Is alkalosis the dominant factor in hypoxia‐induced cognitive dysfunction?

Leacy, Jack K.; Day, Trevor A.; O’Halloran, Ken D.

doi:10.1113/ep087967

Cited by 7 publications

(4 citation statements)

References 5 publications

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“…Arterial blood carbon dioxide partial pressure and/or acid-base status (i.e., alkalosis) not only influences cerebrovascular haemodynamics, but also cognitive performance ( Leacy et al, 2019 ). For example, a recent study demonstrated hyperventilation-induced hypocapnia (~60–80 min) slowed simple and choice reaction time during both normoxia (end-tidal CO 2 of ~33 mmHg) and hypoxia (end-tidal CO 2 of ~38 mmHg), with no differences between conditions ( Friend et al, 2019 ), suggesting an independent effect of hypocapnia on hypoxia-induced cognitive dysfunction.…”

Section: Hypoxia Brain Function and Performancementioning

confidence: 99%

Hypoxic Hypoxia and Brain Function in Military Aviation: Basic Physiology and Applied Perspectives

Shaw

Cabre²

2021

Front. Physiol.

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Acute hypobaric hypoxia (HH) is a major physiological threat during high-altitude flight and operations. In military aviation, although hypoxia-related fatalities are rare, incidences are common and are likely underreported. Hypoxia is a reduction in oxygen availability, which can impair brain function and performance of operational and safety-critical tasks. HH occurs at high altitude, due to the reduction in atmospheric oxygen pressure. This physiological state is also partially simulated in normobaric environments for training and research, by reducing the fraction of inspired oxygen to achieve comparable tissue oxygen saturation [normobaric hypoxia (NH)]. Hypoxia can occur in susceptible individuals below 10,000 ft (3,048 m) in unpressurised aircrafts and at higher altitudes in pressurised environments when life support systems malfunction or due to improper equipment use. Between 10,000 ft and 15,000 ft (4,572 m), brain function is mildly impaired and hypoxic symptoms are common, although both are often difficult to accurately quantify, which may partly be due to the effects of hypocapnia. Above 15,000 ft, brain function exponentially deteriorates with increasing altitude until loss of consciousness. The period of effective and safe performance of operational tasks following exposure to hypoxia is termed the time-of-useful-consciousness (TUC). Recovery of brain function following hypoxia may also lag beyond arterial reoxygenation and could be exacerbated by repeated hypoxic exposures or hyperoxic recovery. This review provides an overview of the basic physiology and implications of hypoxia for military aviation and discusses the utility of hypoxia recognition training.

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Section: Hypoxia Brain Function and Performancementioning

confidence: 99%

Hypoxic Hypoxia and Brain Function in Military Aviation: Basic Physiology and Applied Perspectives

Shaw

Cabre²

2021

Front. Physiol.

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“…Finally, the brain is a high-flow organ that depends on acute increases in regional blood flow and oxygen supply to sustain increases in neuronal activity, a process known as neurovascular coupling. Partial pressure of carbon dioxide in arterial blood and/or acid-base status (i.e., alkalosis) was found to influence not only cerebrovascular hemodynamics but also cognitive performance ( Friend et al, 2019 ; Leacy et al, 2019 ).…”

Section: Physiological and Cognitive Responses To Systemic Environmen...mentioning

confidence: 99%

Sleep loss effects on physiological and cognitive responses to systemic environmental hypoxia

et al. 2022

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In the course of their missions or training, alpinists, but also mountain combat forces and mountain security services, professional miners, aircrew, aircraft and glider pilots and helicopter crews are regularly exposed to altitude without oxygen supplementation. At altitude, humans are exposed to systemic environmental hypoxia induced by the decrease in barometric pressure (<1,013 hPa) which decreases the inspired partial pressure of oxygen (PIO2), while the oxygen fraction is constant (equal to approximately 20.9%). Effects of altitude on humans occur gradually and depend on the duration of exposure and the altitude level. From 1,500 m altitude (response threshold), several adaptive responses offset the effects of hypoxia, involving the respiratory and the cardiovascular systems, and the oxygen transport capacity of the blood. Fatigue and cognitive and sensory disorders are usually observed from 2,500 m (threshold of prolonged hypoxia). Above 3,500 m (the threshold for disorders), the effects are not completely compensated and maladaptive responses occur and individuals develop altitude headache or acute altitude illness [Acute Mountain Sickness (AMS)]. The magnitude of effects varies considerably between different physiological systems and exhibits significant inter-individual variability. In addition to comorbidities, the factors of vulnerability are still little known. They can be constitutive (genetic) or circumstantial (sleep deprivation, fatigue, speed of ascent.). In particular, sleep loss, a condition that is often encountered in real-life settings, could have an impact on the physiological and cognitive responses to hypoxia. In this review, we report the current state of knowledge on the impact of sleep loss on responses to environmental hypoxia in humans, with the aim of identifying possible consequences for AMS risk and cognition, as well as the value of behavioral and non-pharmacological countermeasures.

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“…CO 2 also impacts the oxyhemoglobin curve in a more fundamental way, by altering the affinity of O 2 for hemoglobin. Hypocapnia causes a leftward shift in the oxyhemoglobin curve, reducing the O 2 offload at active tissues; this may cause further reductions in cerebral O 2 availability (Leacy et al 2019 ). Importantly, there is some indication that increasing CO 2 availability during hypoxia can protect cognitive function (Friend et al 2019 ; Stepanek et al 2014 ).…”

Section: Introductionmentioning

confidence: 99%

Carbon dioxide protects simulated driving performance during severe hypoxia

2023

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Purpose We sought to determine the effect of acute severe hypoxia, with and without concurrent manipulation of carbon dioxide (CO2), on complex real-world psychomotor task performance. Methods Twenty-one participants completed a 10-min simulated driving task while breathing room air (normoxia) or hypoxic air (PETO2 = 45 mmHg) under poikilocapnic, isocapnic, and hypercapnic conditions (PETCO2 = not manipulated, clamped at baseline, and clamped at baseline + 10 mmHg, respectively). Driving performance was assessed using a fixed-base motor vehicle simulator. Oxygenation in the frontal cortex was measured using functional near-infrared spectroscopy. Results Speed limit exceedances were greater during the poikilocapnic than normoxic, hypercapnic, and isocapnic conditions (mean exceedances: 8, 4, 5, and 7, respectively; all p ≤ 0.05 vs poikilocapnic hypoxia). Vehicle speed was greater in the poikilocapnic than normoxic and hypercapnic conditions (mean difference: 0.35 km h−1 and 0.67 km h−1, respectively). All hypoxic conditions similarly decreased cerebral oxyhaemoglobin and increased deoxyhaemoglobin, compared to normoxic baseline, while total hemoglobin remained unchanged. Conclusions These findings demonstrate that supplemental CO2 can confer a neuroprotective effect by offsetting impairments in complex psychomotor task performance evoked by severe poikilocapnic hypoxia; however, differences in performance are unlikely to be linked to measurable differences in cerebral oxygenation.

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Is alkalosis the dominant factor in hypoxia‐induced cognitive dysfunction?

Cited by 7 publications

References 5 publications

Hypoxic Hypoxia and Brain Function in Military Aviation: Basic Physiology and Applied Perspectives

Hypoxic Hypoxia and Brain Function in Military Aviation: Basic Physiology and Applied Perspectives

Sleep loss effects on physiological and cognitive responses to systemic environmental hypoxia

Carbon dioxide protects simulated driving performance during severe hypoxia

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