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.