The Role of Cerebral Oxygenation and Perfusion on Tolerance to Central Hypovolemia

Tolerance to central hypovolemia, including hemorrhage, is highly variable between individuals. The role of cerebral oxygenation and regional cerebral perfusion on tolerance to central hypovolemia has not been explored. Protection of posterior cerebral perfusion may be an important factor in tolerance, as the posterior circulation supplies blood to the autonomic and respiratory control centers in the brain stem. Additionally, despite the reduction in cerebral oxygen delivery with central hypovolemia via decreased flow, the role of compensatory increases in oxygen extraction and subsequent cerebral tissue oxygenation on tolerance have not been identified. The oscillatory pattern of cerebral blood flow has recently been identified as a contributing factor to improving tolerance to central hypovolemia, and may be more important than the protection of absolute flow. This finding was demonstrated when comparing high vs. low tolerant individuals, and in subjects who exhibited increased tolerance to central hypovolemia while breathing against inspiratory resistance. We hypothesized that healthy human subjects with naturally high tolerance to central hypovolemia, and subjects breathing against inspiratory resistance under hypovolemic stress would exhibit 1) protection of cerebral oxygen saturation (ScO2); 2) prolonged preservation of cerebral blood flow in the posterior versus anterior cerebral circulation, and; 3) higher LF oscillations in cerebral blood flow. The major findings from these investigations are: 1) subjects with high tolerance to central hypovolemia exhibited protection of ScO2 and velocity in the posterior cerebral circulation; 2) LF oscillations did not play a role in the protection of ScO2; 3) resistance breathing improved tolerance to central hypovolemia, but not via protection of ScO2 or velocity in either the anterior or posterior cerebral circulation, and; 4) resistance breathing was associated with increased high frequency oscillatory power in arterial pressure, anterior and posterior cerebral blood velocity, and ScO2. We conclude that individuals with naturally high tolerance to central hypovolemia exhibit protection of cerebral tissue oxygenation and prolonged preservation of perfusion within the posterior cerebral circulation, but not in the anterior circulation, thus delaying the onset of presyncope. Improved tolerance to central hypovolemia via resistance breathing was not related to these mechanisms, but may have been associated with increased depth of breathing, subsequently decreasing intracranial pressure and increasing cerebral perfusion pressure.