Effect Of Changes In Ventilation On Arterial Carbon Dioxide Levels And Cerebral And Somatic Tissue Oxygenation In Infants Following Cardiopulmonary Bypass And Cardiac Surgery

  • Dr Marino Festa, Children's Hospital at Westmead, Australia
  • Dr Krista Mos, Erasmus MC, The Netherlands
  • Dr Stephanie Fijten, Erasmus MC, The Netherlands
  • Mr Andrew Cole, Children's Hospital at Westmead, Australia
  • A/Prof David Winlaw, Children's Hospital at Westmead, Australia

    • Objective: To study the change in cerebral and somatic tissue oxygenation (rSO2i) in response to alterations in minute volume ventilation and arterial carbon dioxide (PaCO2) concentration in infants following CPB and cardiac surgery.
    Method: Prospective randomised cross-over study in a tertiary cardiac centre, approved by the Local Research and Ethics Committee. Exclusion criteria included age >12 months, univentricular repair, need for extracorporal support and clinical evidence of seizures, focal neurology or raised intracranial pressure.
    Intervention: 50% increase / decrease in minute ventilation to alter PaCO2 levels within normal range at 1 hour and 18-hours post PICU admission.
    Main outcome measurements: Cerebral and Somatic rSO2i (NIRS). Secondary outcome measurements: Haemodynamic status (CI, SVRI, SVI, HR) and amplitude integrated electroencephalography (aEEG) monitoring.
    Results: Eleven infants undergoing biventricular repair of congenital heart lesions on CPB were studied. Mean age 3 months (range 1 – 8). Periods of hyper- and hypoventilation resulted in changed PaCO2 level (median 5.7 mmHg (range 0.6 – 17.0)) from baseline, but did not cause significant changes in overall CI or SVRI. Changes in PaCO2 were associated with significant and linear changes in cerebral but not somatic rSO2i in the 2nd hour and 18th hour after PICU admission. Blinded waveform analysis of aEEG recordings is awaited.
    Conclusion: Post-operative changes in minute ventilation and arterial PaCO2 result in changes in oxygenation in cerebral but not somatic tissues. Post-operative hyperventilation and low arterial PaCO2 is a potential cause of decreased cerebral tissue oxygenation in babies following CPB and biventricular repair.