Abstract

“If you have always done it that way, it is probably wrong.” — Charles F. Kettering, 1876–1958 The morbidity of decompensated heart failure is due to volume overload, a consequence of increased total body sodium.1,2 Failure to adequately reduce total body sodium contributes to progressive ventricular dysfunction, worsening heart failure, and excess morbidity. Ultrafiltration is the gold standard for sodium-volume removal and is the only intervention shown to improve outcomes in a randomized controlled trial of patients hospitalized with decompensated heart failure.3 Diuretics are inherently inferior because they produce hypotonic urine4,5and undesirable hemodynamic and neurohormonal changes.6,7 Therefore, ultrafiltration is the preferred initial treatment for patients hospitalized with decompensated heart failure and sodium-volume overload. Response by Shin and Dec on p 499 The earliest descriptions of heart failure date back more than 3500 years to the Egyptian civilization. Even then, symptoms were correctly attributed to volume excess.8 It was not until the early 20th century that researchers recognized the role of salt in the formation of edema. In 1901, researchers found that salt fed to patients with congestive heart failure could not be recovered as chloride in the urine.8 This represents one of the earliest descriptions of heart failure as a sodium avid state. Later, it was demonstrated that liberal salt intake increased congestive symptoms and pulmonary edema in patients with heart failure whereas patients on salt-restricted diets could tolerate large amounts of water without any further increases in congestion or edema.8 Other studies confirmed the primary role of salt, not water, in the formation of edema in heart failure. By 1948, sodium was widely recognized as the major determinant in extracellular fluid volume.1 Today, it is understood that sodium retention in heart failure is under the influence of the sympathetic and …

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