1 COPD and ASTHMA Nick Weber, MD Chief Medical Resident VA Medical Center February 2, 2011
2 Objectives 1. Distinguish asthma, COPD 2. COPD: Background, RF, pathophysiology, diagnosis, mgmt, complications, prognosis 3. Asthma: Background, RF, pathophysiology, diagnosis, mgmt, complications 4. Conclusions
3 Overlap syndromes Bronchitis: Cough productive of sputum most days for at least 3 months over 2 consecutive years May account for steroid response in subset COPD pts
4 Distinguishing COPD, Asthma ASTHMA Airway inflammation Bronchoconstriction Intermittent Reversible COPD Abn inflammatory response to noxious particles Progressive Not fully reversible Hallmark: Elevated CO2
5 Distinguishing COPD, Asthma Asthma Features COPD Typically begins in Childhood No Direct Relationship Episodic attacks with exposure to allergen, irritant or exercise Typically a dry cough at night AGE? SMOKING? DYSPNEA? COUGH? Patients typically >40 years of age Mainly smokers and ex-smokers Progressive SOB, usually with exertion Productive cough, typically in the morning
6 Objectives 1. Distinguish asthma, COPD 2. COPD: Background, RF, pathophysiology, diagnosis, mgmt, complications, prognosis 3. Asthma: Background, RF, pathophysiology, diagnosis, mgmt, complications 4. Conclusions
7 COPD: Background Approx. 8% of all individuals have COPD, including Approx. 10% individuals >40 y/o. COPD mortality for both men, women increasing. COPD mortality trends several decades behind smoking trends.
8 Percent Change in Age-Adjusted Death Rates, U.S., Proportion of 1965 Rate Coronary Heart Disease Stroke Other CVD COPD All Other Causes % 64% 35% +163% 7% Source:
9 COPD: Risk Factors Smoking Dose-response 90% all COPD pts, smokers Significant slowing in lung function decline w/ cessation Air pollution Occupation (toluene, cotton mills) Genetics (alpha-1 anti-trypsin deficiency)
10 COPD Pathophysiology Starts w/ chronic toxic inhalation Coal dust, occupational, tob Terminal bronchioles trap toxins Initial cilliary clearance, coughing Neutrophil response Over time enzymes digest toxins & normal collagenous support Floppy bronchioles
11 COPD Pathophysiology: Floppy bronchiole Air trapping
12 COPD: Diagnosis, Hx Usually 20+ pack year Chronic pct cough (40), dyspnea (60-70) Pct: normally mucoid but purulent w/ exacerbation Late stage: early AM headaches, weight loss possible
13 COPD: Diagnosis, Exam Tachypneic Mild hypoxemia Cyanotic Pink puffer pink face d/t effort in exhalation Diminished bs, wheezing,hyper resonance Barrel chest Other: digital clubbing, accessory muscle use, pursed lips, cachexia
14 COPD Dx: 3 Presentations 1 - Sedentary lifestyle, few complaints. Unaware of extent of limitations d/t respiratory symptoms. Unknowingly avoiding exertional dyspnea. 2 p/w respiratory symptoms, dyspnea, chronic cough. Dyspnea initially on exertion, progresses. Pct cough. 3 Acutely p/w wheezing, dyspnea, increased pct cough and sputum. Ask if increased pct cough, oxygen req.
15 COPD: Dx, Lab tests PFT s - Diagnose, determine severity, progression COPD dx if Airflow obstruction (FEV1/FVC <.70) AND < 12% reversibility + RF (smoking) and/or sx. Increased RV/TLC suggest hyperinflation Determine DLCO, may be decreased in COPD Sutherland E and Cherniack R. N Engl J Med 2004;350:
16 COPD: Diagnosis, x-ray. Note: Barrel chest and flattened diaphragm
17 COPD: Diagnosis, x-ray. Note: Hyperexpanded lungs, flattened diaphragms, decreased lung markings, ± blebs
18 COPD: Other Diagnostic Tools Routine labs: Polycythemia, elevated bicarb. Arterial Blood Gas In exacerbations may see respiratory alkalosis evolve to respiratory acidosis as pt tires. Hypoxemia Elevated PaCO2 ECG: RAD, RVH, RAE, R heart strain, S1Q3T3, arrhythmias.
