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ARDS
This document discusses ARDS (acute respiratory distress syndrome), including its history, definitions, pathophysiology, and evidence-based treatment strategies. ARDS is characterized by diffuse pulmonary inflammation and reduced lung compliance. Traditional ventilator strategies have been shown to cause ventilator-induced lung injury, so current recommendations focus on lung-protective ventilation with low tidal volumes and high PEEP. Additional rescue therapies for refractory hypoxemia include recruitment maneuvers, proning, and ECMO. Proper diagnosis requires consideration of alternative conditions and use of diagnostic tools like echocardiogram, bronchoscopy, and chest CT scan.
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ARDS
- 1. ARDS Evidence based strategies DR.AMITH SREEDHARAN MD DNB IDCCM EDIC ASTER MIMS, KANNUR
- 2. History In 1967,Ashbaugh and colleagues reported the clinical characteristics of 12 patients with sudden respiratory failure that they called ARDS No underlying cardiac or pulmonary disease Rapidly developed acute hypoxemia, stiff lungs, and diffuse bilateral alveolar infiltrates on chest x-ray a few days following exposure to a precipitating factor. Autopsies revealed a characteristic histological pattern of diffuse alveolar damage (DAD) including hyaline membrane formation, oedema, cell necrosis, or fibrosis (Ashbaugh et al. 1967)
- 3. First clinical definition- AECC (1994) Acute onset of hypoxemia PaO2 to FiO2 ratio ≤ 200 mmHg regardless of PEEP level, Presence of bilateral infiltrates on chest radiograph, and Pulmonary artery wedge pressure ≤ 18 mmHg or no clinical signs of cardiogenic pulmonary oedema ALI ( acute lung injury) ARDS
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- 5. Timing of onset By definition, respiratory symptoms must commence within 7 days of a clinical insult Disease processes developing over several weeks like idiopathic pulmonary fibrosis, nonspecific interstitial pneumonitis and granulomatosis with polyangiitis can be excluded by accurately timing the respiratory symptoms
- 6. Diseases with acuteonset that may mimic ARDS Alveolar hemorrhage due to vasculitis Drug-induced pulmonary toxicity Acute eosinophilic pneumonia Organizing or diffuse interstitial pneumonia A complete diagnostic workup should include Echo,BAL and chest CT scan
- 7. ARDS isan acute inflammatory lung condition ARDS is not a disease Always precipitated by an underlying process • Pneumonia • Aspiration of gastric contents • Contusion,near drowning,inhalational injury pulmonary • sepsis, pancreatitis, major trauma, transfusion-related acute lung injury, severe burns, or drug overdose. Extra pulmonary
- 8. Pathophysioogy ARDS ischaracterized by a marked reduction in lung compliance DAD is the morphological hallmark of the lung in ARDS Diffuse alveolar damage is defined by the presence of hyaline membranes associated with interstitial oedema, cell necrosis and proliferation and then fibrosis at a later stage
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- 10. Mechanisms of hypoxemiain ARDS Loss of lung volume due to alveolar oedema and collapse intrapulmonary shunt and marked alteration in (VA/Q ratio) Surfactant deficiency impairment to the hypoxic pulmonary vasoconstriction response Pulmonary hypertension and positive pressure ventilation Opening of patent foramen ovale intracardiac shunt Increase in the physiological dead space occurs Alteration in lung diffusion
- 11. Traditional ventilator settings TV 12 – 15 ml/kg PEEP 0 - 5 CM H20 FiO2 0.8 - 1.0 PaCO2 < 50, PO2 > 80, spO2 > 98% Ventilator induced lung injury(VILI)
- 12. Volu trauma Ventilator induced lunginjury(VILI) Baro trauma Atelecto trauma Bio trauma Oxygen toxicity
- 14. “Baby lung” UsingCT scan, Gattinoni found that compliance correlated with the normally aerated lung and that the specific compliance (compliance divided by functional residual capacity) was actually normal. The "baby lung" is a physiological concept The remaining normally aerated lung accessible to ventilation is considerably reduced and of similar size as that of a baby ARDS lung is not "stiff" but instead small, with nearly normal intrinsic elasticity
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- 23. Oxygenation strategies Thefirst-line strategy in supporting hypoxemic patients is to provide oxygen oxygen mask oxygen mask plus reservoir High flow canula – 1st line strategy for oxygenation
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- 25. NIV No strongevidence for the use of noninvasive ventilation (NIV) Intubation rates of 40-50% in cases of moderate and severe ARDS Risk of delaying intubation by masking signs of respiratory distress Worsening VILI poor tolerance of the facemask is frequent
- 26. When to intubate? Whatever oxygenation strategy is used, intubation should not be delayed. RR > 35-40 breaths/min Clinical signs of respiratory distress Severe hypoxemia defined as PaO2 < 60 mm Hg or SpO2 < 90% despite high FiO2 Respiratory acidosis, and copious secretions Non-respiratory indications for invasive ventilation are altered consciousness and the occurrence of shock
- 27. Targets of mechanicalventilation To achieve adequate gas exchange whilst avoiding VILI
- 28. Lung protective ventilation Low VTs ( 4 - 6 ml/kg of ideal body weight) High PEEP levels ( 11- 16 cm h2O) Strict monitoring of plateau pressure to avoid exceeding 30 cm H2O
- 29. Mode of ventilation Worldwide assist-control in volume-controlled ventilation (VCV) is the most commonly used mode No difference in outcomes between VCV and (PCV Whatever the ventilator mode used, VTs and end-inspiratory plateau pressure should be limited and continuously monitored.
