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Air trapping and alveolar hyperinflation may occur during mechanical ventilation in the presence of severe airway obstruction, during fast ventilator rates, and when expiratory time is compromised. Inadvertent positive end-expiratory pressure may occur with air trapping and increased mean airway pressure. The pulmonary artery pressure response to air trapping, produced during volume-regulated time-cycled ventilation, was studied in neonatal lamb lungs, isolated in situ, and perfused at a constant flow rate (50-75 ml.kg-1.min-1), both before and after Ca2(+)-channel blockade with verapamil (5 mg). The hub of the endotracheal tube was narrowed to a 1.5-mm orifice to produce fixed proximal airway obstruction. Air trapping was then produced by lengthening inspiratory time from 25 to 80%, at zero end-expiratory pressure. The magnitude of inadvertent positive end-expiratory pressure due to air trapping was estimated by end-expiratory occlusion pressure. End-expiratory occlusion pressure was 0.20 +/- 0.03 kPa (1.7 +/- 0.2 mm Hg) and 1.60 +/- 0.01 kPa (11.8 +/- 1.0 mm Hg), at 25 and 80% inspiratory times, respectively. On lengthening inspiratory time, mean pulmonary artery pressure (mPpa) increased briskly within 30 s followed by a gradual increase over the next 4 min. Verapamil blunted both the brisk and the gradual increase in mPpa on lengthening inspiratory time. Lengthening inspiratory time increased the mPpa by 2.0 +/- 0.1 kPa (14.7 +/- 0.8 mm Hg) from baseline, and verapamil reduced this increase to 1.3 +/- 0.1 kPa (10.1 +/- 0.6 mm Hg; p less than 0.05 by analysis of variance).(ABSTRACT TRUNCATED AT 250 WORDS)

Air Trapping Causes a Ca2+-Channel-Mediated Increase in Pulmonary Vascular Resistance in Neonatal Lambs