Ventilator induced lung injury

1. VENTILATOR INDUCED
LUNG INJURY
Presenter: Dr. Arnab Nandy
Moderator: Dr. Rakesh Lodha
Division of Pediatric Pulmonology and Intensive care, Dept. of Pediatrics,
AIIMS, New Delhi

2. PRELUDE
o Beneficence – “Always do good”
o Non-maleficence – “Do no harm”
o Justice – “Being fair to the patient”
o Autonomy – “Being respectful to an individual’s values and beliefs”
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3. MECHANICAL VENTILATION (MV)
o The use of a device to support, assist or control respiration through the application
of positive pressure to the airway which is delivered via an artificial airway
o Medical or Pharmacological intervention
o Adverse effects
o Therapeutic window and Lung-protective ventilation
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4. Adverse effects of MV
Positive intra-thoracic
pressure
Injury to the
airway
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5. ADVERSE EFFECTS OF MV
o Mechanical lung injury
o Artificial airway
o Muco-ciliary clearance
o Nosocomial infection
o Drug (Oxygen) toxicity
o Pulmonary circulation
o Operational challenges
o Involvement of other organs
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6. 6
Ventilator associated lung injury
(VALI)
Ventilator induced lung injury
(VILI)

7. BACKGROUND AND EPIDEMIOLOGY
o 1744 – John Fothergill – Mouth to mouth resuscitation
o 1952 – Polio epidemic – Structural lung damages by MV
o 1967 – “Respirator lung” – Post mortem lung pathology
o 2000 - ARDSNet trial – Tidal volume
o 2015 – Amato et al (Meta-analysis) – Driving pressure
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8. 8
Prime the immune
system for
initiating a vicious
cascade
Mechanical lung
injury
Concomitant
physiological
insult
(Sepsis, Trauma,
Surgery)
o Lung condition – Normal or Diseased
o Majority of non-ARDS patients at risk
of VILI don’t develop clinically
significant lung injury
o Severity of injury more in diseased
lung compared to normal lung
o Incidence of VILI in 24% of patients
with in first five days of MV
Gajic O, Dara SI, Mendez JL, Adesanya AO, Festic E, Caples SM, et al. Ventilator-associated lung injury in
patients without acute lung injury at the onset of mechanical ventilation. Crit Care Med. 2004 ;32:1817-24
Double hit hypothesis

9. MECHANICAL LUNG INJURY/VILI
 Volutrauma
 Barotrauma
 Atelectrauma
 Biotrauma
 Shear strain
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10. PATHOPHYSIOLOGY
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Under the normal circumstances the alveolar walls ‘unfold’
rather than elastic stretching
Deformation related cell strain causes lipid trafficking to the plasma membranes
Increase cell surface area to prevent plasma membrane rupture and repair the cell when under stress
Any stress that overwhelms these cytoprotective mechanisms by additional inflation directly translate into
Cell detachment from the basement membrane, epithelial and endothelial cell junction breaks, intracapillary
blebs, and alveolar and interstitial oedema

11. 11

12. 12
Overdistension High inflation pressure
Volutrauma Barotrauma
Common link
Trans-pulmonary pressure
(Ptp)

13. 13
Palv
Ppl
Schematic representation of Transpulmonary pressure
(Ptp = Palv – Ppl)
Trans-airway pressure
Alveolus
Visceral pleura
Abbreviation: Paw – Airway pressure; Ppl – Pleural pressure. (Assumption – Paw will equilibrate with Palv at end-inspiration when airflow is zero)
Net pressure at the interface

14. 14
Normal/Quite
breathing
PPV with normal
lung conditions
PPV with chest-
wall stiffness
(Obesity)
PPV with stiff-
lung (ARDS)
Beitler JR, Malhotra A, Thompson T. Ventilator-Induced Lung Injury. Clin Chest Med. 2016 ; 37: 633–646.
Abbreviation: PPV – Positive pressure ventilation

