Asthma and COPD January 6, 2010

Airway hyperresponsivnessBronchoconstrictionReversible airway obstruction

Early asthmatic responseResult of release of preformed

mediators to airway stimulusLate asthmatic response

4-6 hours later as a result of generation and recruitment of other inflammatory mediators in response to airway stimulus

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%

No clinical sign is good enough by itself

Clinical findings correlate poorly with severity of airway obstructionTachypnea (RR>40)Accessory muscle useTachycardia (HR >120bpm)Pulsus paradoxus Upright position/inability to lie supineSweatingDifficulty finishing sentencesCyanosis Decreased LOC“Quiet chest”

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

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

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”

Correlation is better in Severe asthma (FEV <40%)

The greatest utility of PEFR measurements is response to treatment

Asthma PathwayOne exists for adults! (for those with known

asthma) Oxygen PEFR pre-treatment Ventolin by MDI Atrovent (ipratropium bromide) by MDI Prednisone PEFR post-treatment

What diagnostic tests are people doing?

Blood tests rarely indicatedCXR rarely indicated (only to look for

superimposed infection or complications)ABGs rarely indicated

TreatmentOxygenBeta-agonists

No difference between MDI vs nebulizersHospital admissions, time in ED, PEFRSide 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

TreatmentCorticosteroids

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

Re-assessmentCalled 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?

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

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

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

What they’ve done in High River

Ventolin X 3 back to backAtrovent X 3 back to backPrednisone 60 mg High flow oxygen on non-rebreather maskCXR – no infiltrate, no pneumothoraxABG – 7.24/60/85/23

What do you tell them to do?

MagnesiumRowe 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

Epinephrine Epinephrine – B2 effects, but also alpha effect: decreased

airway edema, inflammation, and secretions. Alpha may cause bronchoconstriction.

Nebulized epinephrine not any better than nebulized ventolin 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 nebulized salbutamol on PEFR Excluded severe asthmatics – therefore not useful to our severe

patient population

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

Intravenous VentolinTravers 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

Leukotriene InhibitorsStudies 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

Methylxanthines Not recommended (Evidence A)

National Asthma Education and Prevention Program: Expert Panel Report III. 2007

Cochrane Review: Parameswaran et al. 2000No statistical signficance airflow outcomes More palpitations/arrhythmias

HelioxCochrane Review: Rodrigo et al. 2010

10 trials, 544 patientsNo significant difference in PFTs, admissions to

hospitalSignificant difference in PFT in severe

subgroup (N = 3, SMD 0.61; 95% CI 0.21 to 1.00)

Back to the patient It’s now been 1 hour since the patient received the

back-to-back ventolin/atrovent and steroidsVitals: 37.2oC, RR38, 126bpm, 130/88, 83% on 10L

O2 by maskShallow 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

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 rateSince then, only one study has come out

looking at BiPAP in place of bronchodilators in mild/moderate asthma

WHAT IS STAFF EXPERIENCE WITH BIPAP?

How would you intubate this patient?

KetamineSuccinycholine

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

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

COPD

DefinitionInflammatory lung disease with

progressive airflow limitation that is not fully reversible

Case 151 yo female smoker with 2 days increasing cough,

shortness of breath, and sputum production. Med Hx: COPD (no home O2), HTN, hard of hearingMeds: Ventolin, SpirivaNo allergiesNo chest pain, CHF symptoms, fever/chillsO/E:

375, 139 bpm, RR 36, 210/120,221/123, 45% on RA02, 72% on NRB, 10.5mM

Case 1 Physical ExamAlert, answering appropriately in short phrasesAnxiousCentral and peripheral cyanosis++accessory muscle useDecreased breath sounds throughout Inspiratory and expiratory wheezes throughoutNo extra heart sounds, pulses equal bilat, no

edema

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

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

Results of InvestigationsCBC: Hgb 199, WBC 21.2 (Neuts 18.6), Plt 215Electrolytes: Na 141, K 4.7, Cl 95, HCO3 28Creatinine 101TnT < 0.03CXRay – extensive bilateral nodularity with

confluent opacities at lung basesABG: 7.31/56/80/27 – What is her normal PCO2?

TreatmentOxygen – to maintain saturation ~90%Bronchodilators

Beta-agonists are first-line Improve airway function/reduce hyperinflation

Anticholinergics No difference when compared with beta-agonistsMinimal evidence for synergistic effect with beta-

agonist, but we add it anyways to avoid intubation

TreatmentCorticosteroids

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 patientsFewer treatment failures within 30 days (NNT = 10)Decreased duration hospitalization Improved FEV1, breathlessness, blood gas valuesNo effect on mortalityIncreased adverse events (NNH = 6)

Adverse events: hyperglycemia, increased appetite, weight gain, insomnia

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 ventilationNNT mortality = 8NNT treatment failure = 3Adverse effects: Increased diarrhea

Which antibiotics?Dimopoulos et al. 2007. Comparison of

first-line with second-line antibiotics for acute exacerbations of chronic bronchitis. Chest; 132:447-455More 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

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 cephalosporinYes or >moderate exacerbation?

B-lactam/B-lactamse inhibitor, floroquinolone, 2nd/3rd generation cephalosporin

Who would BiPAP this patient?

Indications for NIPPV Moderate to severe dyspnea

RR>25Accessory muscle useParadoxical abdominal breathing

Moderate severe acidosis pH < 7.35PaCO2 > 45

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

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)

When is BiPAP failing?NIPPV Failure

Lethargy Exhaustion Worsening respiratory rate Worsening oxygen saturation Speechlessness Paradoxical abdominal breathing

Back to our patientAfter 3 hours on BiPAPRepeat ABG: 7.34/53/74/27 with markedly

improved work of breathing. Having conversations in full sentences No longer cyanotic

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

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