Ventilator Associated Lung injury Barotrauma Volutrauma Biotrauma Recruitment derecruitment Oxygen toxicity MODS Shearing injury

1. VENTILATOR ASSOCIATED
LUNG INJURY
DR SURESH KANNA M.D. ,
DR VASIF MAYAN MC
M6 UNIT
MEDICINE DEPT
GMKMCH

2. “…. An opening must be made in the trunk of
the trachea , into which a tube of reed or
cane should be put ; you will then blow into
this, so that the lung may rise again. . . And
the heart becomes strong . . . “
Andreas Vesalius 1555 AD

3. INTRODUCTION
mechanical ventilation with application of pressure to the lung, whether positive or negative,
can cause damage known as ventilator-associated lung injury (VALI)
 VALI may occur in previously normal lungs or worsen pre-existing ARDS
 About 1 in 4 mechanically ventilated patients develop VALI, the risk is likely higher in ARDS
patients
 Ventilator induced lung injury (VILI) is sometimes used as a synonym for VALI, but strictly
speaking VILI is VALI when mechanical ventilation is the proven cause of lung injury

4. DEFINITION
lung damage caused by application of
positive or negative pressure to the lung
by mechanical ventilation.

5. INTRODUCTION
 The purpose of mechanical ventilation is to rest the respiratory muscles while
providing adequate gas exchange.
 Despite the clear benefits of this therapy, many patients eventually die after
the initiation of mechanical ventilation, even though their arterial blood gases
may have normalized.
 This mortality has been ascribed to multiple factors, including complications of
ventilation such as barotrauma (i.e., gross air leaks), oxygen toxicity, and
hemodynamic compromise.
 During the polio epidemic, investigators noted that mechanical ventilation
could cause structural damage to the lung

6.  In 1967, the term “respirator lung” was coined to describe the diffuse alveolar infiltrates and hyaline
membranes that were found on postmortem examination of patients who had undergone
mechanical ventilation
 More recently, there has been a renewed focus on the worsening injury that mechanical ventilation
can cause in normal lungs
 This damage is characterized pathologically by
inflammatory-cell infiltrates
hyaline membranes
increased vascular permeability
pulmonary edema.
 The constellation of pulmonary consequences of mechanical ventilation
has been termed ventilator-induced lung injury

7. PATHOPHYSIOLOGICAL FEATURES
(i) PRESSURES IN THE LUNG
(ii) PHYSICAL FORCES
A. Ventilation in high lung volumes
B. Ventilation in low lung volumes
(iii) BIOLOGIC FORCES

8. Pressures in the lung
 During a lifetime, a person will take approximately 500 million breaths
 For each breath, the pressure necessary to inflate the lungs comprises
 pressure to overcome airway resistance
 Inertance
 pressure to overcome the elastic properties of the lung

9.  When airflow is zero (e.g., at end
inspiration), the principal force
maintaining inflation is the
transpulmonary pressure (alveolar
pressure minus pleural pressure)

10. the same lung while the
patient undergoes
general anesthesia and
positive-pressure
ventilation with the use
of the same tidal
volume

11. In a patient with a stiff chest
wall (e.g., a patient with a
pleural effusion or massive
ascites), a large fraction of
ventilator-delivered pressure is
dissipated in inflating the
chest wall rather than the
lung.

12.  during noninvasive ventilation, if
the patient is markedly distressed
and generating very large
negative pleural pressures,
transpulmonary pressure may be
extremely high, despite low
airway pressures
 and hence lung stretching
increases

13. By analogy, when a
musician plays the trumpet,
airway pressure can reach
150 cm of water
but pneumothorax is
uncommon, because
pleural pressure is also
elevated and there is no
overdistention

14.  Regional lung overdistention is a key factor in generating ventilator-
induced lung injury.
 Since there is no well-accepted clinical method to measuring
regional overdistention, limiting inflation pressure during
mechanical ventilation is used as a surrogate strategy to limit
overdistention
 Alveolar pressure easy to monitor and find out
 Pleural pressure assessment complicated
 Hence true transpulmonary pressure measurement difficult

15. (ii) PHYSICAL FORCES
A. VENTILATION AT HIGH LUNG VOLUMES
 Barotrauma
 REGIONAL Overdistension
 Increased alveolo-capillary permeability
 Pulmonary edema

