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Presentation of Hypoxemia and Cardiorespiratory Compensation in COVID-19 Philip E CLINICAL FOCUS REVIEW Jerrold H. Levy, M.D., F.A.H.A., F.C.C.M., Editor “Silent” Presentation of Hypoxemia and Cardiorespiratory Compensation in COVID-19 Philip E. Bickler, M.D., Ph.D., John R. Feiner, M.D., Michael S. Lipnick, M.D., William McKleroy, M.D. he Coronavirus infection disease 2019 (COVID-19) decline). Simultaneously, even during severe hypoxemia, Tpandemic is bringing unprecedented numbers of cognition can be preserved by autoregulation of cerebral patients with significant hypoxemia to medical care. It is blood flow and brain oxygen delivery. Downloaded from http://pubs.asahq.org/anesthesiology/article-pdf/134/2/262/512654/20210200.0-00020.pdf by guest on 27 September 2021 critical that clinicians caring for hypoxemic patients rec- Another broadly held false belief brought into focus by ognize two facts: (1) it is common for hypoxemia to exist the COVID-19 pandemic is that hypoxia alone causes tis- without dyspnea (“silent hypoxia”); and (2) while patients sue injury. This is rarely the case; rather, acidosis and damage may initially achieve cardiorespiratory compensation to develop when cardiovascular compensation fails, critically hypoxemia, this compensation can fail precipitously. The reducing blood flow and oxygen delivery either globally spectrum of variability in human responses to hypoxemia is or to particular organs.5,6 The critical contribution of car- striking, influenced by differences in respiratory drive (the diovascular compensation to clinical outcome is supported hypoxic ventilatory response) related to age, medications, not only by a large body of experimental evidence, but also coexisting diseases and genetic background. Healthy indi- by our own experience as anesthesiologists, intensivists, and viduals usually respond to acute hypoxemia with dyspnea, scientists studying hypoxia in human subjects. but because of hypoxic suppression of dyspnea (hypoxic The purpose of this focused review is to describe human ventilatory decline) and hypocarbic suppression of dys- response to severe hypoxemia, focusing not on the patho- pnea, profound hypoxemia can be minimally symptomatic physiology of lung injury but on the respiratory system (“silent”), or noticed only during exertion. Cardiovascular response to hypoxemia. In addition, we summarize current compensation for hypoxemia is similarly variable, with the knowledge of the features and limits of human cardiore- normal responses of tachycardia and increased cardiac out- spiratory response and adaptation to profound hypoxemia put limited by age, genetics, and coexisting disease. Failure and describe some of the critical parameters that can help to compensate for decreased oxygen transport is signaled identify when adaptive compensation is failing. by lactic acidosis, bradycardia, and decreased cardiac out- put. The latter may develop rapidly, and all are indicators of Degree of Hypoxemia and Lung Injury in impending tissue injury or death from hypoxemia. Hospitalized Patients with COVID-19 Articles in the popular media1,2 and even a few in med- The available information about the pathophysiology of ical journals3,4 have stated that the symptoms of hypoxemia COVID-19 pneumonia suggests that while key features of in COVID-19 are unique, with minimal dyspnea or cog- the disease are more pronounced than in other viral pneu- nitive depression despite oxygen saturations measured by monias, the pathophysiology is not unique. pulse oximetry of less than 70%. Based on decades of studies The cardinal reason for hospital admission in COVID-19 with healthy volunteers and controlled, severe hypoxemia positive patients is hypoxemia.7–9 Although younger patients at the University of California at San Francisco Hypoxia with no prior history of lung disease can have severe pneu- Research Laboratory and during high-altitude medical monia and require invasive ventilation, elderly patients are research expeditions, it is our experience that while a lack at especially high risk for severe hypoxemia, with mortal- of dyspnea in response to hypoxemia is not typical, it is ity rates of 40 to 80% reported in various cohorts.8,10–12 commonly observed. Preexisting comorbid conditions, including cardiovascular There are several reasons that healthcare providers may be disease, diabetes mellitus, and chronic lung disease, as well surprised by apparently well-tolerated hypoxemia. First, are as male sex and obesity, also confer higher risk of severe several fundamentals related to the regulation of breathing disease and poor outcomes.8,10–12 and the sensation of dyspnea: the suppression of respiratory Hypoxemia is a leading predictor of admission to the drive by the dual effects of reduced carbon dioxide (hypo- intensive care