Article Text

  1. K A de Waal1,
  2. N Evans2,
  3. J H van der Lee3,
  4. A H van Kaam1
  1. 1Department of Neonatology, Emma Children’s Hospital AMC, Amsterdam, The Netherlands,
  2. 2Royal Prince Alfred Hospital, Newborn Care and University of Sydney, Sydney, NSW, Australia,
  3. 3Department of Pediatric Clinical Epidemiology, Emma Children’s Hospital AMC, Amsterdam, The Netherlands


Background: Alveolar recruitment and stabilisation with high mean airway pressures is considered an essential part of lung protective high-frequency ventilation (HFV). This study investigates the effect of these higher mean airway pressures on pulmonary, systemic and ductal blood flow in preterm infants with acute respiratory failure.

Methods: Preterm infants treated with primary HFV were subjected to an individualised recruitment procedure using oxygenation as an indirect marker for lung volume. First the continuous distending pressure (CDP) was stepwise increased until oxygenation no longer improved or the oxygen need was ⩽0.25 (open, CDPo). Next, the CDP was stepwise reduced until oxygenation deteriorated (closing, CDPc). After reopening the lung, the optimal CDP (CDPopt) was set 2 cmH2O above CDPc. Ultrasound measurements of right ventricular output (RVO), superior vena cava flow (SVC) and the ductus arteriosus were performed at the start of the recruitment (CDPs), at CDPo and at CDPopt.

Results: Thirty-four infants (median gestational age 28 weeks (26–29)) were measured at a postnatal age of 5 h (1–10). Starting at CDPs (8 cmH2O), RVO decreased significantly (−51 ml/kg per minute; 95% CI −73 to −29) at CDPo (20 cmH2O) and CDPopt (14 cmH2O). SVC flow remained stable during lung recruitment. The left-to-right ductus arteriosus flow decreased significantly (−30 ml/kg per minute; 95% CI −59 to −2) at CDPo, but normalised at CDPopt.

Conclusions: Optimising lung volume during HFV in preterm infants reduces RVO and left-to-right ductus arteriosus flow, but not SVC flow. The reduction in RVO is modest and most likely caused by an increase in right ventricular afterload.

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