Accuracy of a Cerebral Oximeter in Healthy Volunteers under Conditions of Isocapnic Hypoxia

Henson, Lindsey C.; Calalang, Carolyn C.; Temp, John A.; Ward, Denham S.

doi:10.1097/00000542-199801000-00011

Cited by 109 publications

(55 citation statements)

References 30 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…17 Pollard et al 6 showed that cerebral NIRS oximetry reflected cerebral oxygenation in an AV-ratio of 0.25 in healthy adult volunteers. This fixed AV-ratio is widely accepted in literature, although some studies suggest wide interindividual variation.…”

Section: Reactivity Of Cerebral Nirs Oximetry Assuming a Fixed Av-ratiomentioning

confidence: 99%

Quantifying cerebral hypoxia by near-infrared spectroscopy tissue oximetry: the role of arterial-to-venous blood volume ratio

et al. 2017

View full text Add to dashboard Cite

"Quantifying cerebral hypoxia by near-infrared spectroscopy tissue oximetry: the role of arterial-tovenous blood volume ratio," J. Biomed. Opt. 22(2), 025001 (2017), doi: 10.1117/1.JBO.22.2.025001. Abstract. Tissue oxygenation estimated by near-infrared spectroscopy (NIRS) is a volume-weighted mean of the arterial and venous hemoglobin oxygenation. In vivo validation assumes a fixed arterial-tovenous volume-ratio (AV-ratio). Regulatory cerebro-vascular mechanisms may change the AV-ratio. We used hypotension to investigate the influence of blood volume distribution on cerebral NIRS in a newborn piglet model. Hypotension was induced gradually by inflating a balloon-catheter in the inferior vena cava and the regional tissue oxygenation from NIRS (rStO 2;NIRS ) was then compared to a reference (rStO 2;COX ) calculated from superior sagittal sinus and aortic blood sample co-oximetry with a fixed AV-ratio. Apparent changes in the AV-ratio and cerebral blood volume (CBV) were also calculated. The mean arterial blood pressure (MABP) range was 14 to 82 mmHg. PaCO 2 and SaO 2 were stable during measurements. rStO 2;NIRS mirrored only 25% (95% Cl: 21% to 28%, p < 0.001) of changes in rStO 2;COX . Calculated AVratio increased with decreasing MABP (slope: −0.007 · mmHg −1 , p < 0.001). NIRS estimates that CBV decreased with decreasing MABP (slope: 0.008 ml∕100 g∕mmHg, p < 0.001). Thus, cerebral NIRS oximetry responded poorly to changes in tissue oxygenation during hypotension induced by decreased preload. An increase in the AV-ratio during hypotension due to arterial vasodilation and, possibly, cerebral venous collapse may be a part of the explanation.

show abstract

Section: Reactivity Of Cerebral Nirs Oximetry Assuming a Fixed Av-ratiomentioning

confidence: 99%

Quantifying cerebral hypoxia by near-infrared spectroscopy tissue oximetry: the role of arterial-to-venous blood volume ratio

et al. 2017

View full text Add to dashboard Cite

show abstract

“…NIRS measurements have been well correlated with intracellular O 2 tension in muscle (38) and venous O 2 saturation in both muscle (14) and cerebral tissue (20). However, the relative contribution of skin blood flow to NIRS tissue signals has been questioned because NIRS probes are typically placed on the skin surface.…”

Section: Limitations Of the Study And Technical Considerationsmentioning

confidence: 99%

Effects of normoxic and hypoxic exercise regimens on cardiac, muscular, and cerebral hemodynamics suppressed by severe hypoxia in humans

Wang

Mao

et al. 2010

Journal of Applied Physiology

View full text Add to dashboard Cite

. Effects of normoxic and hypoxic exercise regimens on cardiac, muscular, and cerebral hemodynamics suppressed by severe hypoxia in humans. J Appl Physiol 109: 219-229, 2010. First published April 29, 2010 doi:10.1152/japplphysiol.00138.2010.-Hypoxic preconditioning prevents cerebrovascular/cardiovascular disorders by increasing resistance to acute ischemic stress, but severe hypoxic exposure disturbs vascular hemodynamics. This study compared how various exercise regimens with/without hypoxia affect hemodynamics and oxygenation in cardiac, muscle, and cerebral tissues during severe hypoxic exposure. Sixty sedentary males were randomly divided into five groups. Each group (n ϭ 12) received one of five interventions: 1) normoxic (21% O 2) resting control, 2) hypoxic (15% O2) resting control, 3) normoxic exercise (50% maximum work rate under 21% O 2; N-E group), 4) hypoxic-relative exercise (50% maximal heart rate reserve under 15% O2; H-RE group), or 5) hypoxicabsolute exercise (50% maximum work rate under 15% O 2; H-AE group) for 30 min/day, 5 days/wk, for 4 wk. A recently developed noninvasive bioreactance device was used to measure cardiac hemodynamics, and near-infrared spectroscopy was used to assess perfusion and oxygenation in the vastus lateralis (VL)/gastrocnemius (GN) muscles and frontal cerebral lobe (FC). Our results demonstrated that the H-AE group had a larger improvement in aerobic capacity compared with the N-E group. Both H-RE and H-AE ameliorated the suppression of cardiac stroke volume and the GN hyperemic response (⌬total Hb/min) and reoxygenation rate by acute 12% O2 exposure. Simultaneously, the two hypoxic interventions enhanced perfusion (⌬total Hb) and O 2 extraction [⌬deoxyHb] of the VL muscle during the 12% O2 exercise. Although acute 12% O2 exercise decreased oxygenation (⌬O2Hb) of the FC, none of the 4-wk interventions influenced the cerebral perfusion and oxygenation during normoxic/ hypoxic exercise tests. Therefore, we conclude that moderate hypoxic exercise training improves cardiopulmonary fitness and increases resistance to disturbance of cardiac hemodynamics by severe hypoxia, concurrence with enhancing O2 delivery/utilization in skeletal muscles but not cerebral tissues.oxygen; physical activity; circulation CHRONIC INTERMITTENT HYPOXIA is known to enhance aerobic capacity by increasing pulmonary ventilation, adaptation of the hematopoetic system, and tissue utilization of O 2 in sedentary males (43, 44), endurance athletes (10, 13), and elderly subjects with or without vascular diseases (8). Animal studies have also indicated that hypoxic preconditioning reduced the volume of cerebral infarction and edema (41) and attenuated the loss of myocardial contractility (3) immediately after sublethal ischemic insult. Therefore, we speculate that increased O 2 delivery/utilization and resistance to acute hypoxic/ischemic stresses conferred by hypoxic interventions improves exercise performance and is effective for preventing and treating cerebrovascular/cardiovascular diseases.Howeve...

show abstract

“…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).…”

mentioning

confidence: 99%

Effect of exercise on cerebral perfusion in humans at high altitude

Imray

Myers²,

Pattinson³

et al. 2005

Journal of Applied Physiology

113

View full text Add to dashboard Cite

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...

show abstract

Accuracy of a Cerebral Oximeter in Healthy Volunteers under Conditions of Isocapnic Hypoxia

Cited by 109 publications

References 30 publications

Quantifying cerebral hypoxia by near-infrared spectroscopy tissue oximetry: the role of arterial-to-venous blood volume ratio

Quantifying cerebral hypoxia by near-infrared spectroscopy tissue oximetry: the role of arterial-to-venous blood volume ratio

Effects of normoxic and hypoxic exercise regimens on cardiac, muscular, and cerebral hemodynamics suppressed by severe hypoxia in humans

Effect of exercise on cerebral perfusion in humans at high altitude

Contact Info

Product

Resources

About