Abstract
Since the outbreak of the novel coronavirus disease 2019 (COVID-19),
researchers around the globe are constantly puzzled by a well reported
clinical finding of pronounced arterial hypoxemia, yet without
proportional signs of respiratory distress (i.e. silent hypoxemia or
happy hypoxemia) in this disease. Based upon the findings of increased
intrapulmonary shunt in COVID-19, many proceed to propose the concept of
pulmonary vasoplegia, and not just the loss of hypoxic pulmonary
vasoconstriction, as mechanism behind this phenomenon of silent
hypoxemia. Further, assumptions were made in proposing inflammatory
vasodilators such as prostaglandins and bradykinins to be the
pathological mediators. However, a closer look in to the physiology of
renin-angiotensin system may suggest the predominant role of
angiotensin-converting enzyme and angiotensin II-mediated pulmonary
vasoconstriction to be an early mechanism for silent hypoxia. This
theory not only supports other clinical symptomatology of COVID-19,
including lack of nasal symptoms and absence of asthma as a risk-factor,
but also corelates with the histopathological data and the radiological
findings of COVID-19 disease.