In 2018, the American College of Chest Physician stated that it is presents if there is an inadequate response to high-dose vasopressor therapy defined as ≥ 0.5 mg/kg/min norepinephrine-equivalent dose. Management
Reversing the underlying causes of vasodilatory shock, stabilizing hemodynamic, preventing renal, myocardial, and other organs from injuries due to hypoperfusion and hypoxia, and taking necessary measures to safeguard against complications including venous thromboembolism are served as the top priorities during the treatment.The initial treatment aiming at restoring effective blood pressure in patients that have refractory shock typically starts with introducing norepinephrine and dopamine. Vasopressin comes as the second-line agent.However, high-dose therapy is linked to excessive coronary, splanchnic vasoconstriction, and hypercoagulation. Excessive vasoconstriction can cause cardiac output reduction or even fatal heart complication particularly in those with weak myocardial function.In those whose vasodilatory shock is caused by hypocalcemic cardiomyopathy in the context of dilated cardiomyopathy with documented both reduced heart ejection fraction and contractile performance, the uses of calcium and active vitamin D or recombinant human parathyroid hormone treatment are viable since there were many successful cases reported while given the physiological role of calcium on muscle contraction.A successful treatment requires leveraging the respective unique contributions of a multi-disciplinary team not only critical care doctors and often, infectious disease specialists but also respiratory therapy, nursing, pharmacy and others in collaboration. Epidemiology
Observational studies suggest that, about 6% to 7% of critically ill people may end up developing refractory shock. Prognosis
Early recognition and rapid treatment initiation are crucial to saving life.
Viral cardiomyopathy occurs when viral infections cause myocarditis with a resulting thickening of the myocardium and dilation of the ventricles. These viruses include Coxsackie B and adenovirus, echoviruses, influenza H1N1, Epstein–Barr virus, rubella (German measles virus), varicella (chickenpox virus), mumps, measles, parvoviruses, yellow fever, dengue fever, polio, rabies and the viruses that cause hepatitis A and C, as well as COVID-19, which has been seen to cause this in persons otherwise thought to have a "low risk" of the viruss effects. COVID-19 Cardiomyopathy
Patients with Covid-19 frequently experience heart issues. According to studies, people who have had previous cardiovascular conditions like cardiomyopathy, hypertension, coronary heart disease, or arrhythmia are more likely to become critically ill from SARS-CoV-2 infection. Myocarditis may result from a direct viral infection of the myocardium. Cardiovascular biomarkers like troponin, lactate dehydrogenase, high sensitivity amino-terminal B-type natriuretic peptide, creatinine kinase, and creatinine kinase myocardial band, which indicate myocardial damage, increase in concentration in response to covid-19. Hundreds of studies have reported myocarditis/myopericarditis caused by Covid-19 infection in living patients, with a male predominance (58%), and a median age of 50 years. See also
Coxsackievirus-induced cardiomyopathy
Myocarditis
Pericarditis
Vaccine adverse event

References
External links
Myocarditis on emedicine