'Silent' Presentation of Hypoxemia and Cardiorespiratory Compensation in COVID-19

Philip E. Bickler, M.D., Ph.D.; John R. Feiner, M.D.; Michael S. Lipnick, M.D.; William McKleroy, M.D.

Disclosures

Anesthesiology. 2021;134(2):262-269. 

In This Article

Impairments in Oxygen Uptake Caused by Profound Hypoxemia

Blunting of the hypoxic ventilatory response during prolonged hypoxemia is another factor that can exacerbate existing hypoxemia. Hypoxic ventilatory decline is mediated by the brainstem and cerebrocortex, producing decreased minute ventilation despite significant hypoxemia.[37,42] Hypoxic ventilatory decline appears within about 15 min of sustained hypoxemia and could be present in any patient presenting with hypoxemia due to COVID-19. In addition, hypoxic ventilatory decline, by decreasing chemoreceptor sensitivity to hypoxemia would decrease breathlessness (Figure 1, A and C). Although hypoxic ventilatory decline is overcome during healthy adaptation to hypoxia as in ascent to high altitude,[35] this adaptation fails in chronic mountain sickness and results in worsening hypoxemia, polycythemia, and in severe cases congestive heart failure.[43]

Profound hypoxemia produces irregular or periodic breathing that causes minute-to-minute fluctuations in oxygenation in both sleep and awake states.[44,45] This is observed in both pneumonia and in high altitude hypoxia, and at sea level with hypoxic air breathing.[46] These fluctuations require continuous pulse oximetry to capture the variation and to discern the overall trajectory of saturation values: noting only single values on a digital display may lead to over- or underestimate the degree of hypoxemia. A treating clinician should be aware that the profound hypoxemia noted in COVID-19 may represent a temporary nadir in oxygen saturations that are constantly varying.

Hypoxemia can increase the severity right-to-left shunt by elevating pulmonary artery pressures, increasing blood flow through a patent foramen ovale or other venous channels. Shunting through a patent foramen ovale is observed in about 15% of normal subjects during acute hypoxemia during breathing hypoxic air mixtures to saturations of 70 to 80%. It is also seen during exercise at high altitude. This added intracardiac shunt may worsen hypoxemia out of proportion to the apparent lung injury. Furthermore, because shunt and decreased mixed venous PO 2 shift gas exchange to the steep portion of the oxyhemoglobin dissociation curve, small changes in ventilation, inspired oxygen, and shunt fraction produce large changes in arterial oxygen saturation.

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