Background: Fluid retention in the face of an expanding extracellular fluid volume is a key contributing factor in the development and progression of heart failure.
Methods: We performed a review of clinical texts as well as a Medline investigation for the pathophysiology of fluid and sodium retention in heart failure.
Results: A breakdown in the integrity of the arterial circulation, seen in both high and low output heart failure, triggers a complex cascade of maladaptive events in an effort to maintain cardiorenal homeostasis. The activation of several neurohumoral mechanisms including the sympathetic nervous system, renin-angiotensin-aldosterone axis, nonosmotic arginine vasopressin release, and natriuretic peptide release initially compensates for depressed myocardial function. However, prolonged activation of these systems contributes to sodium and fluid retention, increased preload and afterload, and further damage to the myocardium. Improved understanding of this multifaceted pathophysiology has driven the development of improved treatment modalities, such as beta-blockers and angiotensin converting enzyme inhibitors which are now mainstays of heart failure therapy.
Conclusions: Further investigation into the neurohumoral mechanisms activated in the heart failure patient is a promising avenue for advances in diagnosis, prognosis, and treatment of this prevalent and devastating disease.
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