Near-infrared spectroscopy in the assessment of cerebral oxygenation at high altitude

Imray, Christopher; Barnett, N. J.; Walsh, Sarah; Clarke, T.; Morgan, Jayne; Hale, D. M.; Hoar, Helen; Mole, Damian J.; Chesner, I. M.; Wright, Alex

doi:10.1580/1080-6032(1998)009[0198:nisita]2.3.co;2

Cited by 30 publications

(23 citation statements)

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“…The NIRS method is particularly suitable for multiple measurements of trends rather than single absolute measurements of cerebral oxygenation. We have reported the changes observed on ascent to high altitude and found that the equipment was robust and suitably sensitive for use in the field [15]. In the present study the acute effects of CO # -enriched air on peripheral and cerebral regional oxygenation at high altitude are reported, and the results obtained with CO # are compared with the effects of hyperventilation and administration of oxygen.…”

Section: Introductionmentioning

confidence: 91%

Cerebral oxygenation at high altitude and the response to carbon dioxide, hyperventilation and oxygen

IMRAY¹,

BREAREY²,

CLARKE³

et al. 2000

Clinical Science

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Cerebral oxygenation is likely to be of critical importance in determining function at high altitude. The present study has used the technique of near-IR spectroscopy to monitor changes in cerebral regional oxygenation in response to inhaled carbon dioxide, hyperventilation and supplementary oxygen on ascent to 4680 m over 3 days. At sea level, inhaled CO(2) resulted in a significant rise in cerebral regional oxygenation [from mean 69.6% (S.D. 2.4% to 71. 1+/-2.3%; means+/-S.D.; P<0.001). At 4680 m, CO(2) increased regional cerebral oxygenation (63.8+/-2.5% to 65.9+/-2.2%; P<0.001) and also increased peripheral oxygen saturation (75.1+/-6.1% to 83. 6+/-4.0%; P<0.001). Voluntary hyperventilation resulted in improved peripheral oxygen saturation at 2770 m, 3650 m and 4680 m, whereas cerebral regional oxygenation was reduced at sea level and at 2770 m, unchanged at 3650 m and increased at 4680 m. Supplementary oxygen (6 1itres/min) at 4680 m resulted in greater improvements in peripheral oxygen saturation (76.7+/-7.9% to 98.1+/-1.5%; P<0.001) and cerebral regional oxygenation (64.6+/-3.3% to 70.6+/-2.9%; P<0. 001) than were found with CO(2) or hyperventilation. We conclude that attempts to increase CO(2) inhalation or ventilation at high altitude are likely to be beneficial for cerebral oxygenation in the short term.

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Section: Introductionmentioning

confidence: 91%

Cerebral oxygenation at high altitude and the response to carbon dioxide, hyperventilation and oxygen

IMRAY¹,

BREAREY²,

CLARKE³

et al. 2000

Clinical Science

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“…Impairment in control of cerebral perfusion can cause cerebral ischaemia, with potentially grave consequences (Roach & Hackett, 2001). In healthy lowlanders ascending rapidly to high altitude, non-invasive near-infrared spectroscopy (NIRS) studies using sensors placed on the scalp revealed a considerable reduction in cerebral tissue oxygenation (CTO; Imray et al 1998;Wilson et al 2011;Rupp et al 2014). Whether CTO is also reduced in lifelong residents at high altitude has not been studied, although this might elucidate mechanisms of chronic altitude adaptation and it may guide future research to identify targets for prevention and treatment of altitude-related illness associated with cerebral dysfunction (León-Velarde et al 2005;Wilson et al 2009;Vermeij et al 2012).…”

Section: Introductionmentioning

confidence: 99%

Cerebral oxygenation in highlanders with and without high‐altitude pulmonary hypertension

Furian

Latshang

Aeschbacher

et al. 2015

Experimental Physiology

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New Findings r What is the central question of this study?Cerebral hypoxia impairs cognitive function and exercise performance and may result in brain damage. Residents at high altitude, in particular those with high-altitude pulmonary hypertension, are prone to hypoxaemia due to the exposure to reduced barometric pressure and impaired pulmonary gas exchange. Whether highlanders have a reduced cerebral oxygenation has not been studied. r What is the main finding and its importance?We found that despite a reduced arterial oxygen saturation, healthy highlanders and even those with pulmonary hypertension have a similar cerebral oxygenation to healthy lowlanders, suggesting that compensatory mechanisms protect long-term residents at high altitude from cerebral hypoxia.High-altitude pulmonary hypertension (HAPH), a chronic altitude-related illness, causes hypoxaemia and impaired exercise performance. We evaluated the hypothesis that haemodynamic limitation and hypoxaemia in patients with HAPH are associated with impaired cerebral tissue oxygenation (CTO) compared with healthy highlanders (HH) and lowlanders (LL). We studied 36 highlanders with HAPH and 54 HH at an altitude of 3250 m, and 34 LL at 760 m. Mean(±SD) pulmonary artery pressures were 34(±3), 22(±5) and 16(±4) mmHg, respectively (P < 0.05, all comparisons). The CTO was monitored by near-infrared spectroscopy along with pulse oximetry (peripheral arterial oxygen saturation, S pO 2 ) during quiet breathing of room air (RA) and oxygen for 20 min each, and during hyperventilation with RA and oxygen, respectively. In HAPH, HH and LL breathing RA, S pO 2 was 88(±4), 92(±2) and 95(±2)%, respectively (P < 0.001, all comparisons), and CTO was similar in the three groups, at 68(±3), 68(±4) and 69(±4)%, respectively (n.s., all comparisons). Breathing oxygen increased S pO 2 and CTO significantly more in HAPH than in HH and LL. Hyperventilation (RA) did not reduce CTO in HAPH but did in HH and LL; hyperventilation (oxygen) increased CTO in HAPH only. Highlanders with and without HAPH studied at 3250 m had a similar CTO to healthy lowlanders at 760 m even though highlanders were hypoxaemic. The physiological response to hyperoxia and hypocapnia assessed by cerebral near-infrared spectroscopy suggests that healthy highlanders and even highlanders with HAPH effectively maintain an adequate CTO. This

