The Pathophysiology Of 'happy' Hypoxemia In COVID-19

In early December 2019, the first cases of a pneumonia of unknown origin were identified in Wuhan, the capital of Hubei province in China. The pathogen responsible for coronavirus disease 2019 (COVID-19) has been identified as a novel member of the enveloped RNA betacoronavirus family and named severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), due to similarities with SARS-CoV and Middle East Respiratory Syndrome (MERS) viruses. Although much is known about the epidemiology and the clinical characteristics of COVID-19, little is known about its impact on lung pathophysiology. COVID-19 has a wide spectrum of clinical severity, data classifies cases as mild (81%), severe (14%), or critical (5%) [1,2,3]. Many patients present with pronounced arterial hypoxemia yet without proportional signs of respiratory distress, they not even verbalize a sense of dyspnea [4,5,6,7,8]. This phenomenon is referred as silent or ‘happy’ hypoxemia. Tobin et al. recently presented three cases of happy hypoxemia with PaO2 ranging between 36 and 45 mmHg in the absence of increased alveolar ventilation (PaCO2 ranging between 34 and 41 mmHg) [5]. In patients with COVID-19, the severity of hypoxemia is independently associated with in-hospital mortality and can be an important predictor that the patient is at risk of requiring admission to the intensive care unit (ICU) [9, 10]. Since correct recognition of hypoxemia has such an impact on prognosis and timely treatment decisions, we here offer an overview of the pathophysiological abnormalities in COVID-19 that might explain the disconnect between hypoxemia and patient sensation of dyspnea.