Title: Ventilatorassociated Lung Injury
1Ventilator-associated Lung Injury
2Complications of Mechanical Ventilator
- Barotrauma
- Nosocomial pneumonia
- Oxygen toxicity
- Hypotension
- Stress ulceration cholestasis
3Barotrauma
- High pressure (i.e., gt 50cmH2O)
- Interstitial emphysema
- Pneumomediastinum
- Subcutaneous emphysema
- pneumothorax
4Nosocomial pneumonia
- Patient intubated longer than 72 hours
- Aspiration from the upper airways through small
leaks around the tube cuff - Enteric G(-) rods, S. aureus, anaerobic bacteria
5Oxygen toxicity
- FiO2 gt 60 for more than 72 hours
6Hypotension
- Elevated intrathoracic pressures with decreased
venous return, intravascular volume repletion
7Gastrointestinal effects
- Stress ulcerations
- H2-receptor antagonists or sulcralfate
- Mild to moderate cholestasis
- T-Bil lt 4.0
8Ventilator-associated Lung Injury (VALI)
- Liap Pinhu, Thomas Whitehead, Timothy Evans, Mark
Griffiths - Lancet 2003361332-40 Review
9Ventilator-associated Lung Injury (VALI)
- Definition lung damage caused by application of
positive or negative pressure to the lung by
mechanical ventilation. - oxygen toxicity?
10Mechanisms of VALI1
- Volutrauma damage caused by over-distension.
High volume or high-end inspiratory volume injury - Barotrauma high pressure induced lung damage
- Similar histological appearance,
high-permeability pulmonary edema in uninjured
lung exacerbated damage in injured lung - Alveolar over-distention rather than pressure
itself causes lung injury
11Mechanisms of VALI2
- Atelectotrauma lung injury associated with
repeated recruitment and collapse, low
end-expiratory volume injury - Theoretically prevented by using a level of
positive end-expiratory pressure (PEEP) greater
than the lower inflection point of the pressure
volume curve - The pressure needed to reopen an occluded airway
is inversely proportional to its diameter ?
damage occurs distally
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13Protective ventilation strategy
- PEEP set at 2 cmH2O above the lower inflection
point of the pressure-volume curve - Driving pressure lt 20cmH2O
- Peak pressure lt 40 cmH2O
- Respiratory Rate lt 30/min
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16Conventional v.s. Protective ventilation in
patients with ARDS1
- Spontaneous breathing at rest tidal volume
about 7mL/kg - Conventional ventilation
- tidal volume at least 10mL/kg,
- maintain a normal PaCO2
17Conventional v.s. Protective ventilation in
patients with ARDS2
- Protective ventilation
- Low tidal volume 57mL/kg plateau pressure to
35 cmH2O - permissive hypercapnia
- a non-randomised study in 1990 a consensus
conference recommended in 1993
18Conventional v.s. Protective ventilation in
patients with ARDS3
19Multiple organ failure associated with mechanical
ventilation1
20Multiple organ failure associated with mechanical
ventilation2
- Biotrauma pulmonary and systemic inflammation
caused by the release of mediators from lungs
subjected to injurious mechanical ventilation - Protective ventilation can lower concentration of
cytokines in lung and plasma
21Cellular pathology of VALI
- Physical disruption stress failure
- gt40 mmHg, edema hemorrhage
- Mechanical activation of cellular pathways
mechanotransduction - physical force detected by cells and converted
in biochemical signeals (proinflammatory
mediators, cytokines)
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23Mechanotransduction
- Stretch-activated ion channels
- Extracellular pathways between the matrix,
integrin, and cytoskeleton - Intercellular junctions
- Transcriptional and post-transcriptional
regulations
24Prospects for pharmacotherapy
- After elucidation of the cellular
mechanisms underlying VALI, we can design
effective treatments to block mechanotransduction
and its downstream consequences and further
reduce deaths in patients with ARDS.
25Recommendations
- Protective ventilation is the only
treatment or supportive modality that affects
outcome in patients with ARDS. With few
exceptions, for example patients with underlying
disorders that would be exacerbated by
hypercarpnia (eg, IICP), low tidel volume
ventilation should be used routinely for patients
with injured lungs.
26Thanks you