Lead author Martin J. Tobin, MD, an Edward J. Hines Jr. VAMC pulmonologist and critical care specialist and professor at the Stritch School of Medicine

MAYWOOD, IL — Earlier in the COVID-19 pandemic, physicians were often baffled by patients who presented with extremely low levels of oxygen. Although oxygenation was so low it was potentially life-threatening in some cases, patients showed no obvious difficulty in breathing.

A new study published online by the American Journal of Respiratory and Critical Care Medicine offers a better explanation for silent hypoxemia, which was dubbed “happy hypoxia.” The authors from the Hines VA Hospital and Loyola University of Chicago Stritch School of Medicine suggested their information could help prevent unnecessary intubation and ventilation in patients during the current and expected second wave of coronavirus.1

Lead author Martin J. Tobin, MD, an Edward J. Hines Jr. VAMC pulmonologist and critical care specialist and professor at the Stritch School of Medicine, said the condition “is especially bewildering to physicians as it defies basic biology. In some instances, the patient is comfortable and using a phone at a point when the physician is about to insert a breathing (endotracheal) tube and connect the patient to a mechanical ventilator, which, while potentially lifesaving, carries its own set of risks.”

The small study, which included 16 COVID-19 patients with very low levels of oxygen–in some cases as low as 50%, compared to normal blood oxygen saturation of between 95 and 100%–but without dyspnea, determined that “several pathophysiological mechanisms account for most, if not all, cases of silent hypoxemia.”

Researchers said they conducted an informal poll of 58 hospitalists, emergency physicians and intensivists, inquiring whether they had seen patients who might be regarded as having silent hypoxemia or so-called happy hypoxia.

Of 37 respondents, 15 did not provide useful data, according to the study team, which reported that 16 of 19 patients with arterial blood gas measurement had a PaO2 of less than 60 mm Hg. Yet, they also communicated to a physician that they were not experiencing difficulty with breathing.

In fact, the study noted, 7 of the 16 patients had PaCO2 concentrations above 39 mm Hg (range, 41–49), which, combined with PaO2 of less than 60 mm Hg, would be expected to induce dyspnea. Those were considered to have silent hypoxemia as opposed to nine patients who had PaCO2 concentrations below 39 mm Hg (range, 29–37), which can blunt the respiratory centers.

“A disproportionate number of patients with COVID-19 are elderly and have diabetes,” researchers emphasized. “Both factors blunt the response of the respiratory control system to hypoxia. The ventilatory response to hypoxia is decreased by 50% in people older than 65 years. Given that the dyspnea response to hypoxia parallels the ventilatory response, it is likely that older patients with COVID-19 are more prone to silent hypoxemia. All but two of our seven patients with probable silent hypoxemia were 64 years or older (age range, 59-85 yr).”

In addition, the study recounted how ventilatory response to hypoxia is decreased by more than 50% in diabetes, adding, “ Individuals with diabetes also have a 1.8-fold impaired ability to perceive respiratory sensations. A further confounding factor is the broad range in respiratory drive between individuals). The chemical drive to breathe (in response to hypercapnia and hypoxia) exhibits as much as 300–600% variation between one subject and the next. This wide variability in respiratory drive is another factor that explains why some patients with hypoxia do not develop dyspnea.”

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