Abstract

Beside reduction in tidal volume limiting peak airway pressure minimizes the risk for ventilator-associated-lung-injury in patients with acute respiratory distress syndrome. Pressure-controlled, time-cycled ventilation (PCV) enables the physician to keep airway pressures under strict limits by presetting inspiratory and expiratory pressures, and cycle times. PCV results in a square-waved airway pressure and a decelerating inspiratory gas flow holding the alveoli inflated for the preset time. Preset pressures and cycle times, and respiratory system mechanics affect alveolar and intrinsic positive end-expiratory (PEEPi) pressures, tidal volume, total minute, and alveolar ventilation. When compared with flow-controlled, time-cycled (‘volume-controlled’) ventilation, PCV results in reduced peak airway pressures, but higher mean airway. Homogeneity of regional peak alveolar pressure distribution within the lung is improved. However, no consistent data exist, showing PCV to improve patient outcome. During inverse ratio ventilation (IRV) elongation of inspiratory time increases mean airway pressure and enables full lung inflation, whereas shortening expiratory time causes incomplete lung emptying and increased PEEPi. Both mechanisms increase mean alveolar and transpulmonary pressures, and may thereby improve lung recruitment and gas exchange. However, when compared with conventional mechanical ventilation using an increased external PEEP to reach the same magnitude of total PEEP as that produced intrinsically by IRV, IRV has no advantage. Airway pressure release ventilation (APRV) provides a PCV-like squared pressure pattern by time-cycled switches between two continuous positive airway pressure levels, while allowing unrestricted spontaneous breathing in any ventilatory phase. Maintaining spontaneous breathing with APRV is associated with recruitment and improved ventilation of dependent lung areas, improved ventilation-perfusion matching, cardiac output, oxygenation, and oxygen delivery, whereas need for sedation, vasopressors, and inotropic agents and duration of ventilator support decreases.

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