Pleural and pericardial pressures limit fetal right ventricular output

The chest wall, lungs, and pericardium limit diastolic filling of the left ventricle in the fetus, neonate, and adult. To determine the effect that these tissues have on the fetal right ventricle (RV), we studied six fetal lambs (142 days of gestation)

Pregnant ewes were anesthetized (ketamine and alpha-chloralose), and the fetuses were partially delivered by cesarean section. Fetuses were instrumented to record RV stroke volume, RV end-diastolic pressure (Prved), intrapericardial pressure (Pip), and pleural pressure. Prved was varied between 2 and 20 mm Hg under three conditions: initially with a closed chest and a closed pericardium (CCCP); subsequently with an open chest (chest wall and lungs retracted) and a closed pericardium (OCCP); and finally after the chest wall, lungs, and pericardium were retracted (OCOP). At equal Prved, stroke volume increased substantially when the chest wall and lungs were retracted from the heart and increased further on subsequent retraction of the pericardium (eg, at Prved of 9 mm Hg, stroke volume increased from 1.2 +/- 0.2 mL [mean +/- SEM] in the CCCP condition to 2.9 +/- 0.4 and 4.2 +/- 0.3 mL in the OCCP and OCOP conditions, respectively, P < or = .05). The limitation of stroke volume in the CCCP and OCCP conditions occurred because Pip increased in an almost one-to-one fashion as Prved increased; as a consequence, RV preload (RV end-diastolic transmural pressure, Prved minus Pip) was relatively unchanged.

The chest wall-lung combination and the pericardium each significantly constrain the fetal RV and together limit RV stroke volume.