Haemodynamic effects of altering arterial oxygen saturation in preterm infants with respiratory failure
a Department
Paediatric Cardiology,Freeman
Hospital,Newcastle upon Tyne, b Department
of Paediatric PulmonologyHannover Medical
SchoolGermany, c Newcastle Neonatal
ServiceRoyal Victoria
InfirmaryNewcastle upon Tyne, d Academic Department of
PaediatricsCity General
HospitalStoke on Trent, e Princess Mary Maternity
HospitalNewcastle upon Tyne
Correspondence to: Dr JR Skinner Department of Paediatric Cardiology Green Lane Hospital Green Lane West Auckland 3, New Zealand. email: JSkinner{at}AHSL.co.nz
Accepted 9 September 1998
AIMS
To examine the
haemodynamic effects of brief alteration in arterial oxygenation 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 100%
SaO2, achieved by altering the FIO2. Sixteen were receiving intermittent positive pressure ventilation, median FIO2 0.45 (0.20-0.65), median mean airway pressure 12 cm
H2O (0-20). SaO2 was stable for 15 minutes at
each stage. Four parameters of pulmonary arterial pressure were
measured: peak velocity of tricuspid regurgitation and peak velocity of
left to right ductal flow, TPV:RVET ratio and PEP:RVET ratio, measured
at the pulmonary valve, 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% SaO2, there were no consistent changes, but
in three of the 12 with a patent ductus arteriosus (PDA) there was
ductal constriction, with complete closure in one. Between 96% and
100% SaO2, peak ductal flow velocity rose significantly in
four of eight with a PDA. Ductal 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% SaO2 and pulmonary arterial
pressure fell significantly in seven.
CONCLUSION
A
brief rise in SaO2 within the range maintained by most
neonatal units can cause significant ductal constriction. The fall in
pulmonary arterial pressure with 100% SaO2 seen in most
infants was associated with a fall in pulmonary blood flow (or no
change), rather than a rise, indicating that the dominant haemodynamic effect was ductal constriction rather than pulmonary vasodilation.
© 1999 by Archives of Disease in Childhood
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