Bronchial Asthma
DEFINITION
Asthma is characterised by chronic airway
inflammation and increased airway hyper-
responsiveness leading to symptoms of
wheeze, cough, chest tightness and dyspnoea.
Presence of airflow obstruction is reversible
spontaneously or with treatment.
Aetiology
• Is complex, and multiple environmental and genetic
determinants are implicated
• The hygiene hypothesis
RISK FACTORS & TRIGGERS
Pathophysiology:
Trigger Exposure:
• The process begins when a person with asthma encounters a trigger.
Common triggers include allergens (like pollen, dust mites or pet dander),
irritants (such as cigarette smoke or air pollution), infections, cold air or
exercise.
Immune Activation:
• When the trigger enters the airway, the immune system recognizes it as
harmful.
• Dendritic cells (a type of immune cell) pick up the allergen and present it
to T-helper 2 (Th2) cells in the immune system.
• Th2 cells release signaling molecules called cytokines (specifically IL-4,
Cytokine Effects:
• IL-4 instructs B cells (another immune cell type) to produce IgE
antibodies, which are specific to the allergen.
• IL-5 attracts eosinophils to the airway. These cells release toxic proteins
that damage the airway lining, causing inflammation.
• IL-13 causes excessive mucus production and makes the airway muscles
more sensitive (hyperresponsive) to stimuli.
Mast Cell Activation:
• The IgE antibodies produced earlier attach to mast cells in the airway.
• When the allergen interacts with the mast cells, they "burst open" (a
process called degranulation), releasing chemicals like histamine,
prostaglandins, and leukotrienes.
• These chemicals cause bronchoconstriction (tightening of airway
muscles), swelling of the airway walls, and further mucus production.
Airway Effects:
• The airway becomes narrowed due to three factors:
• Tightening of smooth muscles (bronchoconstriction).
• Swelling of the airway lining (edema).
• Excess mucus clogging the airway (mucus hypersecretion)
Chronic Inflammation:
• Over time, repeated cycles of inflammation lead to airway remodeling,
which causes permanent structural changes:
• Subepithelial fibrosis: Thickening of the airway wall due to collagen
deposition.
• Smooth muscle hypertrophy and hyperplasia: Increase in size and
number of airway muscle cells, making the airway more prone to
narrowing.
• Angiogenesis: Formation of new blood vessels, contributing to swelling
Functional Consequences:
• Airflow limitation: Narrowed airways make it harder for air to flow in and
out of the lungs.
• Airway hyperresponsiveness (AHR): The airway becomes overly
sensitive to even mild triggers, worsening bronchoconstriction
Clinical Manifestations:
The combination of airway obstruction and hyperresponsiveness leads to
the classic symptoms of asthma:
• Wheezing (a high-pitched sound during breathing).
• Shortness of breath.
• Chest tightness.
• Cough, especially at night or early morning.
Clinical features
• Can be discussed under 3 headings
1. Episodic Asthma
2. Chronic Asthma
3. Acute severe Asthma
Episodic Asthma
- episodes with asymptomatic period in between
-symptoms include episodes of wheezing, chest tightness,
breathlessness and cough
- with or without triggers.
Chronic Asthma
- pattern is one of chronic wheeze and breathlessness
- more night symptoms
- repeated attacks of acute severe asthma
Acute severe Asthma
- Severe breathlessness & brochspasm
- sweating, cyanosis, tachycardia, pulsus paradoxus
• Asthma characteristically displays a diurnal pattern, with
symptoms and PEF being worse in the early morning.
• Increased mucus production- with typically tenacious
mucus that is difficult to expectorate
• Auscultation – high pitched polyphonic expiratory &
inspiratory rhonchi are heard.
Clinical manifestations
• Signs:
• Increased respiratory rate along with use of accessory
muscles
• Hyperresonant note on percussion
• Expiratory rhonchi
• No findings when asthma is under control
Classification of asthma severity
INVESTIGATIONS
1. PFT
Peak flow meters - inexpensive and simple
- patients are instructed to record readings after rising in the morning
and before retiring in the evening.
