Ventricular constraint in the fetus and newborn

Birth is accompanied by a series of rapid adaptations of the cardiovascular system, one of the most notable being a doubling of left ventricular (LV) stroke volume. What makes this increase in LV stroke volume remarkable is that before birth the heart functions at a maximal level that cannot easily be increased with acute interventions such as volume infusion. Although changes in heart rate, contractility and afterload contribute to the adaptations of birth they do not adequately explain the doubling of LV stroke volume. Early studies obscured the role that ventricular preload plays in controlling fetal and newborn cardiac function by focusing on these other mechanisms and by failing to appreciate fully the significance of ventricular constraint in limiting heart function. Recent evidence suggests that ventricular constraint, arising from the tissues that surround the heart (chest wall, lungs and pericardium), limits fetal ventricular preload and thus determines the limits of fetal cardiac function. Relief of this constraint at birth, with aeration of the lungs and clearance of the lung liquid associated with the fetal lungs, may be the key mechanism that increases LV preload and thus increases LV stroke volume in the newborn.