Hypercarbic arterial acidemia following resuscitation from severe hemorrhagic shock

Arteriovenous pH and PCO2 gradients can develop during low cardiac output states. We have seen a transient rise in arterial PCO2 and a fall in arterial pH in humans receiving closed-chest cardiopulmonary resuscitation immediately following restoration of spontaneous circulation. Using a hemorrhagic shock model in sheep, serial arterial and mixed venous blood gases were sampled and CO2 elimination was measured. When cardiac output was less than 30% of the baseline value and the arteriovenous PCO2 difference was greater than 20 mmHg, the animals were rapidly resuscitated with intravenous 0.9% NaCl and dopamine. Following resuscitation, there was a transient arterial acidosis and hypercarbia due to passage of venous blood with a high CO2 content into arterial blood. The clinical implications in the setting of hemorrhagic shock are that (1) arterial blood gases are poor indicators of the systemic acid-base state, (2) arterial blood gases drawn immediately following volume resuscitation may be misinterpreted and should probably not be used to guide therapy and (3) there is a transient hypercarbic arterial acidosis following volume resuscitation that may have deleterious effects on cardiac and cerebral function in the early post-resuscitative period.