Organ perfusion in acute heart failure syndromes

Abstract

Acute heart failure syndromes (AHFSs) are associated with some degree of perfusion abnormality that is not necessarily evident. Cardiogenic shock is among the most important manifestations of the AHFS and is defined by clinically obvious or measured inadequate end-organ perfusion and tissue hypoxia with mortality in the range of 50%1. Causes of death are not only cardiogenic shock but also various organ failures despite normalized cardiac index2. Renal dysfunction, for example, is the most frequent and apparent organ dysfunction and is a powerful adverse prognostic factor (reviewed in Gheorghiade et al.3). Low organ perfusion during AHFS (Fig. 15.1) may result from a forward failure (acute coronary syndrome, myocardial failure with cardiogenic shock of various etiologies), from a backward failure with congestion due to global or right heart failure, or from a maladapted peripheral vasoconstriction (hypertensive acute heart failure). Regional redistribution of blood flow toward various vascular beds in the setting of AHFS has been seldom addressed over the last three decades compared to other acute states such as sepsis or hemorrhage, and consequently this chapter focuses on low-output AHFS. © 2008 Springer-Verlag London.