Changes in cerebral saturation profile in response to mechanical ventilation alterations in infants with bidirectional superior cavopulmonary connection.

OBJECTIVES

To document cerebral saturation in response to alterations in mechanical ventilation in infants with bidirectional superior cavopulmonary connection.

DESIGN

Prospective study.

SETTING

Pediatric cardiovascular intensive care unit.

PATIENTS: Children with functional single ventricle who have undergone bidirectional superior cavopulmonary connection.

INTERVENTIONS: We measured cerebral oxygenation using near-infrared spectroscopy in response to three ventilator interventions (change 50% from baseline): a) hyperventilation with increased tidal volume; b) hyperventilation with increased respiratory rate; and c) hypoventilation by decreased respiratory rate. Physiologic variables documented were cerebral oxygenation index (rSO2i), arterial pH, and PCO2.

MEASUREMENTS AND MAIN

RESULTS

Ten patients (eight males and two females) underwent placement of bidirectional superior cavopulmonary connection. There were no mortalities. The mean age was months 8.6 (+/-2.1) months. Hyperventilation (tidal volume increase) caused an increase in pH from 7.35 to 7.42 (p = .001), a decreased PCO2 from a baseline 45.9 to 33.9 mm Hg. (p = .002), a decrease in rSO2i from 64.4 to 52.0 (p < .001), and a decreased Po2 from 52.8 to 46.9 mm Hg (p = .008). Hyperventilation (respiratory rate increase) caused increased pH from 7.35 to 7.39 (p = .002), decreased PCO2 from a baseline 41 to 37 mm Hg. (p = .021), decreased rSO2i from 65.9 to 56.7 (p = .007), and decreased PO2 from 54.9 to 48.9 mm Hg (p = .006). Hypoventilation (respiratory rate decrease) did not change pH did not change from baseline 7.35. The PCO2 increased from 40.8 to 42, and the rSO2i increased from 64.0 to 68.6 (p = .004).

CONCLUSIONS

Hyperventilation can potentially cause a decrease in cerebral oxygenation and should be avoided in children with bidirectional superior cavopulmonary connection. Normoventilation and mild respiratory acidosis, however, preserve cerebral oxygenation in these patients.