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G M C  F I N A L
G M C  F I N A L
G M C  F I N A L
G M C  F I N A L
G M C  F I N A L
G M C  F I N A L
G M C  F I N A L
G M C  F I N A L
G M C  F I N A L
G M C  F I N A L
G M C  F I N A L
G M C  F I N A L
G M C  F I N A L
G M C  F I N A L
G M C  F I N A L
G M C  F I N A L
G M C  F I N A L
G M C  F I N A L
G M C  F I N A L
G M C  F I N A L
G M C  F I N A L
G M C  F I N A L
G M C  F I N A L
G M C  F I N A L
G M C  F I N A L
G M C  F I N A L
G M C  F I N A L
G M C  F I N A L
G M C  F I N A L
G M C  F I N A L
G M C  F I N A L
G M C  F I N A L
G M C  F I N A L
G M C  F I N A L
G M C  F I N A L
G M C  F I N A L
G M C  F I N A L
G M C  F I N A L
G M C  F I N A L
G M C  F I N A L
G M C  F I N A L
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G M C F I N A L

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  • 1. MECHANICAL VENTILATION IN COPD SPEAKER :DR.GOOLAPPA MODERATOR: DR.HARISH R.D.T HOSPITAL, BTP.
  • 2. DEFINITION OF COPD <ul><li>It is chronic </li></ul><ul><li>It is progressive </li></ul><ul><li>Mostly fixed airway obstruction </li></ul><ul><li>Non reversible by bronchodilators </li></ul><ul><li>Exposure to noxious agent is a must </li></ul><ul><li>Chronic obstructive lung disease (COLD) </li></ul><ul><li>Chronic obstructive airways disease (COAD) </li></ul><ul><li>Two entities in COPD – namely </li></ul><ul><ul><li>Chronic Bronchitis 2. Emphysema </li></ul></ul>
  • 3. 2 . CHRONIC BRONCHITIS 1. EMPHYSEMA <ul><li>Productive cough </li></ul><ul><li>For a period of 3 months </li></ul><ul><li>In each of 2 consecutive years </li></ul><ul><li>Absence of any other identifiable cause of excessive sputum production </li></ul><ul><li>Airflow limitation that is not fully reversible </li></ul><ul><li>Abnormal inflammatory response to noxious agent - like smoking </li></ul><ul><li>Alveolar wall destruction </li></ul><ul><li>Irreversible enlargement of the air spaces </li></ul><ul><li>Distal to the terminal bronchioles </li></ul><ul><li>Without evidence of fibrosis </li></ul>
  • 4. SMOKING - THE CULPRIT
  • 5. RISK FACTORS FOR COPD <ul><li>Host Factors </li></ul><ul><ul><li>Genes (alpha 1 - anti-trypsin ↓ ) </li></ul></ul><ul><ul><li>Hyper responsiveness </li></ul></ul><ul><ul><li>Lung growth, low BW, Age </li></ul></ul><ul><li>Exposure </li></ul><ul><ul><li>Tobacco smoke , </li></ul></ul><ul><ul><li>Bio mass fuel smoke, open fires </li></ul></ul><ul><ul><li>Occupational dusts and chemicals </li></ul></ul><ul><ul><li>Chronic uncontrolled asthma </li></ul></ul><ul><ul><li>Infections, overcrowding, damp </li></ul></ul><ul><ul><li>Low socioeconomic status </li></ul></ul><ul><ul><li>Low dietary vegetable and fruit intake </li></ul></ul>MOST IMP RISK
  • 6. CLINICAL FEATURES
  • 7. CHRONIC BRONCHITIS <ul><li>Mild dyspnea </li></ul><ul><li>Cough before dyspnea starts </li></ul><ul><li>Copious, purulent sputum </li></ul><ul><li>More frequent infections </li></ul><ul><li>Repeated resp. insufficiency </li></ul><ul><li>PaCO 2 50-60 mmHg </li></ul><ul><li>PaO 2 45-60 mmHg </li></ul><ul><li>Hematocrit 50-60% </li></ul><ul><li>DLCO is not that much ↓ </li></ul><ul><li>Cor pulmonale common </li></ul>EMPHYSEMA <ul><li>Severe dyspnea </li></ul><ul><li>Cough after dyspnea </li></ul><ul><li>Scanty sputum </li></ul><ul><li>Less frequent infections </li></ul><ul><li>Terminal RF </li></ul><ul><li>PaCO 2 35-40 mmHg </li></ul><ul><li>PaO 2 65-75 mmHg </li></ul><ul><li>Hematocrit 35-45% </li></ul><ul><li>DLCO is decreased </li></ul><ul><li>Cor pulmonale rare. </li></ul>
  • 8. CHRONIC BRONCHITIS EMPHYSEMA BLUE BLOTTER PINK PUFFER
