key: cord-0971151-wn5zoswv
authors: Jounieaux, Vincent; Mahjoub, Yazine; El-Esper, Isabelle; Rodenstein, Daniel Oscar
title: The importance of lung hyperperfusion patterns in COVID-19-related AVDS
date: 2021-07-11
journal: Eur J Nucl Med Mol Imaging
DOI: 10.1007/s00259-021-05451-8
sha: 89ffb9fcb082c7c1f96f87df121f6a009ec7a574
doc_id: 971151
cord_uid: wn5zoswv

nan

between perfusion and ventilation may be attributed to some loss of pulmonary hypoxic vasoconstriction (HPV) and accounts in part in the COVID-19 related hypoxemia. However, using a mathematical model of lung perfusion in normal and injured compartments, Herrmann et al. have concluded that impairment of HPV alone cannot reproduce the same level of severe hypoxia at low values of fraction of injured lung [4] as found by Gattinoni et al. [5] . More, Yao et al. have shown on lung histopathologic pattern of COVID-19 patients that the blood vessels of alveolar septum were congested, oedematous, and widened; and that the COVID-19 infection, while mainly distributed in the lung, involves the vessels, heart, liver, kidney, and other organs [6] . More recently, Ackermann et al. found ultrastructural damages to the endothelium, the presence of Sars-Cov-2 in endothelial cells, as well as a pulmonary angiogenesis observed since day 4 of hospital admission and which significantly increases with time [7] . In COVID-19 patients, Lang et al. observed three major findings from dual-energy CT on the images of pulmonary blood volume perfusion: preferentially increased perfusion of the lungs proximal to areas of lung opacities, areas of decreased perfusion corresponding to peripheral lung opacities, and a halo of increased perfusion surrounding peripheral areas of consolidation [8] . Such vascular abnormalities could be also found in SPECT/CT through an increased perfusion in normally aerated lung regions (or hyperventilated) [9] , as shown, but not described, in Fig. 1a of their letter (areas of augmented perfusion in the right middle lobe despite any evident parenchyma lesions on CT at this level) [1] . We believe that such mismatches may reflect the specific intrapulmonary shunt that we suggest to be the cornerstone of the COVID-19 disease [10] and explain the so-called COVID-19 related "happy hypoxic state." Indeed, we believe that COVID-19 is a vascular disease, inducing an intrapulmonary shunt (as in hepatopulmonary syndrome [11] ) through an increase perfusion of normally (or hyperventilated) lung areas (i.e., without any lung parenchyma lesions) [12] . These mismatches result in a mild initial hypoxemia leading to a compensatory increase in minute ventilation. Because CO 2 is much more diffusible than O 2 , hyperventilation would rapidly lead to hypocapnia which is known to be a powerful inhibitor of the ventilation. We have previously shown that below a PaCO 2 29.3 mmHg, deep oxygen desaturations (up to 64%) are unable to elicit an increase in minute ventilation in normal subjects [13] . This results in the so-called "happy hypoxia" which is a rare situation during hospitalization [14] , as alveolar damage is usually present at this time of the COVID-19 infection. Indeed, associated lung parenchyma lesions limit hypocapnia, aggravate hypoxemia, and hide the presence of the vascular component in the form of intrapulmonary shunting. Among the huge heterogeneity of lung perfusion SPECT/ CT patterns observed in COVID-19 patients, one must be vigilant especially to normal lung areas with increased perfusion; around or at distance of areas of COVID-19 related consolidations. In such situations, it seems crucial for us to track the intrapulmonary shunt, either by performing a planar image of the brain immediately after the lung perfusion SPECT/CT acquisition (to detect an abnormal brain uptake) or through a contrast-enhanced echocardiography [12] .

The authors declare no competing interests.

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On happy hypoxia and on sadly ignored "acute vascular distress syndrome" in patients with COVID-19