Anaesthesia for Patients with COPD

1. Anaesthesia for Patients with COPD Dr SajithDamodaran University College of Medical Sciences & GTB Hospital, Delhi

2. COPD: Pathophysiology, Diagnosis, Treatment

3. Chronic Obstructive Pulmonary Disease Definition: Disease state characterised by airflow limitation that is not fully reversible The airflow limitation is usually progressive and is associated with an abnormal inflammatory response of the lungs to noxious particles or gases, primarily caused by cigarette smoking.

4. Chronic Obstructive Pulmonary Disease Definition: Disease state characterised by airflow limitation that is not fully reversible The airflow limitation is usually progressive and is associated with an abnormal inflammatory response of the lungs to noxious particles or gases, primarily caused by cigarette smoking.

5. COPD: Includes: • Chronic Bronchitis • Emphysema • Peripheral Airways disease Doesn’t include • Asthma, Asthmatic Bronchitis • Cystic Fibrosis • Bronchiactesis • Pulmonary fibrosis due to other • causes

6. COPD Chronic Bronchitis: (Clinical Definition) • Chronic productive cough for 3 months in each of 2 successive years in a patient in whom other causes of productive chronic cough have been excluded. Emphysema: (Pathological Definition) • The presence of permanent enlargement of theairspaces distal to the terminal bronchioles, accompanied by destruction of their walls and without obvious fibrosis

7. Comparative features of COPD

8. COPD: Risk factors • Host factos: • Genetic factors: Eg. α1 Antitrypsin Deficiency • Sex : Prevalence more in males. • ?Females more susceptible • Airway hyperactivity, • Immunoglobulin E and asthma • Exposures: • Smoking: Most Important Risk Factor • Socioeconomic status • Occupation • Environmental pollution • Perinatal events and childhood illness • Recurrent bronchopulmonary infections • Diet

9. Natural History: Fig. 1. - The normal course of forced expiratory volume in one second (FEV1) over time (–––) is compared with the result of impaired growth of lung function (––– ) an accelerated decline (–––) and a shortened plateau phase (–––). All three abnormalities can be combined (KerstjensHAM, Rijcken B, Schouten JP, Postma DS. Decline of FEV1 by age and smoking status: facts, figures, and fallacies. Thorax 1997; 52: 820–827.)

10. Pathophysiology: Pathological changes are seen in 4 major compartments of lungs: • central airways • Peripheral airways • lung parenchyma • pulmonary vasculature.

11. Pathophysiology: Excessive Mucus production • Central Airways: (cartilaginous airways >2mm of internal diameter) • Bronchial glands hypertrophy • Goblet cell metaplasia • Airway Wall Changes: • Inflammatory Cells Loss of cilia and ciliary dysfunction Squamousmetaplasia of the airway epithelium Increased smooth muscle and connective tissue • Peripheral airways (noncartilaginous airways<2mm internal diameter) • Bronchiolitis • Pathological extension of goblet cells and squamousmetaplasia • Inflammatory cells • Fibrosis and increased deposition of collagen in the airway walls Airflow limitation and hyperinflation

12. Pathophysiology: • Lung parenchyma (respiratory bronchioles, alveoli and capillaries) • Emphysema (abnormal englagement of air spaces distal to terminal bronchioles) • occurs in the parenchyma: • 2 Types: Centrilobular and Panlobular • Early microscopic lesion progress to Bullae over time. • Results in significant loss of alveolar attachments, which contributes • to peripheral airway collapse • Inflammatory cells Airflow limitation and hyperinflation • Pulmonary HTN • RV dysfunction (cor Pulmonale) • Pulmonary Vasculature: • Thickening of the vessel wall and endothelial dysfunction • Increased vascular smooth muscle & inflammatory infiltration of the vessel wall • Collagen deposition and emphysematous destruction of the capillary bed

13. Pathogenesis: Alpha 1 antitrypsin def. Tobacco smoke & other noxious gases Proteinase & Antiproteinase imbalance Increased Neutrophils, Lymphocytes & Macrophages Inflammatory response in airways Oxidative Stress Tissue Destruction Impaired defense against tissue destruction Impaired repair mechanisms

