Misconceptions of pathophysiology of happy hypoxemia and implications for management of COVID-19
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LETTER TO THE EDITOR
Open Access
Misconceptions of pathophysiology of happy hypoxemia and implications for management of COVID-19 Martin J. Tobin*, Amal Jubran and Franco Laghi Abstract In the article “The pathophysiology of ‘happy’ hypoxemia in COVID-19,” Dhont et al. (Respir Res 21:198, 2020) discuss pathophysiological mechanisms that may be responsible for the absence of dyspnea in patients with COVID-19 who exhibit severe hypoxemia. The authors review well-known mechanisms that contribute to development of hypoxemia in patients with pneumonia, but are less clear as to why patients should be free of respiratory discomfort despite arterial oxygen levels commonly regarded as life threatening. The authors propose a number of therapeutic measures for patients with COVID-19 and happy hypoxemia; we believe readers should be alerted to problems with the authors’ interpretations and recommendations. Letter We read with interest “The pathophysiology of ‘happy’ hypoxemia in COVID-19” by Dhont et al. [1]. We agree with many of their points but disagree on several important facets. Dhont and colleagues [1] claim that increases in respiratory rate and tidal volume are “the most important clinical signs of impending hypoxemic respiratory failure.” On the contrary, neither rate nor tidal volume are sensitive or specific for hypoxemia. The essential point about happy hypoxemia is that patients can be profoundly hypoxic and yet exhibit no abnormality in breathing pattern [2]. Dhont et al. [1] claim that a leftward shift in the oxyhemoglobin-dissociation curve explains “why SpO2 can be well-preserved in the face of a profoundly low PaO2.” Given that the carotid bodies respond solely to arterial oxygen tension (PaO2), and not to arterial oxygen saturation (SaO2) [1], a leftward shift of the * Correspondence: [email protected] Division of Pulmonary and Critical Care Medicine, Hines Veterans Affairs Hospital and Loyola University of Chicago Stritch School of Medicine, Hines, IL 60141, USA
dissociation curve would increase the likelihood of dyspnea—the opposite of happy hypoxemia. Diagnosis of happy hypoxemia in COVID-19 is typically prompted by low pulse oximeter readings. Pulse oximetry markedly exaggerates the severity of low oxygen saturations when readings are low [2] (and this will not enhance carotid-body stimulation). Additionally, fever (a frequent occurrence in COVID-19) moves the oxygendissociation curve to the right. For example, a temperature of 40 °C will produce a decrease in oxygen saturation of 9.9% without change in PaO2 [2]. This substantial desaturation will not increase carotid-body stimulation—a perfect set-up for happy hypoxemia. Dhont and colleagues [1] claim that increases in negative inspiratory intrathoracic pressure in COVID-19 patients will produce patient self-inflicted lung injury (PSILI). There is no evidence that P-SILI occurs in patients with COVID-19 [3]. Indeed, there is no direct experimental proof for the occurrence of P-SILI in human subjects [4]. Dhont et al. [1] invoke involvement of pulmona
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