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Asthma. J.B. Handler, M.D. Physician Assistant Program University of New England. SOB-shortness of breath ASA- aspirin P.E.- physical exam EOS- eosinophils RR- respiratory rate ABG- arterial blood gas Nl- normal CxR- chest x-ray SaO 2 - saturation of oxygen OP- out patient

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J.B. Handler, M.D.

Physician Assistant Program

University of New England


SOB-shortness of breath

ASA- aspirin

P.E.- physical exam

EOS- eosinophils

RR- respiratory rate

ABG- arterial blood gas

Nl- normal

CxR- chest x-ray

SaO2- saturation of oxygen

OP- out patient

V/Q- ventilation/perfusion

DM- diabetes mellitus

ß- beta

EIA-exercise induced asthma

PRN- as needed

HTN- hypertension

D/C- discontinue

SO2- sulfate

NO2- nitrate

GERD- gastroesophageal reflux disease

PO- by mouth

Alt- alternative

NSAID- non-steroidal anti-inflammatory drug




  • A clinical syndrome of unknown etiology with three components:1. Recurrent episodes of airway obstruction that resolve spontaneously or following treatment.2. Exaggerated bronchoconstrictor response to stimuli that have little/no effect on non-asthmatics.3. Inflammation of the airways.

Case 1

Case 1

  • A 45 y/o white male presents with paroxysms of severe coughing lasting up to 1 hour, resolving spontaneously. He had a recent URI. No prior history of pulmonary problems. No hx of smoking. Currently feels well.

  • P.E: Healthy appearing male, NAD; Vesicular breath sounds throughout both lung fields without wheezing, ronchi or crackles.

  • What is your differential diagnosis?

Differential diagnosis

Differential Diagnosis

  • New/superimposed respiratory infection- bronchitis, pertussis, etc.

  • Asthma

  • Allergies

  • Toxin or pollutant exposure

  • Early signs of new disease

  • Psychogenic cough – dx only of exclusion



  • 5% of child/adult U.S. population

  • Can develop any time in life (often <25 y.o.)

  • 500,000 hospitalizations, 5,000 deaths/yr.

  • 15 million OP visits/yr.

  • >6 billion dollars/annually



  • Genetic predisposition.

  • Inflammatory infiltrates (lymphocytes, neutrophils, eosinophils, mast cells).

  • Injury to airway epithelium; denudation.

  • Thickened airway wall from:

    • Inflammation, collagen deposition, smooth muscle hypertrophy.

    • Hypertrophy and hyperplasia of airway glands.

  • Airway hyperresponsiveness.



  • Episodic airway narrowing: smooth muscle constriction, thickening of airway epithelium and mucus secretion into the airway lumen; mucus inspissates.

  • Local release of bioactive mediators or neurotransmitters during attacks contributes to airway constriction.

  • End result is acute, reversible obstruction of the airway lumen to airflow.



  • Airway resistance; medium and small airwayswork of breathing.

  • Diffuse airway obstruction.

  • Airway reactivity to variety of stimuli.

  • V/Q mismatch: low V/Q contributes to hypoxemia when present.

  • Tachypnea results in PCO2. If PCO2, ominous sign of ventilatory failure.

Airway obstruction

Airway Obstruction

AllRefer Health

Asthma microscopic

Asthma Microscopic

Asthma mucous plugging

Asthma: Mucous Plugging

Mediators acute response

Mediators: Acute Response

  • Acetylcholine: neurotransmitter released via intrapulmonary branches of vagus nerve increases bronchial smooth muscle contraction bronchoconstriction.

  • Histamine: endogenous bronchoconstrictor in mast cells, basophils, lungs. Vasodilator properties promote capillary leakage in presence of inflammation.

Mediators acute response1

Mediators: Acute Response

  • Kinins- bradykinin activated by enzymes (kallikreins) released by mast cells- bronchoconstrictor.

  • Leukotrienes: biochemical mediators released by mast cells, EOS and macrophages-potent smooth muscle constriction; increase mucus secretion and activate airway inflammatory cells.

Asthma triggers

Asthma Triggers

  • “Atopy” association of allergies- inhaled allergens can trigger attacks- dust mites, cats, seasonal pollens, hay fever, etc.

    • Single largest risk factor for developing asthma.

  • Non-specific triggers: URI’s, sinusitis, tobacco smoke, ozone, GERD, weather, stress, exercise, SO2, NO2, and others.

  • Aspirin allergy- cross reactivity with other NSAIDs, but not selective COX-2 agents.

