Congestive Heart Failure in Infants and Children.

Abstract

Congestive heart failure (CHF) refers to a clinical state of systemic and pulmonary congestion resulting from inability of the heart to pump as much blood as required for the adequate metabolism of the body. The clinical picture of CHF results from a combination of “relatively low output” and compensatory responses to increase it. Excellent reviews on CHF in infants and children are available [1, 2]. This article provides core information on selected aspects of CHF. Broadly, heart failure results either from an excessive volume or pressure overload on normal myocardium (left to right shunts, aortic stenosis), or from primary myocardial abnormality (myocarditis, cardiomyopathy). Arrhythmias, pericardial diseases and combination of various factors can also result in CHF. The resultant decrease in cardiac output triggers a host of physiological responses aimed at restoring perfusion of the vital organs [3]. Important among these are renal retention of fluid, renin-angiotensin mediated vasoconstriction and sympathetic overactivity. Excessive fluid retention increases the cardiac output by increasing the end diastolic volume (preload), but also results in symptoms of pulmonary and systemic congestion. Vasoconstriction (increase in afterload) tends to maintain flow to vital organs, but it is disproportionately elevated in patients with CHF and increases myocardial work. Similarly, sympathetic over-activity results in increase in contractility, which also increases myocardial requirements. An understanding of the interplay of the four principal determinants of cardiac output – preload, afterload, contractility and heart rate is essential in optimising the therapy of CHF. It is clinically useful to consider CHF in different age groups separately.