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"Positive ventilation....not always positive


Injury
Mechanism
Minimisation Strategy
Volutrauma
Non-homogenous lung injury
Over-distension of normal alveolar units to trans- pulmonary pressures above ~30 cm H2O (that corresponds to approximate total lung volume) causes basement membrane stretch and stress on intracellular junctions.
Avoid over-distending the “baby lung” of ARDS:
(a) Maintain Plateau Airway pressure under 30 cm H20
(b) Use Tidal volumes 6ml/kg (4- 8ml/kg)
Good evidence to support this strategy (ARDSNet)
Barotrauma
Increasing the trans-pulmonary pressures above 50 cm H2O will cause disruption of the basement membranes with classical barotrauma
Biotrauma
Mechanotransduction and tissue disruption leads to upregulation and release of chemokines and cytokines with subsequent WBC attraction and activation resulting in pulmonary and systemic inflammatory response and multi-organ dysfunction
Protective lung ventilation strategies
?Use of neuromuscular blockers may ameliorate
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Recruitment / Derecruitment Injury
The weight of the oedematous lung in ARDS contributes to collapse of the dependant portions of the lung
Repetitive opening and closing of these alveoli with tidal ventilation will contribute to lung injury.
page19image14900
Consider recruiting collapsed lung +/- employing an open lung ventilation strategy.
This may be achieved by:
(a) Ventilation strategies: Sigh / APRV / “Higher PEEP”
(b) A recruitment manoeuvres: e.g. CPAP 40/40, or stepwise PCV
(c) Prone Positioning (gravitational recruitment manoeuvre)
Good theoretical support and case series / few trials inconclusive outcomes
Shearing injury
This occurs at junction of the collapsed lung and ventilated lung. The ventilated alveoli move against the relatively fixed collapsed lung with high shearing force and subsequent injury.
page19image19132
Oxygen toxicity
page19image19680
Higher than necessary FiO2 overcomes the ability of the cells to deal with free oxygen free radicals and leads to oxygen related free radical related lung injury.
High FiO2 may contribute to collapse through absorption atelectasis.
Limit FiO2 through the use of recruitment, higher PEEP and accepting SaO2 / PaO2 that correspond the the “shoulder” of the oxyhaemoglobin dissociation curve (SaO2 88-94)

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