15. PATIENT SELF INFLICTED LUNG
INJURY (P-SILI)
 Spontaneously breathing patients in ARDS/AHRF
 High flow oxygen/NIV/MV
 Oesophageal pressure (PES) monitoring
 Optimal combination of PS and PEEP
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Grieco DL, Menga LS, Eleuteri D, Antonelli M. Patient self-inflicted lung injury: implications for acute
hypoxemic respiratory failure and ARDS patients on non-invasive support. Minerva Anestesiol. 2019;85:1014-23

16. 16
 Safe range of negative deflection
in esophageal pressure (PES) and
positive swing in trans-pulmonary
pressure (PL)
 HFNC as an alternative to NIV
in meeting the high respiratory
demand in AHRF – Initial
approach

17. 17
Atelectrauma
o Cyclic opening and collapse of the atelectatic lung units during their recruitment through PPV
o Dynamic wave of shear stress generate at the interface between air and collapsed airway
o Inflammatory fluids with in alveolus lead to formation of gas-liquid interface (foam bubbles)
which disrupts plasma membrane and cytoskeletal adhesion
o Target is to reach just about the critical closing pressure for the collapsed lung units with the
setting of low tidal volume
o Sustained recruitment by adjusting PEEP just above the critical closing pressure

18. 18
Dynamic wave of shear stress
Bates JHT, Smith BJ. Ventilator-induced lung injury and lung mechanics. Ann Transl Med. 2018;6:378.
Shear stress by air-fluid interface

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Biotrauma
o Responsible for the injury in regions of the lung which didn’t even face considerable
mechanical lung injury
o Activation and amplification of pro-inflammatory cytokine cascade (TNF-α, IL-6 & 8, MMP-
9, NF-kβ)
o Dissemination of the inflammatory mediators released by the pulmonary epithelial cells into
the other organs through pulmonary circulation
o Extra-pulmonary organ injury – multiorgan dysfunction – increased risk of death
Curley GF, Laffey JG, Zhang H, Slutsky AS. Biotrauma and Ventilator-
Induced Lung Injury: Clinical Implications. Chest. 2016;150:1109-17.

20. 20
Shear strain
o Mechanical alveolar inter dependence - Collapse or flooding of one lung unit induce
deformation of the adjacent units
o The shear strain generated at the inter-alveolar septum cause non-uniform inflation of the
alveolus
o In-vitro model suggest increased damage to the
pulmonary epithelial cells by cyclical deformation
strain compared to tonically sustained deformation
strain of same peak amplitude
Beitler JR, Malhotra A, Thompson T. Ventilator-Induced Lung Injury. Clin Chest Med. 2016 ; 37: 633–46.
Stress multiplication

21. WHEN TO SUSPECT
 Lung condition : Normal or Diseased
 Patient ventilator Asynchrony
 Presence of risk factors (setting) :
Tidal volume, Blood transfusion, Acidemia
 Other causes ruled out for worsening hypoxemia (low PaO2 and SpO2)
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22. ASSESSMENT OF VILI
Evaluation is targeted to rule out the other causes for hypoxemia in mechanically
ventilated patients
o Bedside chest X ray
o U/S lungs and abdomen
o ECG
o Bedside echocardiography
o CT thorax
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Apart from thorough clinical
evaluation the investigations that
would help to constringe the
differentials

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Common differentials:
o Aspiration
o Ventilator associated pneumoniae
o Pneumothorax/Pleural effusion
o ARDS
o Pulmonary haemorrhage
o Pulmonary embolism
o Pulmonary capillary stress failure
o Auto-PEEPing
o Cardiogenic pulmonary oedema
o Intra-abdominal distension

24. Risk for VILI
B. Mechanical ventilation
A. Lung condition
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25. PREDICTION OF VILI
A.1 Lung Injury Prediction Score
(LIPS)
A.2 Early Acute Lung Injury Score
(EALI)
 Oxygen requirement
 Respiratory rate
 Immune suppression
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 Predisposing conditions
(Sepsis, Shock, Trauma, Pneumonia, Aspiration,
Pancreatitis, High-risk elective or emergency surgery)
 Risk modifiers
(Alcohol abuse, Smoking, Hypoalbuminaemia, Diabetes
mellitus, Chemotherapy, Oxygen supplementation,
Tachypnea)
Levitt JE, Calfee CS, Goldstein BA, Vojnik R, Matthay MA. Early acute lung injury: criteria for identifying
lung injury prior to the need for positive pressure ventilation. Crit Care Med. 2013;41:1929-37.

