Hemorrhagic hypotension after brain injury causes an early and sustained reduction in cerebral oxygen delivery despite normalization of systemic oxygen delivery.

Morbidity and mortality are doubled when hemorrhagic hypotension (HEM) accompanies a traumatic brain injury (TBI). Hemorrhagic hypotension initiates a "secondary" injury (SI) that has been attributed to ischemia, but this has not been confirmed in the laboratory. All previous studies have been of relatively short duration (less than 6 hours), allowing insufficient time to study the pathophysiology of SI, since maximal intracranial pressure (ICP) elevations may occur 16 to 20 hours after injury. We hypothesized that HEM combined with TBI would reduce cerebral oxygen delivery (cO2del) and cerebral metabolic rate for oxygen (cMRO2) to a greater degree than would occur with TBI alone. In a porcine model of TBI and HEM we recorded systemic oxygen delivery (sO2del), ICP, cerebral blood flow (CBF), cO2del, cMRO2, brain oxygen extraction ratio (cO2ER), and cortical water content (CWC) over a 24-hour study period. Controls (n = 7) were instrumented only, group 1 (n = 14) received a focal cryogenic lesion only, group 2 (n = 21) received a cryogenic lesion plus hemorrhage to 50 mm Hg for 45 minutes. Animals were resuscitated with crystalloid solutions; shed blood in group 2 animals was returned after one hour. Hemorrhagic hypotension following TBI produced a significant and sustained reduction in cO2del associated with a lower cMRO2 and cO2ER, and higher ICP and CWC, than seen with lesion alone. This occurred despite adequate early restoration of sO2del. This confirms that cerebral ischemia is ongoing despite restoration of systemic hemodynamics.