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ARDS.ppt
- 1. Ian B. Hoffman,MD, FCCP Pulmonary & Critical Care Medicine
- 2. Any disruptionof function of respiratory system – CNS, nerves, muscles, pleura, lungs Any process resulting in low pO2 or high pCO2 – arbitrarily 50/50 Acute respiratory failure can be exacerbation of chronic disease or acute process in previously healthy lungs
- 3. 1940’s –polio, barbiturate OD 1960’s – blood gas analysis readily available, aware of hypoxemia 1970’s – decreased hypoxic mortality, increased multiorgan failure (living longer) 1973 – relationship between resp muscle fatigue and resp failure
- 4. Type 1(nonventilatory) – hypoxemia with or without hypercapnia – disease involves lung itself (i.e, ARDS) Type 2 – failure of alveolar ventilation – decrease in minute ventilation or increase in dead space (i.e. COPD, drug OD)
- 5. Correct hypoxemiaor hypercapnia without causing additional complications Nonivasive ventilation vs. intubation and mechanical ventilation Goal of mechanical ventilation is NOT necessarily to normalize ABGs
- 6. Failure ofrespiratory pump to adequately eliminate CO2 pCO2 : CO2 production alveolar ventilation
- 7. Healthy humanshave V/Q matching High V/Q areas – well ventilated but poorly perfused – wasted ventilation – increased dead space Low V/Q areas – can cause hypercapnia if large amount of venous blood flows through
- 8. Decision tomechanically ventilate is clinical Some criteria Decreased level of consciousness Vital capacity <15 ml/kg Severe hypoxemia Hypercarbia Vd/Vt >0.60 NIF < -25 cm H20
- 9. (formerly Adult RespiratoryDistress Syndrome)
- 10. Severe endof the spectrum of acute lung injury Acute and persistent lung inflammation with increased vascular permeability Diffuse infiltrates Hypoxemia – paO2/FiO2 <200 (i.e. pO2 70 / FiO2 0.5 = 140) No clinical evidence of elevated left atrial pressure (PCWP <18 if measured)
- 11. 1967 –Ashbaugh described 12 pts with acute respiratory distress, refractory cyanosis, decreased lung compliance, diffuse infiltrates 1988 – 4 point lung injury score (level of PEEP, pO2/FiO2, lung compliance, degree of infiltrates) 1994 – acute onset, bilat infiltrates, no direct or clinical evidence of LV failure, pO2/FiO2)
- 12. Annual incidence75 per 100,000 9% of American critical care beds occupied by patients with ARDS
- 13. Clinically andradiographically resembles cardiogenic pulmonary edema PCWP can be misleading – high or low 20% of pts with ARDS may have LV dysfunction
- 17. Direct injuryto the lung Indirect injury to the lung in setting of a systemic process Multiple predisposing disorders substantially increase risk Increased risk with alcohol abuse, chronic lung disease, acidemia
- 18. Direct LungInjury Pneumonia Gastric aspiration Lung contusion Fat emboli Near drowning Inhalation injury Reperfusion injury Indirect Lung Injury Sepsis Multiple trauma Cardiopulmonary bypass Drug overdose Acute pancreatitis Blood transfusion
- 19. Inflammatory injuryto alveoli producing diffuse alveolar damage Proinflammatory cytokines (TNF, IL-1, IL-8) Neutrophils recruited – release toxic mediators Normal barriers to alveolar edema are lost, protein and fluid flow into air spaces, surfactant lost, alveoli collapse Impaired gas exchange Impaired compliance Pulmonary hypertension
- 21. Severe initialhypoxemia Prolonged need for mechanical ventilation Initial exudative stage Proliferative stage resolution of edema, proliferation of type II pneumocytes, squamous metaplasia, collagen deposition Fibrotic stage
- 22. Early Incitingevent, pulmonary dysfunction (worsening tachypnea, dyspnea, hypoxemia) Nonspecific labs CXR – diffuse alveolar infiltrates Subsequent Improvement in oxygenation Continued ventilator dependence Complications Large dead space, high minute ventilation requirement Organization and fibrosis in proliferative phase
