Hyponatremia in heart failure

Mohammad Sarraf, Steven Goldsmith

Research output: Chapter in Book/Report/Conference proceedingChapter

Abstract

Hyponatremia is a common problem in patients with heart failure. Many studies in patients with acute and chronic heart failure have demonstrated a very strong link between hyponatremia and poor outcomes. This link has persisted despite the use of modern neurohormonal blocking agents. Whether there is a causal relationship between hyponatremia and poor outcome in heart failure is uncertain, as hyponatremia is typically found in sicker patients, and it may simply be an association. Nonetheless, there are reasons to suspect a causal relationship, and more research is needed to investigate this possibility. Efforts to more carefully examine the relationship between hyponatremia and outcomes in heart failure have been hampered by the lack of safe and effective treatment for this condition. There are several factors which may influence the development of hyponatremia in heart failure, but since most patients with this condition are either euvolemic or hypervolemic, excess free water reabsorption due to inappropriate levels of the antidiuretic hormone arginine vasopressin is the major factor in most circumstances. The development of antagonists to the renal V2 receptor for vasopressin has now provided an effective and safe therapy for euvolemic and hypervolemic hyponatremia in patients with heart failure. The use of these agents should greatly simplify the treatment of hyponatremia in heart failure when it is symptomatic or interfering with the use of other needed therapies. As well, it may now be possible to undertake studies in which the relationship between hyponatremia and outcomes in heart failure is more fully examined.

Original languageEnglish (US)
Title of host publicationHyponatremia
Subtitle of host publicationEvaluation and Treatment
PublisherSpringer New York
Pages127-143
Number of pages17
ISBN (Electronic)9781461466451
ISBN (Print)9781461466444
DOIs
StatePublished - Jan 1 2013

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