  • 9. ALPHA 1 ANTITRYPSIN ↓ <ul><li>Specific circumstances of Alpha 1- AT ↓include . </li></ul><ul><li>Emphysema in a young individual (< 35) </li></ul><ul><li>Without obvious risk factors (smoking etc) </li></ul><ul><li>Necrotizing panniculitis, Systemic vasculitis </li></ul><ul><li>Anti-neutrophil cytoplasmic antibody (ANCA) </li></ul><ul><li>Cirrhosis of liver, Hepatocellular carcinoma </li></ul><ul><li>Bronchiectasis of undetermined etiology </li></ul><ul><li>Otherwise unexplained liver disease, or a </li></ul><ul><li>Family history of any one of these conditions </li></ul><ul><li>Especially siblings of PI*ZZ individuals. </li></ul><ul><li>Only 2% of COPD is alpha 1- AT ↓ </li></ul>EMPHYSEMA
  • 10. CLINICAL SIGNS <ul><li>Physical exam may be negative </li></ul><ul><li>Hyper-inflated chest, Barrel chest </li></ul><ul><li>Wheeze or quite breathing </li></ul><ul><li>Pursed lip / accessory muscles resp. </li></ul><ul><li>Peripheral edema </li></ul><ul><li>Cyanosis, ↑ JVP </li></ul><ul><li>Cachexia </li></ul><ul><li>Cough, wheeze, dyspnea, sputum </li></ul><ul><li>Decreased FEV 1 </li></ul><ul><li>Decreased FVC </li></ul><ul><li>FEV 1 < 80% </li></ul><ul><li>FEV 1 ÷ FVC < 70% </li></ul><ul><li>Post bronchodilator – no change in FEV 1 </li></ul><ul><li>PEF is decreased </li></ul><ul><li>FET – is prolonged </li></ul><ul><li>V Max - decreased </li></ul>SPIROMETRY
  • 11. MRC DYSPNOEA SCALE Too breathless to leave house or breathless while dressing 4 Stops for breath on walking 100 m or after 2 or 3 minutes continuously 3 Walks slower than contemporaries or has to stop for breath while walking alone 2 Short of breath when walking uphill or while hurrying to catch a bus or train 1 No breathlessness except on strenuous exercise 0 Degree of breathlessness - related activity Grade
  • 12. DIFF. Dx. of COPD & ASTHMA Change > 15% Change < 15% Reversibility ICS IBD (Ipa+Salm) Most IMP Rx. Normal or Obstru. Obstructive Spirometry Useful ad on Rx. Not useful Anti leukotrn. Variable, static Progressive Course Episodic Persistent Dyspnea Mucoid or none Productive Sputum Nearly all Rare Age < 35 May or may not be Nearly all Smoker ASTHMA COPD Clinical
  • 13. CHEST SKIAGRAMS OF EMPHYSEMA
  • 14. CHEST SKIAGRAM OF CHRONIC BRONCHITIS
  • 15. CHEST LATERAL VIEW CHRONIC BRONCHITIS
  • 16. ASSESSMENT OF COPD <ul><li>Diagnosis of COPD </li></ul><ul><li>Spirometry is the Gold Standard </li></ul><ul><li>Every COPD suspect must get spirometry test done </li></ul><ul><li>Like ECG, Spirometry is essential </li></ul><ul><li>Arterial blood gas tensions are needed if the FEV 1 < 40% </li></ul><ul><li>Respiratory failure, Corpulmonale </li></ul>
  • 17. NORMAL AND COPD SPIROMETRY
  • 18. <ul><li>IBD are the main stay </li></ul><ul><li>As when needed basis </li></ul><ul><li>The main drugs are </li></ul><ul><ul><li>β 2 - Agonists (Salbutamol group) </li></ul></ul><ul><ul><li>Anticholinergics (Ipatropium group) </li></ul></ul><ul><ul><li>Their combination </li></ul></ul><ul><ul><li>?? Theophylline </li></ul></ul>MANAGEMENT - IBD
  • 19. Pledge to stop smoking
  • 20. Why use ventilatory assistance ? <ul><li>• patients with COPD are prone to exacerbations of respiratory failure </li></ul><ul><li>• mechanical ventilatory assistance is useful in patients with respiratory failure </li></ul><ul><li>• in COPD, 16-35% of acute exacerbations are intubated </li></ul><ul><li>• overall mortality is high (19-29%) </li></ul>
  • 21. Limitations of invasive ventilation <ul><li>• requirement for sedation (& paralysis) </li></ul><ul><li>• nosocomial infection </li></ul><ul><li>• laryngeal/tracheal injury </li></ul><ul><li>• weaning difficulties </li></ul><ul><li>• progression to tracheostomy </li></ul><ul><li>• prolonged stay in ICU (cost) </li></ul>
  • 22. <ul><li>Advantages of NPPV </li></ul><ul><li>• avoids intubation & potential complications </li></ul><ul><li>• better patient comfort </li></ul><ul><li>• coughing, speech & swallowing preserved </li></ul><ul><li>• little or no sedation required </li></ul><ul><li>• can be used where intubation inappropriate </li></ul><ul><li>• can be used away from ICU & potentially ↓ costs </li></ul>