14. Physiological Effects: • Mucous hypersecretion and cilliary dysfunction • Goblet cell hyperplasia & squamousmetaplasia • Airflow limitation and hyperinflation • Airway remodelling • Loss of eleastic recoil • Destruction of alveolar supports • Accumulation of mucus, inflammatory cells & exudate • Gas exchange abnormalities: (Hypoxemia +/- Hypercapnia) • Abnormal V/Q ratios • Abnormal DLCO • Pulmonary hypertension • Hypoxic Vasoconstrictoin,Endothelial dysfunction • Remodelling of arteries & capillary destruction • Systemic effects

15. Diagnosis Clinical Features: • Physical Examination: • Respiratory Signs • Barrel Chest • Pursed lip breathing • Adventitious Ronchi/Wheeze • Systemic Signs • Cyanosis • Neck vein enlargement • Peripheral edema • Liver enlargement • Loss of muscle mass Symptoms: Cough: Initially intermittent Present throughout the day Sputum: Tenacious & mucoid Purulent Infection Dyspnoea: Progressively worsens Persistant Exposure:Smoking, in pack years

16. Diagnosis • Investigations: • Spirometry • Diagnosis • Assessment of severity • Following progress • Chest Radiograph: To exclude other diseases • Emphysematous changes • Bronchodilator Reversibility • Exclude Bronchial Asthma • <20% • Alpha-1 Antitrypsin levels • Young COPD with Family History

17. GOLD Classification

18. Treatment • Modifying natural history of Disease: • Smoking cessation • Long term oxygen therapy • Symptomatic: • Bronchodilators • Antibiotics • Others • Pulmonary Rehabilitation • Nutrition

19. Treatment: Smoking Cessation • Need: • Most important cause of COPD • Major risk factor for atherosclerotic vascular disease, cancer, peptic ulcer and osteoporosis. • Quitting smoking slows progressive loss of lung function & reduces symptoms • Motivation, Counselling & behavioural support • Nicotine replacement • Patches • chewing gum • Inhaler • nasal spray • lozenges • Bupriopion

20. Effect of smoking and smoking cessation on Lung Function: Loss of lung function over 11 yrs in the Lung Health Study for continuous smokers (–––), intermittent quitters (–––) and sustained quitters (–––). FEV1: forced expiratory volume in one second (AnthonisenNR et al,LungHealth Study Research Group. Smoking and lung function of Lung Health Study participants after 11 years. Am J RespirCrit Care Med 2002; 166: 675–679.

21. Treatment: Oxygen Therapy Long Term Oxygen Therapy(LTOT): • Improves survival, exercise, sleep and cognitive performance. • Oxygen delivery methods include nasal continuous flow, reservoir cannulas and transtracheal catheter. • Physiological indications for oxygen include an arterial oxygen tension (PaO2) <7.3 kPa (55 mmHg). The therapeutic goal is to maintain SpO2 >90% during rest, sleep and exertion.

22. Physiological indications for long-term oxygen therapy (LTOT) PaO2 mmHg SaO2 % LTOT indication Qualifying condition ≤55 ≤88 Absolute None 55–59 89 Relative with qualifier “P” Pulmonale, polycythemia >55% History of edema ≥60 ≥90 None except with qualifier Exercise desaturation Sleep desaturation not corrected by CPAP Lung disease with severe dyspnea responding to O2

23. Treatment: Symptomatic Measures • Bronchodilators: • Anticholinergics • Beta Agonists • Methylxanthines • Corticosteroids • N-Acetyl Cysteine • α1 Antitrypsin augmentation • Vaccination • Others: No proven effect • Leukotriene receptor antagonists/cromones • Maintenance antibiotic therapy • Immunoregulators • Vasodilators: NO, CCB

