Congestive heart failure in children

Abstract

H EART failure in the adult is a well-recognized symptom complex in which the hemodynamic alterations have been documented and the principles of treatment standardized. Heart failure in infants and children is less well recognized despite the fact that it is not uncommon among patients of the pediatric age group requiring hospitalization. In this age group the etiology and clinical manifestations are strikingly different from those in older children and adults and although the principles of treatment are the same, dosage and choice of drugs require special consideration because of the altered physiologic response of the young patient. These differences in the clinical manifestations and in the response to treatment have been noted by several observers,1-4 but documentation of this altered physiology utilizing hemodynamic techniques has not been reported. The study of heart failure in the young patient poses many problems including the modification of available techniques or the introduction of new ones, as well as the development of standards for the normal child. The function of the heart is to maintain adequate output of blood under all circumstances. In heart failure the. cardiac output, which may be decreased (low output failure), normal, or increased (high output failure), is inadequate to sustain normal body functions. The heart is failing when it is unable to increase its output in response to demand and when it is able to maintain its output only by increasing venous filling pressure.6 Heart failure results in inadequate delivery of oxygen to the tissues first during exercise and subsequently at rest. A number of homeostatic mechanisms directed toward increasing the delivery of oxygen to the tissues are available. These homeostatic mechanisms represent “cardiac reserve.” They include: (1) Heart rate and (2) stroke volume both of which affect cardiac output directly, (3) the ability of the tissues to extract larger amounts of oxygen from available blood as reflected by alterations in arteriovenous di$erence, (4) the transport of increased amounts of oxygen to the myocardium by alteration in coronary blood flow, and (5) cardiac hypertrophy. Most of the recognizable manifestations of heart failure are due to the homeostatic mechanisms attempting to restore cardiac output, rather than to a decrease in the output.