  • Absence of triggers not unusual as well.

Clinical presentation

Clinical Presentation

  • History: “attacks” of coughing, wheezing, SOB, anxiety, chest tightness. Associations- allergies, irritants, ASA. Highly variable presentation.

  • Episodes often at night and early AM when airway reactivity is highest.

  • P.E*: P & RR, secretions, expiratory phase, wheezing, mucosal swelling.

  • Note: with severe asthma, wheezing may decrease or stopdecreased airflow.

*During asthma episode/attack

Pulmonary function testing

Pulmonary Function Testing

  • Spirometry easily obtainable – FVC, FEV1, FEV1/FVC.

  • PEFR-Peak expiratory flow rate-(L/min)- varies with age, gender, height; hand-held device good for following asthma severity as an adjunct to PFT’s.

  • Spirometry or PEFR following bronchodilator: assess responsiveness to treatment.

Spirometry of asthmatic

Spirometry of Asthmatic

  • Lung volumes: TLC, FRC, RV; FVC normal or slightly

  • Lung flow:; FEV1, FEV1/FVC (<70% means obstruction), PEFR.

  • DLCO- normal

  • Spirometry in between asthmatic attacks may or may not be normal; depends on asthma severity/classification (see below).

Case 11

Case 1

  • One year ago, he had a similar episode which responded to antibiotics.

  • In the last year he has noted episodic coughing when using a dictaphone or speaking for extended periods of time.

    • Some episodes with exercise- no pattern.

  • PFT’s done on 2 occasions when asymptomatic have been entirely normal.

  • Symptoms rapidly respond to short courses of oral prednisone.

Pulmonary testing

Pulmonary Testing

  • Provocative testing (If spirometry nl)- Methacholine challenge to induce Sx and decrease in FEV1 (by 20% or more). If negative, asthma very unlikely.

  • Arterial blood gases (ABG’s)- measure pH, PCO2, PO2. Respiratory Alkalosis with PCO2 is common during attack. If PCO2 is normal or high during an attack  impending respiratory failure. PO2 indicates severe V/Q mismatch.

  • CxR- Often normal vs hyperinflation.

Case 12

Case 1

  • During methacholine challenge testing, he has abrupt onset of severe coughing with a >20% drop in FEV1 and FEV1/FVC.

  • Treatment with inhaled ß-agonist aborts the attack.

  • PFT’s return to normal following albuterol.

Asthma complications

Asthma Complications

  • Infection including pneumonia

  • Exhaustion, dehydration

  • Oxygenation failure

  • Ventilation failure – lose drive to inflate alveoli

  • Death

Classification of severity

Classification of Severity

  • Applies to clinical features of chronic, stable asthma.

  • Mild intermittent asthma- Symptoms  2x/week- No symptoms and normal PEFR between attacks- Night symptoms  2x/month- FEV1 and PEFR  80% predicted*- PEFR variability 20%

*In between attacks

Current, Chapter 9


  • Mild persistent asthma- Symptoms > 2x/week, <1x/day- Night symptoms > 2x/month- FEV1 or PEFR  80% predicted*- PEFR variability 20-30%

*In between attacks

Current, Chapter 9


  • Moderate persistent asthma- Daily symptoms; daily use of inhaled short acting ß2 agonists - Night symptoms >1x/week- FEV1 or PEFR >60% to <80% * predicted - PEFR variability >30%

*In between attacks

Current, Chapter 9


  • Severe persistent asthma- Symptoms daily and frequent- may be continuous- Frequent night symptoms- FEV1 or PEFR 60% predicted*- PEFR variability >30%

  • Note: Exacerbations of symptoms are common in patients with asthma and often limit activities in moderate to severe forms.

    *In between attacks

Current, Chapter 9

Long term treatment goals

Long Term Treatment Goals

  • Minimize chronic symptoms that impair normal activity.

  • Minimize exacerbations/hospitalizations.

  • Limit side effects of medications.

  • Cornerstone treatment of persistentasthma- daily anti-inflammatory therapy with inhaled corticosteroids.

  • Stepped care approach (Current, table 9-3).

  • Long term control vs. quick relief meds.

Quick relief beta adrenergic agents

Quick Relief: Beta Adrenergic Agents

  • Most efficacious brondchodilators for acute symptoms.

  • Also used to prevent exercise induced asthma (EIA).

  • 2 agonists selectively relax bronchial smooth muscle- bronchodilate while limiting cardiac stimulation.

