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Asthma and COPD

Asthma and COPD . January 6, 2010. Airway hyperresponsivness Bronchoconstriction Reversible airway obstruction. Early asthmatic response Result of release of preformed mediators to airway stimulus Late asthmatic response

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Asthma and COPD

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  1. Asthma and COPD January 6, 2010

  2. Airway hyperresponsivness • Bronchoconstriction • Reversible airway obstruction

  3. Early asthmatic response • Result of release of preformed mediators to airway stimulus • Late asthmatic response • 4-6 hours later as a result of generation and recruitment of other inflammatory mediators in response to airway stimulus

  4. Case 1 • 28 yo female • Known asthmatic • On ventolin inhaler (using every 2-3 hours – 1 puff) • Seasonal allergies, Diabetes Type 1 (insulin) • Cough and runny nose 3 days (nocturnal cough) • 36.7oC, 110bpm, RR36, 120/80, 94% RAO2, 5.7mM • Short sentences, SCM use • BS decreased to bases, expiratory wheezes • PEFR 60%

  5. No clinical sign is good enough by itself • Clinical findings correlate poorly with severity of airway obstruction • Tachypnea (RR>40) • Accessory muscle use • Tachycardia (HR >120bpm) • Pulsusparadoxus • Upright position/inability to lie supine • Sweating • Difficulty finishing sentences • Cyanosis • Decreased LOC • “Quiet chest”

  6. Risk factors for death in Asthma • >2 hospitalizations in the past year for asthma • >3 ED visits in the past year for asthma • Hospitalization/ED visit in past month for asthma • Current/recent systemic steroid use • >2 canisters of beta-agonist use in the past month • Difficulty perceiving severity of airway obstruction • ICU/intubation for asthma • Low socioeconomic status • Significant psychosocial issues • Illicit drug use • Cardiac comorbidity • Chronic lung disease • Severe psychiatric Illness

  7. Any objective measures? • What is your objective measure of choice? • Peak expiratory flow rate (PEFR) vs FEV1 • Spirometry is the gold standard for diagnosing and categorizing severity of airflow limitation in obstructive lung disease • We don’t have ready access to spirometry in the emergency department (RTs have machine in their office but need to carry it up) • We do have ready access to Peak Flow Meters for PEFR measurements

  8. PEFR and FEV1 not interchangeable • Aggarwal AN, Gupta D, Jindal SK. The relationship between FEV1 and peak expiratory flow in patients with airways obstruction is poor. Chest. 2006 Nov;130(5):1454-61. • Cross-sectional, retrospective study • 6,167 adult patients showing obstructive pattern on spirometry over a 6-year period • “we found that in patients with severe airway obstruction (FEV1 < 40% of predicted), PEF% overestimated FEV1 %, whereas exactly the opposite happened in patients with less severe airway obstruction”

  9. Correlation is better in Severe asthma (FEV <40%) • The greatest utility of PEFR measurements is response to treatment

  10. Asthma Pathway • One exists for adults! (for those with known asthma) • Oxygen • PEFR pre-treatment • Ventolin by MDI • Atrovent (ipratropium bromide) by MDI • Prednisone • PEFR post-treatment

  11. What diagnostic tests are people doing? • Blood tests rarely indicated • CXR rarely indicated (only to look for superimposed infection or complications) • ABGs rarely indicated

  12. Treatment • Oxygen • Beta-agonists • No difference between MDI vs nebulizers • Hospital admissions, time in ED, PEFR • Side effects: change in RR, heart rate • Anticholinergics • Synergy with beta-agonist treatment for • Decreasing hospital admissions (NNT = 14) • Increasing PEFR • Especially in those with severe asthma, multiple doses of anticholinergics

  13. Treatment • Corticosteroids • Reduce hospital admissions (NNT = 8) • NNT = 5 in severe asthma • Improve PEFR • Reduce rates of relapse at 7-10 days • Reduce number of relapses requiring admission • Reduce beta-agonist use

  14. Re-assessment • Called back to the bedside, patient done treatment, RAO2 88% • O/E: • Feels better • A/E better, faint wheeze on full end expiration • Decreased work of breathing • What do you want to do? • Why is the RAO2 worse?

