![Low Tidal Volume Ventilation
Calculate ideal body weight (IBW) in pounds
1. Males- 106 + [ 6 x (height in inches 60 inches)]
2. Females- 105 + [ 5 x (height in inches 60 inches)]
Convert into kg by multiplying with 0.453
Set initial tidal volume to 6 ml/kg IBW
Set respiratory rate to < 35 per minute to match baseline minute ventilation](https://image.slidesharecdn.com/ards-satya-220821142805-1bb19916/85/ARDS-Satya-pptx-37-320.jpg)
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ARDS- Satya.pptx
- 1. ACUTE RESPIRATORY DISTRESS SYNDROME Presenter: Dr. SATYAJIT HAJONG Moderator: Dr .Th. BROJENDRO
- 2. The Berlin Definition Of ARDS A clinical syndrome of acute onset dyspnea , severe hypoxemia, diffuse pulmonary infiltrates and decreased respiratory system compliance leading to respiratory failure in absence of evidence of congestive heart failure
- 3. First described in 1967 by Ashbaugh and Petty in The Lancet Incidence (per 1,00,000 person years)- Total- 86.2 Moderate and severe- 64 Dramatically increases between age 75 to 84 yrs - 306
- 4. OLDER DEFINITION According to American European Consensus Conference acute onset of illness , bilateral chest radiographic infiltrates consistent with pulmonary Oedema , poor systemic oxygenation and absence of evidence for left atrial hypertension PaO2/FiO2 if is < 300- Acute Lung Injury, if < 200 then ARDS Cardiogenic pulmonary oedema must be excluded by clinical criteria/ PCWP lower than 18 mm Hg Limitations- subjective variability of CXR interpretation, variable PaO2/FiO2 with PEEP
- 5. THE BERLIN DEFINITION OF ARDS 2012 Clinical variables Parameters Onset Within 1 week of inciting event Chest radiograph (CXR/ CT chest) B/L opacities, not explained by effusion, atelectasis or nodules Non-cardiac aetiology Respiratory failure not fully explained by cardiac failure or fluid overload Hypoxemia (PaO2/FiO2) </= 300 mmHg at PEEP >/= 5 cm H2O
- 6. ARDS Severity ARDS Severity PaO2/FiO2 in mmHg (at PEEP>/= 5cm H2O) Mortality Mild 200-300 26% Moderate 100-200 32% Severe <100 45-58%
- 7. Etiology Direct causes Indirect causes Pneumonia(40 to 50)% Aspiration of gastric contents Pulmonary contusion Fat , amniotic fluid or air embolism Near drowning Inhalational injury Reperfusion injury High altitude pulmonary oedema Neurogenic pulmonary oedema Re-expansion pulmonary oedema Sepsis- most common cause Multiple Trauma Burns Acute pancreatitis Post cardiopulmonary bypass Toxic ingestions- aspirin, TCAs Transfusion of blood products
- 8. Factors Influencing The Risk and Mortality Advanced age Chronic liver disease Hypoproteinaemia Increased severity and extent of illness as measured by APACHE score Hyper transfusion of blood products Chronic alcohol abuse Cigarette smoking Long hospital stay prior to the development of ARDS
- 9. The natural history of ARDS is marked by three phases 1.Exudative (First 7 days) 2.Proliferative (After 7-21 days) 3.Fibrotic (After 3-4 weeks) Pathophysiology
- 10. Initial Exudative" phase-diffuse alveolar damage within the first week
- 11. Alveolar capillary membrane(ACM) integrity is lost, interstitial and alveolus fills with proteinaceous fluid, surfactant can no longer support alveolus Ware et al. NEJM 2000; 342:1334
- 12. Direct or indirect injury to the alveolus causes alveolar macrophages to release pro- inflammatory cytokines Ware et al. NEJM 2000; 342:1334
- 13. Cytokines attract neutrophils into the alveolus and interstitum, where they damage the alveolar-capillary membrane (ACM). Ware et al. NEJM 2000; 342:1334
- 14. Most patient recover in this stage Signs of resolution and lung repair * Neutrophil to lymphocytes predominant infiltrates * Type II pneumocytes proliferation and differentiation into type I pneumatocytes * New pulmonary surfactant Proliferative phase
- 15. Require long term airway support(mechanical/supplemental O2) Histologically-alveolar duct and interstitial fibrosis Pulmonary hypertension from intimal fibroproliferation Pulmonary fibrosis= increased mortality Fibrotic phase
