Inpatient management of patients with volume overload and high filling pressures

J Hosp Med. 2008 Nov;3(6 Suppl):S25-32. doi: 10.1002/jhm.396.


The majority of patients with acute decompensated heart failure are admitted with symptoms of congestion. The classic symptoms of "congestive" heart failure reflect fluid overload, that is, orthopnea, paroxysmal nocturnal dyspnea, and peripheral edema; these symptoms can be so dramatic that it is not surprising that patients seek hospitalization. Activation of the renin angiotensin system coupled with sympathetic hyperactivity results in marked sodium retention and high filling pressures that ultimately bring about these congestive symptoms. The treatment goal of patients hospitalized with volume overload and high filling pressures is to improve symptoms by normalizing the filling pressure and volume status without worsening renal function. The current use of diuretics, vasodilators, and ultrafiltration, as well as potential future use of investigational agents such as oral vasopressin antagonists and adenosine A1-receptor antagonists, is surrounded by the important issues of when to stop intravenous therapy in hospitalized patients and the exact mechanism by which the filling pressures are normalized. New data from evidence-based clinical trials and optimal strategies for monitoring fluid overload will help define this issue and ultimately reduce mortality in these patients.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Acute Disease
  • Adenosine A1 Receptor Antagonists
  • Diuretics / therapeutic use
  • Evidence-Based Medicine
  • Heart Failure / diagnosis*
  • Heart Failure / drug therapy*
  • Hospitals / standards
  • Humans
  • Medication Therapy Management
  • Patient Care Management / standards*
  • Practice Guidelines as Topic*
  • Renin-Angiotensin System / drug effects
  • Ultrafiltration
  • Vasodilator Agents / therapeutic use
  • Vasopressins / antagonists & inhibitors


  • Adenosine A1 Receptor Antagonists
  • Diuretics
  • Vasodilator Agents
  • Vasopressins