Resp Care
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With a high-frequency percussive ventilator and a mechanical lung model, to measure tidal volume (V(T)), pulsatile pressure amplitude (difference between peak and nadir pulsatile pressure [DeltaP];), and mean airway pressure (P (aw)) at various pulsatile frequencies, pulsatile inspiratory-expiratory ratios (I:E(p)), and pressures (measured at the interface between the pulse-generator and the endotracheal tube [P(vent)]). ⋯ During high-frequency percussive ventilation, the pulsatile frequency is inversely related to V(T). Partial cuff deflation reduces the delivered F(IO(2)).
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High-frequency ventilation can be delivered with either oscillatory ventilation (HFOV) or jet ventilation (HFJV). Traditional clinician biases may limit the range of function of these important ventilation modes. We hypothesized that (1) the jet ventilator can be an accurate monitor of mean airway pressure (P (aw)) during HFOV, and (2) a mathematical relationship can be used to determine the positive end-expiratory pressure (PEEP) setting required for HFJV to reproduce the P (aw) of HFOV. ⋯ HFJV is an accurate monitor during HFOV. These measurements can be used to calculate the predicted PEEP necessary to match P (aw) on the 2 ventilators. Replicating the P (aw) with adequate PEEP on HFJV may help simplify transitioning between ventilators when clinically indicated.
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The time course of the physiological derangements that result from ventilator-induced lung injury has not been adequately described. Similarly, the regional topographies of pleural pressure and tissue edema have not been carefully mapped for this injury process. ⋯ Following the induction period, the development of ventilator-induced lung injury progressed steadily and then plateaued, as assessed by quantitative physiology variables during 6 hours of ventilation at a transpulmonary pressure of 35 cm H(2)O. Greater injury developed in animals that had a coexisting potential insult (thoracotomy). Injury development was not paralleled by bloodborne inflammatory cytokines.