Potentially Harmful Effects of Hypoxemia
Severe hypoxemia can result in cellular hypoxia, organ dysfunction, and death. The degree of organ dysfunction is determined by the rapidity of onset, severity, and duration of hypoxemia and individual susceptibility. An extreme example of ischemia-hypoxia tolerance is iatrogenically induced hypothermic circulatory arrest during cardiothoracic surgery. Sudden exposure to severe atmospheric hypoxia will cause rapid unconsciousness secondary to cerebral hypoxia, while gradual acclimatization to a comparable level of hypoxia can be well tolerated. In a report detailing 22 clinical cases of profound hypoxemia (PaO2 < 20.3 mm Hg [2.7 kPa]), 13 of the patients survived, ten of whom were seemingly unaffected by the event. The lowest reported PaO2 was 7.5 mm Hg (1.0 kPa), in a 20-yr-old male patient breathing room air following a heroin overdose yet he made an unremarkable recovery.
Much of the concern regarding extreme hypoxemia is focused upon recovery of neurological function. It is difficult to attribute cognitive deficits occurring after critical illness directly to hypoxemia, when other factors such as hypotension, infection, electrolyte abnormality, and drug effects may have contributed. Whether hypoxemia reduces long-term cognitive function after sustained exposure to extreme high altitude is disputed.[77–80] In a study of healthy volunteers breathing 7% oxygen, no electroencephalogram abnormalities were detectable. Furthermore, postmortem examinations of young adults following severe and prolonged hypoxemia prior to death from sudden cardiac failure revealed no specific pathological cerebral changes that might be attributed to hypoxia. Hypoxemia tends to increase blood flow to tissues ensuring an adequate oxygen supply for metabolism, and this has been clearly demonstrated in the severely hypoxemic brain. Thus, when untangling the literature it is important to differentiate the subtle but important differences between hypoxemia and ischemia. "Hypoxic brain injury" in the absence of hypoperfusion is a much-feared consequence of a prolonged reduction in arterial oxygenation, yet there is little evidence for its existence and it should not be mistaken for ischemic cerebral injury that occurs post cardiac arrest.
Crit Care Med. 2013;41(2):423-432. © 2013 Lippincott Williams & Wilkins