Presented by:

Dr. Christopher Ekpo

An airway disorder that causes:
• respiratory hypersensitivity,
•inflammation, and
•intermittent obstruction
Chronic inflammatory airway disorder
characterized by
 airflow obstruction and
 airway hyper-responsiveness to a
multiplicity of stimuli.
 Image of the airway during asthmatic
attack: courtesy, clivir.com
• Airflow obstruction usually reversible,
either spontaneously or with treatment.

• Clinical course unpredictable with

periods of adequate control to
exacerbations of dyspnoea, wheezing
and chest tightness
• A chronic inflammatory disorder of the
airways in which many cells and cellular
elements play a role, in particular, mast
cells, eosinophils, T lymphocytes,
macrophages, neutrophils, and
epithelial cells.
• In susceptible individuals, this
inflammation causes recurrent episodes
of wheezing, breathlessness, chest
tightness and coughing, particularly at
night or in the early morning.
 Theseepisodes are usually associated
with widespread but variable airflow
obstruction that is often reversible either
spontaneously or with treatment.
 Theinflammation also causes an
associated increase in the existing
bronchial responsiveness to a variety of
stimuli.
 Reversibility of airflow limitation may be
incomplete in some patients with
asthma.
 Boys
more affected than girls (2:1) before
puberty.
 After
puberty more women are affected
than men.
 Women have increased risk for death than
men.
 50% of asthmatics are younger than 10yrs.
 Annually, the World Health Organization
(WHO) has estimated that 15 million
disability-adjusted life-years are lost and
250,000 asthma deaths are reported
worldwide

(Bateman et al, 2008).

 Intrinsic allergens

 Emotional stress
 Fatigue
 Endocrine changes
 Temperature variations
 Humidity variations
 Anxiety
 Genetic factors
 Extrinsic allergens
 Pollen
 Animal dander
 House dust or mold
 Kapok or feather pillows
 Food additives containing sulfites & other
sensitizing substances
 Exposure to noxious fumes (air pollution)
 Irritants

Courtesy, onlinehomeopathiccare.com
 Intrinsic
asthma reacts to internal,
nonallergenic factors, external factors not
implicated.

 Extrinsic
asthma commonly accompanied
by other hereditary allergies.

 Environmental factors interact with

inherited factors to cause asthmatic
reactions.
◦ Environmental allergens: House dust
mites, animal allergens (especially cat
and dog), cockroach allergens and
fungi are most commonly reported.
◦ Viral respiratory tract infections
◦ Exercise; hyperventilation
◦ Gastroesophageal reflux disease
◦ Chronic sinusitis or rhinitis
• Aspirin or nonsteroidal anti-
inflammatory drug (NSAID)
hypersensitivity, sulfite sensitivity

◦ Use of beta-adrenergic receptor

blockers (including ophthalmic
preparations)
 Obesity:
Based on a prospective cohort study of
86,000 patients, those with an elevated
body mass index are more likely to have
asthma.
 • Environmental pollutants, tobacco
smoke
• Occupational exposure
--Irritants (eg, household sprays,
paint fumes).
Emotional factors or stress
-Various high and low molecular weight
compounds: A variety of high and low
molecular weight compounds are
associated with the development of
occupational asthma, such as insects,
plants, latex, gums, diisocyanates,
anhydrides, wood dustand fluxes.
-Environmental allergen exposure
(dust mites, pet dander, pollens)

-Occupation

-Medications

-Exercise
• Viral upper respiratory tract infections

• Strong emotional expression

• Menstrual cycles

• Airborne dusts or chemicals

 Complex and involves the following
components:

 Airway inflammation.

 Intermittent airflow obstruction.

