ventilator associated lung injury

VENTILATOR ASSOCIATED LUNG INJURY

DR SURESH KANNA M.D. ,

DR VASIF MAYAN MC

M6 UNIT

MEDICINE DEPT

GMKMCH

“…. 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

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

DEFINITION

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

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

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 infiltrateshyaline membranesincreased vascular permeabilitypulmonary edema.

The constellation of pulmonary consequences of mechanical ventilation has been termed ventilator-induced lung injury

PATHOPHYSIOLOGICAL FEATURES

(i) PRESSURES IN THE LUNG(ii) PHYSICAL FORCES

A. Ventilation in high lung volumesB. Ventilation in low lung volumes

(iii) BIOLOGIC FORCES

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

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

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

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.

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

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

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

(ii) PHYSICAL FORCESA. VENTILATION AT HIGH LUNG VOLUMES Barotrauma

REGIONAL Overdistension

Increased alveolo-capillary permeability

Pulmonary edema

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

(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

TYPES OF VALI

Ventilator Associated Lung Injury (VALI) can occur due to:VolutraumaBarotraumaBiotraumaOxygen toxicityRecruitment/ derecruitment injury (atelectotrauma)Shearing injury

1. VOLUTRAUMAMECHANISM Over-distension of normal alveolar units to trans- pulmonary

pressures above ~30 cm H2O causes basement membrane stretch and stress on intracellular junctions.

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

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

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

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

1. VOLUTRAUMA

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 FACTORSLarge tidal volumeselevated peak inspiratory pressures

2. BAROTRAUMA

2. BAROTRAUMAMECHANISM Increasing the trans-pulmonary pressures above 50 cm H2O will

cause disruption of the basement membranes with classical barotrauma

• 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)

Effect of 45 cmH2O Peak Inspiratory Pressure

Control 5 min 20 min Control 5 min 20 min

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)

3. BIOTRAUMAMechanism – 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

AlveolarSpace

A-CMembrane

3. BIOTRAUMA strategies

Protective lung ventilation strategiesUse of neuromuscular blockers may

ameliorate (ACURASYS trial)

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 .

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

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.

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)

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

• The difficulty is finding the “Sweet Spot”

Multiple organ failure associated with mechanical ventilation1

VENTILATION STRATEGIES

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

VENTILATOR OPTIONS

A. Low tidal volumeB. High PEEP and recruitmentC. 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

VENTILATOR OPTIONSA. Low tidal volume

B. High PEEP and recruitmentC. 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

VENTILATOR OPTIONSA. Low tidal volumeB. 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

• 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

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2.ADJUNCTIVE STRATEGIESProne positionPartial 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

PHARMACOLOGICAL

A. Neuromuscular Blocking AgentsB. Anti inflammatoryC. 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

Minimising inflammation and BIOTRAUMA

Anti inflammatories tried

Mesenchymal stem cells are studied in animal models

Clinical benefit unproven.

Studies need to be conducted

PHARMACOLOGICALa.Neuro muscular blocking agents

b. Anti inflammatoryc. Stem cells

references

ICU Manual ; Paul marino

Millers Anaesthesia

Thank you