Question 10

Outline the potential mechanisms of ventilator associated lung injury in patients with Acute Respiratory Distress Syndrome and the steps that can be taken to minimise them.

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College Answer

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






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.	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.









Oxygen toxicity	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)

Discussion

This question interrogates one's understanding of ARDS ventilation strategies.

Its difficult to add to the already comprehensive list of answers provided by the college.

Here is a good review article on ventilator-associated lung injury in general.

A more recent discussion is also available.

The combination of these two articles was the source of my own summary, which was supposed to trim the theoretical fat away, and leave behind dry factual bones... Pity it never turns out like that. I think the word count of this "summary" far exceeds the combined word count of both the publications.

References

Rocco PR, Dos Santos C, Pelosi P. Pathophysiology of ventilator-associated lung injury. Curr Opin Anaesthesiol. 2012 Apr;25(2):123-30

Caironi P et al, Lung opening and closing during ventilation of acute respiratory distress syndrome. Am J Respir Crit Care Med. 2010;181(6):578.

The Acute Respiratory Distress Syndrome Network.Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. N Engl J Med. 2000;342(18):1301.

Brower RG, Lanken PN, MacIntyre N, et al: Higher versus lower positive end-expiratory pressures in patients with the acute respiratory distress syndrome. N Engl J Med 351:327–336, 2004.

Pinhu, Liao, et al. "Ventilator-associated lung injury." The Lancet 361.9354 (2003): 332-340.

Tremblay, Lorraine N., and Arthur S. Slutsky. "Ventilator-induced lung injury: from the bench to the bedside." Applied Physiology in Intensive Care Medicine 1. Springer Berlin Heidelberg, 2012. 343-352.

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