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“…Cerebral spectroscopy has been shown to track changes in jugular venous bulb saturations in healthy volunteers under conditions of isocapnic hypoxia (12) and has also been validated by comparison with PET scanning, with 133 Xe washout methods and with internal carotid artery stump pressures (54). We have used this technique during dynamic studies of cerebral oxygenation at altitude and assessed the effects of hyperventilation, oxygen therapy, and CO 2 supplementation (19,20) and during assessment of the effects of pressurization in a portable hyperbaric chamber (21). Assessments of cerebral blood flow and cerebral oxygenation during exercise and under field conditions have proven challenging.…”

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confidence: 99%

Effect of exercise on cerebral perfusion in humans at high altitude

Imray

Myers²,

Pattinson³

et al. 2005

Journal of Applied Physiology

113

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Society. Effect of exercise on cerebral perfusion in humans at high altitude. J Appl Physiol 99: 699 -706, 2005. First published May 26, 2005 doi:10.1152/japplphysiol.00973.2004.-The effects of submaximal and maximal exercise on cerebral perfusion were assessed using a portable, recumbent cycle ergometer in nine unacclimatized subjects ascending to 5,260 m. At 150 m, mean (SD) cerebral oxygenation (rSO2%) increased during submaximal exercise from 68.4 (SD 2.1) to 70.9 (SD 3.8) (P Ͻ 0.0001) and at maximal oxygen uptake (V O2 max) to 69.8 (SD 3.1) (P Ͻ 0.02). In contrast, at each of the high altitudes studied, rSO2 was reduced during submaximal exercise from 66.2 (SD 2.5) to 62.6 (SD 2.1) at 3,610 m (P Ͻ 0.0001), 63.0 (SD 2.1) to 58.9 (SD 2.1) at 4,750 m (P Ͻ 0.0001), and 62.4 (SD 3.6) to 61.2 (SD 3.9) at 5,260 m (P Ͻ 0.01), and at V O2 max to 61.2 (SD 3.3) at 3,610 m (P Ͻ 0.0001), to 59.4 (SD 2.6) at 4,750 m (P Ͻ 0.0001), and to 58.0 (SD 3.0) at 5,260 m (P Ͻ 0.0001). Cerebrovascular resistance tended to fall during submaximal exercise (P ϭ not significant) and rise at V O2 max, following the changes in arterial oxygen saturation and end-tidal CO 2. Cerebral oxygen delivery was maintained during submaximal exercise at 150 m with a nonsignificant fall at V O2 max, but at high altitude peaked at 30% of V O2 max and then fell progressively at higher levels of exercise. The fall in rSO2 and oxygen delivery during exercise may limit exercise at altitude and is likely to contribute to the problems of acute mountain sickness and highaltitude cerebral edema. maximal oxygen uptake; cerebral oxygenation; cerebral blood flow; cerebrovascular resistance; cerebral oxygen delivery ALTERED CEREBRAL FUNCTION on ascent to altitude was part of the first description of mountain sickness in 1913 (40), and acute mountain sickness (AMS) and high-altitude cerebral edema (HACE) have been shown to be potentially serious clinical conditions that may occur on acute exposure to altitudes above 2,500 -3,000 m. Exercise at altitude causes further decreases in arterial oxygenation and so may exacerbate cerebral hypoxia. However, the fall in arterial saturation that occurs during exercise at high altitude (14) might not affect cerebral oxygenation to the same extent as it does in peripheral tissues due to a compensatory increase in cerebral blood flow (24). Nevertheless, avoidance of strenuous exercise during ascent, and on arrival at altitude, is standard advice for reducing the risk of AMS and HACE. Evidence from clinical studies is conflicting. Higher AMS symptom scores were found in subjects exercising four times a day for 30 min at 50% of their altitude-specific maximal oxygen consumption (V O 2 max ), compared with no exercise, in a chamber study at simulated altitude of 4,800 m (41). Another study of mountaineers, however, showed that physical fitness and exercise intensity during ascent to 4,559 m were of minor importance for the development of AMS (3). It is also possible that other neurological conditions falling outside the usual def...

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Near-infrared spectroscopy in the assessment of cerebral oxygenation at high altitude

Cited by 30 publications

References 13 publications

Cerebral oxygenation at high altitude and the response to carbon dioxide, hyperventilation and oxygen

Cerebral oxygenation at high altitude and the response to carbon dioxide, hyperventilation and oxygen

Cerebral oxygenation in highlanders with and without high‐altitude pulmonary hypertension

Effect of exercise on cerebral perfusion in humans at high altitude

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