24. Surgical Treatment Bullectomy • short-term improvements in • airflow obstruction • lung volumes • hypoxaemia and hypercapnia • exercise capacity • dyspnoea Lung Volume Reduction Surgery • potentially long-term improvement in survival • short-term improvements in • Spirometry • lung volumes • exercise tolerance • dyspnoea Lung Transplantation

25. COPD: Exacerbations Definition: • An exacerbation of COPD is an event in the natural course of the disease characterised by a change in the patient’s baseline dyspnoea, cough and/or sputum beyond day-to-day variability sufficient to warrant a change in management. Precipitating Causes: • Infections: Bacterial, Viral • Air pollution exposure • Non compliance with LTOT

26. COPD: Exacerbations Indication for Hospitalisation: • The presence of high-risk comorbid conditions • pneumonia, • cardiac arrhythmia, • congestive heart failure, • diabetesmellitus, • renal or liverfailure • Inadequate response to outpatient management • Marked increase in dyspnoea, orthopnoea • Worsening hypoxaemia & hypercapnia • Changes in mental status • Uncertain diagnosis.

27. COPD: Exacerbations Indication for ICU admission: • Impending or actual respiratory failure • Presence of other end-organ dysfunction • shock • renal failure • liver failure • neurological disturbance • Haemodynamic instability

28. Treatment • Supplemental Oxygen (if SPO2 < 90%) • Bronchodilators: • Nebulised Beta Agonists, • Ipratropium with spacer/MDI • Corticosteroids • Inhaled, Oral • Antibiotics: • If change in sputum characteristics • Based on local antibiotic resistance • Amoxycillin/Clavulamate, Respiratory Flouroquinolones • Ventillatory support: NIV, Invasive ventillation

29. In a nutshell Optimal disease management entails redesigning standard medical care to integrate rehabilitative elements into a system of patient self-management and regular exercise

30. ………. Preparation for Anaesthesia

31. Anaesthetic Considerations in patients with COPD undergoing surgery: Patient Factors: • Advanced age • Poor general condition, nutritional status • Co morbid conditions • HTN • Diabetes • Heart Disease • Obesity • Sleep Apnea • Weak HPV, blunted Ventilatory responses to hypoxia and CO2 retention

32. Age Related Pulmonary Changes:

33. Anaesthetic Considerations in patients with COPD undergoing surgery: • Problems due to Disease • Exacerbation of Bronchial inflammation • d/t Airway instrumentation • preoperative airway infection • surgery induced immunosuppression • increased WOB • Increased post operative pulmonary complications

34. Anaesthetic Considerations in patients with COPD undergoing surgery: • Problems due to Anaesthesia: • GA decreases lung volumes, promotes V/Q mismatch • FRC reduced during anaesthesia, CC parallels FRC • Anaesthetic drugs blunt Ventilatory responses to hypoxia & CO2 • Postoperative Atelectasis & hypoxemia • Postoperative pain limits coughing & lung expansion • Problems due to Surgery: • Site : most important predictor of Post op complications • Duration: > 3 hours • Position

35. Pre-operative assessment: History: • Smoking • Cough: Type, Progression, Recent RTI • Sputum: Quantity, color, blood • Dyspnea • Exercise intolerance • Occupation, Allergies • Symptoms of cardiac or respiratory failure

36. Pre-operative assessment: Examination Physical Examination: Better at assessing chance of post op complications Airway obstruction • hyperinflation of chest, Barrel chest • Decreased breath sounds • Expiratory ronchi • Prolonged expiration: Watch & Stethoscope test, >4 sec ↑WOB • ↑ RR, ↑HR • Accessory muscles used • Tracheal tug • Intercostal indrawing • Tripod sitting posture

37. Pre-operative assessment: Examination • Respiratory failure • Hypercapnia • Hypoxia • Cyanosis • Cor Pulmonale and Right heart failure Dependant edema tender enlarged liver • Pulmonary hypertension • Loud P2 • Right Parasternal heave • Tricuspid regurgitation • Body Habitus Obesity/ Malnourished • Active infection • Sputum- change in quantity, nature • Fever • Crepitations

