الفهرس 
Pathophysiology of heart failureOnly 14 pages are availabe for public view
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Abstract
Heart failure results from any structural or functional disorder that impairs the ability of the ventricles to fill or eject blood .It comprises a heterogenous group of syndromes with different pathophysiology, clinical presentations and response to specific therapies.(Hunt et al,2009).
In the later stages of heart failure (i.e decompensated heart failure), Resting flow decreases to vital organs and inotropic therapy is frequently considered in hopes that these agents could increase cardiac contractility, enhance the cardiac output ( Sandham et al, 2003) and perfusion of vital organs. Thus, inotropic agents could convert decompensated heart failure patients into a more compensated form (Warner, 2003).
Despite the short-term benefits of conventional inotropes, the clinical utility of inotropic agents is compromised by their potentially deleterious effects on calcium handling and oxygen consumption, resulting in an increased risk of serious ventricular arrhythmias and death (Murdoch and McMurray, 2000).
As, current inotropic drugs have consistently failed to show beneficial effects beyond short term haemodynamic improvement in patients with heart failure, Newer agents targeting different mechanisms of action were developed and hold new promise for the future, as long as complications of myocardial ischaemia, arrhythmias, and hypotension can be avoided. (Hasenfuss and Teerlink, 2011).