30 Congestive Heart Failure in the Fetus
I. INTRODUCTION
1. Fetal echocardiography can now diagnose many forms of congenital heart disease and assess the prognosis of cardiac lesions based on their anatomy and presentation in utero.
2. However, the presence of signs of fetal heart failure, such as hydrops or valvar regurgitation, makes the assessment of prognosis more difficult.
3. A tool for this assessment is the cardiovascular profile score, which combines ultrasonic markers of fetal cardiovascular unwellness based on univariate parameters that have been correlated with perinatal mortality.
4. This profile could then become the heart failure score and could potentially be used in much the same way as, and in combination with, the biophysical profile score.
5. This chapter presents a straightforward method for rapid evaluation of the fetus with possible fetal congestive heart failure (CHF).
II. FETAL CIRCULATION AND HEART FAILURE
1. Fetal ventricles pump blood in parallel rather than in series.
2. Three shunts (ductus venosus, foramen ovale, and ductus arteriosus) allow the fetal heart to work with two parallel rather than one series circulation.
3. The left ventricle (LV) pumps to the aorta and upper body, and the right ventricle (RV) pumps to the ductus arteriosus and the lower body and placenta.
4. The lungs have a high resistance in utero, and the placenta fulfills the role of oxygenating the blood and ridding the body of wastes.
5. Highly oxygenated blood from the placenta passes to the ductus venosus, where a portion bypasses the liver and passes predominantly to the left atrium (LA).
6. Deoxygenated blood from the upper body passes to the tricuspid valve and then to the ductus arteriosus and lungs.
7. Deoxygenated blood from the inferior vena cava (VC) and the right hepatic veins is directed to the right atrium (RA) and predominantly to the tricuspid valve.
8. The IVC connects directly to the foramen ovale and the superior portion of the atrial septum, the crista dividens, which overlies the IVC, effectively dividing it into two streams.
9. Right and left atrial pressures are almost equal because of the presence of the foramen ovale, and right and left ventricular pressures are equal due to the ductus arteriosus.
III. FACTORS AFFECTING PERINATAL CARDIAC OUTPUT
1. Fetal myocardium develops less active tension than the adult’s at similar muscle lengths. Structural differences, such as less T-tubular system and fewer organized myofibrils, are observed, but there are also differences in calcium uptake into the sarcoplasmic reticulum.
2. Decreased sympathetic innervation in the immature myocardium could influence the stress response of the myocardium.
3. Fetal myocytes are smaller, have fewer mitochondria, smaller sarcoplasmic reticulum, fewer myofilaments, fewer α- and β-adrenoceptors, fewer T-tubules, and higher concentrations of DNA, reflecting a larger number of nuclei.
4. Growth or increased work load in the fetus results in hyperplasia of the myocardium, with an increased number of cells. In contrast, after birth, the myocardium increases only by increased cell size or hypertrophy (increased protein content of each cell).
5. In the very immature heart, myofilaments are arranged in a more chaotic way, but they become better organized as gestation advances.
6. The metabolic source of energy for the fetal myocardium is glucose almost exclusively. In adults, fatty acids are the major source of energy for the myocardium.
7. The fetus has a range of heart rates between 50 and 200, at which the stroke volume of the ventricular chambers can adapt to maintain adequate combined ventricular output (CVO) and tissue perfusion. Outside of this range, heart failure will often result.
8. In summary, the major determinant of cardiac output is the afterload of the fetal ventricle. Any influence that raises the impedance to ejection will inversely lower the ventricular stroke volume by the effect on both the systolic and diastolic function of the heart.
V. ETIOLOGY
A. Hydrops fetalis
1. All of these factors contribute to decreased cardiac reserve in response to stress and to a higher susceptibility of the fetus to cardiac failure:
a. The reduced ability of the fetal heart to contract and to generate force.
b. The lower myocardial compliance and the diminished Starling mechanism.
c. The higher dependence of cardiac output on heart rate.
2. All of these factors favor fluid movement out of the capillary into tissue, causing fluid accumulation in fetal tissue:
a. The younger the fetus, the higher its extracellular water content and the lower its tissue pressure.
b. Fluid movement between intravascular and extravascular space is dependent on intra- and extravascular hydrostatic and oncotic pressure and the fluid filtration coefficient.
3. Faced with a fetus with hydrops fetalis, one must first determine if the hydrops is cardiac, inflammatory, or metabolic. There are several possibilities for the cause of heart failure in the fetus after ruling out fetal infection.
