![]() ![]() Reynolds and colleagues also found that the number of microbubbles was inversely correlated with oxygenation (Pa O 2:F i O 2 ratio) and lung compliance, suggesting that microbubbles may be a marker of disease severity from both a gas exchange and lung mechanics perspective ( 4). To further support this hypothesis, pulmonary vascular dilatation and altered perfusion has also recently been identified as a radiographic finding in COVID-19 pneumonia ( 6). Although more information regarding ventilator settings, pulmonary hemodynamics, and the presence or absence of patent foramen ovale would have been helpful to characterize the patients, these findings suggest that intrapulmonary vasodilatation could play an important role in the pathogenesis of hypoxemia associated with COVID-19. Notably, these prior studies also used the less sensitive method of CE-TTE for microbubble detection. Although this is a small pilot study, this prevalence is much higher than that reported in prior studies of patients with ARDS ( 3). Reynolds and colleagues found that the majority (15/18, 83%) of patients with COVID-19 had detectable microbubbles in the cerebral circulation by TCD ( 4). Compared with CE-TTE, TCD is more sensitive but less specific and unfortunately cannot distinguish intracardiac from intrapulmonary shunting ( 5). In patients with intracardiac shunting or intrapulmonary vasodilatation, however, the bubbles transit through the pulmonary circulation and can be visualized downstream in the left heart (as detected by contrast-enhanced transthoracic echocardiography ) or middle cerebral artery (as detected by TCD). Normally, the microbubbles, whose diameter exceeds the pulmonary capillaries, are trapped in the pulmonary circulation. With this method, agitated saline microbubbles are injected into a central or peripheral venous catheter and TCD is used to detect and quantify microbubbles that appear in the cerebral circulation. 1037–1039), in a pilot study, used automated transcranial Doppler (TCD) ultrasound to define the prevalence of intracardiac or intrapulmonary shunting in patients with COVID-19 ( 4). In this issue of the Journal, Reynolds and colleagues (pp. Although both intrapulmonary and intracardiac shunting have been described in classical ARDS, they are generally present in a minority of patients and are not a predominant feature ( 3). In a study by Guan and colleagues, only 18.7% of 1,099 hospitalized patients with COVID-19 reported dyspnea despite the majority having abnormal chest imaging ( 2). Hypoxemia in COVID-19 can also be disproportionate to the degree of symptoms and impairment in lung mechanics. Gattinoni and colleagues initially described this unique phenomenon of large shunt fractions and severe hypoxemia in patients with COVID-19 as compared with “typical” acute respiratory distress syndrome (ARDS) ( 1). Frontline healthcare workers witness this shunt physiology on a regular basis while caring for hospitalized patients with coronavirus disease (COVID-19). Right-to-left shunts may be intracardiac or intrapulmonary and are characterized by a reduced or absent response to supplemental oxygen. In training, we learn that there are five causes of hypoxemia: V ˙ /Q mismatch, right-to-left shunt, diffusion impairment, hypoventilation, and low F i O 2.
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