  15. What if this patient was pregnant? • Conflicting studies • Possible IUGR, preterm delivery, preeclampsia in those with poorly controlled asthma • Therapy as is • Potential harmful role of systemic epinephrine on uterine vasoconstriction

  16. Discharge Instructions? Discharge Medications? • 2 puffs ventolin q4-6h depending on symptoms • Return to ER if >16 puffs day • Check sugars more frequently (QID) because of corticosteroids • WHAT ARE STAFF IN THE ROOM DOING? • When do you prescribe something in addition to their Ventolin? • WHAT ARE STAFF IN THE ROOM DOING? • If using SABA >2days/week, add low dose corticosteroid (Flovent) • If using SABA daily, add low dose corticosteroid + LABA (Advair/Symbicort) • Referral to Calgary COPD & Asthma Program • Spirometry, Education, Smoking Cessation, Action Plan

  17. Case 2 • RAPID call from High River • 18yo male with known asthma • 1 week of increasing wheezing, shortness of breath, cough • Increasing ventolin use, 2 puffs every hour since yesterday • Meds: Ventolin, Advair, Singulair • Past Med Hx: 2 asthma ED visits last year, 1 admission at age 15 (+ICU/not intubated) • Smoker • Vitals: 37.2oC, RR40, 132bpm, 130/88, 85% on 10L O2 by mask • Shallow fast breathing, minimal wheezes, very minimal air entry, drowsy

  18. What they’ve done in High River • Ventolin X 3 back to back • Atrovent X 3 back to back • Prednisone 60 mg • High flow oxygen on non-rebreather mask • CXR – no infiltrate, no pneumothorax • ABG – 7.24/60/85/23 • What do you tell them to do?

  19. Magnesium • Rowe et al. Magnesium sulfate for treating exacerbations of acute asthma in the emergency department. Cochrane Airways Group Cochrane Database of Systematic Reviews. 2000. • Pooled study results show no significant difference • Reduces hospitalizations and improves pulmonary function scores in those with “severe” asthma • Severe asthma defined as PEFR < 25% post-treatment with beta-agonists

  20. Epinephrine • Epinephrine – B2 effects, but also alpha effect: decreased airway edema, inflammation, and secretions. Alpha may cause bronchoconstriction. • Nebulized epinephrine not any better than nebulizedventolin • Plint et al. 2000. Prospective RCT - No difference in pulmonary index score, O2 sat, O2 requirements, admission rates, length of ED stay, length of hospital stay • SC epinephrine equivalent to nebulized beta-agonist in in mild/moderate asthma • Sharma and Madan 2001 Indian Journal of Pediatrics Vol 68. Prospective randomized study • SC epinephrine equivalent to nebulizedsalbutamol on PEFR • Excluded severe asthmatics – therefore not useful to our severe patient population

  21. Epinephrine • IM epinephrine • No evidence for IM epinephrine • Extrapolated from SC data/Anaphylaxis data • IV epinephrine • No evidence for IV epinephrine • Theoretical benefits and used only in severe refractory cases • Serious adverse events are somewhere <4% • SVT, chest pain with ECG changes, increased TnT, hypotension • Putland et al. 2006. Vol 47(6) Annals of Emergency Medicine

  22. Intravenous Ventolin Travers et al. 2002 Systematic Review • Looked at population with ‘severe’ asthma (defined differently – HR, pulmonary index scores, PFT) in EDs. • No benefit for IV beta-agonists compared to nebulized beta agonists with non-statistically significant increase autonomic adverse effects, but no data on IV in addition to inhaled. • 3 of 9 studies in children

  23. Leukotriene Inhibitors • Studies showing modest improvements in PEFR but no effect on hospitalizations • We also do not have the IV montelukast or PO zafirlukast on our formulary used in the studies

  24. Methylxanthines • Not recommended (Evidence A) • National Asthma Education and Prevention Program: Expert Panel Report III. 2007 • Cochrane Review: Parameswaran et al. 2000 • No statistical signficance airflow outcomes • More palpitations/arrhythmias

