Respiratory Response to Acute Progressive Pneumothorax

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Abstract
The respiratory effects of increasing pneumothorax have been studied using anesthetized dogs. The pneumothorax was produced by insufflation of a volume of air into the intrapleural space equal to a definite multiple of the functional residual capacity. Minute and tidal volumes, intrapleural pressures and percentage of lung collapse were measured. Arterial blood was analyzed for O2 content, O2 saturation, CO2 content, pH and hematocrit. It was found that dogs would tolerate a pneumothorax caused by air insufflation equal to twice the functional residual capacity with little distress. With this pneumothorax the physiologic compensation consisted of hyperventilation and chest expansion. With higher degrees of pneumothorax physiologic compensation failed, resulting in respiratory acidosis and elevated hematocrit. The tolerance limit for pneumothorax was an air insufflation equal to 2.5–3.5 times the functional residual capacity. Vagotomy and O2 breathing had no significant effect on this tolerance. Submitted on March 10, 1958

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