- 16. Stages of ARDS EXUDATIVE PROLIFERATIVE FIBROTIC 0-6 days Accumulation of excess fluid in the lung Hypoxemia is maximum at this stage Some individuals recover from this stage 3 stages of oedema- Stage 1- drained by lymphatic Stage2- interstitial Stage 3- alveolar 7-21 days Connective tissue, fibroblasts proliferation Termed as stiff lung/ shock lung Abnormally enlarged air spaces and fibrotic tissue are increasingly apparent > 21 days Oxygenation improves and extubation becomes possible Lung function continue to improve over as long as 6-12 months Varying levels of residual fibrotic changes remain
- 17. Resolution of ARDS Removal of alveolar oedema fluid (10-20% per hour) via 5 routes- lymphatics, blood vessels, airways, pleural space and mediastinum Mechanism- activated NaCl transporter Protein removal- (1-2% per hour)- mostly as intact- f/b phagocytosis Removal of interstitial fluid- in blood vessels or mediastinum 25-30% of oedema fluid- leaves into pleural space- pleural effusion
- 20. Clinical Presentation Acute dyspnoea within 7 days of an inciting event Hypoxemia resistant to oxygen therapy (d/t large R->L shunt)- Need for high fraction of inspired O2(*FiO2) to maintain O2 saturation Tachypnoea (earliest sign), tachycardia, cyanosis Restlessness, confusion, disorientation Hypertension or low BP when in shock Bilateral fine crepitation on chest auscultation Other manifestations of the underlying cause
- 22. Differential Diagnosis Most common Less frequent Cardiogenic pulmonary oedema Diffuse pneumonia Alveolar haemorrhage Acute interstitial lung disease Hypersensitivity pneumonitis Radiation pneumonitis B/L lower lobe atelectasis Severe U/L lower lobe atelectasis Massive pulmonary embolism
- 23. Chest Radiograph in ARDS Diffuse bilateral lung infiltrates extending to the lung margins Early in the course infiltrates may have patchy peripheral distribution CT scan of chest- more informative Drawbacks- oedema may not be visible until lung water increases upto 30% and upto 12 hours after onset of dyspnoea
- 28. Chest x ray in ARDS
- 29. Arterial Blood Gas Hypoxemia- PaO2/FiO2 <300 mm Hg Initially respiratory alkalosis However if ARDS is due to sepsis- metabolic acidosis with or without respiratory compensation As the condition progresses the work of breathing increases and pCO2 begins to rise- respiratory acidosis
- 30. Broncho alveolar lavage Most reliable to confirm or exclude ARDS Neutrophils- in normal individuals <5% whereas in ARDS upto 80% Total protein- lavage fluid rich in protein is evidence of inflammation When protein in lavage fluid expressed as a fraction of serum protein concentration- If <0.5 indicates hydrostatic oedema If >0.7 indicates lung inflammation
- 31. Other Investigations CBC- leukopenia/ leucocytosis, thrombocytopenia (in DIC) RFT and LFT- deranged in acute tubular necrosis and hepatocellular injury respectively Cytokines- IL-1, IL-6, IL-8 levels are elevated Pro calcitonin- marker of sepsis Von Willebrand Factor & plasma angiopoietin 2 : markers of impending ARDS with non pulmonary sepsis- poor outcome Plasma BNP- to exclude cardiogenic pulmonary oedema <100 pg/ml- unlikely heart failure >500 pg/ml- heart failure is likely Echocardiography - to exclude cardiogenic pulmonary edema
- 32. Complications COMMON OTHERS Nosocomial pneumonia Barotrauma SIRS and MODS 1. Renal- 40-55% 2. Liver- reversible , enzyme changes in 95%, fulminant hepatitis in 10% 3. Myocardial depression by TNF- 10-23% 4. DIC- 26% 5. GIT- 7-30% as haemorrhage, ileus, malabsorbtion Oxygen toxicity Stress ulcers Tracheal ulcerations Deep vein thrombosis Pulmonary embolism Pressure sores
- 33. Management of ARDS Goals : To diagnose and treat the precipitating cause To maintain oxygenation To prevent ventilator induced lung injury (VILI) Hemodynamic management To keep pH in normal range without compromising goal to prevent VILI Prevention of other complications
- 35. Mechanical Ventilation No role of NIPPV (Only one comparative study by Ferrer et.al) To enhance patient ventilator synchrony and patient comfort by sedation, amnesia, opioid analgesia, antipyretics and pharmacological paralysis- also decreases oxygen consumption To apply PEEP to maximize alveolar recruitment & minimize cyclic atelectasis Wean from mechanical ventilation when patient can breathe without assisted ventilation to the earliest
