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Ventilator associated lung injury
The document discusses ventilator-associated lung injury (VALI), which can result from mechanical ventilation and may occur in normal or previously injured lungs, particularly in patients with acute respiratory distress syndrome (ARDS). Complications such as volutrauma, barotrauma, and biotrauma can lead to further lung injury, while various ventilation strategies like low tidal volume and high PEEP aim to minimize such damage. The importance of protective ventilation and adjunctive therapies, including neuromuscular blocking agents and prone positioning, is emphasized to improve patient outcomes.
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Ventilator associated lung injury
- 1. VENTILATOR ASSOCIATED LUNG INJURY DRSURESH KANNA M.D. , DR VASIF MAYAN MC M6 UNIT MEDICINE DEPT GMKMCH
- 2. “…. An openingmust 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 withapplication 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 causedby application of positive or negative pressure to the lung by mechanical ventilation.
- 5. INTRODUCTION The purposeof 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) PRESSURESIN THE LUNG (ii) PHYSICAL FORCES A. Ventilation in high lung volumes B. Ventilation in low lung volumes (iii) BIOLOGIC FORCES
- 8. Pressures in thelung 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 airflowis zero (e.g., at end inspiration), the principal force maintaining inflation is the transpulmonary pressure (alveolar pressure minus pleural pressure)
- 10. the same lungwhile the patient undergoes general anesthesia and positive-pressure ventilation with the use of the same tidal volume
- 11. In a patientwith 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 noninvasiveventilation, 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, whena 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 lungoverdistention 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 ATLOW 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 VentilatorAssociated 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 amechanical 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 increasedlocal 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 hasgained 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 alveolifrom 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 Increasingthe trans-pulmonary pressures above 50 cm H2O will cause disruption of the basement membranes with classical barotrauma
- 29. • Barotrauma • Airleaking 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 45cmH2O 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.
- 34. 3. BIOTRAUMA strategies Protectivelung 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 atelectotraumaand 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 difficultyis finding the “Sweet Spot”
- 44. Multiple organ failureassociated with mechanical ventilation1
- 46.
- 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. Lowtidal 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. Lowtidal 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. Lowtidal 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 withSurfactant 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 Partialor 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 BlockingAgents 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 inflammationand 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.