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ARDS Ventilation Stategy

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  1. 1. ARDS.. Definition •ARDS: acute respiratory distress syndrome Criteria : - Acute onset - Bilateral infiltrates on chest radiograph - Exclusion of left Atrial hypertension Two categories.. Acute Lung Injury - PaO2/FiO2ratio <300 RDS - PaO2/FiO2ratio <200 American European consensus conference (AECC) 1994
  2. 2. Other CriteriaChest Radiograph OxygenationSource Impaired pulmonary compliance Marked difference in inspired vs. arterial oxygen tensions Diffuse alveolar infiltrates on frontal chest radiograph Cyanosis refractory to oxygen therapy Petty and Ashbau, 1971 PEEP and respiratory system compliance (by quintiles) Preexisting direct or indirect lung injury Nonpulmonary organ dysfunction No. of quadrants of alveolar consolidation on frontal chest radiograph Hypoxemia (PaO2/FIO2), by quintiles Murray et al, Older diagnostic Criteria for ARDS
  3. 3. Other CriteriaChest Radiograph OxygenationSource PCWP <18 mm Hg if measured or no clinical evidence of left atrial hypertension Bilateral infiltrates on frontal chest radiography ALI: PaO2/FIO2 <300, regardless of PEEP level ARDS, PaO2/FIO2 <200, regardless of PEEP level Bernard et al, Older diagnostic Criteria for ARDS
  4. 4. ARDS… ‘Berlin definition’ Adopted in 2011; initiated by European Society Of Intensive Care Medicine 3 mutually exclusive categories.. based on PaO2/FIO2 (at PEEP> 5) • Mild- Between 300 and 200 mmHg. • Moderate- Between 100 and 200 mmHg. • Severe- Less than 100 mmHg. Initially 4 ancillary criterions( radiographic severity, respiratory system compliance, PEEP, and corrected expired minute volume) were also included, but later dropped as they did not contribute to predictive validity of severe ARDS. JAMA. 2012;307(23):2526-2533/ doi:10.1001/jama.2012.5669
  5. 5. ARDS… ‘Berlin definition’ Differences • Acute Lung Injury.. No longer exists. It is replaced by mild ARDS. • Onset must be within 7 days of some defined event, like sepsis, pneumonia or worsening of respiratory symptoms. • Bilateral opacities consistent with Pulmonary edema must be present, but may be detected on CT scan. • There is no need to exclude heart failure in this new definition. Patients with CHF or high PCOP can still have ARDS. JAMA. 2012;307(23):2526-2533/ doi:10.1001/jama.2012.5669
  6. 6. ARDS.. Etiology Direct Injury Common Causes • Pneumonia 28% • Gastric aspiration 14% Less Common Causes • Pulmonary contusion • Fat emboli • Near drowning • Inhalational injury Indirect Injury Common Causes •Sepsis 32% •Shock after severe trauma 5% Less Common Causes •Cardiopulmonary Bypass •Drug overdose •Acute pancreatitis •Massive blood transfusions Davis et al., J Peds1993;123:35
  7. 7. ARDS.. Stages Acute, exudative - inflammatory phase • Rapid onset of respiratory failure after trigger • Diffuse alveolar damage with inflammatory cell infiltration • Hyaline membrane formation • Capillary injury • Protein-rich edema fluid in alveoli • Disruption of alveolar epithelium
  8. 8. ARDS.. Stages Sub-acute, Proliferative phase:4-10 days • Persistent hypoxemia • Development of hypercarbia • Further decrease in pulmonary compliance • Pulmonary hypertension
  9. 9. ARDS.. Stages Chronic phase above 10 days • Fibrosing alveolitis • Obliteration of alveolar and bronchiolar spaces and pulmonary capillaries Recovery phase • Gradual resolution of hypoxemia • Improved lung compliance • Resolution of radiographic abnormalities
  10. 10. ARDS.. Pathophysiology • Abnormalities of gas exchange • Oxygen delivery and consumption • Cardiopulmonary interactions • Multiple organ involvement
  11. 11. Abnormalities in Gas Exchange Hypoxemia: HALLMARK of ARDS • Increased capillary permeability • Interstitial and alveolar exudate • Surfactant damage • Decreased FRC • Diffusion defect and right to left shunt
  12. 12. Oxygen delivery and consumption • VO2 is dependent on DO2 over a wide range of DO2 values in acute respiratory failure. This dependency phenomenon is much stronger in ARDS than in respiratory failure due to other causes. • Because of alterations in ventricular function, DO2 may be inadequate to satisfy oxygen demand and may contribute to multiple-system organ failure (MSOF). • Due to the abnormal dependency of VO2 on DO2, changes in the oxygenation status may not be reflected by changes in mixed venous oxygen saturation in ARDS
  13. 13. Cardiopulmonary interactions • A = Pulmonary hypertension resulting in increased RV afterload • B = Application of high PEEP resulting in decreased preload • A+B = Decreased cardiac output
  14. 14. Innovations: •iNO •PLV •Proning •Surfactant •Anti- Inflammatory Gentle ventilation: •Permissive hypercapnia •Low tidal volume •Open-lung •HFOV ARDS Extra Corporeal Membrane Oxygenator ARDS.. Therapies
  15. 15. Mechanical Ventilation in ARDS Injurious ventilator associated lung injury Necessary to reverse Hypoxaemia
  16. 16. • The lung with ALI or ARDS are particularly prone to ventilator associated lung injury: (Baby lung)  Collapsed, consolidated, less compliant areas (Dependant)  Normal areas (non dependant)
  17. 17. A, The chest radiograph shows bilateral pulmonary infiltrates that appear to be diffuse. B, A computed tomographic scan of the thorax from the same patient demonstrates that the distribution of the bilateral infiltrates is predominantly in dependent regions with more normal-appearing lung in nondependent regions.
