During the past decade a serious and often irreversible syndrome has been recognized with increasing frequency in patients with long-standing congestive heart failure. Clinically these patients are characterized by extensive disease of the heart, prolonged histories of recurrent episodes of circulatory failure, and intractable edema. Chemically they present considerable reductions in the serum sodium and chloride concentrations and signs of increasing renal failure. Admission to the hospital is generally prompted by increasing edema and fastness to mercurial diuretics.
The precise mechanism whereby prolonged congestive heart failure terminates in this therapeutic paradox remains obscure. The past 10 to 15 years have been noteworthy for the development of several concepts in the management of congestive heart failure. These therapeutic usages have appreciably prolonged the life of the cardiac patient. This very prolongation, however, by exposing tissues to the sequellae of perpetuated ischemia and anoxia, may have rendered these tissues subject to alterations
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