
Congestive heart failure, by reason of its frequency of occurrence and the distress and suffering entailed, remains the cardinal problem in cardiac thera¬peutics. Recent advances in our knowledge have brought better understanding of its genesis and of the causation of the oedema and dyspnoea which are two of its features. Its management, while still largely on traditional lines, has changed considerably in detail in recent years, particularly since the advent of new diuretic agents and the introduction of the refined digitalis glycosides. Yet it remains a condition difficult to treat effectively, and in which the results of treatment are extremely variable. Congestive cardiac failure, while commonly a terminal process, is not necessarily a precursor of early death. If relieved by treatment, it may resolve completely, and when a precipitating factor has been dealt with may not recur for many years, if ever ; but from the nature of things the failure may be irreversible: e.g. a grossly scarred heart muscle following repeated infarction's or rheumatic inflammation may have insufficient healthy contractile tissue to meet the needs of the body even at rest. Again the valve lesion may be of such severity that no muscle can cope with the burden. Such may be the case in aortic stenosis; when failure eventually occurs in patients with this lesion it may prove intractable and progresses to death within a few months. It is quite otherwise with mitral disease, in which repeated bouts of congestive failure may occur over a period of years, each possibly more severe and more resistant than the last, but with long intervening periods of reasonably good health. The general course is, however, downhill and leads eventually to a terminal state of intractable failure. At the other extreme, cardiac failure precipitated by a remediable cause such as thyrotoxicosis may be permanently abolished by efficient therapy. The importance of full and accurate diagnosis as stressed in the preamble is apparent.
The recognition of congestive heart failure presents no difficulty. The assessment of its severity may be less easy, but is of great importance, since it has a bearing on the urgency with which treatment is prosecuted. Congestive teardiac failure is seen in all grades, from a slight increase in the venous pressure in the neck with some enlargement and tenderness of the liver to the grossly water-logged patient, with sacral pad, gross hepatic enlargement, ascites, bilateral hydrothorax and accompanied by orthopnoea, insomnia and vomiting. It is important that the type of cardiac failure should be recognized, since not every patient with congestive failure has a low cardiac output. In patients with valvular disease, hypertension and ischaemic heart disease, failure with low output is the rule, but in other conditions, notably thyrotoxicosis and in some'patients with heart failure secondary to respiratory disease, the cardiac output is actually above normal despite the occurrence of oedema and other features of heart failure. It is important to recognize this high-output type since its management differs from that of conventional low-output failure.
Further in every patient presenting with cardiac! failure it is important that a search be made for a precipitating cause. For example, a patient known to have a valvular lesion with which he has lived in reasonable equilibrium for many years, probably with some restriction of activity but with little serious disability, develops gross congestive failure, it may be in the course of a day or two or dramatically in a few hours. The doctor must always ask himself what circum¬stance has determined this sudden deterioration. Commonly an intercurrent respiratory infection is responsible, and this may well escape detection unless specifically sought for, since the signs are obscured by those of failure. Pul¬monary infarction is another common cause, as is a relapse of rheumatic infection in the vounger age-group or the onset of an abnormal rhythm, particularly atrial fibrillation. In women of child-bearing age pregnancy is a recognized hazard to the cardiac patient. In older patients, particularly hypertensives, the sudden development of cardiac failure may have been determined by a myocardial infarction, often without pain and therefore easily overlooked, or by the occurrence of an abnormal rhythm, such as atrial fibrillation or paroxysmal tachycardia. Lastly, and especially in the older age-group, thyrotoxicosis as a cause of unexplained failure must be kept in mind. The diagnosis of such hyperthy-roidism is not always obvious, since in elderly patients the conventional eye signs and nervousness may be minimal. Clearly the detection of a precipitating cause which can be dealt with while the congestive failure is being treated has an important bearing on the eventual outcome.
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