The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) virus enters pulmonary and myocardial cells by the binding of the spike viral protein to the ACE2 (angiotensin-converting enzyme 2) receptor, a key actuator in the renin-angiotensin-aldosterone system (RAAS). Thus, in coronavirus disease (COVID-19), RAAS has been directly implicated in the pathogenesis of acute respiratory distress syndrome (ARDS) as part of the host tissue response. ACE2 catalyzes the conversion of angiotensin II (AngII) to Ang-(1-7). When ACE2 is not present, AngII remains at increased levels, stimulating vasoconstriction, the production of inflammatory cytokines, and pulmonary fibrosis (1). Ongoing investigations of the RAAS in COVID-19 include how this pathway regulates susceptibility to SARS-CoV-2 infection, severity of illness, and how therapeutics might prevent or mitigate severe disease. Even with a unifying cause of COVID-19, SARS-CoV-2 infection has one of the most protean presentations of any disease, and studies have found that COVID-19 ARDS phenotypes are also heterogeneous