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Published on: October 11, 2011
Haemodynamic effects of altering arterial oxygen saturation in preterm infants with respiratory failure
J R Skinner1, S Hunter, C F Poets
1Department Paediatric Cardiology, Freeman Hospital, Newcastle upon Tyne. JSkinner@AHSL.co.nz
Insights
A small increase in blood oxygen levels (SaO2) in preterm infants with respiratory failure can cause significant ductal constriction. This constriction, not pulmonary vasodilation, primarily affects pulmonary arterial pressure and blood flow.
Area of Science:
- Neonatal Physiology
- Cardiovascular Research
- Respiratory Medicine
Background:
- Preterm infants often experience respiratory failure requiring respiratory support.
- Arterial oxygenation (SaO2) management is critical in neonates.
- The ductus arteriosus (DA) is a vital fetal blood vessel that typically closes after birth.
Purpose of the Study:
- To investigate the hemodynamic impact of short-term changes in arterial oxygenation in preterm infants with respiratory failure.
- To assess the effect of varying SaO2 levels on ductal patency and pulmonary arterial pressure.
Main Methods:
- Doppler echocardiography was used to assess hemodynamic parameters in 18 preterm infants.
- Measurements were taken at stable SaO2 levels of 86%, 96%, and 100%.
- Key parameters included ductal flow velocity, pulmonary arterial pressure indicators, and aortic flow integrals.
Main Results:
- Increasing SaO2 from 96% to 100% led to significant increases in peak ductal flow velocity in some infants with a patent ductus arteriosus (PDA).
- Ductal constriction was observed in four infants, associated with reduced aortic flow and increased aortic pressure.
- Pulmonary arterial pressure significantly decreased in seven infants as SaO2 increased from 86% to 100%.
Conclusions:
- Even brief increases in SaO2 within typical neonatal unit ranges can induce significant ductal constriction.
- The observed decrease in pulmonary arterial pressure at 100% SaO2 is primarily attributed to ductal constriction, not pulmonary vasodilation.
- These findings highlight the sensitivity of the ductus arteriosus to oxygen levels in preterm infants with respiratory compromise.
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.
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