38. Preoperative Assessment: Investigations • Complete Blood count • Serum Electrolytes • Blood Sugar • Urinalysis • ECG • Arterial Blood Gases • Diagnostic Radiology • Chest X Ray • Spiral CT • Preoperative Pulmonary Function Tests • Tool for optimisation of pre-op lung function • Not to assess risk of post op pulmonary complications

39. Investigations: Chest X-Ray • Overinflation • Depression or flattening of diaphragm • Increase in length of lung • ↑ size of retrosternal airspace • ↑ lung markings- dirty lung • Bullae +/- • Vertical Cardiac silhouette • ↑ transverse diameter of chest, ribs horizontal, square chest • Enlarged pulmonary artery with rapid tapering in MZ

40. Pulmonary Function Tests:

41. Litres 0 FEV1 FVC FEV1/FVC 1 Normal 4150 5200 80% COPD 2350 3900 60% 2 FEV1 3 COPD FVC 4 FEV1 NORMAL FVC 5 seconds 1 2 3 4 5 Spirometric tracing in COPD patients

42. Maximum inspiratory and expiratory flow-volume curves (i.e., flow-volume loops) in four types of airwayobstruction.

43. Preoperative Assessment: Investigations ECG • Signs of RVH: • RAD • p Pulmonale in Lead II • Predominant R wave in V1-3 • RS pattern in precordial leads Arterial Blood Gases: • In moderate-severe disease • Nocturnal sample in cor Pulmonale • Increased PaCO2 is prognostic marker • Strong predictor of potential intra op respiratory failure & post op Ventilatory failure • Also, increased d/t post op pain, shivering, fever,respiratory depressants

44. Pre-operative preparation • Cessation of smoking • Dilation of airways • Loosening & Removal of secretions • Eradication of infection • Recognition of Cor Pulmonale and treatment • Improve strength of skeletal muscles – nutrition, exercise • Correct electrolyte imbalance • Familiarization with respiratory therapy, education, motivation & facilitation of patient care

45. Effects of smoking: • Cardiac Effects: • Risk factor for development of cardiovascular disease • CO decreases Oxygen delivery & increases myocardial work • Catecholamine release, coronary vasoconstriction • Decreased exercise capacity • Respiratory Effects: • Major risk factor for COPD • Decreased Mucociliary activity • Hyperreactive airways • Decreased Pulmonary immune function • Other Systems • Impairs wound healing

46. Smoking cessation and time course of beneficial Effects

47. Dilatation of Airways: • Bronchodilators: • Only small increase in FEV1 • Alleviate symptoms by decreasing hyperinflation & dyspnoea • Improve exercise tolerance • Anticholinergics • Beta Agonists • Methylxanthines

48. Anticholinergics: • Block muscarinic receptors • Onset of action within 30 Min • Ipratropium – • 40-80 μg by inhalation • 20 μg/ puff – 2 puffs X 3-4 times • 250 μg / ml respirator soln. 0.4- 2 ml X 4 times daily • Tiotropium - long lasting • Side Effects: • Dry Mouth, metallic taste • Caution in Prostatism & Glaucoma

49. Beta Blockers: • Act by increasing cAMP • Specific β2 agonist – • Salbutamol : • oral 2-4 mg/ 0.25 – 0.5 mg i.m /s.c 100-200 μg inhalation • muscle tremors, palpitations, throat irritation • Terbutaline : • oral 5 mg/ 0.25 mg s.c./ 250 μg inhalation • Salmeterol : • Long acting (12 hrs) • 50 μg BD- 200 μg BD • Formeterol, Bambuterol

50. Bronchodilators: methylxathines • Mode of Action – inhibition of phospodiesterase,↑ cAMP, cGMP – Bronchodilatation • Adenosine receptor antagonism • ↑ Ca release from SR • Oral(Theophyllin) & Intravenous (Aminophylline, Theophyllin) • loading – 5-6 mg/kg • Previous use – 3 mg/kg • Maintenace – • 1.0mg/kg h for smokers • 0.5mg/kg/h for nonsmokers • 0.3 mg/kg/h for severely ill patients.