Abstract
This chapter discusses the myofibrillar alterations of heart in hemorrhagic shock. The chapter presents an experiment in which myocardial alterations were investigated in dogs after hemorrhagic hypotension. Hypotension was induced by bleeding through the femoral artery, and shed blood was stored at room temperature. The blood pressure of the animals was adjusted to 40 mmHg, and the period of hypotension was maintained until the spontaneous withdrawal of 30% of the blood drawn off. The average duration of the hypotonic period was 2.675 ± 0.242 h. Development of metabolic acidosis with increased lactate concentration was observed in all cases. Focal hemorrhages and hypoxic changes developed in the subendocarial region. Typical so-called zonal lesions were demonstrable in the mural myopardium of both ventricles. The hypoxia, increased level of catecholamines, metabolic disturbances, and probably cardiotoxlc products may play a role in the pathomechanism. The alterations that are potentially reversible are transformed into irreversible damage only in most severe cases. The necrosis is of hypercontraction type, and is associated with rapid calcification and mononuclear cell infiltration. The morphologic changes may explain the circulatory disturbances of cardiac origin and may represent the basis of development of the low cardiac output syndrome in hemorrhagic shock.
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