Aim: To determine whether the use of a respiratory function monitor (RFM) during PPV of extremely preterm infants at birth, compared with no RFM, leads to an increase in percentage of inflations with an expiratory tidal volume (Vte) within a predefined target range. Methods: Unmasked, randomised clinical trial conducted October 2013 -May 2019 in 7 neonatal intensive care units in 6 countries. Very preterm infants (24-27 weeks of gestation) receiving PPV at birth were randomised to have a RFM screen visible or not. The primary outcome was the median proportion of inflations during manual PPV (face mask or intubated) within the target range (Vte 4-8 mL/kg). There were 42 other prespecified monitor measurements and clinical outcomes. Results: Among 288 infants randomised (median (IQR) gestational age 26 +2 (25 +3 -27 +1 ) weeks), a total number of 51,352 inflations were analysed. The median (IQR) percentage of inflations within the target range in the RFM visible group was 30.0 (18.0-42.2)% vs 30.2 (14.8-43.1)% in the RFM non-visible group (p = 0.721). There were no dierences in other respiratory function measurements, oxygen saturation, heart rate or FiO 2 . There were no dierences in clinical outcomes, except for the incidence of intraventricular haemorrhage (all grades) and/or cystic periventricular leukomalacia (visible RFM: 26.7% vs non-visible RFM: 39.0%; RR 0.71 (0.68-0.97); p = 0.028). Conclusion:In very preterm infants receiving PPV at birth, the use of a RFM, compared to no RFM as guidance for tidal volume delivery, did not increase the percentage of inflations in a predefined target range. Trial registration: Dutch Trial Register NTR4104, clinicaltrials.gov NCT03256578.

During oxygen therapy, preterm infants spent more time within the SpO target range after implementation of automated oxygen control, with a significant reduction in hyperoxaemia, but not hypoxaemia.

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Some neural circuits within infants are not fully developed at birth, especially in preterm infants. Therefore, it is unclear whether reflexes that affect breathing may or may not be activated during the neonatal stabilisation at birth. Both sensory reflexes (eg, tactile stimulation) and non-invasive ventilation (NIV) can promote spontaneous breathing at birth, but the application of NIV can also compromise breathing by inducing facial reflexes that inhibit spontaneous breathing. Applying an interface could provoke the trigeminocardiac reflex (TCR) by stimulating the trigeminal nerve resulting in apnoea and a reduction in heart rate. Similarly, airflow within the nasopharynx can elicit the TCR and/or laryngeal chemoreflex (LCR), resulting in glottal closure and ineffective ventilation, whereas providing pressure via inflations could stimulate multiple receptors that affect breathing. Stimulating the fast adapting pulmonary receptors may activate Head’s paradoxical reflex to stimulate spontaneous breathing. In contrast, stimulating the slow adapting pulmonary receptors or laryngeal receptors could induce the Hering-Breuer inflation reflex or LCR, respectively, and thereby inhibit spontaneous breathing. As clinicians are most often unaware that starting primary care might affect the breathing they intend to support, this narrative review summarises the currently available evidence on (vagally mediated) reflexes that might promote or inhibit spontaneous breathing at birth.

RationaleAntenatal inflammation, usually associated with chorioamnionitis, is a major cause of premature birth. As inflammation could depress respiratory drive, we have examined the effect of clinical chorioamnionitis (CCA) on spontaneous breathing in premature infants at birth.MethodsInfants with CCA born <30 weeks’ gestation were matched with control infants based on gestational age (±6 days), birth weight (±300 g), antenatal corticosteroids, sex and general anaesthesia. The primary outcome was breathing effort, assessed as minute volume (MV) of spontaneous breathing. We also measured tidal volume (Vt), respiratory rate (RR) and apnoea in the first 5 min and additional physiological parameters in the first 10 min after start of respiratory support.ResultsNinety-two infants were included (n=46 CCA infants vs n=46 controls; median (IQR) gestational age 26+4(25+0–27+6) vs 26+6(25+1–28+3) weeks). MV and Vt were significantly lower (MV: 43 (17–93) vs 70 (31–119) mL/kg/min, p=0.043; Vt: 2.6 (1.9–3.6) vs 2.9 (2.2–4.8) mL/kg/breath, p=0.046), whereas RR was similar in CCA infants compared with controls. Incidence of apnoea was higher (5 (2-6) vs 2 (1-4), p=0.002), and total duration of apnoea was longer (90 (21-139) vs 35 (12-98) s, p=0.025) in CCA infants. CCA infants took significantly longer to reach an oxygen saturation >80% (3:37 (2:10–4:29) vs 2:25 (1:06–3:52) min, p=0.016) and had a lower oxygen saturation at 5 min (77 (66–92) vs 91 (68–94) %, p=0.028), despite receiving more oxygen (62 (48-76) vs 54 (43-73) %, p=0.036).ConclusionCCA is associated with reduced breathing effort and oxygenation in premature infants at birth.