Respiratory and cardiovascular effects of COVID-19 infection
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The virus SARS-CoV-2 causes multiorgan damage and primarily damages airway epithelium, small intestine epithelium, and vascular endothelium, which are organs with high angiotensin-converting enzyme. The most affected organ is the lungs, and the cardiovascular system follows it closely.

In the second clinical stage of established pulmonary disease, viral multiplication occurs, and there is respiratory inflammation. Lung inflammation is mediated by proinflammatory macrophages and granulocytes. Antigen presentation stimulates the body's humoral and cellular immunity, and this immune response is mediated by virus-specific B and T cells.

The ACE2 receptors act as an entry point to the myocardial cells causing direct injury in them. The severe cytokine surge results in injury to multiple organs, including cardiac myocytes. Increased metabolic demand associated with systemic infection and decreased supply, due to the ongoing hypoxia, results in myocardial damage. Many cardiovascular complications such as myocardial injury, myocarditis, arrhythmias, and venous thromboembolism (VTE) are associated with COVID-19 infection.

Supplemental oxygen therapy must be administered to the following category of patients - severe acute respiratory infection, obstructed or absent breathing, respiratory distress, central cyanosis, shock, coma or convulsions, respiratory distress, and hypoxemia or shock. Tracheal intubation should be performed as the risk of lung injury increases. A conservative fluid management strategy is recommended to ensure adequate tissue perfusion. The preferred fluid should be buffered/balanced crystalloids. Vasopressin or epinephrine must be administered as the first-line vasoactive agent.