Differential effects of acute hypoxia and high altitude on cerebral blood flow velocity and dynamic cerebral autoregulation: alterations with hyperoxia

Abstract

We hypothesized that 1) acute severe hypoxia, but not hyperoxia, at sea level would impair dynamic cerebral autoregulation (CA); 2) impairment in CA at high altitude (HA) would be partly restored with hyperoxia; and 3) hyperoxia at HA and would have more influence on blood pressure (BP) and less influence on middle cerebral artery blood flow velocity (MCAv). In healthy volunteers, BP and MCAv were measured continuously during normoxia and in acute hypoxia (inspired O2 fraction = 0.12 and 0.10, respectively; n = 10) or hyperoxia (inspired O2 fraction, 1.0; n = 12). Dynamic CA was assessed using transfer-function gain, phase, and coherence between mean BP and MCAv. Arterial blood gases were also obtained. In matched volunteers, the same variables were measured during air breathing and hyperoxia at low altitude (LA; 1,400 m) and after 1-2 days after arrival at HA ( approximately 5,400 m, n = 10). In acute hypoxia and hyperoxia, BP was unchanged whereas it was decreased during hyperoxia at HA (-11 +/- 4%; P < 0.05 vs. LA). MCAv was unchanged during acute hypoxia and at HA; however, acute hyperoxia caused MCAv to fall to a greater extent than at HA (-12 +/- 3 vs. -5 +/- 4%, respectively; P < 0.05). Whereas CA was unchanged in hyperoxia, gain in the low-frequency range was reduced during acute hypoxia, indicating improvement in CA. In contrast, HA was associated with elevations in transfer-function gain in the very low- and low-frequency range, indicating CA impairment; hyperoxia lowered these elevations by approximately 50% (P < 0.05). Findings indicate that hyperoxia at HA can partially improve CA and lower BP, with little effect on MCAv.

Effects of Hypobaric Hypoxia on Cerebral Autoregulation

“…Our data differ from previous studies [11][12][13] that have reported moderate associations between CA and AMS scores. Variations in methodology and interpretation may explain the different conclusions.…”

“…9 Ensuing meningeal stress or increased intracranial pressure, if cerebral compliance is limited, 10 could be responsible for headache, dizziness, and nausea that define AMS. This hypothesis appears to be supported by a few studies showing that CA is impaired after AMS has developed (6 -48 hours) and that the degree of CA impairment is moderately correlated with AMS symptomology (r 2 ϭϷ0.20 -0.50); [11][12][13] however, no studies have reported serial measurements of CA as AMS develops to establish a definitive link between impairment of CA and onset of AMS. Additionally, because CA remains impaired after successful acclimatization to high altitude 14 -16 and persists in life-long residents of high altitude, 15,17 a relationship between CA and AMS remains questionable.…”

Cerebral Pressure–Flow Relationship in Lowlanders and Natives at High Altitude

“…Out of these five, three studies assessed the dynamic cerebral pressure-flow relationship at one time point after arrival (between 1 to 10 days) to HA. 5,9,10 Upon initial arrival to HA, Van Osta et al 5 reported that there was an altered cerebral autoregulatory response, as measured using the autoregulatory index, in proportion to the severity of AMS in an individual. However, consistent with our initial arrival findings (o20 hours), they did not note any overall subject differences for the BP or MCAv at HA from SL.…”

“…1 Using this approach, a number of studies have reported that the dynamic cerebral pressure-flow relationship is impaired in conditions of hypobaric hypoxia, and may 4,5 or may not [6][7][8] be an important underlying mechanism in the pathophysiology of acute mountain sickness (AMS). A limitation in the majority of these studies, however, is that this impaired relationship upon initial exposure 9,10 or after acclimatization 11,12 has been inferred from TFA under spontaneous conditions (as reported by decreases in phase (i.e. the time lag) or increases in gain (i.e.…”

Ocular morbidity among porters at high altitudes

“…Many tissues in the eye are affected by high-altitude related hypoxia, with effects that can be observed with the conjunctiva, cornea, intraocular pressure, lens, uvea, retina and the optic nerve (Karakucuk et al, 2000). Most published reports on the effects of high altitude focus on high-altitude retinal haemorrhage (Frayser et al, 1970(Frayser et al, , 1971, systemic side effects, such as increased blood pressure (Ainslie et al, 2008, Hainsworth et al, 2007, and cardiac side effects (Bernardi, 2007), which can lead to mountain sickness.…”