Sebastiaan Dhont, Eric Derom, Eva Van Braeckel, Pieter Depuydt & Bart N. Lambrecht
Respiratory Research volume 21, Article number: 198 (2020)
Abstract
![](https://media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs12931-020-01462-5/MediaObjects/12931_2020_1462_Fig1_HTML.png?as=webp)
The novel coronavirus disease 2019 (COVID-19) pandemic is a global crisis, challenging healthcare systems worldwide. Many patients present with a remarkable disconnect in rest between profound hypoxemia yet without proportional signs of respiratory distress (i.e. happy hypoxemia) and rapid deterioration can occur. This particular clinical presentation in COVID-19 patients contrasts with the experience of physicians usually treating critically ill patients in respiratory failure and ensuring timely referral to the intensive care unit can, therefore, be challenging. A thorough understanding of the pathophysiological determinants of respiratory drive and hypoxemia may promote a more complete comprehension of a patient’s clinical presentation and management. Preserved oxygen saturation despite low partial pressure of oxygen in arterial blood samples occur, due to leftward shift of the oxyhemoglobin dissociation curve induced by hypoxemia-driven hyperventilation as well as possible direct viral interactions with hemoglobin. Ventilation-perfusion mismatch, ranging from shunts to alveolar dead space ventilation, is the central hallmark and offers various therapeutic targets.
Take home message
This review describes the pathophysiological abnormalities in COVID-19 that might explain the disconnect between the severity of hypoxemia and the relatively mild respiratory discomfort reported by the patients.