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

Introduction Trauma‐induced hemorrhage can occur at high altitude from a variety of causes, including battlefield injuries, motor vehicle accidents, air accidents, and major falls. The hypoxic environment of high altitude can limit the ability of the cardiovascular system to compensate for blood loss injuries, due, in part, to the reduced arterial oxygen content. In humans, the effect of sustained hypoxia on tolerance to hemorrhage and the cardiovascular and cerebrovascular responses to this stress are unknown. 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 high altitude would be similar compared to low altitude due to increased cerebral blood flow and oxygen delivery, and the subsequent preservation of cerebral tissue oxygenation. Methods Healthy human subjects (N=8; 4F, 4M) participated in LBNP protocols to presyncope at low altitude (1045 m, Calgary, Canada) and at high altitude (3800 m, White Mountain, California) following 4–5 days of acclimatization. LBNP chamber pressure was initially reduced to −60 mmHg for 10‐min followed by decreases every 5‐min to −70, −80, −90 and −100 mmHg, until the onset of presyncopal symptoms. Arterial pressure, heart rate, internal carotid artery blood flow, and cerebral oxygen saturation were measured continuously. Stroke volume was derived from the arterial pressure waveform, and systemic vascular resistance was calculated from cardiac output and mean arterial pressure. Time to presyncope and cardiovascular responses were compared between the low and high altitude conditions. Results Time to presyncope was similar between conditions (low altitude: 1276 ± 108 s vs. high altitude: 1208± 108 s; P=0.58). Similar responses to LBNP were observed between low and high altitudes in mean arterial pressure (low altitude: −16±2 % vs. high altitude: −16±2 %; P=0.85), stroke volume (low altitude: −57±5 % vs. high altitude: −60±5 %; P=0.39), systemic vascular resistance (low altitude: +23±9 % vs. high altitude: +38±12 %; P=0.21), and heart rate (low altitude: +69±12 % vs. high altitude: +65±8 %; P=0.71). Internal carotid artery blood flow was higher at high altitude vs. low altitude (condition effect, P=0.01), and decreased with LBNP under both conditions (P≤0.005). There was no effect of high altitude on cerebral oxygen saturation at baseline and presyncope (altitude Effect, P=0.73). Conclusion These findings suggest that the hypoxia induced by ascent to high altitude (3800 m) does not affect tolerance to simulated hemorrhage in young healthy adults, which may be due to 1) similar cardiovascular reflex responses to central hypovolemia, and/or 2) the compensatory increase in cerebral blood flow and subsequent maintenance of oxygen delivery to the tissues, resulting in the preservation of cerebral oxygen saturation. Support or Funding Information AHA 17GRNT33671110

Fetched live from OpenAlex and de-inverted. Abstracts are not stored in this database: the inverted indexes are 8.6 GB of the frame’s 9.3 GB of text, and the host has 13 GB free.