Jr. Skinner et al., Haemodynamic effects of altering arterial oxygen saturation in preterm infants with respiratory failure, ARCH DIS CH, 80(2), 1999, pp. F81-F87
Aims-To examine the haemodynamic effects of brief alteration in arterial ox
ygenation in preterm infants with respiratory failure.
Methods-Eighteen preterm infants with respiratory failure, aged 9-76 hours,
underwent detailed Doppler echocardiographic assessment at 86%, 96%, and 1
00% SaO(2),, achieved by altering the FIO2. Sixteen were receiving intermit
tent positive pressure ventilation, median FIO2, 0.45 (0.20-0.65), median m
ean airway pressure 12 cm H2O (0-20). SaO(2) was stable for 15 minutes at e
ach stage. Four parameters of pulmonary arterial pressure were measured: pe
ak velocity of tricuspid regurgitation and peak velocity of left to right d
uctal flow, TPV:RVET ratio and PEP:RVET ratio, measured at the pulmonary va
lve, along with flow velocity integrals at the aortic and pulmonary valves,
and systemic arterial pressure. Ductal size was graded into closed, small,
moderate, large with imaging, pulsed and continuous wave Doppler.
Results-Between 86% and 96% SaO(2), there were no consistent changes, but i
n three of the 12 with a patent ductus arteriosus (PDA) there was ductal co
nstriction, with complete closure in one. Between 96% and 100% SaO(2), peak
ductal flow velocity rose significantly in four of eight with a PDA. Ducta
l constriction occurred in four infants; in three this was associated with
a significant fall in aortic flow integral and a rise in aortic pressure (4
-6 mm Hg). Overall, 11 infants went from 86% to 100% SaO(2) and pulmonary a
rterial pressure fell significantly in seven.
Conclusion-A brief rise in SaO(2), within the range maintained by most neon
atal units can cause significant ductal constriction. The fall in pulmonary
arterial pressure with 100% SaO(2) seen in most infants was associated wit
h a fall in pulmonary blood flow (or no change), rather than a rise, indica
ting that the dominant haemodynamic effect was ductal constriction rather t
han pulmonary vasodilation.