16. B. VENTILATION AT LOW LUNG VOLUMES
 lung injury via repeated opening
and closing of lung
(atelectrauma)
 Lung inhomogeneity as in ARDS
can lead on to atelectasis and
pulmonary edema

17. (iii) BIOLOGIC FORCES
 Epithelial microtears due to the physical forces can activate the
immune response
 Translocation of
 Inflammatory chemokines
 Bacteria
 Lipopolysaccharide
 ARDS
 PULMONARY FIBROSIS
 MODS

21. TYPES OF VALI
Ventilator Associated Lung Injury (VALI) can occur due to:
 Volutrauma
 Barotrauma
 Biotrauma
 Oxygen toxicity
 Recruitment/ derecruitment injury (atelectotrauma)
 Shearing injury

22. 1. VOLUTRAUMA
 MECHANISM
 Over-distension of normal alveolar units to trans- pulmonary
pressures above ~30 cm H2O causes basement membrane stretch
and stress on intracellular junctions.

23.  When a mechanical ventilation breath is forced into
patient - positive pressure tends to follow path of
least resistance to normal or relatively normal alveoli,
potentially causing overdistention.
 This overdistention l/t inflammatory cascade that
augments the initial lung injury, causing additional
damage to previously unaffected alveoli.
1. VOLUTRAUMA

24.  The increased local inflammation lowers
the patient's potential to recover from
ARDS.
 The inflammatory cascade occurs
locally and may augment the systemic
inflammatory response as well.
1. VOLUTRAUMA

25.  Volutrauma has gained recognition
over last 2 decades d/t importance
of lung protection ventilation with
low tidal volumes of 6–8 mL/kg.
1. VOLUTRAUMA

26. PEEP prevents alveoli from totally
collapsing at the end of
exhalation and may be beneficial
in preventing this type of injury.
1. VOLUTRAUMA

27.  Barotrauma - rupture of alveolus with
subsequent entry of air into pleural
space (pneumothorax) and/or tracking
or air along the vascular bundle to
mediastinum (pneumomediastinum).
 RISK FACTORS
Large tidal volumes
elevated peak inspiratory pressures
2. BAROTRAUMA

28. 2. BAROTRAUMA
MECHANISM
 Increasing the trans-pulmonary pressures above 50 cm H2O will
cause disruption of the basement membranes with classical
barotrauma

29. • Barotrauma
• Air leaking into
pleural space
• Air leaking into
interstitial space
• Tearing at Bronchio-
Alveolar Junction as
lung is recruited and
allowed to collapse
• Most occurs in
dependent lung
zones (transition
zone)

30. Effect of 45 cmH2O Peak Inspiratory
Pressure
Control 5 min 20 min

31. Barotrauma and volutrauma
 MINIMISATION STRATEGY
 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 ARMA trial)

32. 3. BIOTRAUMA
 Mechanism – MECHANOTRANSDUCTION-physical forces
are detected by cells and converted into biochemical
signals
 Mechanotransduction and tissue disruption leads to
upregulation and release of chemokines and cytokines
with subsequent chemoattraction and activation resulting
in pulmonary and systemic inflammatory response and
multi-organ dysfunction

33. Alveolar
Space
A-C
Membrane

34. 3. BIOTRAUMA strategies
Protective lung ventilation strategies
Use of neuromuscular blockers may
ameliorate (ACURASYS trial)

35. 4. Oxygen toxicity
 Oxygen toxicity is due to production of oxygen
free radicals, such as superoxide anion, hydroxyl
radical, and hydrogen peroxide.
 Oxygen toxicity can cause a variety of
complications
 mild tracheobronchitis
 absorptive atelectasis
 diffuse alveolar damage .

36. 4. Oxygen toxicity
 It is adviced to attain an FIO2 of 60% or less within
the first 24 hours of mechanical ventilation.
 If necessary, PEEP should be considered a means
to improve oxygenation while a safe FIO2 is
maintained.
 Oxygen toxicity
FiO2 > 60% for more than 72 hours

37. 5. Recruitment / Derecruitment Injury aka
atelectotrauma
 lung injury associated with repeated recruitment and collapse
 low end-expiratory volume injury
6. 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.