unit, mechanical ventilation, and death.12,13 carbia), as well as by hypoxemia itself (hypoxic ventilatory Arterial blood gas and oxygen saturation (pulse oximetry) This article is featured in “This Month in Anesthesiology,” page 1A. Submitted for publication July 8, 2020. Accepted for publication September 2, 2020. Published online first on September 24, 2020. From the Hypoxia Research Laboratory, Department of Anesthesia and Perioperative Care (P.E.B., J.R.F., M.S.L., W.M.), and the Division of Critical Care Medicine (M.S.L., W.M.), Department of Medicine, University of California at San Francisco, California. Copyright © 2020, the American Society of Anesthesiologists, Inc. All Rights Reserved. Anesthesiology 2021; 134:262–9. DOI: 10.1097/ALN.0000000000003578 262 FEBRUARY 2021 ANESTHESIOLOGY, V 134 • NO 2 Copyright © 2020, the American Society of Anesthesiologists, Inc. Unauthorized reproduction of this article is prohibited. Hypoxemia and COVID-19 data often show severe hypoxemia at time of presentation, suffer decreased compliance as disease progresses,26 rep- 27 with wide alveolar-arterial Po2 gradients and low Pao2/Fio2 resenting a diversity of pathology. Appropriate manage- ratios. Increased oxygen requirements have been addressed ment of invasive ventilation in ARDS has been recently with increased use of noninvasive oxygen therapy (including reviewed and no strong data exist to support modifi- high flow nasal oxygen), prone positioning, invasive ventila- cation of existing ARDS protocols for COVID-19.28,29 tion, and in some cases, extracorporeal membrane oxygen. Readers are referred to the frequently updated consensus Hypercarbic respiratory failure has not been a prominent statements concerning treatment of COVID-19 by the presenting feature in existing reports or in our experience World Health Organization: (https://www.who.int/publi- at University of California at San Francisco. cations/i/item/clinical-management-of-covid-19; accessed Intrapulmonary shunt and ventilation/perfusion mis- September 24, 2020). match are the chief gas exchange abnormalities causing Downloaded from http://pubs.asahq.org/anesthesiology/article-pdf/134/2/262/512654/20210200.0-00020.pdf by guest on 27 September 2021 hypoxemia in COVID-19, as they are in other viral pneu- Hypoxemia and Breathlessness: Variability in monias, bacterial pneumonias,14 and acute respiratory distress Humans 15 syndrome. However, some features of COVID-19 may be Hypoxemia can present in a highly variable manner, with more pronounced than in other viral pneumonias, including some patients dyspneic with labored breathing and pan- substantial endothelial damage and micro-/macro-emboli icked, and others calm, despite oxygen saturations in the 16 formation. Limitation of diffusion across the alveolar mem- 70% range or below. The processes that produce intrapul- brane can cause hypoxemia, but while this is seen in humans monary shunt do not necessarily decrease lung compliance ,17 in at high altitude due to low inspired and alveolar Po2 or produce dyspnea. For many hypoxemic patients, oxygen patients with loss of functional lung units (such as in inter- saturations less than 70% can be tolerated for some time stitial lung disease or emphysema), and in some elite athletes with only moderate and transient alterations in mentation 18 at extremely high levels of cardiac output it does not sig- or other signs and symptoms.30 Dyspnea may only occur 15 nificantly contribute to hypoxemia in ARDS. Unique to with exertion, although decreased exercise tolerance is a shunt physiology is that increased ventilation decreases car- nonspecific symptom in acute illness. Decreased lung com- bon dioxide more than it increases oxygenation. The reduced pliance contributes to dyspnea, but as previously discussed, carbon dioxide limits respiratory drive and dyspnea (fig. 1). early COVID-19 pneumonia may present with shunt and Although intrapulmonary shunt is the dominant present- normal lung compliance.26 In our experience with pro- ing gas exchange abnormality in COVID-19, dead space may found experimental hypoxemia to oxygen saturations as significantly worsen with progression of ARDS. Hypoxemia low as 50% in healthy humans, subjective symptoms of that does not resolve with supplemental oxygen clearly indi- hypoxia may go unnoticed in some individuals, with no cates that gas exchange impairment has progressed beyond appearance of discomfort and minimal hyperpnea.30 Given · · ventilation/perfusion ration (V/Q ) mismatch and includes this variability in individual responses to hypoxemia, it is substantial intrapulmonary shunt. Alveolar filling, a cardi- not surprising that some COVID-19 patients have been nal feature of ARDS, correlates with lung radiographs and described as asymptomatic “silent” or “happy hypoxia.”3 impaired
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