- 24. Ventilator inducedlung injury Sedation and neuromuscular blockade Nosocomial infection Pulmonary emboli Multiple organ dysfunction
- 25. Improved survivalin recent years – mortality was 50-60% for many years, now 25-40% Improvements in supportive care, newer ventilatory strategies Early deaths (3 days) usually from underlying cause of ARDS Later deaths from nosocomial infections, sepsis, MOSF Severity of gas exchange at admission does not correlate with mortality Respiratory failure only responsible for ~16% of fatalities Long-term survivors usually show mild abnormalities in pulmonary function (DLCO), impaired neurocognitive function
- 26. Failure toimprove over 1st few days Initially increased dead space Advanced age Sepsis Multiple organ dysfunction (higher APACHE) Steroids given prior to onset of ARDS Blood transfusion Not managed by Intensivist
- 27. Provide adequateoxygenation without causing damage related to: Oxygen toxicity Hemodynamic compromise Barotrauma Alveolar overdistension
- 28. Reliable oxygensupplementation Decrease work of breathing Increased due to high ventilatory requirements, increased dead space, and decreased compliance Recruit atelectatic lung units Decreased venous return can help decrease fluid movement into alveolar spaces
- 29. Low tidalvolume, plateau pressure <30 (less alveolar overdistension) PEEP – enough, not too much Pressure controlled vs. volume cycled Open lung strategy PC-IRV ventilation Vt < 6ml/kg, PEEP 16, RR <30, Peak pressure <40
- 30. Prolong inspiratorytime (increase mean airway pressure and improve oxygenation) Permissive hypercapnia Secondary effect of low tidal volumes Maintain adequate oxygenation with less risk of barotrauma Sedation/paralysis usually necessary
- 31. Decreases peakairway pressure Improves alveolar recruitment Increases ventilation of dependent lung zones Improves oxygenation BUT – no evidence yet of improved outcome
- 33. Increases FRC– recruits “recruitable” alveoli Decreases shunt, improves V/Q matching No consensus on optimal level of PEEP
- 34. Initial tidalvolume of 6 ml/kg IBW and plateau pressure <30 vs. Initial tidal volume of 12 ml/kg IBW and plateau pressure <50 Reduction in mortality of 22% (31% vs 40%)
- 36. APRV High-frequencyventilation ECMO Beta agonists Nitric Oxide Surfactant Steroids (possible benefit if given early -or- in late fibroproliferative phase) ?benefit from tube feeds containing combination of eicosapentaenoic acid and gamma-linolenic acid (?antiinflammatory effects)
- 37. Selectively dilatesvessels that perfuse better ventilated lung zones, resulting in improved V/Q matching, improved oxygenation, reduction of pulmonary hypertension Less benefit in septic patients No clear improvement in mortality
- 38. Known fordecades that high levels of positive pressure ventilation can rupture alveolar units In 1950’s became apparent that high FiO2 can produce lung injury
- 39. Macrobarotrauma Pneumothorax,interstitial emphysema, pneumomediastinum, SQ emphysema, pneumoperitoneum, air embolism ? resulting from high airway pressures, or just a marker of severe lung injury Higher PEEP predicts barotrauma
- 40. Microbarotrauma Alveolaroverinflation exacerbating and perpetuating lung injury – edema, surfactant abnormalities, inflammation, hemorrhage Less affected lung accommodates most of tidal volume – regional overinflation Cyclical atelectasis (shear) – adds to injury Low tidal volume strategy (initial tidal volume 6 ml/kg IBW, plateau pressure <30) – lower mortality
- 41. Prophylaxis forDVT Prophylaxis for GI bleeding Measures to avoid nosocomial pneumonia Treat nosocomial pneumonia Nutritional support Sedation and paralysis Treating hypoxemia Diuresis Prone positioning Decrease oxygen consumption