19 GOLD Classification of COPD Severity by Spirometry Stage I: Mild FEV1/FVC < 0.70 FEV1 > 80% pred Stage II: Moderate FEV1/FVC < % < FEV1 < 80% pred Stage III: Severe FEV1/FVC < % < FEV1 < 50% pred Stage IV: Very Severe FEV1/FVC < 0.70 FEV1 < 30% pred or FEV1 < 50% pred + chronic resp failure
20 COPD: Treatment Smoking cessation: Slows FEV1 decline, decrease mortality. O2: If Pa02 <55mmhg or Sa02 <89%. (Annals 1980, Lancet 1981) Decrease mortality. Medications: Inh steroids, bronchodilators (sx relief) Steroids slow FEV1 decline
21 COPD: Treatment Pulmonary Rehabilitation Prevention: Influenza vax yearly for all Pneumovax all. Repeat if vx before 65 y/o and 5 yr since last dose Surgery Transplantation vs. lung volume reduction surgery
22 COPD: Treatment by Stage Stage FEV1; FEV1/FVC Tx 0 Nml but sx none I-Mild >80% ; <70% Bronchodil. prn IIA-Mod 50-80% ; <70% Scheduled dilator, trial inh steroids, rehab IIB-Mod 30-50% ; <70% Above + inh steroids if many exac III-Severe <30% ; <70% Above + O2 if resp failure
23 COPD: Treatment, Exacerbation Oxygen (titrate SaO %) Bronchodilators (beta2 agonist + anticholin) Nebulizer or MDI + spacer Steroids, 7-10 d. IV, PO Approx. 30% reduced death, intubation, readmissions. Decreases LOS. Antibiotics No single abx superior. Amox, Bactrim, doxy, if mod disease. Severe exac: azithro, Levo.
24 COPD: Treatment, Ventilation NIPPV : Initiate if mod/severe dyspnea, acidosis w/ CO2 retention on ABG or RR>25. 58% decrease in intubations. Mortality benefit observed. Note contraindications: AMS, hemodynamic instability, UGIB. Intubation: Consider if pt failing NIPPV. Clinical decision.
25 COPD: Complications Infections: bronchitis, pneumonia Pulmonary embolus Pulmonary hypertension Chronic hypercarbic and/or hypoxic respiratory failure Spontaneous pneumothorax
26 COPD: Prognosis, FEV1 Predictors of mortality in chronic obstructive pulmonary disease. A 15-year follow-up study. Traver GA; Cline MG; Burrows B SO Am Rev Respir Dis 1979 Jun;119(6):
27 Objectives 1. Distinguish asthma, COPD 2. COPD: Background, RF, pathophysiology, diagnosis, mgmt, complications, prognosis 3. Asthma: Background, RF, pathophysiology, diagnosis, mgmt, complications 4. Conclusions
28 Asthma: Definition/Background Chronic inflammatory disorder of airways involving mast cells, eosinophils, T lymphocytes. Inflammation causes recurrent wheezing, SOB, chest tightness, cough particularly at night and/or in early morning. a/w variable airflow obstruction, hyperresponsiveness at least partly reversible.
29 Asthma: Background Classically a disease of childhood Increasingly common to have adult onset Affects 4-5% of the population Higher mortality rate, African- Americans Several syndromes (i.e GERD, VCD)
30 Asthma: Risk factors, triggers Allergens Drugs (ASA via leukotrienes) BB via bronchospasm Morphine via histamine release Environmental (cold air, smoke) Occupational Infections Exercise Stress
31 Asthma: Pathophysiology Inflammatory response occurs in both terminal bronchioles and interstitium Inflammation increases permeability of capillaries, fluid leaks into the interstitium Increase in wall thickness, bronchoconstriction impairs oxygen exchange Mucous plugging makes much worse Inflammation persists
32 Asthma: Diagnosis, hx Increasing SOB, wheezing w/ identifiable trigger (i.e. cold, occupational, infxn, etc) Recurrent symptoms Cough, wheeze, SOB relieved w/ bronchodilator Symptoms worse at night Chest tightness
33 Asthma: Diagnosis, exam Hypoxia Wheezing bilateral lungs Hyperventilation Difficulty speaking (severe if two word sentences) Tachycardiac Diaphoresis Accessory muscle use Look for boggy turbinates etc (allergy)
34 Asthma: Diagnosis, Tests PFTS: Decreased FEV1/FVC AND bronchodilator response > 12% Flow volume loop: Decreased peak expiratory flow rate Methacholine challenge: To see if symptoms triggered
35 Asthma: Diagnosis Peak flow: Helps diagnose exacerbation, monitor tx response in known asthmatic. If suspect allergy: Check serum IgE, eos, skin testing. >3% sputum eos 86% sens, 88% spec.
