tetano
Editor, Senior Moderator
J Med Virol
. 2020 Jul 24.
doi: 10.1002/jmv.26342. Online ahead of print.
SARS-Cov-2 infection causes pulmonary shunt by vasodilatation
Anderson Brito-Azevedo[SUP] 1 2 3 [/SUP], Eduardo Costa Pinto[SUP] 1 4 [/SUP], Gabriel Angelo de Cata Preta Corr?a[SUP] 4 [/SUP], Eliete Bouskela[SUP] 3 [/SUP]
Affiliations
Abstract
Patients with SARS-CoV-2 may present a significant hypoxemia. The exactly mechanism of such hypoxemia in Covid-19 patients is not well described. It has been suggested that microthrombosis contributes to this mechanism, increasing pulmonary dead space. However, dead spaces would not be sensible to oxygen supplementation, and also, enlargement of pulmonary vessels it has been evidenced. Shunt mechanism by vasodilatation, instead, could explain decubitus dependence in oxygenation by blood redistribution as observed in these patients, and moreover, would be more sensible to oxygen supplementation than dead spaces. We hypothesized that SARS-Cov-2 causes an intrapulmonary vascular dilatation (IPVD), determining a shunt mechanism by vasodilatation. We performed contrast-enhanced transthoracic echocardiography to search IPVD shunt in patients with confirmed COVID-19, hospitalized in an intensive care unit. Ten patients were recruited; one patient was excluded due to low quality of echocardiographic image, and nine patients were included. IPVD was found in seven (78%) patients, with different grades, including patient with normal compliance and the one without invasive ventilation. We demonstrated that shunt by IPVD is present among Covid-19 patients, and this mechanism is probably implicated in significant hypoxemia observed. This article is protected by copyright. All rights reserved.
Keywords: ACE-2; ARDS; COVID-19; angiotensin-converting enzyme; bradykinin; coronavirus.
. 2020 Jul 24.
doi: 10.1002/jmv.26342. Online ahead of print.
SARS-Cov-2 infection causes pulmonary shunt by vasodilatation
Anderson Brito-Azevedo[SUP] 1 2 3 [/SUP], Eduardo Costa Pinto[SUP] 1 4 [/SUP], Gabriel Angelo de Cata Preta Corr?a[SUP] 4 [/SUP], Eliete Bouskela[SUP] 3 [/SUP]
Affiliations
- PMID: 32706407
- DOI: 10.1002/jmv.26342
Abstract
Patients with SARS-CoV-2 may present a significant hypoxemia. The exactly mechanism of such hypoxemia in Covid-19 patients is not well described. It has been suggested that microthrombosis contributes to this mechanism, increasing pulmonary dead space. However, dead spaces would not be sensible to oxygen supplementation, and also, enlargement of pulmonary vessels it has been evidenced. Shunt mechanism by vasodilatation, instead, could explain decubitus dependence in oxygenation by blood redistribution as observed in these patients, and moreover, would be more sensible to oxygen supplementation than dead spaces. We hypothesized that SARS-Cov-2 causes an intrapulmonary vascular dilatation (IPVD), determining a shunt mechanism by vasodilatation. We performed contrast-enhanced transthoracic echocardiography to search IPVD shunt in patients with confirmed COVID-19, hospitalized in an intensive care unit. Ten patients were recruited; one patient was excluded due to low quality of echocardiographic image, and nine patients were included. IPVD was found in seven (78%) patients, with different grades, including patient with normal compliance and the one without invasive ventilation. We demonstrated that shunt by IPVD is present among Covid-19 patients, and this mechanism is probably implicated in significant hypoxemia observed. This article is protected by copyright. All rights reserved.
Keywords: ACE-2; ARDS; COVID-19; angiotensin-converting enzyme; bradykinin; coronavirus.