 Bronchial hyperresponsiveness.
 Pathophysiologic changes during asthma:
courtesy, healthlifestyletips.com
 Environmental factors interact with
inherited factors.
 Bronchial linings overreact to stimuli
causing episodic smooth-muscle spasms
that severely constrict the airways.
 Mast cells degranulate, release histamine
and leukotrienes.
 Histamine causes swelling in smooth
muscles.
 Mucous membranes become inflammed,
irritated and swollen.
 Leukotrienes attach to receptor sites in
the smaller bronchi & cause swelling of
the smooth muscle
 Leukotrienes also cause prostaglandins
to travel through the bloodstream to the
lungs to enhance histamine’s effect.
 Wheezing during coughing occurs.
 Histamine stimulate excessive mucus
secretion further narrowing the bronchial
lumen.
 Goblet cells secret viscous mucus that is
difficult to cough up resulting in rhonchi,
increased pitch-wheezing & increased
respiratory distress.
 On inhalation, narrowed bronchial lumen
can still expand slightly.
 On exhalation, increased intrathoracic
pressure closes bronchial lumen
completely.
 Air enters but cannot escape.
 Patient develops barrel chest &
hyperresonance to percussion.
 Mucus fills lung bases.
 Intrapleural & alveolar gas pressures
rise.
 There is ventilation-perfusion mismatch.
 Hypoxia triggers hyperventilation
 Respiratory alkalosis result.
 Ventilation & perfusion remain
inadequate resulting in co₂ retention.
 Respiratory acidosis results
 May result in respiratory failure.
 - Intermittent asthma
• Intermittent symptoms occurring no more than
once per week
• Brief exacerbations
• Nocturnal symptoms occurring less than twice a
month
• Asymptomatic with normal lung function
between exacerbations
• No daily medication needed
• FEV1 or PEF rate greater than 80%, with less than
20% variability
- Mild persistent asthma

• Symptoms occurring more than once a week but

less than once a day
• Exacerbations affect activity and sleep
• Nocturnal symptoms occurring more than twice
a month
• FEV1 or PEF rate greater than 80% predicted,
with variability of 20-30%
- Moderate persistent asthma

• Daily symptoms
• Exacerbations affect activity and sleep
• Nocturnal symptoms occurring more than once a
week
• FEV1 or PEF rate 60-80% of predicted, with
variability greater than 30%.
- Severe persistent asthma
• Continuous symptoms
• Frequent exacerbations
• Frequent nocturnal asthma symptoms
• Physical activities limited by asthma symptoms
• FEV1 or PEF rate less than 60%, with variability
greater than 30%.
 Sudden dyspnoea  Rapid pulse
 Wheezing  Profuse perspiration
 Tightness in the chest  Hyperresonant lung
 Coughing –produce fields
thick, clear or yellow  Diminished breath
sputum. sounds.
 Tachypnoea  Increased anxiety
 Restlessness
 Clinicalmanifestations
 Health history
 Physical examination
 Increase IgE levels from allergic reaction.
 Totalserum immunoglobulin E levels
greater than 100 iu are frequently
observed in patients experiencing
allergic reactions, but this finding is not
specific for asthma and may be observed
in patients with other conditions (eg,
allergic bronchopulmonary aspergillosis,
Churg-Strauss syndrome(Bateman, 2008).
 Pulmonary function studies- FEV₁, PEFR,
FVC, etc.( forced expiratory volume in 1
second, peak expiratory flow rate, forced
vital capacity).
 Spirometry assessments should be
obtained as the primary test to establish
the asthma diagnosis.
 Should be performed prior to initiating
treatment in order to establish the
presence and determine the severity of
baseline airway obstruction

(Enright, Lebowitz & Cockroft, 1994).

Spirometry measures how fast and how much air
can be breathed out of the lungs. Courtesy,
wvasthma.wordpress.com
 Spirometry measures the forced vital
capacity (FVC), the maximal amount of
air expired from the point of maximal
inhalation, and the forced expiratory
volume in one second (FEV1). A reduced
ratio of FEV1 to FVC, when compared
with predicted values, demonstrates the
presence of airway obstruction.
 Increase eosinophil count on CBC.
 Blood eosinophilia greater than 4% or
300-400/μL supports the diagnosis of
asthma, but an absence of this finding is
not exclusionary. Eosinophil counts
greater than 8% may be observed in
patients with concomitant atopic
dermatitis ( Morris et al, 2012).
 The British Thoracic Society
recommends using sputum eosinophilia
determinations to guide therapy in
assessing asthma control.
 Animprovement in asthma control, a
decrease in hospitalizations, and a
decrease in exacerbations were noted in
those patients in whom sputum-guided
therapy was used

(Bacci, et al, 2006)

 Sputum analysis- presence of
Curschmann’s spirals i.e. cast of airways.
Also Charcot-Leyden crystals &
eosinophils.
 Chest X-ray- may show hyperinflation
with areas of atelectasis
 Arterialblood gas (ABG)
measurement provides important
information in acute asthma. This test
may reveal dangerous levels of
hypoxemia or hypercarbnia secondary to
hypoventilation;
 Typically, results are consistent with
respiratory alkalosis.
 Pulse oximetry measurement is desirable
in all patients with acute asthma to
exclude hypoxemia.
 The hypoxemia of uncomplicated acute
asthma is readily reversible by oxygen
administration.
 In children, pulse oximetry is often used
to grade severity of acute asthma.
 Oxygen saturation of 97% or above
constitutes mild asthma,
 92-97% constitutes moderate asthma,
 Less than 92% signifies severe asthma

(Morris, et al, 2012).

