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MECHANICAL VENTILATION: IN SEARCH OF TRUE SURROGATE TO PREVENT VILI

 
From respirator lung to ventilator induced lung injury, we have travelled a long distance from the concept of barotrauma-volutrauma to stress-strain. Stress is defined as equal and opposite force developed in a material, when exposed to external force, while strain is change in the area or volume from baseline, brought about in this process. Stress-strain relationship is a function of material property, solid, viscous or viscoelastic.

Current strategy of mechanical ventilation as endorsed by ARDS net, is limiting the tidal volume and plateau airway pressure to 6 ml per kg of predicted body weight and 30 cmH2O.

Baby lung volume in ARDS is variable with severity of disease, worse is the ARDS, smaller is the baby lung. As baby lung has normal compliance, setting tidal volume according to predicted body weight, may be safe to unsafe depending upon baby lung volume.

Lung behaves like viscoelastic material, which makes pulmonary mechanics time dependent. For a constant tidal volume, stress (transpulmonary pressure) increases with respiratory rate. In other words, for a set tidal volume, transpulmonary pressure which is safe at lower respiratory rate, may become unsafe at higher respiratory rate, thus predisposing to VILI.

Thus, tidal volume per kg predicted body weight, is not a reliable surrogate of lung stress-strain and VILI.

As per the stress-strain relationship of human lung, a transpulmonary pressure of 17 cmH2O will inflate lung from functional residual capacity to total lung capacity, the limit of structural damage. As baby lung is physiologically normal, transpulmonary pressure of 17 cmH2O will increases its volume to the limit, irrespective of its volume. But in ARDS, alveolar heterogeneity acts as stress riser, multiplying global stress at regional level. Therefore, in ARDS, critical transpulmonary pressure to develop VILI would be lower than 17 cmH2O.

Therefore, Safe strategy of mechanical ventilation to prevent VILI in ARDS would be limitation of transpulmonary pressure (stress) to less than 17 cmH2O.

Driving pressure is recently proposed surrogate of transpulmonary pressure aimed at limitation of transpulmonary pressure. In quantitative terms, driving pressure is plateau pressure above PEEP.

Conceptually, driving pressure strategy differs from currently practiced ARDS net, so that driving pressure becomes the independent variable and tidal volume assumes the role of derived variable.
In a recently published study in NEJM, limiting driving pressure to less than 14 cmH2O predicted improved survival. Though driving pressure concept seems promising, it is still to be subjected to randomized controlled trials.

Precaution must be exercised in interpreting driving pressure in patients with reduced chest wall compliance. As driving pressure is the distending pressure of respiratory system, its relation to transpulmonary pressure is dependent upon chest wall compliance. If chest wall compliance is low, as in obesity, chest wall deformity or increased intraabdominal pressure, a higher driving pressure would be needed to achieve similar transpulmonary pressure, as in patient with normal chest wall compliance.

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