Effect of rapid-rate ventilation on the experimental diseased lung caused by meconium aspiration.
We compared rapid-rate ventilation using a conventional ventilator with slow-rate ventilation in the normal lung of 7 newborn pigs and in the diseased lung model instilled with 25% meconium solution into the trachea. The flow rate (7.5 1/min) and inspiratory:expiratory ratio (1:3) were kept constant during the experiments by using a constant-flow and time-cycled ventilator; the only change in settings was the rate. Transthoracic electrical impedance at end-expiration increased in the normal and in the diseased lung. Both mean intratracheal pressure and end-expiratory esophageal pressure increased significantly (p less than 0.05) in both models upon changing to rapid-rate ventilation. Following the increase in ventilatory rates from an initial frequency of 37.5 breaths/min to a rapid rate of 150 breaths/min, there was a significant rise in both PaO2 and PaCO2 in the normal and diseased lung models. Although rapid-rate ventilation was maintained for 1 h, the improvement in oxygenation progressively deteriorated and PaCO2 also increased further. This rise in PaCO2 returned to the control levels by decreasing ventilation to the initial rate of 37.5/min. This study demonstrates that rapid-rate ventilation using a constant-flow and time-cycled ventilator is inferior to slow-rate ventilation in the diseased lung model.
D000818:Animals; D000831:Animals, Newborn / Q000502:physiology*; D002245:Carbon Dioxide / Q000097:blood; D004195:Disease Models, Animal; D004947:Esophagus; D007700:Kinetics; D008171:Lung Diseases / Q000209:etiology / Q000503:physiopathology / Q000628:therapy*; D008470:Meconium; D010100:Oxygen / Q000097:blood; D011312:Pressure; D012121:Respiration, Artificial / Q000379:methods*; D013552:Swine; D014132:Trachea
D002245:Carbon Dioxide; D010100:Oxygen