Heart failure is a syndrome of cardiac dysfunction that, left untreated, results in the myocardium’s inability to maintain adequate cardiac output.¹ It may present as systolic and/or diastolic dysfunction. With progressive dysfunction, cardiac output is further diminished, resulting in impaired oxygen delivery to the body. As a result, many patients present to the pediatric intensive care unit or cardiac intensive care unit with signs and symptoms of cardiogenic shock (see Chapter 28).

The heart failure syndrome may result from several etiologies, including states of altered preload, afterload, contractility, and abnormal heart rate or rhythm.² The most common etiology of heart failure in children is secondary to congenital malformations and cardiomyopathies.³ Additional etiologies include arrhythmias, ischemia, toxins, or infections.²

In the setting of decreased cardiac output and decreased oxygen delivery to the kidney, the renin-angiotensin-aldosterone system is activated by the juxtaglomerular apparatus.¹ This adaptive response leads to increased sodium and water retention, thus increasing circulating blood volume. Initially, stroke volume is increased as a result of this increased volume by way of the Frank-Starling mechanism.¹ However, as volume overload develops, there is increased stretch of the ventricle, leading to decreased ejection fraction, increased wall stress, and increased myocardial oxygen consumption.⁴