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Asthma and COPD January 6, 2010
Airway hyperresponsivness
Bronchoconstriction
Reversible airway obstruction
Early asthmatic responseResult of release of preformed
mediators to airway stimulus
Late asthmatic response4-6 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 indicated
CXR rarely indicated (only to look for superimposed infection or complications)
ABGs rarely indicated
TreatmentOxygen
Beta-agonists No difference between MDI vs nebulizers
Hospital 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 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?
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 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
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?
How would you intubate this patient?
Ketamine
Succinycholine
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 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
Case 1 Physical ExamAlert, 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
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 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?
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. 200910 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 ventilation
NNT mortality = 8
NNT treatment failure = 3
Adverse 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 cephalosporin
Yes 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 BiPAP
Repeat 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