Quick relief beta adrenergic agents1

Quick Relief: Beta Adrenergic Agents

  • Albuterol, others: Rapid onset of action (<5”); most effective agents for acute bronchospasm. Use of a spacer may improve delivery.

  • MDI 1-2 puffs (0.18mg) up to 6+ puffs q6hr; delivery may improve with spacer.

  • Nebulizer doses (2.5 mg) are 14x more potent than MDI (2 inhalations)- more effective for severe asthmatic exacerbations (ED, hospitalized).

Inhalers and spacers

Inhalers and Spacers

AllRefer Health

Quick relief anticholinergic meds

Quick Relief: Anticholinergic Meds

  • Reverse vagally mediated bronchoconstriction and mucus production.

  • Ipratropium bromide (Atrovent) via inhaler 2-4 puffs (18mcg/puff) q6h as an alternative or adjunct (in moderate to severe exacerbations) to short acting B-agonists; not as effective.

    • Not useful for EIA or allergy induced asthma

Long term control inhaled corticosteroids

Long Term Control: Inhaled Corticosteroids

  • Low to high dose, local Corticosteroids: most importantandeffective for long term control in persistent asthma.

  • Reduce chronic and acute inflammation; mild persistent asthma and worse.

  • Inhaled preparations for prevention; dose titrated to symptom relief; may take weeks for optimal efficacy; adrenal suppression unlikely.

Inhaled corticosteroids

Inhaled Corticosteroids

  • Several agents- varying potency (Fluticasone, Beclomethazone, Flunisolide et. al.).

  • Usually 2x or 3x daily dosing

  • Follow by H2O or mouth wash gargle to avoid local yeast (Candida) infection.

Long term control long acting agonists

Long Term Control: Long Acting -agonists

  • Used for long term (8-12 hrs) bronchodilation and EIA; not for acute episodes.

    • Especially beneficial for night time symptoms.

  • Salmeterol (Serevent): 50mcg 2x/d. Formoterol is new with similar effects.

Salmeterol safety concerns

Salmeterol Safety Concerns

  • Two large clinical trials salmeterol s asthma exacerbations and asthma related deaths (small number of patients, but statistically significant).

  • Black-box warning on labeling since 2005

    • Little change in prescribing since.

  • Message: Use with caution. Confine use only to patients already on inhaled corticosteroids with ongoing symptoms.

Leukotriene modifiers

Leukotriene Modifiers

  • Leukotriene modifiers: Inhibit synthesis (Zileuton/Zyflow) or action (Zafirlukast/Accolade) of leukotrienes; inhibit inflammatory mediators; decreases need for rescue inhaler. Modest efficacy for patients with mild persistent asthma.

    • Alternative to low dose inhaled steroids in treatment of mild persistent asthma.

Mediator inhibitors

Mediator Inhibitors

  • Chromolyn, Nedocromil- mild improvement in airway function in mild persistent or EIA. Inhibit mast cell release of mediators of inflammation; inhibit asthmatic response to allergens.

  • Alternative to IC for some patients with mild persistent asthma and allergies. Limited usefullness.

  • Excellent safety profile

Systemic corticosteroids

Systemic Corticosteroids

  • Systemic steroids are used in Rx of moderate to severeasthmaexacerbations; marked anti-inflammatory properties speed (6+ hours) the resolution of airway obstruction and reduce rate of relapse; oral or IV dosing.

  • Long term use may be required in some patients with severe persistent asthma.

Systemic corticosteroids1

Systemic Corticosteroids

  • Prednisone et. al. (40-60 mgs/daily for out-patient care); higher doses required if severity requires hospitalization.

  • Safe when used for short term treatment (see below) of moderate to severe exacerbations.

  • May occasionally be needed (short term course) in some patients with mild asthma during severe exacerbations.

Systemic corticosteroids2

Systemic Corticosteroids

  • Dangers: Supraphysiologic dosing over time leads to long term risks: Adrenal suppression, HTN, osteoporosis, glucose intolerance/DM, easy bruisability, weight gain, etc.

  • Goal: Pulse dosing followed by taper and D/C, overlapping with  dosing of inhaled agents whichhave minimal systemic side effects.

  • Tapering dose (days to weeks) allows return of adrenal-pituitary axis.

Interest only

Interest Only

  • Phosphodiesterase inhibitors- aminophylline, theophylline- less effective and potentially toxic; adjunctive Rx for mod to severe persistent asthma.

  • Toxicity- Low therapeutic/toxic ratio- GI (nausea, abd. pain), CNS stimulation (anxiety, HA,tremors, seizures)and Cardiac (arrhythmias, tachycardia).

