White Mountain Expedition 2019: The Impact of Sustained Hypoxia on Cerebral Blood Flow Responses and Tolerance to Simulated Hemorrhage

Trauma-induced hemorrhage can occur at high altitude (HA) from a variety of causes, including battlefield injuries, motor vehicle/air accidents, and major falls. Based on the known compensatory increases in cerebral blood flow that occur with exposure to hypoxia, we hypothesized that tolerance to simulated hemorrhage (via application of lower body negative pressure, LBNP) at HA would be similar compared to low altitude (LA) due to increased cerebral blood flow and oxygen delivery, and the subsequent preservation of cerebral tissue oxygenation. Healthy human subjects (N=8; 4F/4M) participated in LBNP protocols to presyncope at LA (1045 m) and at HA (3800 m) following 4-5 days of acclimatization. Arterial pressure, heart rate, stroke volume, internal carotid artery (ICA) blood flow, and cerebral oxygen saturation were measured continuously. Time to presyncope was similar between conditions (LA: 1276±108s vs. HA: 1208±108s; P=0.58). Similar responses to LBNP were observed at LA and HA in mean arterial pressure (LA: -16±2% vs. HA: -16±2%; P=0.85), stroke volume (LA: -57±5% vs. HA: -60±5%; P=0.39), and heart rate (LA: +69±12% vs. HA: +65±8%; P=0.71). ICA blood flow was higher at HA vs. LA (P=0.01), and decreased with LBNP under both conditions (P≤0.005), with no effect of altitude on cerebral oxygen saturation (P=0.73). These findings suggest that hypoxia with ascent to 3800 m does not affect tolerance to simulated hemorrhage in young healthy adults, which may be due to 1) similar cardiovascular reflex responses, and/or 2) compensatory increases in cerebral blood flow and subsequent preservation of cerebral tissue oxygenation.