Physiology Guides You Best!

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Ventilating Smoothly: Physiology Guides You Best!
From：Peter M. Suter, MD
Since the discovery of the harmful effects of mechanical
ventilation (MV) on lung tissue and function
many years ago, a number of elements responsible for
these changes have been identified. Many investigations
into the mechanisms of so-called ventilator-induced lung
injury (VILI) have been performed in animal models or intensive
care unit (ICU) patients presenting with acute lung
injury (ALI) or acute respiratory distress syndrome
(ARDS). In these clinical situations, high tidal volumes
(Vt), increased inflation pressures, as well as low or zero
positive end-expiratory pressure (PEEP) levels were found
to be associated with more severe forms of VILI.1–4 In
contrast to MV in lungs with acute diseases such as ALI
and ARDS, ventilation of normal, healthy lungs during
anesthesia may cause less tissue injury and distant organ
dysfunction. Here, the occurrence, risk factors, and determinants
of lung damage of the VILI type are less well
examined. Although animal experiments in ex vivo isolated
“normal” lungs and in vivo situations have shown similar
types of damage to the parenchyma by MV and a preventive
effect of PEEP, much remains to be clarified. Indeed,
experimental conditions do not always reflect the physiologic
situation. Isolated lungs are partly collapsed and the
Vt used was sometimes markedly above the normal range,
2 factors known to enhance VILI. Clinical studies performed
in adults or children undergoing MV for anesthesia
and a surgical procedure have yielded conflicting results
with regard to the effects of Vt and PEEP on lung inflammation
and other signs of VILI.