Cerebral oxygenation and hyperthermia

Abstract

Hyperthermia is associated with marked reductions in cerebral blood flow (CBF). Increased distribution of cardiac output to the periphery, increases in alveolar ventilation and resultant hypocapnia each contribute to the fall in CBF during passive hyperthermia; however, their relative contribution remains a point of contention, and probably depends on the experimental condition (e.g., posture and degree of hyperthermia). The hyperthermia-induced hyperventilatory response reduces arterial CO2 pressure (PaCO2) causing cerebral vasoconstriction and subsequent reductions in flow. During supine passive hyperthermia, the majority of recent data indicate that reductions in PaCO2 may be the primary, if not sole, culprit for reduced CBF. On the other hand, during more dynamic conditions (e.g., hemorrhage or orthostatic challenges), an inability to appropriately decrease peripheral vascular conductance presents a condition whereby adequate cerebral perfusion pressure may be compromised secondary to reductions in systemic blood pressure. Although studies have reported maintenance of pre-frontal cortex oxygenation (assessed by near-infrared spectroscopy) during exercise and severe heat stress, the influence of cutaneous blood flow is known to contaminate this measure. This review discusses the governing mechanisms associated with changes in CBF and oxygenation during moderate to severe (i.e., 1.0°C to 2.0°C increase in body core temperature) levels of hyperthermia. Future research directions are provided.

Keywords: cerebral blood flow; cerebral oxygenation; heat stress; hemorrhage; hyperthermia; syncope.

Figure 1

Representation of the reported percent reductions in middle cerebral artery blood velocity (MCAv) (x axis) as a function of delta core temperature (esophageal, gastrointestinal, or rectal) (y axis) during supine passive hyperthermia up to +2°C.

Figure 2

Change in middle cerebral artery blood velocity (MCAv), posterior cerebral artery blood velocity (PCAv), internal carotid artery blood flow (QICA) and vertebral artery blood flow (QVA) following a 2.0°C rise in esophageal temperature with and without restoration of end-tidal CO₂. Adapted from (Bain et al., 2013).

Figure 3

Simplified schematic of the mechanisms and modifying factors involved with reductions in cerebral blood flow and ultimately cerebral oxygenation during whole-body hyperthermia. Global cerebral oxygenation is likely impaired when CBF is reduced beyond 50%, i.e., a critical blood flow is reached at maximal levels of oxygen extraction. Changes in cerebral metabolism will alter the theoretical critical blood flow limit, while regional changes in metabolism and blood flow can yield regional differences in cerebral oxygenation.