Abstract
The pathophysiological model for cardiogenic shock was first described by Hollenberg and colleagues,1 in which severely depressed myocardial contractility, due to acute coronary thrombosis, initiates progressive worsening of systolic and diastolic dysfunction. These impairments result in systemic hypoperfusion, coronary ischaemia, increased ventricular filling pressures, multiorgan system failure, and death.1 A key premise to this paradigm has been the maladaptive role that systemic vasoconstriction (a compensatory response to reduced cardiac output) has in perpetuating this cascade through its adverse effects on afterload and myocardial oxygen demand.
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