Haemodynamic effects of altering arterial oxygen saturation in preterm infants with respiratory failure
- Jonathan R Skinnera,
- Stewart Huntera,
- Christian F Poetsb,
- David W A Milliganc,
- David Southalld,
- Edmund N Heye
- aDepartment Paediatric Cardiology,Freeman Hospital,Newcastle upon Tyne, bDepartment of Paediatric PulmonologyHannover Medical SchoolGermany, cNewcastle Neonatal ServiceRoyal Victoria InfirmaryNewcastle upon Tyne, dAcademic Department of PaediatricsCity General HospitalStoke on Trent, ePrincess Mary Maternity HospitalNewcastle upon Tyne
- 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
Abstract
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.
