Effect of inspiratory flow pattern and inspiratory to expiratory ratio on nonlinear elastic behavior in patients with acute lung injury.

Ventilatory modes employing different inspiratory flow patterns and inspiratory to expiratory ratios may alter lung strain in acute lung injury patients. To determine whether variations in lung strain existed between pressure-controlled, volume-controlled, and pressure-controlled inverse ratio modes of ventilation, we randomly applied each for 30 minutes in 18 acute lung injury patients, keeping tidal volume, respiratory rate, fractional inspired oxygen, and total positive end-expiratory pressure constant. After each mode, a multiple linear regression analysis of dynamic airway pressure and airflow was performed with a volume-dependent single compartment model of the equation of motion, and an index of nonlinear elastic behavior was calculated. In five additional patients, concurrent dynamic computerized axial tomography scanning at juxtadiaphragmatic and subcarinal levels was added. Although static mechanics, oxygenation, and hemodynamics were no different between pressure-controlled, volume-controlled, and pressure-controlled inverse ratio ventilation, we found significant differences in nonlinear behavior. This was least with pressure-controlled followed by volume-controlled ventilation, and pressure-controlled inverse ratio ventilation had the greatest nonlinear elastic behavior. Dynamic computerized axial tomography analysis revealed more overinflated units in the left subcarinal slice with pressure-controlled inverse ratio ventilation. Ventilator flow pattern and inspiratory to expiratory ratio independently influence lung strain in acute lung injury; however, further studies are needed to determine the biologic significance.

The effect of buprenorphine on the analgesic and respiratory depressant effects of pethidine: a preliminary study.

The effects on respiration and pain perception of giving 0.6 mg buprenorphine alone and of giving the same dose after the administration of pethidine intravenously to achieve a steady-state blood pethidine level (mean blood level 0.29-0.47 microgram/ml) were studied in 3 healthy male volunteers. Depression of ventilation occurred with both pethidine and buprenorphine, and the combination produced greater depression than did either drug alone. Times to onset of, and tolerance to, experimental pain increased with pethidine and buprenorphine, a greater increase occurring when both drugs were combined. There was no evidence that buprenorphine reversed the respiratory depression produced by pethidine, while maintaining analgesia.