Tolerance to central hypovolemia: the influence of oscillations in arterial pressure and cerebral blood velocity

Abstract

Higher oscillations of cerebral blood velocity and arterial pressure (AP) induced by breathing with inspiratory resistance are associated with delayed onset of symptoms and increased tolerance to central hypovolemia. We tested the hypothesis that subjects with high tolerance (HT) to central hypovolemia would display higher endogenous oscillations of cerebral blood velocity and AP at presyncope compared with subjects with low tolerance (LT). One-hundred thirty-five subjects were exposed to progressive lower body negative pressure (LBNP) until the presence of presyncopal symptoms. Subjects were classified as HT if they completed at least the -60-mmHg level of LBNP (93 subjects; LBNP time, 1,880 ± 259 s) and LT if they did not complete this level (42 subjects; LBNP time, 1,277 ± 199 s). Middle cerebral artery velocity (MCAv) was measured by transcranial Doppler, and AP was measured at the finger by photoplethysmography. Mean MCAv and mean arterial pressure (MAP) decreased progressively from baseline to presyncope for both LT and HT subjects (P < 0.001). However, low frequency (0.04-0.15 Hz) oscillations of mean MCAv and MAP were higher at presyncope in HT subjects compared with LT subjects (MCAv: HT, 7.2 ± 0.7 vs. LT, 5.3 ± 0.6 (cm/s)(2), P = 0.075; MAP: HT, 15.3 ± 1.4 vs. 7.9 ± 1.2 mmHg(2), P < 0.001). Consistent with our previous findings using inspiratory resistance, high oscillations of mean MCAv and MAP are associated with HT to central hypovolemia.

Comparison of compensatory reserve during lower-body negative pressure and hemorrhage in nonhuman primates

“…Since stroke volume and compensatory reserve are both calculated from features of the arterial waveform, there was a high correlation between the two measures. However, consistent with previous observations in humans (6,9,25), data from this study reaffirmed that stroke volume failed to distinguish low-from high-tolerant baboons (Fig. 4A).…”

The physiology of blood loss and shock: New insights from a human laboratory model of hemorrhage

“…Similar arterial blood pressure oscillations are highly associated with an increased tolerance to central hypovolemia. [14][15][16] Figure 6(b) represents two arterial pressure tracings taken from healthy human subjects during a standard LBNP protocol. The top panel represents a LT subject who experience decompensation at 30 mmHg LBNP which equated to a blood loss of only $450 mL.…”

“…As such, pronounced oscillatory patterns of circulatory pressure and flow represent a sensitive ''on-off'' sympathetically mediated feedback mechanism designed to maintain tissue oxygenation despite the compromise to blood flow under severe hypovolemic conditions. 15 In addition, there is evidence that maintaining coherence between arterial pressure and sympathetic nerve activity represents an important compensatory mechanism during hypovolemia. 16 The same relationship between oscillations in arterial blood pressure and tolerance to central hypovolemia also translates to protection of cerebral blood flow.…”

Autonomic mechanisms associated with heart rate and vasoconstrictor reserves

“…All experimental procedures were conducted under a protocol reviewed and approved by the Brooke Army Medical Center Institutional Review Board, and in accordance with the approved protocol. Data from these subjects are also reported as a subgroup of a larger cohort in a related study [36]. Prior to inclusion, all subjects underwent a medical history and physical examination by a physician to ensure that they had no previous or current medical conditions that might preclude their participation.…”