  25. Heliox • Cochrane Review: Rodrigo et al. 2010 • 10 trials, 544 patients • No significant difference in PFTs, admissions to hospital • Significant difference in PFT in severe subgroup (N = 3, SMD 0.61; 95% CI 0.21 to 1.00)

  26. Back to the patient • It’s now been 1 hour since the patient received the back-to-back ventolin/atrovent and steroids • Vitals: 37.2oC, RR38, 126bpm, 130/88, 83% on 10L O2 by mask • Shallow fast breathing, minimal wheezes, very minimal air entry, drowsy (but less so than before) • ABG – 7.24/60/85/23 and Pulse oximeter reading 85% • You’re working with Arun, explain the ABG/O2 discrepancy

  27. Would anyone BiPAP this patient? • Cochrane Review, Ram et al. 2005 • 1 study, N=30 • BiPAP (8/5 to 15/3 max) vs Sham (1/1 with holes in tube) • No intubations, deaths • Decreased hospital admissions, PEFR, RR • No difference treatment failure, length of ICU stay, heart rate • Since then, only one study has come out looking at BiPAP in place of bronchodilators in mild/moderate asthma • WHAT IS STAFF EXPERIENCE WITH BIPAP?

  28. How would you intubate this patient? • Ketamine • Succinycholine

  29. How would you set your ventilator settings? • FiO2 100% • RR 6-8 • Small tidal volumes 6-8cc/kg (partly guided by evidence in ALI) • Long expiratory times (I:E ratio > 1:2) • PEEP < 5 cm H20 (start with 0) • Target plateau pressures < 20 cm H20 • Oxygenation > 90% • Permissive hypercapnea (pH >7.20) to prevent barotrauma

  30. Once intubated, patient becomes hypotensive and O2 sats decreasing • What do you do? • Disconnect the patient from the ventilator • Decompress the Chest • Consider bilateral chest tubes • Fluid bolus • Suction tube

  31. COPD

  32. Definition • Inflammatory lung disease with progressive airflow limitation that is not fully reversible

  33. Case 1 • 51 yo female smoker with 2 days increasing cough, shortness of breath, and sputum production. • Med Hx: COPD (no home O2), HTN, hard of hearing • Meds: Ventolin, Spiriva • No allergies • No chest pain, CHF symptoms, fever/chills • O/E: • 375, 139 bpm, RR 36, 210/120,221/123, 45% on RA02, 72% on NRB, 10.5mM

  34. Case 1 Physical Exam • Alert, answering appropriately in short phrases • Anxious • Central and peripheral cyanosis • ++accessory muscle use • Decreased breath sounds throughout • Inspiratory and expiratory wheezes throughout • No extra heart sounds, pulses equal bilat, no edema

  35. What is your definition of AECOPD? • Acute exacerbation of COPD • A change in the patient’s dyspnea, cough, or sputum that is beyond normal day-to-day variation

  36. Investigations • Bloodwork usually not helpful • PFTs not as helpful as in asthma; majority of disease is non-reversible • Arterial Blood Gas usually not helpful unless • Unable to obtain O2 sat • Severe exacerbation • Hospitalization • Prior to NIPPV • CXRay • Helpful in decision making and ruling out DDx • Changes management in ~15-20% cases • What would you expect to see on an ECG? • ECG • Right axis deviation, RVH, Right atrial enlargement, low voltage • Atrial arrhythmias are most common: A. Fib, MAT

  37. Results of Investigations • CBC: Hgb 199, WBC 21.2 (Neuts 18.6), Plt 215 • Electrolytes: Na 141, K 4.7, Cl 95, HCO3 28 • Creatinine 101 • TnT < 0.03 • CXRay – extensive bilateral nodularity with confluent opacities at lung bases • ABG: 7.31/56/80/27 – What is her normal PCO2?

