Increased right ventricular power and ductal characteristic impedance underpin higher pulmonary arterial blood flow after betamethasone therapy in fetal lambs.

BACKGROUND: The glucocorticosteroid betamethasone is routinely administered prior to anticipated preterm birth to enhance lung maturation. While betamethasone also increases fetal pulmonary blood flow and reduces pulmonary vascular resistance (PVR), we investigated whether alterations in right ventricular (RV) function and ductal characteristic impedance (Zc ) additionally contributed to rises in pulmonary flow.

METHODS: Anesthetized preterm fetal lambs with (n = 10) or without (n = 8) betamethasone pretreatment were instrumented with a pulmonary trunk micromanometer and ductus arteriosus and left pulmonary artery (PA) flow probes to calculate Zc , and obtain RV output and hydraulic power.

RESULTS: Betamethasone (1) increased systolic and pulse arterial pressures (P ≤ 0.04), heart rate (P = 0.02), and lowered PVR (P = 0.04), (2) increased mean (P = 0.008) and systolic (P = 0.004), but not diastolic PA flow or PA Zc , (3) increased ductal Zc (P < 0.05), but not ductal flow, (4) increased RV output (P = 0.03) and the proportion of PT flow distributed to the lungs (P = 0.02), and (5) increased RV power (P ≤ 0.002).

CONCLUSION: An increased fetal PA blood flow after betamethasone therapy was confined to the systole and underpinned not only by decreased PVR, but also greater RV power and preferential distribution of an augmented RV systolic outflow to the lungs due to higher ductal Zc .