SARS-CoV2 Happy Hipoxemia: is it really happy? - Abstract
A significant number of patients affected by COVID-19 present a pattern of severe respiratory failure, with heterogeneous characteristics of acute respiratory distress syndrome (ARDS) [1]. Many of them show a marked alteration in the ventilationperfusion ratio (V/Q) and, consequently, an increase in the shunt and intrapulmonary dead space with impaired oxygenation; on the other hand, different reports [2-4], show the presence of thrombosis and diffuse alveolar damage, which translates into an increase in dead space and shunt too, which reduces CO2 elimination and, probably, an increase in respiratory rate. In some patients, relatively preserved compliance values have been observed and, additionally, a reduction in the
hypoxic vasoconstriction mechanism has been postulated as a consequence of an alteration in the carotid bodies function [5]. Thus, we would be in the presence of patients showing hypoxemia and hypercapnia with no more functional alteration
than an increase in respiratory rate. This is what was called happy hypoxemia. This clinical picture usually presents greater severity around 7-10 days from the onset of symptoms.