Saturday, September 29, 2012

Pathophysiology of Lower Extremity Edema in Acute Heart Failure Revisited.

Pathophysiology of Lower Extremity Edema in Acute Heart Failure Revisited.

Aug 2012


Department of Internal Medicine, University Hospital, Basel, Switzerland; Department of Renal Medicine, Royal Derby Hospital, Derby, United Kingdom; Department of Nephrology, University Hospital, Basel, Switzerland.



The pathophysiology and key determinants of lower extremity edema in patients with acute heart failure are poorly investigated.


We prospectively enrolled 279 unselected patients presenting to the Emergency Department with acute heart failure. Lower extremity edema was quantified at predefined locations. Left ventricular ejection fraction, central venous pressure quantifying right ventricular failure, biomarkers to quantify hemodynamic cardiac stress (B-type natriuretic peptide), and the activity of the arginine-vasopressin system (copeptin) also were recorded.


Lower extremity edema was present in 218 (78%) patients and limited to the ankle in 22%, reaching the lowerleg in 40%, reaching the upper leg in 11%, and was generalized (anasarca) in 3% of patients. Patients in the 4 strata according to the presence and extent of lower leg edema had comparable systolic blood pressure, left ventricular ejection fraction, central venous pressure, and B-type natriuretic peptide levels, as well as copeptin and glomerular filtration rate (P=NS for all). The duration of dyspnea preceding the presentation was longer in patients with more extensive edema(P=.006), while serum sodium (P=.02) and serum albumin (P=.03) was lower.


Central venous pressure, hemodynamic cardiac stress, left ventricular ejection fraction, and the activity of the arginine-vasopressin system do not seem to be key determinants of the presence or extent of lower extremity edemain acute heart failure.

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