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Ventilatorassociated Lung Injury

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Patient intubated longer than 72 hours. Aspiration from the upper airways through small ... Enteric G(-) rods, S. aureus, anaerobic bacteria. Oxygen toxicity ... – PowerPoint PPT presentation

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Title: Ventilatorassociated Lung Injury


1
Ventilator-associated Lung Injury
  • Ri ???

2
Complications of Mechanical Ventilator
  • Barotrauma
  • Nosocomial pneumonia
  • Oxygen toxicity
  • Hypotension
  • Stress ulceration cholestasis

3
Barotrauma
  • High pressure (i.e., gt 50cmH2O)
  • Interstitial emphysema
  • Pneumomediastinum
  • Subcutaneous emphysema
  • pneumothorax

4
Nosocomial 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

5
Oxygen toxicity
  • FiO2 gt 60 for more than 72 hours

6
Hypotension
  • Elevated intrathoracic pressures with decreased
    venous return, intravascular volume repletion

7
Gastrointestinal effects
  • Stress ulcerations
  • H2-receptor antagonists or sulcralfate
  • Mild to moderate cholestasis
  • T-Bil lt 4.0

8
Ventilator-associated Lung Injury (VALI)
  • Liap Pinhu, Thomas Whitehead, Timothy Evans, Mark
    Griffiths
  • Lancet 2003361332-40 Review

9
Ventilator-associated Lung Injury (VALI)
  • Definition lung damage caused by application of
    positive or negative pressure to the lung by
    mechanical ventilation.
  • oxygen toxicity?

10
Mechanisms 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

11
Mechanisms 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

12
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13
Protective 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

14
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16
Conventional 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

17
Conventional 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

18
Conventional v.s. Protective ventilation in
patients with ARDS3
19
Multiple organ failure associated with mechanical
ventilation1
20
Multiple 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

21
Cellular 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)

22
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23
Mechanotransduction
  • Stretch-activated ion channels
  • Extracellular pathways between the matrix,
    integrin, and cytoskeleton
  • Intercellular junctions
  • Transcriptional and post-transcriptional
    regulations

24
Prospects 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.

25
Recommendations
  • 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.

26
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