Arterial and Cerebral Venous Blood Gases Differ in Acute Tension Pneumothorax

Tension pneumothorax (TP) complicates the course of respiratory distress syndrome in about 13% of low birth weight infants. If TP is accompanied by hypotension the majority of infants will develop large intraventricular hemorrhages or cerebral ischemic lesions. Severe TP likely produces cerebral ischemia as a consequence of systemic hypotension, but in a previous clinical study we did not demonstrate accompanying abnormalities in the arterial blood gases. Because of the possibility that arterial blood gases do not reflect tissue acid-base abnormalities during TP, this study was designed to compare sagittal sinus blood gases with arterial gases during and following recovery from severe TP in 5-7 day piglets.

During a 4 minute TP mean blood pressure and common carotid blood flow dropped by 75% and 73%, respectively, and the electroencephalogram became isoelectric. Also sagittal sinus pCO₂ rose (from 45.7 to 63.4 mmHg, P < 0.02) and pH fell (from 7.31 to 7.23, P < 0.02). During TP, end-tidal CO₂ decreased (from 47.5 to 27.0 mmHg, P < 0.005) indicating that the rise in venous (and tissue) pCO₂ was a consequence of reduced CO₂ excretion by the lungs. However, as sagittal sinus pCO₂ rose, arterial pCO₂ fell (from 41.6 to 32.4 mmHg, P < 0.02). Thus, as in other clinical conditions where the circulation is markedly compromised, during severe TP, venous and arterial pCO₂ and pH diverge and arterial blood gases cannot be used to evaluate tissue acidosis.