Digitalis and Intractable Heart Failure

Judicious digitalis therapy still remains the most important factor in the management of con- gestive heart failure at all its stages.Digitalis acts directly on the heart muscle, increasing the output of the failing heart in the presence of congestion, thereby restoring cardiac compensation (Harvey et al., 1949).As a result, therapeutic doses slow the pulse.Dosage required for adequate digi- talization cannot be predicted with certainty, although body weight may be a guide (Eggleston, 1915).Therapeutic trial alone may indicate if digitalis is likely to be beneficial.Moreover, experience shows that digitalis requirements may vary from time to time during the course of congestive heart failure: any procedure that helps to determine these for patients requiring urgent help is a significant therapeutic advance, as it provides a basis for rational therapy.We have used the digitalis tolerance test (Lown and Levine, 1955) in assessing the digitalis requirements of nine cases of intractable congestive heart failure.Therapy based on the results benefited the patients, and allowed us to make certain deductions, which we believe to be important, about the nature of disturbances of rhythm occurring in congestive failure and their management.It may be opportune at this stage to examine some of the important factors that play a role in the evolution of intractable congestive failure in so far as they affect digitalis therapy.A profound relationship exists between potassium metabolism and digitalis toxicity (Lown et al., 1951) with regard to the action of the drug on isolated groups of cardiac cells producing ectopic foci.Deple- tion of myocardial potassium sensitizes the heart to digitalis, so narrowing the margin between its therapeutic and toxic action.Potassium loss may render a therapeutic dose a toxic dose.During the development of congestive failure, total body potassium is reduced (Burrows and Sisson, 1950).A negative potassium balance is also favoured by nutritional problems in advanced congestive failurepoor appetite, monotonous diets, nausea, impaired absorption, and deranged liver function.Per- haps most important of all, therapeutic measures aimed at reducing the work of the heart may be responsible for substantial potassium loss, e.g.rigid salt restriction and administration of ammonium chloride during mercurial diuresis (Lesser et al., 1952).In addition diamox (Berliner et al., 1951), steroid hormones (Lown et al., 1951), ion exchange resins, and mechanical fluid drainage (paracentesis, acupuncture) deplete body stores of potassium.It would appear that the above factors play an important part in the evolution of intractable congestive failure as they may adversely modify the response of the heart to digitalis.In this connection also special reference must be made to coronary arterial disease.There is experimental evidence to show that myocardial ischmnia is associated with loss of intracellular myocardial potassium (Dennis and Moore, 1938).The pro- gressive loss of myocardial potassium associated with advancing coronary disease may help to explain the changing sensitivity of the heart to digitalis.Toxic doses of digitalis may also deplete the myocardial cells of potassium (Calhoun and Harrison, 1931) and potassium administration will abolish toxic arrhythmias caused by digitalis (Sampson et al., 1943).We have utilized the complex relationship between digitalis and potassium metabolism in the management of our cases.This paper is concerned with the particular problem of the digitalis status of patients admitted to hospital with intractable heart failure.Enquiry often reveals a long history of congestive failure, often for months or years, with varying response to digitalis and diuretic treatment.Frequently