Elevated Intracranial Pressure Masks Hemorrhagic Hypotension in a Canine Model

Abstract

Previous clinical studies of blunt trauma patients with severe brain injuries have demonstrated that emergency department vital signs failed to consistently identify life-threatening abdominal injury. One hypothesis to explain this is that bradycardia and systemic hypertension from brainstem injury (the Cushing response) may mask the tachycardia and hypotension ordinarily manifested by hemorrhagic hypovolemia. This would result in inappropriately normal or near-normal emergency department vital signs for otherwise clinically apparent hypovolemia. To test this hypothesis, splenectomized dogs (n = 9) were phlebotomized to a systolic blood pressure (SBP) of 60 mm Hg. Subsequently, intracranial pressure (ICP) was artificially elevated in a controlled, incremental fashion. From a mean SBP of 58.4 +/- 3.9 mm Hg at a baseline ICP of 8.1 +/- 4.2 mm Hg, increases in ICP of only 20 mm Hg significantly raised SBP (in some animals). When ICP reached 70 mm Hg, mean SBP reached 95.1 +/- 8.7 mm Hg (p < 0.001) in spite of profound hemorrhagic hypovolemia. In all subjects, the tachycardia that accompanied hypovolemia tended towards normal with incremental increases in ICP. However, this did not reach statistical significance. In response to elevations in ICP, this hypovolemic canine model displayed normalization of SBP with variable changes in heart rate. These changes could mask hemorrhagic hypotension in humans sustaining multiple system trauma. These experimental data support clinical studies advocating immediate definitive abdominal evaluation in unconscious blunt trauma patients, regardless of vital signs.

Changes in the intracranial rheoencephalogram at lower limit of cerebral blood flow autoregulation

“…Without intervention, SAP increase can lead to herniation and death (Bakay and Lee 1965). Related clinical aspects can be found elsewhere (Prall et al 1995, Jones 1989, Strandgaard and Paulson 1989, Griswold et al 1981.…”