  • Must monitor serum theophylline levels to maintain therapeutic range (10-20 ug/ml).

Still other io

Still Other……IO

  • Oral -agonists- terbutaline, albuterol tablets- usually add little to inhaled agents; may be useful as an adjunct; terbutaline causes tremors.

  • Immunosuppresive agents: Methotrexate, cyclosporine, trolandomycin- for patients unresponsive to other drugs or where steroids contraindicated.

Combination meds

Combination Meds

  • Advair Diskus: Combination inhaler with Fluticasone in varying strengths combined with a fixed dose (50mcg) of Salmeterol, one inhalation b.i.d, decreases number of inhalers and inhalations.

  • Combivent: Albuterol + ipratropium

Case 1 many years later

Case 1: Many Years Later

  • He remains asymptomatic and has reduced meds over time. Rare coughing episodes rapidly respond to albuterol inhaler.

  • Meds:

    • Fluticasone MDI 220mcg 2x/d

    • Abuterol MDI (90mcg/puff)- 2-3 puffs prn

  • Notes breathing is best when teaching PA students at UNE!

Mild persistent asthma

Long Term Control:

Daily meds

Either low dose inhaled steroid or Cromolyn/Nedocromil

Alternative: Leukotriene modifier

If needed increase dose of IC’s

Quick Relief:

Short acting B2 agonist

Frequent or increasing use of B2 agonist suggests need for additional therapy.

Mild Persistent Asthma

Current, Chapter 9

Moderate persistent asthma

Long Term Control:

Daily meds

Low, medium or high dose inhaled streroid

If needed, add long acting bronchodilator-B2 agonist (esp for night time Sx)

Alt: SR theophylline

Quick Relief:

Short acting inhaled B2 agonist

Frequent or increasing use of B2 suggests need for additional therapy

Moderate Persistent Asthma

Current, Chapter 9

Severe persistent asthma

Long Term Control:

Daily meds

High dose inhaled corticosteroid

Long acting bronchodilator-B2 agonist

Alt: SR theophylline

Oral steroid therapy often needed for long periods.

Quick Relief:

Short acting B2 agonist

Frequent or increasing use of B2 suggests need for additional therapy

Severe Persistent Asthma

Current, Chapter 9

Mild asthma exacerbations

Mild Asthma Exacerbations

  • Stepped care incremental therapy

  • Most are treated at home with quick response to ’d dose/frequency of short acting “rescue” ß-agonist.

  • These drugs may be needed every 3-6 hours for a short course.

  • Inhaled corticosteroids may need to be added (*MIA) or dose ’d (x2) if already taken (*PA); full effect will take weeks.

*PA- persistent asthma

*MIA- mild intermittent asthma

Mild asthma exacerbations1

Mild Asthma Exacerbations

  • If already taking an inhaled corticosteroid, the dose is doubled during an acute exacerbation until PEFR return to normal.

  • If unresponsive, an oral systemic corticosteroid may be needed for a short course, then tapered, returning to inhaled corticosteroids.

Moderate severe attacks

Moderate/Severe Attacks

  • Some patients (caution) managed as out patient- require very close monitoring via phone.

  • Most patients warrant hospitalization.

  • Supplemental O2 as needed to maintain SaO2>90%.

  • Continuous O2 saturation monitoring via oximetry if hospitalized.

Moderate severe attacks1

Moderate/Severe Attacks

  • Reversal of airway obstruction- repetitive/continuous use of high dose ß-agonists usually via nebulizer.

  • Early administration of systemic corticosteroids IV; high dose.

  • Serial measurement of lung function: PEFR or spirometry to monitor course.

  • ABG’s often helpful: pH, PO2, PCO2.

Moderate severe attacks2

Moderate/Severe Attacks

  • Never sedate during acute asthma exacerbation; will ventilatory drive.

  • Dropping PO2 <60mm Hg (O2 sat<90%) and rising PCO2> 42mm Hg are evidence of impending respiratory/ventilatory failure and warrant treatment in the ICU.

  • Intubation may be required- initiate before patient has respiratory arrest.

Moderate severe attacks3

Moderate/Severe Attacks

  • Rehydration IV usually warranted- BP will drop once on ventilator.

  • Bronchodilators are maintained on ventilator.

  • IV Magnesium Sulfate has some usefulness for bronchial relaxation.

  • Once improved, discharge considered once FEV1 or PEFR70% of predicted or personal best.

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