Spirometry - measurement of FEV1 and VC - demonstration of airflow
obstruction, and following the administration of a bronchodilator,
confirms the diagnosis when a 15% (and 200 ml) improvement in
FEV1 is noted
Forced expiratory volume in 1 second: (FEV1)
• Volume of air forcefully expired from full inflation in the first second
2.Measurement of allergic status
Elevated sputum or peripheral
blood eosinophil count in
atopic asthma
Skin prick tests are simple and
provide a rapid assessment of
atopy
Management
• Patient education
-Avoidance of aggravating factors
Education
• About the condition
• On use of a bronchodilator and any other medication
• How to prevent chest infection from occurring
• Correct posture in standing and sitting which assists in the
management of asthma attacks by allowing the chest to expand
appropriately and the lungs to function optimally
Non-pharmacological management
• Reduce exposure to indoor allergens
• Avoid tobacco smoke
• Avoid vehicle emission
• Identify irritants in the workplace
• Explore role of infections on asthma development in
children and young infants
• Influenza vaccine: routine vaccination
Bronchodilator Therapies
• β2-Agonists - relax airway smooth-muscle cells
Short-acting β 2-agonists (SABAs)- albuterol and terbutaline rapid
onset of bronchodilation and used as needed for symptom relief.
Long-acting 2-agonists (LABAs) - salmeterol and formoterol, duration
of action over 12 hours and are given twice daily
• Anti-Cholinergics- ipratropium bromide, prevent cholinergic
nerve–induced bronchoconstriction and mucus secretion
• Theophylline
- due to inhibition of phosphodiesterases in airway smooth-muscle
cells
- Oral theophylline is usually given as a slow-release preparation
once or twice daily
- Iv aminophylline used for the treatment of severe asthma
Controller Therapies
• Inhaled Corticosteroids - anti-inflammatory agents - usually given
twice daily
• Systemic Corticosteroids
- iv (hydrocortisone or methylprednisolone) in acute severe asthma
- course of oral corticosteroids - prednisolone for 5–10 days used to
treat acute exacerbations.
• Antileukotrienes - montelukast and zafirlukast
add-on therapy if not controlled with low doses of inhaled steroids
• Cromones - Cromolyn sodium and nedocromil sodium , inhibit mast
• Oxygen-to maintain the oxygen
saturation > 92%
• High doses of inhaled
bronchodilators
nebuliser driven by oxygen for
salbutamol + Ipratropium.
• Systemic corticosteroids - orally
(prednisolone 30-60 mg) or iv
hydrocortisone 200 mg
PHYSIOTHERAPY MANAGEMENT
Breathing retraining Techniques:
Breathing techniques may have more benefit on mild – moderate asthma.
The aim of breathing retraining is to normalise breathing patterns by stabilising
respiratory rate and increasing expiratory airflow.
Instructions are given from the physiotherapist on how to complete this technique,
with the following components:
Decreasing breaths Taken (Reducing Respiratory Rate)
• Taking Smaller Breaths (Reducing Tidal Volume)
• Deep Breathing (Diaphragmatic breathing through use of abdominal muscles
and lower thoracic chest movement)
• Breathing through the Nose (Nasal Breathing)
• Relaxation (Relaxed, controlled breathing)
• Controlled exhalation (Decreased expiratory flow through pursed lip breathing)
• These retraining techniques help control breathing and reduce airflow
turbulence, hyperinflation, variable breathing pattern and anxiety.
Buteyko Breathing Technique
• The Buteyko technique aims to reduce ventilation and subsequently lung
volume, as a treatment for asthma and other respiratory diseases.
• A qualified practitioner is necessary to train the patient.
• Breathe normally through the nose for 2-3 mins – Breathe out normally, close
nose with fingers, and hold – Record number of seconds – On first need to
breathe, release nose and return to nasal breathing (Control Pause) – Wait 3
minutes – Repeat and hold breath for as long as possible (Maximum Pause)
Breathing pattern retraining and relaxed breathing techniques
• This is usually accomplished by slowing the breathing rate, and
encouraging relaxed, ‘abdominal’ breathing.
• Another potential mechanism for breathing pattern retraining is that
by encouraging a longer expiratory time, the effects of any static/
dynamic hyperinflation may be reduced.
