American journal of respiratory and critical care medicine
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Am. J. Respir. Crit. Care Med. · May 1994
Tidal ventilation at low airway pressures can augment lung injury.
Intermittent positive pressure ventilation with large tidal volumes and high peak airway pressures can result in pulmonary barotrauma. In the present study, we examined the hypothesis that ventilation at very low lung volumes can also worsen lung injury by repeated opening and closing of airway and alveolar duct units as ventilation occurs from below to above the infection point (Pinf) as determined from the inspiratory pressure-volume curve. We ventilated isolated, nonperfused, lavaged rat lungs with physiologic tidal volumes (5 to 6 ml/kg) at different end-expiratory pressures (above and below Pinf) and studied the effect on compliance and lung injury. ⋯ The group ventilated without PEEP had significantly greater respiratory and membranous injury to bronchioles, while the group ventilated with PEEP of 4 cm H2O had significantly greater alveolar duct injury. In conclusion, ventilation at lung volumes below those found at Pinf caused a significant decrease in lung compliance and progression of lung injury. Therefore, in addition to high airway pressures, end-expiratory lung volume is an important determinant of the degree and site of lung injury during positive-pressure ventilation.
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Am. J. Respir. Crit. Care Med. · May 1994
Effects of PEEP on VA/Q mismatching in ventilated patients with chronic airflow obstruction.
Recent work in patients with acute respiratory failure (ARF) due to exacerbation of chronic airflow obstruction (CAO) suggests that application of low degrees of positive end-expiratory pressure (PEEP) can improve rather than impair respiratory mechanics, because PEEP replaces intrinsic PEEP (PEEPi). However, the impact of PEEP on pulmonary gas exchange has not been fully investigated. ⋯ Respiratory mechanics, hemodynamics, respiratory blood gases, and VA/Q distributions were measured during each ventilatory mode. At low values of PEEP (PEEP-50%) no changes in respiratory mechanics nor in hemodynamics were observed, but PaO2 moderately increased (from 103 +/- 25.2 to 112 +/- 29.6 mm Hg) and PaCO2 slightly decreased (from 42 +/- 3.7 to 40 +/- 3.3 mm Hg) essentially because of an increase in the mean VA/Q ratio (first moment) of both flood flow (Q, from 0.65 +/- 0.28 to 0.78 +/- 0.29) and ventilation (V, from 4.02 +/- 1.55 to 4.93 +/- 2.00) distributions (p < 0.05, each).(ABSTRACT TRUNCATED AT 250 WORDS)
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Am. J. Respir. Crit. Care Med. · Mar 1994
Ventilatory responses during wakefulness in children with obstructive sleep apnea.
The pathophysiology of the obstructive sleep apnea syndrome (OSAS) is not fully understood. In children, airway obstruction secondary to tonsilloadenoidal hypertrophy is the leading cause of OSAS. However, not all children with tonsilloadenoidal hypertrophy develop OSAS. ⋯ There was a weak inverse correlation between the slope of the hypercapnic ventilatory response and the duration of hypoventilation during polysomnography (r = -0.44, p < 0.05). We conclude that children with OSAS have normal ventilatory responses to hypercapnia, and they may have normal ventilatory responses to hypoxia. We speculate that abnormal central ventilatory drive plays little if any role in the pathogenesis of pediatric OSAS.(ABSTRACT TRUNCATED AT 250 WORDS)