006439:Hemodynamics; D007022:Hypotension / Q000150:complications*; D000860:Hypoxia / Q000150:complications*; D010100:Oxygen / Q000378:metabolism; D011030:Pneumothorax / Q000209:etiology / Q000503:physiopathology*; D011175:Positive-Pressure Respiration; D013552:Swine; D013898:Thoracic Injuries / Q000150:complications
chemical_list: D010100:Oxygen