  38. Treatment • Oxygen – to maintain saturation ~90% • Bronchodilators • Beta-agonists are first-line • Improve airway function/reduce hyperinflation • Anticholinergics • No difference when compared with beta-agonists • Minimal evidence for synergistic effect with beta-agonist, but we add it anyways to avoid intubation

  39. Treatment • Corticosteroids • Moderate/Severe AECOPD (Evidence 1A) • dose/duration/type needs to be individualized • 7 to 10 days recommended (GOLD Guidelines 2009) • Cochrane Review: Walters et al. 2009 • 10 RCTs, 1051 patients • Fewer treatment failures within 30 days (NNT = 10) • Decreased duration hospitalization • Improved FEV1, breathlessness, blood gas values • No effect on mortality • Increased adverse events (NNH = 6) • Adverse events: hyperglycemia, increased appetite, weight gain, insomnia

  40. Who do you give antibiotics to? • 3 of 3 for: dyspnea, sputum volume, sputum purulence • Sputum purulence if accompanied by dyspnea or sputum volume • Mechanical ventilation • NNT mortality = 8 • NNT treatment failure = 3 • Adverse effects: Increased diarrhea

  41. Which antibiotics? • Dimopoulos et al. 2007. Comparison of first-line with second-line antibiotics for acute exacerbations of chronic bronchitis. Chest; 132:447-455 • More treatment failures with 1st line Abx VS 2nd line Abx (OR 0.51, 95% CI 0.34 to 0.75) • No differences in adverse effects

  42. What antibiotics? • Depends on the presence of high risk features: • Severe COPD • Recent antibiotic use (<3 months) • Frequent exacerbations (>3/year) • Presence of comorbid disease • No and mild exacerbation? • B-lactam/B-lactamase inhibitor, tetracycline, TMP-SMX, macrolide, 2nd/3rd generation cephalosporin • Yes or >moderate exacerbation? • B-lactam/B-lactamse inhibitor, floroquinolone, 2nd/3rd generation cephalosporin

  43. Who would BiPAP this patient? • Indications for NIPPV • Moderate to severe dyspnea • RR>25 • Accessory muscle use • Paradoxical abdominal breathing • Moderate severe acidosis • pH < 7.35 • PaCO2 > 45

  44. Which patients would you not BiPAP? • Exclusion Criteria • Systemic • Respiratory arrest • Hemodynamic instability (hypotension, arrhythmia, MI) • Change in mental status/uncooperative patient • Anatomic • High aspiration risk • Copious/viscous secretions • Recent facial/GI surgery • Craniofacial trauma • Fixed nasopharyngeal abnormality • Extreme obesity • Burns

  45. What does BiPAP do for you? • Cochrane Review, Ram et al. 2004 • Respiratory failure patients due to AECOPD with PaCO2 >45 • Excluded patients with primary diagnosis of pneumonia • 14 studies (758 patients) • Outcomes • Decreased mortality (NNT 10) • Decreased need for intubation (NNT 4) • Decreased treatment failures (NNT 5) • More rapid improvement in first hour of pH, PaCO2, RR • Decreased complications associated with treatment • Decreased hospital length of stay (pH<7.30 subgroup only)

  46. When is BiPAP failing? • NIPPV Failure • Lethargy • Exhaustion • Worsening respiratory rate • Worsening oxygen saturation • Speechlessness • Paradoxical abdominal breathing

  47. Back to our patient • After 3 hours on BiPAP • Repeat ABG: 7.34/53/74/27 with markedly improved work of breathing. • Having conversations in full sentences • No longer cyanotic

  48. Not recommended • Methylxanthines • No difference FEV1 • No difference hospital admissions/length of stay • No difference relapses • Increased adverse effects with methylxanthine • Heliox (insufficient evidence to support use) • No clinical outcomes reported (mortality, intubation) • Improved peak inspiratory flow rate • Decreased PaCO2 • Decreased dyspnea scores • Respiratory Stimulants • Doxapram • Improved blood gas exchange in first few hours of treatment, but NIPPV may be more effective

  49. What is your approach to intubating this patient? • Much the same as intubating the asthma patient • Want to avoid intubation if possible • Same RSI technique • Same ventilator settings • Want to avoid hyperventilation alkalosis • These patients usually have metabolic alkalosis (compensation for chronic respiratory acidosis) • Can result in seizures, dysrhythmias

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