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
THERAPEUTIC OPTIONS FOR ACUTE HEART FAILURE
The goal of acute heart failure treatment is to maintain or restore adequate oxygen delivery to end organs. This may be accomplished by improving oxygen delivery (DO2) or decreasing oxygen consumption (VO2) by decreasing the metabolic demands of the patient.
INCREASING OXYGEN DELIVERY
This strategy is aimed at improving oxygen delivery to the tissues. It may be accomplished by augmenting preload, decreasing afterload, or augmenting cardiac contractility to improve cardiac output.2 Continuous infusions of catecholamines/catecholamine analogs (e.g., epinephrine, dopamine, or dobutamine) may be used for their beta-effects to increase cardiac contractility. However, these agents may increase myocardial oxygen consumption (VO2), resulting in myocardial cell apoptosis.2
Milrinone, a phosphodiaesterase-3 inhibitor, is increasingly being used after cardiac surgery and in cases of heart failure.5,6 It acts as an inodilator, resulting in improved myocardial contractility as well as pulmonary and systemic vasodilatory effects.2 This vasodilation results in decreased afterload to the right and left sides of the heart, leading to increased cardiac output. Additionally, it improves diastolic relaxation (lusitropy) of the myocardium through its enhanced reuptake of calcium. Each of these effects occurs without increasing myocardial oxygen consumption. In many cases of acute decompensated heart failure, milrinone is used in combination with an inotrope (e.g., epinephrine).
DECREASING OXYGEN CONSUMPTION
This strategy is aimed at decreasing the metabolic demands of the ...