Loss of hypoxic pulmonary vasoregulation has been attributed as a mechanism in this scenario. It is postulated that hypoxemia in COVID-19 is resultant of a V/Q mismatch due to a vascular pathology, 1 especially in the early stages. The rapidly evolving data on the subject has prompted us to postulate a multifold pathophysiologic approach to these mechanism/s and their dynamic transition as well as overlap. One of the more enigmatic unknowns for clinicians worldwide in the pathophysiology of COVID-19 is the mechanism/s by which it causes severe hypoxia with relatively preserved lung mechanics, especially in the early stages. Indian J Crit Care Med 2020 24(10):967–970.ĭespite the circadian increase in the available literature on coronavirus disease-2019 (COVID-19), we are far from having a thorough understanding of its pathophysiology or established protocols for management. Mechanisms of Hypoxia in COVID-19 Patients: A Pathophysiologic Reflection. How to cite this article: Nitsure M, Sarangi B, Shankar GH, Reddy VS, Walimbe A, Sharma V, et al. In this hypothesis paper, we attempt to gather and explain these observations within a unified conceptual framework by invoking the relative contributions of microvascular thrombosis, along with two proposed vascular mechanisms of capillary flow redistribution and flow through intrapulmonary arteriovenous anastomoses (IPAVA). The scant but rapidly evolving data available on the pathophysiology are seemingly conflicting, indicating the relative dominance of intrapulmonary shunting or dead space in different studies. The combination of factors including low P/F ratios, high A-a gradient, relatively preserved lung mechanics, and normal pulmonary pressures may imply a process occurring on the vascular side of the alveolar–capillary unit. Coronavirus disease-2019 (COVID-19) causes severe hypoxemia which fulfills the criteria of acute respiratory distress syndrome (ARDS) but is not accompanied by typical features of the syndrome.
0 kommentar(er)
