There is a growing body of evidence that implicates mechanical pulmonary ventilation (MV) at high peak airway pressures as the major contributing element that can transform a mild acute respiratory failure (ARF), into a severe respiratory failure with multiorgan system failure (MOSF), with a very high mortality. We have now shown in animal studies that evolution of the injury process is greatly dependent on the respiratory rate, and pressure settings. While we have reproduced pulmonary dysfunction at peak inspiratory pressures (PIP) as low as 30 cm H20, the injury process is greatly accelerated at frequencies above 8/min, and PIP near 50 cm H20. This poses a practical dilemma as current technology is not capable of providing mechanical ventilation without encroaching on those boundaries. We have now developed a novel approach to MV in which fresh air/oxygen is fed directly into the trachea through a small catheter, placed at the level of the carina. In this method (Intratracheal Pulmonary Ventilation - ITPV), using healthy sheep we were able to use tidal volumes as low as 10% of normal; the dead space in the frequency range under 20/min. was below zero, and at higher RR average 0.4 ml/kg. We have applied this technique to the management of lungs in which ARF was induced by MV and high PIP. When switched to ITPV at low PIP, the bulk of pulmonary ventilation was directed to the still normal remaining parts of the lungs. In parallel, the bulk of pulmonary blood flow on its own was directed to the same parts of the lungs, effecting good oxygenation, and control of C02. We believe ITPV is likely to impact pulmonary ventilation at all stages of current practice in MV.
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