- 36. 1. Maintaining adequate oxygenation- Positive end expiratory pressure (PEEP) is employed When utilized in sufficient amount PEEP allows lowering of FiO2 from high, potentially toxic concentrations Lung protective mechanical ventilation- Mechanical ventilation using limited tidal volume The goal is to avoid injury to the alveoli 1. By overexpansion during inspiration (volu-trauma) 2. Due to repetitive opening and closing during inspiration and expiration (atelecta-trauma)
- 37. Low Tidal Volume Ventilation Calculate ideal body weight (IBW) in pounds 1. Males- 106 + [ 6 x (height in inches 60 inches)] 2. Females- 105 + [ 5 x (height in inches 60 inches)] Convert into kg by multiplying with 0.453 Set initial tidal volume to 6 ml/kg IBW Set respiratory rate to < 35 per minute to match baseline minute ventilation
- 38. Ventillator Mode - Volume Assist / control Tidal Volume (VT) 6ml/kg of IBW Measure pleatue pressure (Pplat 0.5 sec inspiratory pause ) every 4hrs and after each change in PEEP and VT Goal is to maintain plateau pressure(Pplat) </= 30 cm of H2O If Pplat rises above 30cm of H2O decrease tidal volume to 5 or to 4ml/kg IBW If Pplat is below 25cm of H2O increase tidal volume by 1ml /kg IBW to keep Pplat >25cm of H2O
- 39. Positive end expiratory pressure (PEEP) is employed I:E ratio -1: to 1:3 Maintain PaO2 : ( 50 to 60) mm of Hg SpO2 : ( 88 to 95) % FiO2 30 to 40 % 40% 50% 60% 70% 80% 90% 100 % PEEP 5to8 8 to 14 8 to 16 10 to 20 10 to 20 14 to 22 16 to 22 18 to 25
- 40. Acidosis management If pH < 7.3 increase RR until pH >7.3 or RR 35 If pH remains < 7.3 with RR 35 consider bicarbonate infusion If pH < 7.15, VT may be increased( (Pplat may exceed 30cm of water)
- 41. Alkalosis management If pH >7.4 and paient not triggering ventillator decrease set RR but not below 6/min
- 42. Weaning from Mechanical Ventillation Daily interruption of sedation Daily screen for spontenous breathing trial Give spontenous breathing trial when all of the following criteria are present 1. FiO2<40% PEEP <8cm of H2O 2. Not receiving neuro mascular blocking agent 3.Patient is awake and following commands 4.Systolic arterial pressure >90mm of Hg without vasopressors 5.Tracheal secretions are minimal and patient have a good cough and gag reflex
- 43. Spontaneous Breathing Trial 1. Place patient on 5mm Hg pressure support with 5mm of Hg PEEP 2. Monitor HR , RR, SPO2 for 20 to 30 min 3. Extubate if there is no signs of distress ( tachycardia , tachypnea , agitation , diaphoresis )
- 46. Open Lung Ventilation Combines LTVV with enough applied PEEP LTTV- mitigates alveolar over distention and PEEP- minimizes cyclic atelectasis PEEP is set at least 2 cm above the lower inflection point of the pressure volume curve If the point is uncertain- PEEP of 16 cm of H2O is to be applied Drawback -it has the potential to cause barotrauma and decrease cardiac output
- 47. Adjuncts to lung protective ventilation 1. Permissive hypercapnia LTVV causes reduction of CO2 elimination- allowing this to persist in favour of maintaining lung protective LTVV is known as permissive hypercapnia Can be minimized by highest respiratory rate that does not induce auto PEEP Also by changing from a heat & moisture exchanger to a heated humidifier Can cause hyperventilation (brainstem stimulation)- neuromuscular blockade Data shows arterial pCO2 levels of 60-70 mmHg is safe
- 48. 2. Recruitment manoeuvres- intermittent increase of PEEP, by maintaining CPAP of 35 to 40cm of H2O for 30 seconds 3. Prone positioning- About 66% of the patients improve oxygenation with this Mechanisms - 1. Increase in functional residual capacity 2. Change in regional diaphragmatic motion 3. Perfusion redistribution 4. Improve clearance of secretions
- 49. Extra Corporeal Membrane Oxygenation Modified heart lung machine- gas exchange and circulatory support Veno-venous(VV) ECMO- for gas exchange Veno-arterial(VA) ECMO- for both gas exchange and circulatory support ARDS with pneumonia is the commonest situation needing ECMO
- 50. Newer therapeutic strategies 1. Intra venous mesenchymal stromal (stem) cells(START Trial) being tested in phase 2 clinical trial have pleotropic protective and reparative effect in the lungs 2. Use of pulmonary vasodialators - inhaled nitric oxide and prostacyclin 3. Glucocorticoids ( methylprednisolone ) hastens resolution of late fibroproliferative ARDS not recommended for routine use
