Fetal right ventricular myocardial function is better preserved by fibrillatory arrest during fetal cardiac bypass

Protection and preservation of fetal myocardial function are important for successful fetal intracardiac repair. Our objective was to determine fetal biventricular cardiac performance after two cardiac-arrest techniques.

Three groups of midterm ovine fetuses underwent 90-minute bypass. A control group (no arrest shams, n = 3), and two groups that included 20 minutes of arrest, using fibrillatory (n = 3) or blood cardioplegia (n = 3), were compared. Blood cardioplegia consisted of 4:1 cold blood to crystalloid solution induction every 10 minutes, followed by a warm shot terminal dose before clamp removal. Myocardial function variables from biventricular intracardiac pressure catheters, and 3-axes cardiac sonomicrometry, fetal hemodynamics, and arterial blood gases were continuously recorded. Fetal myocardium was collected for troponin-I analysis at 90 minutes. Statistical analysis was by two-way analysis of variance for repeated measures.

Compared with sham, right ventricular myocardial contractility was reduced with plegia but not fibrillation at 90 minutes after arrest: dP/dt max (511 ± 347 vs 1208 ± 239, p < 0.01) and preload-recruitable stroke work (7.2 ± 8.5 vs 32.3 ± 14.6, p < 0.01). Right ventricular end diastolic pressure-volume relationship (ventricular stiffness) worsened by 90 minutes for plegia vs fibrillation (0.84 ± 0.18 vs 0.25 ± 0.16, p < 0.05). There were no differences in left ventricle performance between groups. Fetal heart rate increased in shams by 30 minutes after arrest compared with both arrest groups (p < 0.05). Right ventricular troponin-I degradation increased with plegia, but not fibrillation, compared with sham (p < 0.05).

In vivo, fetal right ventricular contractile function deteriorates with a common blood-plegia regimen. Fibrillatory arrest better preserves right ventricular function, the dominant ventricle in fetal life, for short arrest periods.