Immediate cardiovascular effects of tension pneumothorax.

We studied the immediate cardiovascular effects of unilateral tension pneumothorax in sheep, a species with an intact mediastinal pleura similar to that in humans. Adult animals were restrained in the prone position and studied in the conscious state to permit spontaneous respiratory adjustments. We measured pressures in the ipsilateral pleural space (Ppli), contralateral pleural space (Pplc), esophagus (Pes), pulmonary artery (Ppa), superior vena cava (Pcv), carotid artery (Ps), as well as thermodilution cardiac output (CO) and heart rate (HR). Acute unilateral pneumothorax of 0, 10, and 20 cmH2O tension produced no significant changes in mean Ps, Pcv, and CO at any level of tension, but it did produce a marked increase in HR at 10 and 20 cmH2O tension (p less than 0.05). Similar observations were made with unilateral pneumothorax of 15 cmH2O for 30 min. These results suggested that tension was transmitted incompletely to the mediastinum and contralateral hemithorax. This was confirmed by an increase from baseline of mean (+/- SE) end-expiratory Pes by 6.6 +/- 4.9 cmH2O and Pplc by 6.7 +/- 6.0 cmH2O, for an increase in Ppli by 20.5 +/- 4.0 cmH2O. The respiratory intrathoracic pressure fluctuations were accentuated with mean increases of 211, 78, and 117% in the ipsilateral pleural space, esophagus, and contralateral pleural space, respectively (p less than 0.05). When the increase in respiratory intrathoracic pressure fluctuations was prevented by artificial hyperventilation, CO decreased. We conclude that unilateral tension pneumothorax does not directly lower CO and Ps because of (1) incomplete transmission of the ipsilateral pleural pressure to the mediastinum and contralateral hemithorax, (2) marked respiratory intrathoracic pressure swings, and (3) compensatory tachycardia.