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B.1 Mechanical Power
 Tidal volume (∆V)
 Driving pressure (∆P or Vt/ELrs)
 Flow (F)
 PEEP
 Respiratory rate (RR)
Gattinoni L, Tonetti T, Cressoni M, Cadringher P, Herrmann P, Moerer O, et al. Ventilator-
related causes of lung injury: the mechanical power. Intensive Care Med. 2016;42:1567-75.
B.2 Dynamic compliance (Crs) for
nature and degree of lung injury
 Tidal volume (∆V)
 Peak inspiratory pressure (PIP)
PEEP
f (t)

27. EQUATION OF MOTION
TRANS AIRWAY
PRESSURE TO
OVERCOME AIRWAY
RESISTANCE
TRANS THORACIC
PRESSURE TO OVERCOME
ELASTIC RECOIL OF
CHEST WALL
POSITIVE END
EXPIRATORY PRESSURE
TO PREVENT ALVEOLAR
COLLAPSE
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28. 28
Resistive pressure
Elastic pressure
P = V/ELrs + Raw * F + PEEP
[∆P]
[Ppeak − Pplat]
[(Ppeak − Pplat) = Raw*F]
P
T
[(Pplat − PEEP) = V/ELrs]
Driving pressure (∆P)
Trans airway pressure (Pta)
Trans thoracic pressure (Ptt)

29. PREVENTIVE/RESCUE STRATEGIES
Strategy Mechanism Implementation/Monitoring
Limit tidal volume Prevent barotrauma, volutrauma, and
minimise shear forces
Avoidance of tidal recruitment of
atelectatic alveoli
Tidal volume scaled to
functional lung size
Limit inspiratory pressure - Do - Transpulmonary driving pressure
PEEP Increase in aerated functional lung size,
prevent tidal collapse during expiration,
improving lung homogeneity to reduce
shear strain
PEEP-FiO2 table, Oesophageal
pressure guided, pressure-
volume curve
Limit respiratory rate Limit stress frequency Minimum allowable pH or
maximum allowable PaCO2
Limit spontaneous respiratory
effort
Limiting inspiratory effort to avoid occult
high tidal volumes from breath stacking
and forced expiration to prevent cyclic de-
recruitment
Sedation and neuro-muscular
blockade in severe ARDS
Prone position (in ARDS) Improving lung homogeneity to decrease
shear strain
P/F ratio
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30. RECENT DEVELOPMENTS
o Particle flow rate (PFR)
- To guide individualisation of ventilator settings
- To monitor response after changing ventilator mode/setting
- To identify VILI
o Time controlled adaptive ventilation (TCAV)
- To maintain stable inflation and lung homogeneity
- To reduce the regional dynamic strain around the atelectatic alveolus
- To reduce tidal recruitment/de-recruitment and stress multiplication
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- Nieman GF, Gatto LA, Andrews P, Satalin J, Camporota L, Daxon B, et al. Prevention and treatment of acute lung injury with time-
controlled adaptive ventilation: physiologically informed modification of airway pressure release ventilation. Ann Intensive Care. 2020;10:3.
- Hallgren F, Stenlo M, Niroomand A, Broberg E, Hyllén S, Malmsjö M, Lindstedt S. Particle flow rate from the airways as fingerprint
diagnostics in mechanical ventilation in the intensive care unit: a randomised controlled study. ERJ Open Res. 2021;7:00961-2020.
Monitoring
Rescue strategy

31. TCAV
o Viscoelastic properties of terminal
airspaces
o Based on the principle of APRV
o Keeping the inspiratory time span
higher in each cycle
o Brief period of release phase
o Configuring each breath guided by
previous breath
o Limitations
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…“gradually nudge alveoli and alveolar ducts
open with an extended inspiratory duration and
prevent alveolar collapse using a brief (sub-
second) expiratory duration that does not allow
time for alveolar collapse”…

32. SUMMARY
 Clinical judgement before starting MV
 Continuous monitoring
 Minimal setting of MV as per the patient condition
 Early detection and possible intervention
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33. THANK YOU
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