Pathophysiology of volume overload in acute heart failure syndromes.
The inability to effectively regulate volume status is a major consequence of acute heart failure syndromes (AHFS). A variety of pathophysiologic processes contribute to this impairment, most notably neurohormonal activation of the renin-angiotensin-aldosterone system, arginine vasopressin, and the sympathetic nervous system. As a result, addressing volume overload is one of the most challenging aspects of AHFS management. Neurohormonal activation leads to substantial changes in hemodynamics and myocardial remodeling, which further contribute to the severity of heart failure (HF) disease and thereby cyclically increase the risk of further neurohormonal activation. Pulmonary capillary wedge pressure is a dependable reflection of volume status and has been used as a surrogate marker in recent studies to assess disease progression in response to innovative HF treatment strategies. Future approaches to HF treatment should focus on the more accurate assessment and management of volume status in an effort to improve patient care.[1]References
- Pathophysiology of volume overload in acute heart failure syndromes. Chen, H.H., Schrier, R.W. Am. J. Med. (2006) [Pubmed]
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