Pathogenesis of Cardiac OedemaBr Med J 1972; 1 doi: https://doi.org/10.1136/bmj.1.5794.222 (Published 22 January 1972) Cite this as: Br Med J 1972;1:222
- Jan Brod
When the heart ceases to meet the requirements of the body for oxygen, the sympathetic-adrenal system is activated. This occurs in people with a healthy heart when the demands for oxygen are excessive—for example, in heavy muscular work—and in subjects with a failing heart when the demands are normal or small. Eventually, when the heart is unable to meet even the ordinary requirements of everyday life, the sympathetic activity becomes more or less continuous. It may lessen during rest at night, but with a further failing of the heart its output may become inadequate even in complete rest.
The sympathetically-medicated renal vasoconstriction, with reduction of the glomerular sodium load, redistribution of the blood flow in the renal cortex to the juxtamedullary glomeruli, and the mobilization of the renin-angiotensin-aldosterone system, is responsible for the salt and water retention which will ultimately become clinically manifest as oedema—especially when it is no longer counteracted by the tidal output of water and sodium at night. A by-product of this continuing dehydration reaction is a cumulative potassium loss which may lead to disastrous consequences if untreated.
↵* Lecture at the First Conference of the European Association of Internal Medicine, held at the Royal College of Physicians, London, 13 May 1972.