 Chest radiography usually is more useful
in the initial diagnosis of bronchial
asthma than in the detection of
exacerbations
 It is valuable in excluding complications
such as pneumonia and asthma mimics,
even during exacerbations
 Mediastinal air is noted adjacent to the
anteroposterior window and airtrapping
extends to the neck, especially on the right
side. Courtesy, emedicine.com
Chest CT scanning(HRCT):
 A second line examination but useful in
patients with chronic or recurring
symptoms and in those with possible
complications such as allergic
bronchopulmonary aspergillosis and
bronchiectasis

(Woods & Lynch, 2009).

Peak flow monitoring:
 Peak expiratory flow (PEF) measurement
is common in the A & E.
 Serial measurements document response
to therapy and along with other
parameters, are helpful in determining
whether to admit the patient to the
hospital or discharge from the A & E.
A peak flow meter calibrated to ensure
accuracy. Courtesy, allsportmedical.co.uk
 Electrocardiography
 MRI
 Nuclear imaging
 Allergy skin testing
 Bronchoprovocation which includes
exercise testing and allergen inhalation
challenge, etc
 Exhaled Nitric Oxide
 Sinus CT Scanning
 24 hrs pH monitoring
Step 1: mild intermittent-

 Quick relief: Short-acting beta-agonists

 Long term: No daily medication needed.

-course of systemic
corticosteroids recommended in severe
exacerbations.
Step 2: Mild persistent-

 Quickrelief: Short-acting inhaled beta-

agonist.

 Long term: daily low-dose inhaled

corticosteroids OR cromolyn, leukotriene
modifier, sustained release theophylline.
Step 3: Moderate persistent:

 Quick relief: Short-acting inhaled beta-

agonists.
 Long term: Low to medium dose inhaled
corticosteroids and long-acting inhaled
beta-agonists OR increase inhaled
corticosteroids within medium dose
range and either leukotriene modifier or
theophylline.
Step 4: Severe persistent-

 Quickrelief: Short-acting inhaled B₂-

agonists.

 Long term: High dose inhaled

corticosteroids and long-acting inhaled
B₂-agonists and, if needed, oral
corticosteroids.
 Short-acting bronchodilators by
inhalation.

 Beta₂-
adrenergic agonists- albuterol
(Proventil, Ventolin).

 Anticholinergic
agent- ipratropium
bromide (Atrovent).

 Systemic corticosteroids ( short course).

 Inhaled corticosteroids- triamcinolone
(azmacort), beclomethasone (Vanceril,
Beclovent), fluticasone ( Flovent), etc.

 Long-acting inhaled beta-agonists-

salmeterol (Serevent)

 Combination inhalers- fluticasone &

salmeterol (Advair).
 Leukotriene modifiers- Montelukast
(Singulair), Zafirlukast (Accolate).

 Inhaled
mast cell stabilizers- Cromolyn
sodium (Intal).

