Viral myocarditis is the result of a viral infection that produces myocardial necrosis and triggers an immune response to eliminate the viral agent. Many pathogenic mechanisms may contribute to myocardial cell loss including the following: cytokine production contributing to disease severity; viral persistence, which may produce an autoimmune response to cardiac myosin; and viral invasion of vascular endothelium causing vascular spasm with reperfusion injury. The compensatory response of the myocardium to these mechanisms of cell loss is hypertrophy, which results in fibrosis, scarring, and dilation. The myocardial cell loss and physiological response produces a child with fever, lethargy, symptoms of congestive heart failure, cardiogenic shock, or new onset arrhythmias. The initial presentation may be subtle, but if left untreated will go on to produce severe symptoms. The focus of diagnostic studies is to evaluate cardiac function, identify the viral agent, and eliminate other causes of global cardiac dysfunction. Treatment must provide for support of cardiac function through inotropic and afterload-producing agents while providing rest for the stressed cardiac muscle. The nursing care of children with viral myocarditis must focus on continual assessment of the cardiovascular system while supporting the recovery of myocardial function.

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