- 51. Fluid management Golden rule- hydrostatic pressure to be kept as low as possible provided that oxygen delivery to the tissues is not compromised Tailored systemic fluid restriction to achieve lowest intravascular volume that maintain adequate tissue perfusion The lung infiltration in ARDS is an inflammatory process- diuretics dont reduce this , but helps in lowering intra vascular volume To maintain CVP < 4 2 ,MAP> 65 mmHg and Urine output > 0.5 ml/kg/hour
- 52. Nutrition High fat and low carbohydrate diet reduces the duration of mechanical ventilation by reduction in carbon dioxide production and reduction in respiratory quotient
- 53. Other agents Agent Mechanism of action Recommendation Glucocorticoids Anti-inflammatory NO Neuromuscular blockers Promotes ventricular synchrony, decrease oxygen consumption YES Statins Antagonising inflammatory cytokines Under experimentation Beta-agonists Fluid removal by activated sodium pump via cAMP NO Macrolide antibiotics Unknown Under experimentation
- 54. Mortality and Functional Recovery Mortality- ARDS Network published in 2012 , 60 day mortality was 23% 1 year mortality is 41% 32% for mild ARDS , 58 to 60 % for moderate to severe ARDS Early death - due to the underlying cause of ARDS most commonly Death in later course- nosocomial pneumonia and sepsis causing MODS
- 55. Mortality and Functional Recovery Functional recovery- Maximum lung function- by 6 months One year after extubation over 33% survivors have normal spirometry and diffusion capacity Most of the remaining survivors have only mild abnormalities- others low exercise capacity Significant rate of post traumatic stress disorder in the form of depression and anexity
- 56. Conclusion ARDS is a multisystem syndrome Characterised by accumulation of fluid in the lungs with resulting hypoxemia and some degree of fibrotic changes The most frequent causes - sepsis, pneumonia, aspiration and severe trauma Treatment- supportive, ventilation and oxygenation strategies Despite many theoretical therapies the best proven strategy to improve survival is LOW TIDAL VOLUME VENTILATION Despite all advances mortality is still very high ranging from 26-58%
- 57. References Fishmans Pulmonary Diseases and Disorders 5th Edition Harrisons Principles of Internal Medicine 20th edition The ICU book,3rd edition- Paul L. Marino JAMA, June 20th, 2012- vol 307, no 23: Berlin definition Finks Textbook of Critical care 7th edition
- 58. THANK YOU
- 59. Pathophysiology Normally small amount of fluid leaking into the interstitium is drained by lymphatic system In ARDS- diffuse alveolar injury (T1 pneumocytes)-> release of cytokines-> recruitment and activation of neutrophils Neutrophils release toxic mediators (ROS, proteases)-> capillary endothelium and alveolar epithelium damage-> protein loss into interstitium Loss of oncotic gradient-> fluid pours into interstitium overwhelming the lymphatic system Epithelial breakage- alveoli get filled with oedema fluid and debris
- 60. In addition surfactants are lost resulting in alveolar collapse These result in impaired gas exchange, decreased compliance and increased pulmonary arterial pressure Physiological shunt- continued perfusion of non ventilated alveoli (V/Q=0) Microscopically- 1. Widespread alveolar and interstitial oedema, inflammation & haemorrhage 2. Hyaline membrane composed of plasma proteins, fibrin & necrotic debris- the footprint of a pathologic finding- diffuse alveolar damage (DAD) MODS- due to increased concentration of biologically active soluble Fas ligand (sFasL 45 kD)- apoptosis
- 62. Time course of evolution of ARDS
- 65. Effective anti sepsis interventions Antibodies against macrophage migration inhibitory factor Antibodies against high mobility group B1 protein Stem cell therapy- Human Mesenchymal Stem Cells for Acute Respiratory Distress Syndrome (START trial)
Editor's Notes
- #3: Synonyms- sponge lung/ shock lung/ non cardiogenic pulmonary oedema/ capillary leak syndrome/ adult hyaline membrane disease/ wet lung/ da nang lung
- #4: Non-cardiogenic pulmonary edema Profound hypoxemia difference between ali and ards.
- #21: due to hyper adrenergic state),
- #23: Alveolar haemorrhage (especially in post bone marrow transplantation) pneumonia (often with autoimmune diseases/post bone marrow transplantation ) Severe U/L lower lobe atelectasis (especially when on vasodilators- blunting hypoxic vasoconstriction)