Abstract
We are living and suffering a unique medical experience right now. A small virus, of no more than 100 nanometers, from the coronavirus family, known as SARS-COV 2 or COVID-19 (Coronavirus Disease, 2019) began its expansion around the world, starting from the city of Wuham in China in the last months of 2019. In December of that year it was already recognized by the WHO authorities as a possible serious disease. Its extension has been gradual, but explosive, by more than 200 countries on all continents. Most of the infected (up to 80%) will pass their process asymptomatic. But the sick who develop the disease will do so to varying degrees. 40% mildly, paucisymptomatic, while the other 60% will present respiratory symptoms that in 15% will be severe and in 5% will place the patient in a critical situation. The most common clinical presentation is in the form of progressive bilateral bronchopneumonia, with hypoxemia and severe acute respiratory distress, which compromises the patient’s life. These are patients who will need hospital admission for treatment with respiratory assistance, and in critical situations, admission to intensive care units, to connect to assisted breathing, and if it is complicated by cardiac pathology, which can accompany a significant percentage of these severe patients, for circulatory support. These are the patients that reach a high mortality. The virus has a characteristic structure in which the single-stranded chain of RNA is enveloped by a series of proteins, among which the surface spicules that give it the characteristic shape, or S proteins, stand out. They serve as binding to specific receptors cells of the Angiotensin 2 Converting Enzyme, ECA2, with which it interacts. Through them it is introduced into the respiratory epithelial cells or the cardiovascular system and other organs. It uses the genetic structure of invaded cells to replicate and spread throughout the affected organ and throughout the body. The immune response system, both humoral and cellular, tries to stop the replicative stimulus of the virus. The resistance of the virus to limit its replication causes the uncontrolled response of anti-inflammatory mediators to continue, which is summarized in what is called a cytokine storm. This is the most important damage mechanism produced by the body’s response. Homeostatic balances are decompensated, both in maintaining blood pressure with critical hypotension and shock situations, and in the balance of pro and anticoagulant systems, with a general production of thrombi that produces the most serious complications, as well as the destruction of own anti-infective barriers. Pulmonary pathology progresses progressively from pneumonia to fibrosis, complicating many of the critically ill patients with pulmonary thromboembolism. Myocardial damage occurs in the circulatory system, with criteria for thrombosis and inflammation in the form of ischemic damage and different forms of cardiomyopathy. One of the most unique occurs specifically in the young population, in the form of a multisystemic hyperinflammatory response. But they can also damage the liver, kidney, central nervous system and other non-vital organs and systems.
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