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The Pathophysiology of 'Happy' Hypoxemia in COVID-19

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Dhont et al. Respiratory Research (2020) 21:198 https://doi.org/10.1186/s12931-020-01462-5 REVIEW Open Access The pathophysiology of ‘happy’ hypoxemia in COVID-19 Sebastiaan Dhont1* , Eric Derom1,2, Eva Van Braeckel1,2, Pieter Depuydt1,3 and Bart N. Lambrecht1,2,4 Abstract 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’sclinical 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. Keywords: COVID-19, SARS-CoV-2, Respiratory failure, Hypoxemia, Dyspnea, Gas exchange Take home message COVID-19, little is known about its impact on lung This review describes the pathophysiological abnormal- pathophysiology. COVID-19 has a wide spectrum of ities in COVID-19 that might explain the disconnect be- clinical severity, data classifies cases as mild (81%), se- tween the severity of hypoxemia and the relatively mild vere (14%), or critical (5%) [1–3]. Many patients present respiratory discomfort reported by the patients. with pronounced arterial hypoxemia yet without propor- tional signs of respiratory distress, they not even verbalize a sense of dyspnea [4–8]. This phenomenon is Background referred as silent or ‘happy’ hypoxemia. Tobin et al. re- In early December 2019, the first cases of a pneumonia cently presented three cases of happy hypoxemia with of unknown origin were identified in Wuhan, the capital PaO2 ranging between 36 and 45 mmHg in the absence of Hubei province in China. The pathogen responsible of increased alveolar ventilation (PaCO2 ranging between for coronavirus disease 2019 (COVID-19) has been iden- 34 and 41 mmHg) [5]. In patients with COVID-19, the tified as a novel member of the enveloped RNA betacor- severity of hypoxemia is independently associated with onavirus family and named severe acute respiratory in-hospital mortality and can be an important predictor syndrome coronavirus 2 (SARS-CoV-2), due to similar- that the patient is at risk of requiring admission to the ities with SARS-CoV and Middle East Respiratory Syn- intensive care unit (ICU) [9, 10]. Since correct recogni- drome (MERS) viruses. Although much is known about tion of hypoxemia has such an impact on prognosis and the epidemiology and the clinical characteristics of timely treatment decisions, we here offer an overview of the pathophysiological abnormalities in COVID-19 that * Correspondence: [email protected] 1Department of Internal Medicine and Paediatrics, Ghent University, Corneel might explain the disconnect between hypoxemia and Heymanslaan 10, 9000 Ghent, Belgium patient sensation of dyspnea. Full list of author information is available at the end of the article © The Author(s). 2020 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data. Dhont et al. Respiratory Research (2020) 21:198 Page 2 of 9 Dyspnea as a sensation 4 (too dyspneic to leave house or breathless when dress- Breathing is centrally controlled by the respiratory cen- ing) in relation to subjects of the same age [15, 16]. ter in the medulla oblongata and pons regions of the Various sensory, pain and emotional stimuli affect the brainstem (see Fig. 1) that control the ‘respiratory drive’ sensation of breathing via the cerebral cortex and hypo- to match respiration to the metabolic demands of the thalamus [17, 18]. The abnormal sense of muscle effort body [11, 12]. The main input affecting the respiratory is another contributor to dyspnea. Conscious awareness drive is derived from chemical feedback among periph- of the activation of respiratory muscles is absent in eral and central chemoreceptors. The center is, however, healthy breathing. However, when the respiratory mus- also influenced by higher brain cortex, hypothalamic in- cles are fatigued or weakened due to altered lung me- tegrative nociception, feedback from mechanostretch re- chanics (e.g. decreased thoracic compliance), breathing ceptors in muscle and lung, and metabolic rate. The may be perceived as a substantial effort [12]. Dyspnea output of the respiratory center can be divided into can also be caused by input from the mechanoreceptors rhythm- (e.g. respiratory rate) and pattern generating in the respiratory tract and the chest wall. Stimulation of (e.g. depth of breathing effort) signals, and these outputs vagal irritant receptors (e.g. bronchoconstriction, breath- may be controlled independently [11, 13, 14]. Dyspnea is ing through an external resistance) appears to intensify generally defined as a sensation of ‘uncomfortable, diffi- dyspnea [12, 19, 20]. The contribution of metabolic rate cult, or labored’ breathing and occurs, in general, when in modulating sense of dyspnea in critically ill patients the demand for ventilation is out of proportion to the remains unclear, despite its well-established role during patient’s ability to respond. It should be distinguished exercise [11, 21]. The best-known determinants of the from tachypnea (rapid breathing) or hyperpnea (in- respiratory drive are the central and peripheral chemore- creased ventilation). Dyspnea grading relates to whether ceptors. Changes in partial gas pressure of dissolved car- this feeling occurs in rest or upon exercise. This semi- bon dioxide in the blood (PaCO2) seem the most quantitative approach of scoring is best exemplified by important component, causing shifts in pH at the level the frequently used modified Medical Research Council of both the peripheral and central chemoreceptors [11, (MRC) dyspnea scale, which categorizes dyspnea from 12, 22]. At steady state, the arterial PaCO2 is determined grade 0 (dyspnea only with strenuous exercise) to grade by the following equation: Fig. 1 Main inputs affecting respiratory center (RCC) Dhont et al. Respiratory Research (2020) 21:198 Page 3 of 9 K:VCO ratios, abnormal CT scans (86%) and common require- .2 PaCO2 ¼ : ment for supplemental oxygen (41%) [31]. Happy or silent Ve: − Vd 1 Vt hypoxemia is not exclusively seen in COVID-19, but may also occur in patients with atelectasis, intrapulmonary shunt (i.e. arterio-venous malformations) or right-to-left intracardiac shunt. The adequacy of gas exchange is pri- K constant (863 mmHg) marily determined by the balance between pulmonary VCO2 Rate of CO2 production ventilation and capillary blood flow, referred as ventila- tion/perfusion (V/Q) matching [32]. In the initial phase of VE minute ventilation COVID-19, several mechanisms contribute to the devel- V dead space D opment of arterial hypoxemia (see Fig. 2), without a con- Vt tidal volume comitant increase in work of breathing. Rapid clinical deterioration may occur. The normal response to hypercapnia (caused by increased VD, hypoventilation or increased VCO2) is an increase in Changes in oxyhemoglobin dissociation curve respiratory drive and minute volume ventilation [23]. Oxygen saturation measured by pulse oximetry Hypoxemia itself rather plays a limited role in the sensation (SpO2) is often used to detect hypoxemia. However, of breathlessness experienced by patients with SpO2 should be interpreted with caution in COVID- cardiopulmonary disease on the opposite of hypercapnia that 19. The sigmoid shaped oxyhemoglobin dissociation creates per se dyspnea [12, 24, 25]. In healthy subjects, the curve seems to shift to the left, due to induced re- respiratory drive shifts minimally in mild hypoxemia (PaO2 spiratory alkalosis (drop in PaCO2) because of 60–65 mmHg), such as resulting from stays at high altitude hypoxemia-driven tachypnea and hyperpnea. During or experimental hypoxic chambers [11, 26]. Many patients hypocapnic periods, the affinity
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