 Methylxanthines- Theophylline (Theo-

24,Theodur, Uniphyl).
 Environmental control
 Immunotherapy
 Exercise- regular aerobic
 Use of inhaled beta-agonist 15-20 min
before exercise.
 Avoidance of foods that contain tartrazine
in aspirin-sensitive clients.
 Complementary and alternative
therapies- yoga, acupuncture,
chiropracture, herbs, etc.
 Assessment- Health history (involve
students)
- physical examination
-laboratory/ other findings.
 Assess the severity of asthma.
 Monitor vital signs.
 Place patient in high Fowler’s position.
 Administer prescribed treatment and
assess patient’s response- nebulizers, etc.
 Encourage patient to use pursed-lip and
diaphragmatic breathing.
 Administer humidified oxygen as
ordered by physician.
 Pursed-lipbreathing: courtesy,
livestrong.com
 Encourage fluid intake (3L) to liquefy
secretions and maintain hydration.
 Monitor vital signs frequently.
 Monitor airway functioning through peak
flow meter or pulmonary function test.
 Auscultate lungs frequently noting
degree of wheezing & quality of air
movement.
 Teach patient how to use metered-dose
inhaler.
 Discuss environmental control.
 Explain use of peak flow meter to
measure degree of airway obstruction.
 Teach patient and family to avoid known
allergens and irritants.
 Educate patient on prescribed drugs-
names, dosages, actions, adverse effects
etc.
 Monitor ABG levels, oxygen saturation
regularly.
Client using a peak flow meter: courtesy,
consumerreports.org
 Severe and persistent asthma that does
not respond to conventional therapy.
 Attacks occur with little or no warning
 Can progress rapidly to asphyxiation.
 Likely contributing factors are: infection,
anxiety, nebulizer abuse, dehydration,
nonspecific irritants, etc.
 Supplemental oxygen should be used in
most patients to maintain oxygen
saturations greater than 90%.
 Inhaled short-acting beta-agonists are
the initial treatment.
• Repetitive or continuous administration by
nebulizer.
• In the emergency department, 3 treatments
every 20-30 minutes as initial therapy.
• High-dose (6-12 puffs) beta-agonist by MDI or
nebulizer therapy (Nebulizer is most effective with
more severe exacerbations.)
 Consider inhaled ipratropium bromide
(Atrovent) in patients with severe
exacerbations.
 Methylxanthines (theophylline) can be
considered in patients with severe
exacerbations, but their use is
controversial.
 Treatment based on the severity of the
asthma exacerbation.
 Administer systemic corticosteroids
early in the course of disease in patients
with an incomplete response to beta-
agonists. Oral administration is
equivalent in efficacy to intravenous
administration. Corticosteroids speed the
resolution of airway obstruction and
prevent a late-phase response.
 Rapidly worsening asthma or a lack of
response to the initial therapy in the
emergency department is an indication
for ICU admission.
 If patients have confusion, drowsiness,
signs of impending respiratory arrest, or
loss of consciousness, they should be
admitted to the ICU.
 Pneumonia
 Pneumothorax
 Respiratory failure
 Status asthmaticus
 Previous severe asthma exacerbation (eg,
intubation or ICU admission for asthma)
 Two or more hospitalizations for asthma
in the past year
 Three or more emergency department
visits for asthma in the past year
 Hospitalization or emergency
department visit for asthma in the past
month.
 Usingmore than 2 canisters of short-
acting beta-agonists per month

 Difficulty
perceiving asthma symptoms
or severity of exacerbations

 Otherrisk factors - Lack of a written

asthma action plan, sensitivity to
Alternaria( natural part of fungal flora
almost everywhere).
 Socialhistory - Low socioeconomic status
or inner-city residence, illicit drug use, or
major psychosocial problems

 Comorbidities - Cardiovascular disease,

other chronic lung disease, chronic
psychiatric disease.
 Nocturnal asthma: A large percentage
of patients with asthma experience
nocturnal symptoms once or twice a
month.
 Bronchoconstriction is highest between
the hours of 4:00 am and 6:00 pm (the
highest morbidity and mortality from
asthma is observed during this time).
 Nocturnalasthma is a significant clinical
problem that should be addressed
aggressively.
 Pregnancy: Asthma complicates 4-8% of
pregnancies.
 Pregnant women with asthma are safer to
be treated with asthma medications than
to have asthma symptoms and
exacerbations.
 Poorly controlled asthma can result in
-low birth weight,
-increased prematurity, and
-increased perinatal mortality.
 OXYGEN
 Ineffective airway clearance Rt.
Excessive production of mucus AEB
adventitious breath sounds, ……

 Ineffective
breathing pattern Rt.
bronchospasm AEB SOB, use of
accessory muscles of breathing, ……
 Please involve the learners here
Bacci E, et al.(2006).Low sputum
eosinophils predict the lack of response
to beclomethasone in symptomatic
asthmatic patients. Chest.129(3):565-72.
Bateman ED, et al. (2008).Global strategy
for asthma management and prevention:
GINA executive summary. European
Respiratory Journal 1(1):143-78.
Enright, P.L; Lebowitz, M.D; Cockroft, D.W.
(1994).Physiologic measures:
pulmonary function tests. Asthma
outcome. Am J Respir Crit Care
Med 149(2 Pt 2):S9-18
Morris, M. et al. (2012). Asthma

http://emedicine.medscape.com/article/
296301
Woods, A.Q; Lynch, D.A. (2009). Asthma: an
imaging update. Radiol Clin North Am.
47(2):317-29