( A) Hypoxemia is sensed primarily at the carotid body (“peripheral”) chemoreceptors, and the gain of the carotid body response to hypoxia is increased by increasing Pa co 2 and decreasing pH. Sensation of and response to arterial hypoxemia. The latter may develop rapidly, and all are indicators of impending tissue injury or death from hypoxemia. Failure to compensate for decreased oxygen transport is signaled by lactic acidosis, bradycardia, and decreased cardiac output.
Cardiovascular compensation for hypoxemia is similarly variable, with the normal responses of tachycardia and increased cardiac output limited by age, genetics, and coexisting disease. Healthy individuals usually respond to acute hypoxemia with dyspnea, but because of hypoxic suppression of dyspnea (hypoxic ventilatory decline) and hypocarbic suppression of dyspnea, profound hypoxemia can be minimally symptomatic (“silent”), or noticed only during exertion. The spectrum of variability in human responses to hypoxemia is striking, influenced by differences in respiratory drive (the hypoxic ventilatory response) related to age, medications, coexisting diseases and genetic background. It is critical that clinicians caring for hypoxemic patients recognize two facts: (1) it is common for hypoxemia to exist without dyspnea (“silent hypoxia”) and (2) while patients may initially achieve cardiorespiratory compensation to hypoxemia, this compensation can fail precipitously. The Coronavirus infection disease 2019 (COVID-19) pandemic is bringing unprecedented numbers of patients with significant hypoxemia to medical care.
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