  • 23. Limitations of NPPV <ul><li>• need patient co-operation </li></ul><ul><li>• patient must protect upper airway </li></ul><ul><li>• no direct access to airway (secretion clearance) </li></ul><ul><li>• risk of mask dislodgment </li></ul><ul><li>⇒ inadequate ventilation </li></ul><ul><li>• not all patients tolerate NPPV (up to 20% fail) </li></ul><ul><li>• appropriately skilled staff required </li></ul>
  • 24. Current Recommendations - NPPV in ARF <ul><li>• Strong Evidence – Level A (multiple controlled trials) </li></ul><ul><li>• Acute hypercapnic COPD </li></ul><ul><li>• Acute cardiogenic Pulmonary Oedema – most evidence for CPAP </li></ul><ul><li>• Immunocompromised patients </li></ul><ul><li>• Less strong – Level B (single controlled trials, multiple case series) </li></ul><ul><li>• Asthma </li></ul><ul><li>• Community Acquired Pneumonia in COPD patients </li></ul><ul><li>• Facilitation of weaning in COPD </li></ul><ul><li>• Avoidance of extubation failure </li></ul><ul><li>• Post Operative Respiratory Failure </li></ul><ul><li>• Do not intubate patients </li></ul>
  • 25. NPPV in COPD <ul><li>Mechanism of action </li></ul><ul><li>• multifactorial, controversial and poorly understood </li></ul><ul><li>• ↓ work of breathing </li></ul><ul><li>• ‘ rest’ respiratory muscles </li></ul><ul><li>• ↓ respiratory muscle fatigue </li></ul><ul><li>• ↓ dyspnoea </li></ul><ul><li>• counter intrinsic PEEP </li></ul><ul><li>• reverses acidosis </li></ul><ul><li>• allows time for conventional therapy to work </li></ul><ul><li>• avoid death by intubation </li></ul>
  • 26. NPPV in acute COPD – results <ul><li>• reduction in mortality - 48% </li></ul><ul><li>• reduction in intubation rates – 59% </li></ul><ul><li>• significant improvements in pH, PaCO2, & PaO2 & </li></ul><ul><li>respiratory rate </li></ul><ul><li>• reduction in hospital length of stay > 3 days </li></ul><ul><li>• only 1 negative study – here less sick, & delay ~12 </li></ul><ul><li>hours to commencement of NPPV </li></ul>
  • 27. NPPV – How to Make it work in ARF <ul><li>• Patient factors </li></ul><ul><li>• diagnosis </li></ul><ul><li>• clinical characteristics </li></ul><ul><li>• lower APACHE score </li></ul><ul><li>• no pneumonia </li></ul><ul><li>• pH > 7.10, PaCO2 < 92mmHg </li></ul><ul><li>• better neurological state </li></ul><ul><li>• good initial response to NPPV </li></ul>
  • 28. <ul><li>• Staff </li></ul><ul><li>need adequate training </li></ul><ul><li>Site for NPPV </li></ul><ul><li>need to be able to monitor patient properly </li></ul><ul><li>need expertise in intubation – especially with </li></ul><ul><li>conditions where failure more likely e.g. asthma </li></ul>
  • 29. Contraindications <ul><li>• patients requiring >50% oxygen </li></ul><ul><li>• thoracic / gastric surgery / pneumothorax </li></ul><ul><li>• patients unable to maintain patent airway / clear secretions </li></ul><ul><li>• significant hypotension induced by NPPV therapy </li></ul><ul><li>• fractured base skull / facial fractures / ↑ Intracranial pres </li></ul><ul><li>• respiratory arrest </li></ul>
  • 30. Interfaces:-Nasal & Full Face masks
  • 31. Implementation - Hypercapnoeic RF <ul><li>• sit patient upright & explain procedure </li></ul><ul><li>• commence and titrate up to maximum tolerated level </li></ul><ul><li>• full face masks get better control of leaks </li></ul><ul><li>• apply chin strap if required / instruct patient to close mouth </li></ul><ul><li>• apply oxygen to machine end of tubing if required </li></ul>
