Impact of Sleep Quality on Cardiovascular Responses to Simulated Hemorrhage in Humans

Abstract

Introduction Sleep is an important determinant of cardiovascular health. Poor sleep quality, including sleep restriction, is associated with impairments in cardiovascular function, and may limit cardiovascular responsiveness to physiological stress. As hemorrhage is one of the leading causes of preventable civilian death, and a major cause of death from trauma in the military, it is important to assess the impact of sleep quality on cardiovascular responses to this stress. We hypothesize that human subjects who report poor sleep quality will be less tolerant to simulated hemorrhage, which will be associated with lower arterial pressure and cerebral blood flow, and higher heart rates compared to subjects who report good sleep quality. Methods Healthy human subjects (10F; 10M) participated in a graded pre-syncopal lower body negative pressure (LBNP) protocol to simulate hemorrhage. Sleep quality was assessed pre-experiment using the Pittsburgh Sleep Quality Index (PSQI). Subjects were categorized in two groups: POOR sleep quality (Global PSQI score ≥ 5) or GOOD sleep quality (Global PSQI score < 5). Arterial pressure, heart rate, stroke volume, and middle cerebral artery velocity (MCAv) were measured continuously throughout the LBNP protocol. The protocol was terminated if systolic arterial pressure was < 80 mmHg, or if subjects reported symptoms such as lightheadedness, nausea, dizziness, or vision disturbances. Results Of the 20 subjects tested, 5 were in the POOR sleep quality group (5M; 0F), and 15 were in the GOOD sleep quality group (5M; 10F). Sleep quality had no effect on tolerance to LBNP (POOR: 1453 ± 223 s vs. GOOD: 1535 ± 88 s; P = 0.34), and there were no differences in the magnitude of central hypovolemia at presyncope (%Δ stroke volume, POOR: -53 ± 8 % vs. GOOD: -49 ± 4 %; P = 0.32). However, there were differences in the magnitude of hypotension (%Δ mean arterial pressure, POOR: -18 ± 3 % vs. GOOD: -22 ± 2 %; P = 0.08), cerebral blood flow reduction (%Δ MCAv, POOR: -19 ± 6 % vs. GOOD: -28 ± 2 %; P = 0.03), and reflex tachycardia (% Δ heart rate, POOR: 103 ± 30 % vs. GOOD: 72 ± 9 %; P = 0.09). There was a moderate association between sleep quality and the magnitude of MCAv reduction at presyncope (r = 0.53; P = 0.02), where poorer sleep quality was associated with a smaller reduction in MCAv at presyncope. All 5 (100%) subjects in the POOR group terminated the experiment based on subjective symptoms (i.e., they did not reach the systolic arterial pressure threshold of 80 mmHg), compared to 2 of the 15 subjects (13%) in the GOOD group (P=0.001). Conclusion: Sleep quality did not affect tolerance to simulated hemorrhage in healthy human subjects. While there were differences in hemodynamic responses, this may be related to premature termination of the LBNP protocol based on the early onset of subjective presyncopal symptoms. A larger sample size may help to further investigate these observations.