Abstract

In this discussion of some of the points that have interested us in the correction of electrolyte deficits in cardiovascular-renal disease, we briefly reviewed the salt-losing syndrome in terminal nephritics and in hypertensives with advanced renal damage, and incidentally delved into the concepts of edema formation as we discussed its opposite mechanism. We found ourselves drawn into a discussion of potassium metabolism in the process, touching on the subject of "potassium losers." Next in the panorama of this multifaceted problem came the management of edematous patients who developed hyponatremia on the diuretic egimen (without losing their edema) or who became mercurial fast in "midstream"; i.e., after losing about half their edema. Under such dire circumstances, we showed how sodium chloride might be used to good advantage. The promising use of corticotropin (ACTH) in hopelessly resistant cases of cardiac edema or in near-terminal severe cases of myocardial insufficiency, with incidental correction of a coexisting hyponatremia (accomplished without the use of sodium supplements) was described. Finally, we discussed in detail our use mainly of hypotonic solutions of sodium salts in correcting concentration as well as pattern and volume disturbances of the extracellular fluid in cardiovascular-renal patients who develop serious gastrointestinal and surgical complications. We emphasized that in such patients we have obtained the best end results with mainly hypotonic and isotonic, rather than hypertonic salt solutions. With this form of electrolyte replacement therapy, we have seen more floating on water and less drowning in brine!

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