RESISTANT CARDIAC FAILURE

RESISTANT CARDIAC FAILURE : SALT DEPLETION SYNDROME
While in the majority of patients with congestive cardiac failure there is a prompt and adequate response to the usual measures of rest, digitalis and diuretics, there is a proportion in whom these remedies lose their effect, in whom oedema persists or increases, in whom the response to individual doses of powerful diuretics is negligible, and who pass into a state of resistant cardiac failure. In some there is biochemical evidence of a profound upset of the blood and tissue electrolytes, the so-called " salt depletion syndrome " It was at one time believed that this refractory state was induced by the treatment, and that depletion of sodium and chloride was responsible for it as well as for some of the untoward accompanying symptoms. It is now clear that a complex mechanism is involved and that while depletion of sodium and chloride may occur this is rare and commonly sub-terminal. On the other hand potassium depletion is recognized as a common and often dominant feature.
In a patient under treatment with a standard regimen of digitalis and diuretics, successive doses of diuretics tend to produce progressively smaller responses as the total accumulation of salt and water in the tissue spaces is reduced; the net water output falls and with it the daily output of sodium and chloride. As the patient approaches his dry weight—that is his weight free from oedema—the increase in water, sodium and chloride output after each injection of a mercurial or oral dose of a sulphamyi diuretic may become negligible. Thus depletion of body stores of sodium and chloride seldom occurs from the action of diuretics, unless drastic salt deprivation has been imposed, or until the terminal stages of the illness are reached. On the other hand potassium excretion is increased as an integral part of the action of diuretics, and despite the decreased excretion of water and sodium referred to above, potassium excretion in response to each dose may remain high. This leads eventually to a state of profound potassium depletion which may readily escape detection, since un¬happily the serum potassium level does not reflect the tissue level and a normal blood potassium may be found when the cells are severely potassium-deficient. The potassium content of the cells becomes largely replaced by sodium, with serious effects on their metabolism and therefore on the body as a whole. The demonstration that such depletion of total body potassium has occurred may only be achieved by careful balance studies over a long period, during which the net daily intake and output of potassium are carefully measured. Such studies may reveal that the body avidly absorbs and retains potassium without a corresponding rise in the blood level, indicating diffusion of the absorbed potassium into the depleted cells.
In certain persons a low blood chloride and low blood sodium may be demonstrated—the so-called salt depletion syndrome. Such patients are ill, commonly nauseated, weak, drowsy or confused and the condition is attended by a rising blood urea and evidence of azotasmia, progressing it may be to ursemic coma. This perilous state of affairs may be aggravated in such a patient by any measure which drastically upsets the body equilibrium in respect of fluid and salt—for example, the withdrawal of a large quantity of fluid by abdominal or thoracic paracentesis. Even the use of Southey's tubes to drain subcutaneous oedema from the legs may result in a curious reaction on the part of the kidney, with active retention of ingested water leading to hydrsemia, the consequent dilution lowering the blood sodium and chloride levels. This fall in the levels of sodium and chloride, formerly attributed to excessive urinary losses, is now realized to be due to a bizarre and active water retention by the body in the later stages of heart failure. An example of such hyponatrsemia and hypochlorasmia is shown in Fig. 3 (p. 579). In this case, as in many similar ones, the patient died.

Management of " Resistant " Failure.—The successful management of
a patient with resistant cardiac failure is a difficult therapeutic problem. Before concluding that an individual patient is actually in this resistant phase, however, every care should be taken to ensure that the diagnosis is accurate and that a false impression of resistance has not been produced. Each case should be carefully reviewed to ensure that a cause of continuing failure is not still operative, undetected and untreated. For example, it may be that the patient is the victim of an active rheumatic carditis, or that he has a respiratory infection with toxaemia. A painless myocardial infarction which may have escaped notice may be the underlying cause, and there is a proportion of patients in whom undetected thyrotoxicosis may be operative having excluded such factors, the next step is to review critically the treatment which the patient has had. Many patients, resistant under home conditions, respond rapidly to a hospital regimen, and it is clear that the complete rest enforced under ward discipline is commonly a major factor in the changed status. Particular attention should also be paid to the dose of digitalis which the patient has been having, and it should be ascertained that he has actually taken the drug in the quantity prescribed and has not for one reason or another modified this dosage on his own initiative. Attention should also be paid to his intake of salt, since many patients reputedly on a salt-poor diet in fact take much more than is prescribed. Consumption of porridge made with salt, salt butter, certain proprietary fruit drinks and other articles of diet, may push the daily intake up to an undesirably high level. Lastly, in every resistant patient a check should be made of the blood levels of sodium, potassium and chloride to establish whether salt depletion is present, bearing in mind the caveat that the level of blood potassium is not always an accurate guide to its concentration in the cells.
The first few days of treatment should be devoted to securing complete rest, to adequate digitalization and to the restriction of salt in the diet to a maximum of 0-5 g. daily. After a few days during which the patient is stabilized on this regimen, and the response noted, diuretics should be given—mersalyl, thiazides, chlorthalidone, triamterene or frusemide in usual dosage (p. 577). If the resulting diuresis is unsatisfactory, adjuvant measures should be tried, e.g. the administration of ammonium chloride before the injection of mersalyl may lead to dramatic diuresis. Alternatively, the administration of theophylline, i g. intravenously in 10 ml. water an hour before 2 ml. of mersalyl is given intra¬muscularly may lead to a brisk diuresis.
It is in patients of this group that recourse may be had to the specific antagonist to aldosterone—a spironolactone. Aldactone-A, four times as potent as the original preparation, is given in 25 mg. doses together with a conventional diuretic. The drug is non-toxic and may induce a satisfactory diuresis in a patient otherwise resistant to mercurials or thiazides.
The crux of the matter in handling patients with resistant cardiac, failure is attention to detail—to strict rest, to digitalization, to salt restriction, to diuretic administration with such adjuvant therapy as outlined above. The truly resistant patient in whom cardiac failure defeats all attempts at treatment is generally in the terminal stage of his illness.