Tracheal Gas Insufflation as an Adjunct to Conventional Ventilation

  • A. Nahum
  • J. J. Marini
Conference paper
Part of the Yearbook of Intensive Care and Emergency Medicine 1994 book series (YEARBOOK, volume 1994)


Improved understandig of the potential for ventilator-induced lung damage has inspired recent therapeutic innovations whose value currently remains unproven. It is now known that the manifestations of acute lung injury (ALI) are not homogeneously distributed [1, 2]. Only a fraction of the injured lung is accessible to inspired gas; in severe cases, no more than one third of all alveoli remain patent. Because ventilated lung units may be normally elastic and fragile, the apparent “stiffness” of the lung in ALI may be better explained by fewer functional alveoli than by a generalized increase in elastic recoil [1]. The small functional compartment that remains must receive the entire tidal volume (VT) and may therefore be subjected to overdistension, local hyperventilation, and inhibition of surfactant [3]. Injurious shear stresses may result from rapid inflation to high transalveolar pressures, especially at the junctions of structures that are mobile (aerated alveoli) with those that are immobile (collapsed or consolidated alveoli, conducting airways). In diverse animal models, transalveolar cycling pressures approximating those that normally correspond to total lung capacity (≈ 30 cm H2O) can diffusely injure normal alveoli over 15–60 min-periods; even lower pressures may damage normal lung tissues when sustained for several days [3, 4]. Conversely, failure to maintain a certain minimum lung volume in the setting of pre-existing ALI or an excessive inflation pressure may also produce or accentuate lung damage [2–4].


Acute Lung Injury Dead Space Conventional Ventilation Alveolar Pressure Permissive Hypercapnia 
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Copyright information

© Springer-Verlag Berlin Heidelberg 1994

Authors and Affiliations

  • A. Nahum
  • J. J. Marini

There are no affiliations available

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