  18. 18. Ventilator associated lung injury  High inflation pressure Barotrauma  Over distension Volutrauma  Repetitive opening & closing of alveoli Atelect-trauma  SIRS & cytokines release Biotrauma.
  19. 19. Ventilator--Associated Lung Injury • Barotrauma - Extra-alveolar air (pneumo-…) • Volutrauma - Regional lung over-distension (stretch injury) • Alelectrauma - Cyclic closure & reopening of terminal units (shear injury) • Biotrauma - Inflammatory mediators transmigrate to systemic circulation, causing multiple organ-system failure
  20. 20. Lung Protection strategy • Implemented immediately on intubation • Limit tidal volume 6-8 ml/kg • PEEP above inflection point • FiO2 <0.6 and saturation (88-90%) • Permissive hypercapnia NIH study NEJM 2000;342:1301-8
  21. 21. Lung protective ventilation strategy  Pressure & volume limitation  Higher PEEP  Recruitment maneuvers (Dynamic process of reopening collapsed alveoli through increase in trans pulmonary pressure)
  22. 22.  Which Recruitment maneuvers to be Used ? 1. The most well Known method of recruitment maneuver is sustained application of CPAP of 30- 50 Cm H2O for 30 seconds 2. Periodic recruitment with a series of traditional sigh breaths 3. Intermittently raising PEEP over several breaths 4. Extended sigh maneuver with step wise increase in PEEP while Vt is decreased 5. Intermittent application of pressure controlled ventilation with incremental high PEEP Lung protective ventilation etiology
  23. 23.  Permissive hypercapnea (acute respiratory acidosis) Treatment : Increase respiratory rate in a stepwise up to 35 Bicarbonate infusion Increase Vt  Worsened oxygenation & transient desaturation  Increased sedation or analgesia  Hypotension & arrhythmias  Barotraumas (Pneumothorax)  Bacterial translocation Consequences of lung protective ventilation
  24. 24. • High-frequency Ventilation (Jet, Oscillation, or Percussive ventilation) • HFOV allows for higher mean airway pressures & markedly reduced tidal volumes (1-3 ml/kg) Lung recruitment & reduce lung injury. Alternative Approaches to Lung Protection
  25. 25. High frequency oscillatory ventilation (HFOV) • Advantage:- Can provide enhanced gas exchange Protective lung strategy for poor compliance of lung • Disadvantage:- High lung volume may cause decreased venous return and hypotension IV fluids and vasopressors may be required
  26. 26. Gas entering the lungs travels centrally, while gas leaving the lungs swirls around it
  27. 27. Airway pressure release ventilation (APRV) • It provides two levels of airway pressure (P high & P low) during two time periods (T high & T low) , usually a long Thigh & short Tlow with spontaneous breathing during both. • Advantages: Decrease barotrauma, provide better V/P matching, cardiac filling & patient comfort. Alternative Approaches to Lung Protection
  28. 28. APRV
  29. 29. APRV Cautions • Hemodynamic compromise • Changing expiratory time constant • Change in resistance • Change in compliance • Auto-PEEP • Excessive release VT??
  30. 30. Open lung ventilation technique • Advantages of high PEEP to • Recruit more alveoli • Reduce atelactasis • Reduce stretch sheering injury • Disadvantages • Reduces cardiac output • Increases airway pressure Alternative Approaches to Lung Protection
  31. 31.  Prone positioning: Recruitment of dorsal (nondependent) atelectatic lung units, improved respiratory mechanics, decreased ventilation- perfusion mismatch, increased secretion drainage, reduced and improved distribution of injurious mechanical forces (Pelozi P et al, 2002) Adjunctive therapies to lung-protective Ventilation
  32. 32. Inhaled nitric oxide : Selective VD in ventilated lung units improving V/Q mismatch, decrease PaO2 & pulmonary hypertension ( no sustained clinical benefit) (Tayler RW et al, 2004) Adjunctive therapies to lung-protective Ventilation
  33. 33. Irrespective of this controversy as to whether the exact ARDSNet protocol should be adopted, the existing evidence supports that clinicians should change their practice and adopt volume and pressure limited ventilation for patients with ALI or ARDS. As additional evidence emerges, ongoing reassessment and evolution of these protocols will be necessary.
  34. 34. 1. Mechanical ventilation, although life saving, can contribute to patient morbidity and mortality 2. Volume and pressure limited ventilation clearly leads to improved patient survival 3. The role of re-cruitment maneuvers, higher levels of PEEP, or both remain controversial 4. At this time, use of alternative modes of ventilation (e.g., HFOV) and adjunctive therapies (e.g., inhaled nitric oxide and prone positioning) should be limited to future clinical trials and rescue therapy for patients with ALI or ARDS with life threatening hypoxemia failing maximal conventional lung protective ventilation. Conclusions and Future Considerations
  35. 35. A R D S N E T P r o t o c o l
  36. 36. ARDS Patient Manage ment Protocol
  37. 37. The Puzzle keep getting tougher with each step…