  • 32. Monitoring <ul><li>• Observations </li></ul><ul><li>• BP, RR, HR & rhythm, O2 saturation, conscious state </li></ul><ul><li>• Treatment tolerance, complications </li></ul><ul><li>• Initially, 15 minutely for 1 hour, 30 minutely for 2 </li></ul><ul><li>hours, Hourly for 2 hours, then 4 hourly </li></ul><ul><li>• ABGs – measured prior to commencement, at 1 hour, </li></ul><ul><li>within 1 hour of setting changed, then as clinically needed </li></ul>
  • 33. Weaning in Acute COPD Exacerbation <ul><li>• Aim to remove NPPV within 48hours </li></ul><ul><li>• weaning is commenced </li></ul><ul><li>• once reversal of acute factors & improved ABGs </li></ul><ul><li>• after consultation with medical team </li></ul><ul><li>• weaning carried out during day initially and then night </li></ul><ul><li>• ↑ ing time off ventilation rather than ↓ing pressures </li></ul><ul><li>• monitor clinically and with ABGs as required </li></ul>
  • 34. The Decision To Intubate <ul><li>Initiation of mechanical ventilation in COPD patients is associated with high patient mortality and poor potential for weaning </li></ul><ul><li>Indications: (E.B.M. vs. clinical gestalt ) </li></ul><ul><ul><li>Patient failed conservative management </li></ul></ul><ul><ul><li>Severe, persistent acidosis </li></ul></ul><ul><ul><li>Continued arterial hypoxemia despite initial therapy </li></ul></ul><ul><ul><li>Patient fatigue </li></ul></ul><ul><ul><li>Altered mental status </li></ul></ul><ul><ul><li>Additional major illness (pulmonary embolism, AMI) </li></ul></ul>
  • 35. Goals for COPD patients <ul><li>Adequate patient monitoring </li></ul><ul><li>Optimize ventilator settings to minimize excessive work of breathing </li></ul><ul><li>Assure Synchrony </li></ul><ul><li>Detect auto-PEEP and prevent barotrauma </li></ul><ul><li>Prevent further respiratory muscle atrophy </li></ul><ul><li>Intubate using the widest diameter ET tube possible (R = 8nl / π r 4 ) </li></ul>
  • 36. Vent Guidelines <ul><li>Emphasis on assisted modes of ventilation (patient initiated), institution preference for A/C vs. IMV with PSV (to overcome ET tube) </li></ul><ul><li>SIMV: probably causes excess work, b/c of high resistance circuit but debatable; requires close patient monitoring </li></ul>
  • 37. Vent Guidelines <ul><li>Tidal Volume: 5-7 ml/kg </li></ul><ul><li>Set Rate: 4 less than spontaneous rate </li></ul><ul><li>FiO2: adjust to PaO2 of at least 60 mmHg </li></ul><ul><li>Triggering: -1 to -2 cm H2O </li></ul><ul><li>Prevent Auto-PEEP with sufficient PEEP </li></ul><ul><li>Flow rate: Increase to provide increased expiratory time (70-90 lpm) </li></ul><ul><li>Continue inhaled medications: requires sufficient tidal volume and inspiratory time </li></ul>
  • 38. Summary <ul><li>The need to initiate mechanical ventilation in patients with obstructive lung disease in the emergency department is associated with a higher inpatient mortality </li></ul><ul><li>Patients with obstructive lung disease require close monitoring of all physiologic parameters to prevent complications associated with positive pressure ventilation </li></ul><ul><li>Assessing a distressed ventilator dependent patient requires an organized approach </li></ul><ul><li>In general: low tidal volumes, higher flow rates and application of a conservative amount of PEEP are appropriate initial settings for patients with obstructive lung disease </li></ul>
  • 39. References <ul><li>“ The ICU Book” Marino PL, 2 nd Edition </li></ul><ul><li>“ Respiratory Physiology” West JB, 5 th Edition </li></ul><ul><li>“ Pulmonary Pathophysiology” Grippi MA </li></ul><ul><li>“ Textbook of Medical Physiology” Guyton and Hall 9 th Edition </li></ul><ul><li>“ Chest Radiology Companion” Stern EJ, White CS </li></ul><ul><li>Harrison’s Principles of Internal Medicine 16 th Edition </li></ul>
  • 40.  
  • 41. THANK YOU

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