Objective: We hypothesized that spontaneous inspiratory effort transmitted to the pleural space during airway pressure release ventilation would result in increased lung perfusion after surgery for tetralogy of Fallot or following a cavopulmonary shunt as a consequence of transient decreases in intrapleural pressure.
Design: Prospective crossover cohort study.
Setting: A tertiary care cardiac pediatric intensive care unit.
Patients: Children after tetralogy of Fallot repair, cavopulmonary shunt, or Fontan operation.
Interventions: Lung perfusion and cardiac output were measured during airway pressure release ventilation and pressure control ventilation with pressure support, both with and without spontaneous ventilation. Oxygen consumption was measured (mass spectrometer) and lung perfusion/cardiac output calculated (Fick equation). Constant levels of CO2 and mean airway pressure were targeted in all study phases.
Measurements and Main Results: Twenty patients were enrolled in the study, nine after repair of tetralogy of Fallot and 11 after a cavopulmonary shunt. In the absence of spontaneous ventilation, there were no differences in lung perfusion or any of the measured gas exchange or hemodynamic parameters. In the presence of spontaneous ventilation for all patients, mean pulmonary blood flow increased from 2.4 to 2.9 L·min−1M−2 (p = .02). Oxygen delivery increased from 594 to 774 mL/min/m2 (p = .05) in the patients with tetralogy of Fallot patients and from 473 to 518 L·min−1M−2 (p = .07) in the cavopulmonary shunt group.
Conclusion: Ventilation with airway pressure release ventilation (at comparable mean airway pressure) improves lung perfusion compared with pressure control ventilation in children after tetralogy of Fallot repair and cavopulmonary shunt operations. Although this study focused on tetralogy of Fallot and cavopulmonary shunt operations, the improved cardiopulmonary interactions may be beneficial in other situations in which hemodynamics are impaired by positive pressure ventilation.
From the Division of Cardiology (MAW, GLR, ANR), Labatt Family Heart Centre, Cardiovascular Surgery (CAC, GSVA), and the Departments of Paediatrics (MAW, GLR, ANR), Cardiovascular Surgery (CAC, GSVA), Anesthesia (MM, PJ, VJ, TT, SJ, BPK), and Critical Care Medicine (MM, PJ, VJ, TT, SJ, BPK), The Hospital for Sick Children and The University of Toronto, Toronto, Canada.
Dr. Van Arsdell holds equity interest in Boston Scientific, Cellaegis, and Medtronic. The remaining authors have not disclosed any potential conflicts of interest.
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