Pulmonary artery blood flow patterns in fetuses with pulmonary outflow tract obstruction

Abstract

Objectives: Fetuses with pulmonary outflow tract obstruction (POTO) have altered blood flow to the pulmonary vasculature. We sought to determine whether pulmonary vascular impedance, as assessed by the pulsatility index (PI), is different in fetuses with POTO compared with normal controls.

Methods: Branch pulmonary artery PI was evaluated in age-matched normal control fetuses (n=22) and 20 POTO fetuses (pulmonary stenosis n=15, pulmonary atresia n=5). Pulsed-wave Doppler was performed in the proximal (PA1), mid (PA2) and distal (PA3) branch pulmonary artery. The direction of flow in the ductus arteriosus was noted. The study and control groups were compared with Student's t-test and ANOVA. A linear mixed model evaluated the relationship between PI and ductus arteriosus flow patterns.

Results: There was no difference in PI between control, pulmonary stenosis and pulmonary atresia subjects at PA1 and PA2; however, there was a significant difference at PA3. Subjects with pulmonary atresia had a lower PI at PA3 than did controls (P=0.003) and pulmonary stenosis subjects (P=0.003). Subjects with retrograde flow in the ductus arteriosus had lower PIs in PA2 and PA3 than did those with antegrade flow (P=0.01 and 0.005, respectively). The PI in PA3 was lower in fetuses that required prostaglandin postnatally than in those that did not (P=0.008).

Conclusions: Fetuses with pulmonary atresia or severe pulmonary stenosis with retrograde flow in the ductus arteriosus have decreased PI in the distal pulmonary vasculature. Our findings indicate the capacity of the fetal pulmonary vasculature to vasodilate in response to anatomical obstruction of flow.

Keywords: congenital heart disease; fetal echocardiography; pulmonary vascular resistance; pulsatility index.

Figure 1

Sites of pulmonary artery sampling in a) 2D and b) color Doppler echocardiography in a patient with tetralogy of Fallot and pulmonary stenosis. Sampling was performed in the right pulmonary artery.

Figure 1

Sites of pulmonary artery sampling in a) 2D and b) color Doppler echocardiography in a patient with tetralogy of Fallot and pulmonary stenosis. Sampling was performed in the right pulmonary artery.

Figure 2

Distal pulmonary artery Doppler flow patterns; a) Doppler pattern in a normal fetus (top panel) and a fetus with pulmonary stenosis that did not require prostaglandin or intervention in the neonatal period (bottom panel), demonstrating rapid systolic velocity acceleration and deceleration with a small amount of forward flow in diastole; b) Doppler pattern in a fetus with pulmonary atresia (top panel) and a fetus with pulmonary stenosis that required a neonatal intervention to improve pulmonary blood flow (bottom panel), demonstrating a broad, blunted systolic acceleration and deceleration with a moderate amount of forward flow in diastole.

Figure 3

Boxplots of pulsatility index for site PA3 in control, pulmonary stenosis and pulmonary atresia subjects demonstrating no significant overlap in the 25–75^th interquartile range when comparing the pulmonary atresia group to the pulmonary stenosis and control groups. Patients with pulmonary atresia had a lower pulsatility index in PA3 when compared to those with pulmonary stenosis (p =0.003) and controls (p= 0.003).

Figure 4

Boxplots of pulsatility index in PA3 in subjects that required prostaglandin (PGE1) postnatally and those that did not demonstrating no significant overlap in the 25–75^th percentile interquartile range when comparing the two groups. Subjects that required PGE1 in the postnatal period had a lower pulsatility index in PA3 as compared to subjects that did not require PGE1 (p= 0.0075).

Figure 4

Boxplots of pulsatility index in PA3 in subjects that required prostaglandin (PGE1) postnatally and those that did not demonstrating no significant overlap in the 25–75^th percentile interquartile range when comparing the two groups. Subjects that required PGE1 in the postnatal period had a lower pulsatility index in PA3 as compared to subjects that did not require PGE1 (p= 0.0075).