36 Moderate airflow reduction noted as nonlinear flow with expiration. Scooped out Improved w/ bronchodilator.
37 Asthma: Diagnosis, exacerbation Generally, clinical diagnosis CXR rarely helpful (only to exclude other dx) Can assess peak flow Assess ABG: Resp alk if hyperventilating May become normal as pt tiring and accumulating CO2 (warning sign)
38 Asthma: Severity. Clinical Tool In the past four weeks, how much of the time did your asthma keep you from getting as much done at work or at home? During the past four weeks, how often have you had shortness of breath? During the past four weeks, how often did your asthma symptoms (wheezing, coughing, shortness of breath, chest tightness or pain) wake you up at night or earlier than usual in the morning? During the past four weeks, how often have you used your rescue inhaler or nebulizer medication (such as albuterol)? How would you rate your asthma control during the past four weeks?
39 Asthma: Diagnosis, severity Mild intermittent: 2/wk Nocturnal: 2x/mo Mild persistent: > 2/wk (< 1/d) Noct: 3-4/mo Moderate persistent: Daily Noct: > 1/wk (not daily) Severe persistent: Throughout day Nocturnal: 7d/wk
40 Asthma: Treatment Antiinflamatory tx is foundation Bronchodilators play supporting role
41 Asthma: Treatment Prevent/reverse inflammation Glucocorticoids (inh, oral) Mast cell-stabilizing agents (cromolyn, nedocromil) Leukotriene receptor antagonists (montelukast) Inhibit smooth muscle contraction Beta-agonists (albuterol, salmeterol) Methylxanthines (theophylline) Anticholinergics (ipratropium)
42 Asthma: Treatment, Step-up Step 1: SABA prn Step 2: Low dose ICS Step 3: Low dose ICS + LABA Step 4: Medium dose ICS + LABA Step 5: High dose ICS + LABA* Step 6: High dose ICS + LABA + PO CS* If uses SABA > 2 d/wk, step up Step down trial if stable 3 mo *± Omalizumab (allergies)
43 Large study of 26,000 patients with asthma who were randomized to salmeterol versus placebo Revealed small inc in asthma-related deaths and/or life-threatening experiences in pts on salmeterol alone LABA should not be used w/o concomitant inhaled corticosteroids.
44 Asthma: Treatment, Exacerbations Management: Bronchodilators: SABA + anticholinergics Systemic steroids, po or IV Oxygen, SaO2>90% Magnesium, 2gm IV (dilates sm muscle) Frequent reassessment NIPPV, intubation (clinical decision) No benefit w/ abx? if LTRA, heliox beneficial
45 Asthma: Complications Decline in lung function Greater than normal pts. Rate of decline: May be greatest in new asthmatics and in pts w/ more severe disease Frequent hospitalizations, missed work/school Death Side effects of chronic medications
46 Objectives 1. Distinguish asthma, COPD 2. COPD: Background, RF, pathophysiology, diagnosis, mgmt, complications, prognosis 3. Asthma: Background, RF, pathophysiology, diagnosis, mgmt, complications 4. Conclusions
47 Conclusions Asthma and COPD differentiated by: Degree of reversibility History, age 0f presentation Intermittent vs progressive symptoms
48 Conclusions: COPD Smoking greatest RF Loss elastic recoil chronic toxin exposure Hx: Pct cough, DOE Exam: Barrel chest, hyperresonant, clubbing, wheezing Tests: FEV1/FVC < 70%, < 12% response Flat diaphragms, dec markings, Inc PaCO2, RAD, RVH
49 Conclusions: COPD Variety of staging: GOLD Criteria Treatment: Smoking cessation, O2 (most beneficial) Other: Bronchodilators, anticholinegrics, steroids, rehab, reduction/txp, antibiotics Complications: R heart failure, PE, infections. Prognosis: Varies based on degree of lung function decline
50 Conclusions: Asthma Variety of RF, triggers (i.e cold, viral, etc) Acute bronchiole inflammation cap permeability, constriction Hx: Cough, wheeze, SOB. Often worse at night. Exam: Wheezing, hypoxia, hyperventilation, accessory muscles Tests: FEV1/FVC decreased, > 12% response Abnormal peak flow, flow volume (exp)
51 Conclusions: Asthma Variety of staging: based on exac frequency Treatment: Step up approach Steroids (other anti-inflamm), bronchodilators O2 Avoid LABA w/o inh steroids Complications: Decline in lung fct, loss of work/school
52 That s the end! Thank you!