Basically cardiogenic shock results from profound reduction in cardiac output. This is usually caused by marked reduction of left or right ventricular systolic func¬tion, despite adequate ventricular filling pressures, and there is a failure of compensatory vasoconstrictive mech¬anisms that are overwhelmed by inappropriate vasodilation in large, nonvital vascular beds. Thus this deprivescri-tical areas like the heart ,brain, and kidney of perfusion. Hochman points out that data from the shock trial and registry indicate that cardiogenic shock is often not simply due to extensive myocardial infarction with pump failure, ‘‘but also involves inflammatory mediators. These mediators induce nitric oxide synthase (iNOS) expres¬sion, increasing nitric oxide (NO) and peroxynitrite levels, resulting which results in further myocardial dysfunc¬tion and failure of an appropriate peripheral circulatory response.’’

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