Congestive Heart Failure in the Fetus

Published on 07/06/2015 by admin

Filed under Neonatal - Perinatal Medicine

Last modified 07/06/2015

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30 Congestive Heart Failure in the Fetus

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