'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.


Anesthesiology. 2021;134(2):262-269. 

In This Article

Predicting the Limits of Cardiovascular Compensation in Profound Hypoxemia

The precise limits of tolerance of reduced oxygen delivery are difficult to predict in an individual patient, but a critical threshold is when oxygen delivery is reduced to less than 25% of normal.[59] The clinical assessment of the transition from compensated to poorly compensated cardiovascular adaptation to hypoxemia includes the following: (1) worsened acidemia or plasma lactate;[60,61] (2) decreased mixed venous PO2 or decreased tissue oximetry (near infrared spectroscopy); (3) increased requirements for vasoactive medications to support blood pressure despite adequate fluid resuscitation; (4) increase in blood pressure reactivity to changes in body position, e.g., not tolerating prone or head-up positions; (5) bradycardia, arrhythmias, electrocardiogram changes concerning for ischemia, and increased in heart rate variability; and (6) increased troponin levels or ultrasound evidence of decreased myocardial contractility. These assessments reflect a focus on the cardiovascular compensation/tissue oxygen delivery for hypoxemia rather than on the degree of hypoxemia or hypercarbia per se. Bradycardia and decreased cardiac output/myocardial function are described in severe cases of hypoxemic respiratory failure, including COVID-19 disease, and often represent premorbid events.[62] Given reports of acute cardiomyopathy among patients with COVID-19,[62,63] clinicians must be keenly aware that the changes listed above may also reflect development or progression of myocardial injury; similarly, patients with low ejection fraction may have significantly less ability to augment cardiac output to compensate for any degree of hypoxemia.