39. Strategies against atelectotrauma and
shearing injury
 The pressure needed to reopen an occluded airway is inversely
proportional to its diameter → damage occurs distally
 This may be achieved by:
(a) Ventilation strategies: “Higher PEEP”
(b) A recruitment manoeuvres: e.g. CPAP
(c) Prone Positioning (gravitational recruitment manoeuvre)

40. Protective ventilation strategy
 PEEP set at 2 cmH2O above the lower inflection point of the
pressure-volume curve
 Peak pressure < 40 cmH2O
 Respiratory Rate < 30/min

43. • The difficulty is finding the “Sweet Spot”

44. Multiple organ failure associated with
mechanical ventilation1

46. VENTILATION
STRATEGIES

47. OPTIONS
 VENTILATOR OPTIONS
 A. Low tidal volume
 B. High PEEP and recruitment
 C. HFOV ( High Frequency Oscillatory ventilation)
 ADJUNCTIVE STRATEGIES
 Prone position
 Partial or total extracorporeal
 PHARMACOLOGICAL
 Neuro muscular blocking agents
 Anti inflammatory
 Stem cells

48. VENTILATOR OPTIONS
A. Low tidal volume
B. High PEEP and recruitment
C. HFOV ( High Frequency Oscillatory ventilation)
 Patients with ARDS have
 Relatively nonaerated dependent lung regions
 Aerated non dependent lungs
 Smaller volume available for ventilation BABY LUNG
 Low tidal volume should be used to prevent overinflation of normally aerated lung

49. VENTILATOR OPTIONS
A. Low tidal volume
B. High PEEP and recruitment
C. HFOV ( High Frequency Oscillatory ventilation)
 Pulmonary edema and end-expiratory alveolar collapse characterize several forms of
respiratory failure
 Low PEEP may cause atelectrauma and collapse
 High PEEP can impair venous return and cause pulmonary overdistension
 Studies show 5% reduced mortality with Higher PEEP setting

51. VENTILATOR OPTIONS
A. Low tidal volume
B. High PEEP and recruitment
C. HFOV ( High Frequency Oscillatory ventilation)
technique in which very small tidal volumes
(sometimes less than the anatomic dead space) are
applied at high frequencies (up to 15 per second).
Theoretically, this technique should be ideal for
minimizing ventilator-induced lung injury

52. • HFOV with Surfactant as Compared
to CMV with Surfactant in the
Premature Primate
– HFOV resulted in
• Less Radiographic Injury
• Less Oxygenation Injury
• Less Alveolar Proteinaceous
Debris
• HFOV Stimulates Significantly Less
Neutrophil Activity Than CMV
Alveolar Protein
0%
5%
10%
15%
20%
25%
30%
CMV
CMV-S
HFOV
HFOV-S
Mode
PercentDebris

53. 2.ADJUNCTIVE STRATEGIES
Prone position
Partial or total extracorporeal
 PRONE POSITION
 70% of patients with ARDS have improved oxygenation in prone position
 Increase end expiratory lung volume
 Less effect of mass of lung on the heart
 Improved V – P quotient
 Increase homogeneity of ventilation
 PARTIAL OR TOTAL EXTRACORPOREAL
 intensity of ventilation is decreased
 carbon dioxide is removed through an extracorporeal circuit
 Tidal volumes can be reduced hence reduced injury

54. PHARMACOLOGICAL
A. Neuromuscular Blocking Agents
B. Anti inflammatory
C. Stem cells
 Due to extreme dyspnea, patients with ARDS often “fight the ventilator”
 Papazian et al.51 found that the adjusted 90-day mortality was lower among those who
received a neuromuscular blocking agent for 48 hours than among those who received
placebo
 reduced serum cytokine levels among patients receiving a neuromuscular blocking agent
 BIOTRAUMA reduced

55.  Minimising inflammation and BIOTRAUMA
 Anti inflammatories tried
 Mesenchymal stem cells are studied in animal models
 Clinical benefit unproven.
 Studies need to be conducted
PHARMACOLOGICAL
a.Neuro muscular blocking agents
b.Anti inflammatory
c. Stem cells

56. references
ICU Manual ; Paul marino
Millers Anaesthesia

57. Thank you