title: Elevated intra-abdominal pressure in acute decompensated heart failure: a potential contributor to worsening renal function?
abstract: OBJECTIVE
  This study sought to determine whether changes in intra-abdominal pressure (IAP) with aggressive diuretic or vasodilator therapy are associated with improvement in renal function in acute decompensated heart failure (ADHF).
  
  
  BACKGROUND
  Elevated IAP (>or=8 mm Hg) is associated with intra-abdominal organ dysfunction. There is potential for ascites and visceral edema causing elevated IAP in patients with ADHF.
  
  
  METHODS
  Forty consecutive patients admitted to a specialized heart failure intensive care unit for management of ADHF with intensive medical therapy were studied. The IAP was measured using a simple transvesical technique at time of admission and before removal of the pulmonary artery catheter.
  
  
  RESULTS
  In our study cohort (mean age 59 +/- 13 years, mean left ventricular ejection fraction 19 +/- 9%, baseline serum creatinine 2.0 +/- 0.9 mg/dl), the mean baseline IAP was 8 +/- 4 mm Hg, with 24 (60%) patients having elevated IAP. Elevated IAP was associated with worse renal function (p = 0.009). Intensive medical therapy resulted in improvement in both hemodynamic measurements and IAP. A strong correlation (r = 0.77, p < 0.001) was observed between reduction in IAP and improved renal function in patients with baseline elevated IAP. However, changes in IAP or renal function did not correlate with changes in any hemodynamic variable.
  
  
  CONCLUSIONS
  Elevated IAP is prevalent in patients with ADHF and is associated with impaired renal function. In the setting of intensive medical therapy for ADHF, changes in IAP were better correlated with changes in renal function than any hemodynamic variable.
authors.affiliation: Section of Heart Failure and Cardiac Transplantation, the Cleveland Clinic, Cleveland, Ohio 44195, USA.
authors.forename: Wilfried
authors.initials: W
authors.lastname: Mullens
authors.forename: Zuheir
authors.initials: Z
authors.lastname: Abrahams
authors.forename: Hadi N
authors.initials: HN
authors.lastname: Skouri
authors.forename: Gary S
authors.initials: GS
authors.lastname: Francis
authors.forename: David O
authors.initials: DO
authors.lastname: Taylor
authors.forename: Randall C
authors.initials: RC
authors.lastname: Starling
authors.forename: Emil
authors.initials: E
authors.lastname: Paganini
authors.forename: W H Wilson
authors.initials: WH
authors.lastname: Tang
mesh_terms: D000005:Abdomen / Q000503:physiopathology*; D000208:Acute Disease; D000368:Aged; D003404:Creatinine / Q000097:blood; D004232:Diuretics / Q000627:therapeutic use*; D004359:Drug Therapy, Combination; D005260:Female; D006333:Heart Failure / Q000150:complications / Q000188:drug therapy / Q000503:physiopathology*; D006439:Hemodynamics / Q000187:drug effects; D006801:Humans; D007674:Kidney Diseases / Q000097:blood / Q000209:etiology*; D008297:Male; D008875:Middle Aged; D015588:Observer Variation; D011312:Pressure; D011446:Prospective Studies; D013318:Stroke Volume; D014665:Vasodilator Agents / Q000627:therapeutic use*
chemical_list: D004232:Diuretics; D014665:Vasodilator Agents; D003404:Creatinine