BACKGROUND: The reduction of instrumental dead space is a recognized approach to preventing ventilation-induced lung injury in premature infants. However, there are no published data regarding the effectiveness of instrumental dead-space reduction in endotracheal tube (ETT) connectors. We tested the impact of the Y-piece/ETT connector pairs with reduced instrumental dead space on CO 2 elimination in a model of the premature neonate lung. METHODS: The standard ETT connector was compared with a low-dead-space ETT connector and with a standard connector equipped with an insert. We compared the setups by measuring the CO 2 elimination rate in an artificial lung ventilated via the connectors. The lung was connected to a ventilator via a standard circuit, a 2.5-mm ETT, and one of the connectors under investigation. The ventilator was run in volume-controlled continuous mandatory ventilation mode. RESULTS: The low-dead-space ETT connector/Y-piece and insert-equipped standard connector/Y-piece pairs had instrumental dead space reduced by 36 and 67%, respectively. With set tidal volumes (V T ) of 2.5, 5, and 10 mL, in comparison with the standard ETT connector, the low-dead-space connector reduced CO 2 elimination time by 4.5% (P < .05), 4.4% (P < .01), and 7.1% (not significant), respectively. The insert-equipped standard connector reduced CO 2 elimination time by 13.5, 25.1, and 16.1% (all P < .01). The low-dead-space connector increased inspiratory resistance by 17.8% (P < .01), 9.6% (P < .05), and 5.0% (not significant); the insert-equipped standard connector increased inspiratory resistance by 9.1, 8.4, and 5.9% (all not significant). The low-dead-space connector decreased expiratory resistance by 6.8% (P < .01) and 1.8% (not significant) and increased it by 1.4% (not significant); the insert-equipped standard connector decreased expiratory resistance by 1.5 and 1% and increased it by 1% (all not significant). The low-dead-space connector increased work of breathing by 4.7% (P < .01), 3.8% (P < .01), and 2.5% (not significant); the insert-equipped standard connector increased it by 0.8% (not significant), 2.5% (P < .01), and 2.8% (P < .
IntroductionVentilator-induced lung injury is considered an important causative factor in the pathophysiology of bronchopulmonary dysplasia (BPD) in premature infants. 1 Limiting ventilator-associated lung overdistention/damage is a well-recognized approach for the prevention of BPD, but Dr Ivanov is affiliated with the Section