- 30. Gas exchange targets Target a PaO2 of at least 60 mm Hg and SaO2 of at least 90% No studies have shown that increasing PaO2 improves outcome Protective ventilation using low VTs may induce respiratory acidosis pH should usually be maintained above 7.2.
- 31. Driving pressure Drivingpressure (plateau pressure – PEEP) major determinant of outcome it has been suggested that the mechanical power transferred to the respiratory system from the ventilator plays a key factor in VILI Not only the strain (change in lung volume) but both high flow and respiratory rate are potentially harmful to the lungs
- 33. Rescue therapies toimprove oxygenation
- 34. Recruitment maneuvers Transientincreases in trans-pulmonary pressure in an attempt to open collapsed alveoli. When performing a recruitment manoeuvre the pressure reached at the end of inspiration surpasses the recommended safety thresholds for short time periods Sigh breaths, extended sigh breaths, Increased inspiratory pressures and PEEP, Sustained inflation Staircase Recruitment Manoeuvre. There is currently minimal evidence to recommend a particular method of recruitment.
- 35. Recruitment maneuvers Oxygenationbenefits may be short-lived and of uncertain signifiance, There are no studies showing patient outcome benefits, It is uncertain how to differentiate responders from non-responders There is no evidence for when, how often they should be performed There is no evidence of reducing VILI The ART trial found increased mortality with staircase recruitment manoeuvre. Experts made recently a conditional recommendation for using recruitment maneuver (Fan et al. 2017 Recruitment maneuvers can be considered as rescue therapyin the most severely hypoxemic patients No single method can be recommended.
- 36. Proning Advocated foralmost 40 years Oxygenation improves dramatically The dorsum of the lung has a larger volume than the anterior and apical areas Better ventilating the dorsal regions of the lung in the prone position improves ventilation, reduces intrapulmonary shunt leading to an improvement in V/Q matching.
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- 39. Hemodynamics of proning Afterload to the right ventricle is reduced Lower pulmonary vascular resistance Reduced levels of PEEP Improves preload
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- 42. PROSEVA trial PROSEVA:Prone Positioning in Severe Acute Respiratory Distress Syndrome Guerin et al for the PROSEVA Study Group. NEJM 2013;368:2159-68. Proning in severe ARDS reduces mortality without an increase in adverse outcomes. Further studies are required to confirm these findings but in the mean time these results are difficult to ignore
- 43. ECMO CESAR EOLIA Early transfer to ecmo centre and VV ecmo improve survival
- 44. Early applicationof airway pressure release ventilation may reduce the duration of mechanical ventilation in acute respiratory distress syndrome Zhou. Intensive Care Medicine 2017; 43:1648-1659.
- 45. APRV (Airway PressureRelease Ventilation)
- 46. Sedation The useof sedation improves patient tolerance of positive pressure ventilation and allows resting of respiratory muscles and the reduction of oxygen consumption by these muscles.
- 47. Neuro muscular blockers Neuromuscular blocking agent cisatracurium used for 48 hours in severe ARDS patients Improved oxygenation ( ACURASYS trial) Reduced lung and systemic inflammation Improved patient survival after adjusting for confounding factors
- 48. steroids Clear indicationsfor steroid therapy for diseases that may mimic ARDS include Alveolar hemorrhage due to vasculitis, Drug-induced toxic pneumonia with a lymphocytic pattern Organized pneumonia Acute eosinophilic pneumonia
- 49. Steroids in ARDS Useof steroids in ARDS is unresolved Mortality was significantly higher when steroid therapy was started 2 weeks after the onset Studies showing beneficial outcomes started low dose steroids early in the course of the disease High doses of steroids has been associated with either worse outcomes
- 50. Other adjunct therapies HFOV - High frequency oscillatory ventilation - found harmful Inhaled nitric oxide - no proven benefit Restricted fluid regimen - beneficial
- 51. SUMMARY Bed sideecho ,BAL and CT thorax for complete work up HFNC is first line oxygenation method in mild ARDS Do not delay intubation Lung protective ventilation strategy Recruitment during early disease as rescue oxygenation Early proning in case of poor response Consider early ecmo if poor response to proning
- 52. This Photo byUnknown Author is licensed under CC BY-NC-ND