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Published in Michael Hehenberger, Zhi Xia, Huanming Yang, Our Animal Connection, 2020
Michael Hehenberger, Zhi Xia, Huanming Yang
Another mammalian high altitude challenge is associated with cerebral dysfunction. Again, birds have an advantage: several differences in the brain physiology of birds compared with mammals may protect against cerebral dysfunction under hypoxic conditions, at high altitude. In birds, unlike in mammals, cerebral blood flow is not inhibited by respiratory hypocapnia, defined as a state of reduced carbon dioxide in the blood.l This should improve brain oxygenation during environmental hypoxia. Avian neurons also appear to have an inherently higher tolerance of low cellular oxygen levels, and therefore appear to be well protected from cellular damage induced by O2 limitation. A still unanswered question is whether birds can suffer hypoxic cerebral edema, one of the biggest risks of human high-altitude exposure.
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Published in Michael Hehenberger, Zhi Xia, Our Animal Connection, 2019
Another mammalian high altitude challenge is associated with cerebral dysfunction. Again, birds have an advantage: several differences in the brain physiology of birds compared with mammals may protect against cerebral dysfunction under hypoxic conditions, at high altitude. In birds, unlike in mammals, cerebral blood flow is not inhibited by respiratory hypocapnia, defined as a state of reduced carbon dioxide in the blood.l This should improve brain oxygenation during environmental hypoxia. Avian neurons also appear to have an inherently higher tolerance of low cellular oxygen levels, and therefore appear to be well protected from cellular damage induced by O2 limitation. A still unanswered question is whether birds can suffer hypoxic cerebral edema, one of the biggest risks of human high-altitude exposure.
Panic attacks and anxiety disorders
Published in Herman Staudenmayer, Environmental Illness, 2018
Scientific theories of panic attack have biological and physiological evidence to support the postulated mechanisms. In a series of studies employing the method of magnetic resonance spectroscopy imaging (MRI), Dager and colleagues have demonstrated that panic patients are more prone to react with panic to lactate infusion than non-panic comparison subjects (Dager et al., 1987a, 1994). There is evidence that the effects of lactate are occurring directly in the brain in that hyperventilation induced significantly greater brain lactate elevations in panic patients than in non-panic controls (Dager et al., 1995). Shortness of breath (hypocapnia) induced by hyperventilation is a potent stimulus for decreasing cerebral blood flow and may be the mechanism responsible for brain lactate elevations in response to hyperventilation. Decreased cerebral blood flow is also associated with under-activation of cognitive processes which could explain some of the symptoms of central nervous system dysfunction such as difficulty concentrating and poor memory.
Normobaric hypoxia training in military aviation and subsequent hypoxia symptom recognition
Published in Ergonomics, 2021
Antti Leinonen, Nikke Varis, Hannu Kokki, Tuomo K. Leino
Hypoxia symptoms can vary from one training exposure to another, and this variation may affect the pilots’ ability to recognise the symptoms. One of the reasons for this may be increased ventilation rates resulting in a combination of hypoxia and hypocapnia (Loeppky et al. 1997; Temme et al. 2017). This combination may lead to respiratory alkalosis, which shifts the O2 dissociation curve to the left. Initially, with decreased O2 tension, unloading of O2 at peripheral tissues is favoured, but in hypoxia and hypocapnia haemoglobin has an increased affinity for O2 and unloads it more reluctantly. Consistent with our findings, others have shown that there is considerable variation in response to hypoxia, and people tend to forget their symptoms of hypoxia (Woodrow, Webb, and Wier 2011).
Integrating physiological monitoring systems in military aviation: a brief narrative review of its importance, opportunities, and risks
Published in Ergonomics, 2023
David M. Shaw, John W. Harrell
Hypocapnia and hypercapnia are states of low and high arterial partial pressures of carbon dioxide (PCO2), respectively. Hypocapnia results from hyperventilation, such as in response to hypoxia (Friend, Balanos, and Lucas 2019), prolonged hyperoxia (Becker et al. 1996; Marczak and Pokorski 2004), vibration (Lamb and Tenney 1966) or psychological stressors (e.g. anxiety) (Suess et al. 1980). Hypocapnia presents similarly to hypoxia (Shaw, Cabre, and Gant 2021), whereas hypercapnia presents with tachycardia, confusion, shortness of breath, and headaches. Hypercapnia results from inhibited ventilation and limited carbon dioxide off-loading, such as restricted breathing systems (e.g. mask air flow resistance) or due to an inability for full ventilation (e.g. atelectasis). Carbon dioxide has a strong influence on ventilation, CBF (Ogoh 2019), and haemoglobin affinity for oxygen (Stepanek et al. 2020). Arterial PCO2 is the gold standard measurement, but it can also be inferred from the end-tidal partial pressure of carbon dioxide (McSwain et al. 2010), although this may not be reliable across all aerospace conditions (Shykoff et al. 2021). Hypocapnia reduces CBF, whereas hypercapnia increases CBF (Ito et al. 2003). Heart rate increases in hypocapnia (Rutherford, Clutton-Brock, and Parkes 2005) and appears unaffected in hypercapnia (Brown, Barnes, and Mündel 2014). Heart rate variability appears unaltered in both, although both low- and high-frequency components of HRV increase with added carbon dioxide compared to normal and reduced carbon dioxide levels (Pöyhönen et al. 2004). Electroencephalogram measures are altered in hypocapnia and hypercapnia, despite no difference in cognitive performance (Bloch-Salisbury, Lansing, and Shea 2000). Considering the above, measuring arterial PCO2 is likely as important as oximetry to determine physiological and functional states.