Coronavirus disease 2019 (COVID-19) has been compared to high altitude pulmonary edema (HAPE) Multiple similarities between the two conditions were drawn in the past This article seeks to further clarify potential underlying mechanisms related to hypoxia and pulmonary vascular responses It does so by looking at perfusion imaging of patients with COVID-19 and comparing them with patterns observed in HAPE and hypoxic exposure Two separate clinical cases are reviewed The salient aspect of each case that is emphasized is the perfusion scintigraphy results that revealed heterogeneous perfusion patterns in both patients Heterogeneous or non-homogeneous perfusion is also observed in HAPE A detailed clinical course of each patient is described Medications utilized to treat the conditions are outlined as well as laboratory parameters and clinical findings Interestingly, both of these patients were treated with calcium channel blockers and this class of medications is utilized to prevent HAPE as well Discussion following the case presentations attempts to contextualize possible implications of this and other studies on the broader pathophysiology of COVID-19 disease Findings related to pathophysiologic patterns and treatment strategies are also described Micro-thrombi formation has been reported in both COVID-19 and HAPE as well and may be an accessory complication of perfusion compromise In a separate study, vasodilatation with calcium channel blocker (CCB) therapy has been associated with improved mortality in COVID-19 and potential pathophysiologic mechanisms were previously presented This case report provides further clinical findings that support the notion that perfusion deficits are an integral component of hypoxia in COVID-19 It also advances the basis for use of vasodilator therapy as part of treatment regimens in COVID-19 Vasodilators may improve micro-perfusion In this way, oxygenation may be promoted by decreasing impedance and improving flow via the alveolar-capillary unit
Heterogeneous Perfusion in COVID-19 and High Altitude Pulmonary Edema: A Review of Two Cases Followed by Implications for Hypoxic Pulmonary Vasoconstriction, Thrombosis Development, Ventilation Perfusion Mismatch and Emergence of Treatment Approaches