ASTHMA AND COPD
DR SANJENA MITHRA, FY1
Objectives
 Differentiate severity of acute asthma exacerbations
 Pathophysiology of Asthma and COPD
 Discuss CXR and ABG
 Type 1 vs Type 2 respiratory failure
 5 mins – pretest
 10 mins – case 1
 10 mins – case 2
 5 mins – end of session test
 feedback
Pretest
 Define asthma
 What constitutes COPD?
 Briefly outline the pathophysiology of asthma
 Describe 4 differences in the airways of acute and
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chronic asthmatics.
How can you categorise severity of acute asthma attacks?
List 4 classes of drug used to treat Asthma/COPD
What are their mechanisms of action and side effects?
How can you determine severity of COPD?
Compare type 1 and type 2 respiratory failure
Take a history from this patient who is short of
breath…
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Cough +/- sputum
Chest pain (pleuritic)
Wheeze
SMOKING
Allergies, Pets
Foreign travel
History of DVT, PE
*Compliance with
meds*
 Weight loss
 Haemoptysis
 Atopy
 Family history
 Exercise tolerance
 Diurnal variation
 Complications:
 Oedema
 SOBOE
 Recurrent infections
 Fever
CASE 1- Summary
 28 year old lady presents to A&E after becoming short of
breath whilst visiting friends. She was feeling well during
the day and had been to work. Non-smoker
 PMH: Asthma since childhood – Salbutamol PRN
 Inhaler currently not relieving symptoms; SOB worse
over last 2 hours. Chest starting to feel tight, she is
getting lightheaded.
 On examination:
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T 36.2
BP 124/71
HR 90
RR26
96% sats on air
 Alert, talking in full sentences but distressed.
 CVS and Abdo – NAD
 Resp – widespread wheeze, no crackles, no friction rub
 What are your differentials for this patient and why?
 Acute asthma exacerbation (non-life threatening)
 PE
 Inhaled foreign body
 Allergic reaction
 Anxiety
 Pathophysiology
 Define asthma
 4 characteristics of acute and chronic asthma
Asthma
 ASTHMA – chronic, inflammatory
disease of the airways resulting in
variable, often reversible airflow
obstruction and airway
hyperresponsiveness.
 Acute asthma airway changes
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Airway constriction, microvascular leakage /
oedema, vasodilation, mucus hypersecretion
IgE mediated inflammatory response. Crosslinking of IgE results in degranulation of
mast cells, histamine release and
inflammatory cell infiltration
 Chronic asthma airway changes–
airway remodelling
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Subepithelial fibrosis, smooth muscle
hyperplasia / hypertrophy, goblet cell
hyperplasia, new vessel formation
Investigations
 What investigations would you like to do?
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Bedside: Peak flow – 45% of best
Bloods: ABG, FBC, U&E, CRP
Imaging: CXR
 ABG:
 pH 7.46
 pCO2 4.1
 pO2 10.3
 HCO3 26
Respiratory
Acidosis
Respirator
y Alkalosis
Metabolic
Acidosis
Metabolic
Alkalosis
pH ↓
pH ↑
pH ↓
pH ↑
Primary
problem:
pCO2 ↑
Primary
problem:
pCO2 ↑
Primary
problem:
HCO3 ↓
Primary problem:
HCO3 ↑
Compensatio
n:
HCO3 ↑
Compensatio
n
HCO3 ↓
Compensati Compensation:
pCO2 ↑
on:
pCO2 ↓
Reading Chest X-Rays
RIP...ABCDE
Adequacy:
-Rotation (symmetry of
clavicles)
-Inspiration (ribs)
-Penetration (vertebral
bodies)
-Mention central lines,
NG tubes, pacemakers
etc
-Airway: is the trachea
central?
-Boundaries and
Both lungs: lung
borders, consolidation,
hazy etc
-Cardiac: Heart size
-Diaphragm
-Everything else: soft
tissue mass, fractures
 What investigations would you like to do?
 Bedside: Peak flow – 45% of best
 Bloods: ABG, FBC, U&E, CRP
 Imaging: CXR
Allergic bronchopulmonary aspergillosis: refractory asthma with fever,
cough and sputum. Eosinophilia and raised IgE
Acute severe asthma
 How would you like to manage this patient?
 Immediate
 A to E
 Salbutamol 5mg via oxygen driven nebuliser
 Repeat obs (SpO2, HR, RR) and PEF to assess for progression
of severity and risk to life
 If clinically stable and PEF >75%, can repeat Salbutamol nebs
and consider oral prednisolone 40-50mg
Moderate
PEF >50-75%
SpO2 >92%
No features of severe
Acute Severe
PEF 33-50%
RR >25
SpO2 >92%
HR >110
Cannot complete
sentences
Life threatening
33-92-CHEST
PEF <33%
SpO2 <92%
Cyanosis/Confusion,
Hypotension,
Exhaustion, Silent
chest, Tachycardia
Salbutamol 4 puffs, then
2 puffs every 2 mins
Salbutamol 5mg via O2
driven nebuliser
Senior help (ITU,
anaesthetics)
If life threatening
features present
Repeat salbutamol nebs,
give oral prednisolone
40-50mg
ABG, CXR
O SHIT!
•O2 to maintain sats 94-98%
•Salbutamol 5mg via O2 driven nebs
•Hydrocortisone IV/oral prednisolone
•Ipratropium via O2 driven nebs
•Consider Magnesium Sulphate IV
Long term management
 Long term
 Conservative: Follow up by GP, check inhaler technique, refer
to chest clinic/asthma liaison nurse
 Medical: If PEF <50% on admission, can consider
prednisolone, adequate inhaler supply
 Stepwise treatment of asthma
Communication
 Please explain to Mr X how to correctly use his inhaler
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Check understanding
If you haven’t used it for a while, spray in the air to check it works
Shake it
As you breathe in, simultaneously press down on the inhaler
Continue to breathe deeply
Hold your breath for 10 seconds or as long as you comfortably can,
before breathing out slowly.
If you need to take another puff, wait for 30 seconds, shake your
inhaler again then repeat
Advise on using a spacer
Chronic Management of Asthma
Case 2 – Summary
 A 64 year old gentleman presents to A&E with increasing SOB
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over the last 3 days. This is associated with a cough productive
of thick, green sputum.
Gets SOB normally after about 5-10 mins walking on the flat
PMH: “asthma”
SH: 50 cigarettes a day for the past 40 years.
On examination he is alert but visibly SOB

T 37.7
RR 25
HR 110
O2 sats 89% on air, you
notice he is using his accessory muscles to breathe.
 Resp: hyperinflated chest, diffuse coarse crepitations,
widespread wheeze, reduced air entry bilaterally
 CVS: JVP raised, ankle oedema (non-pitting)
 Abdo SNT
Case 2
 What are your differentials for this patient and why?
 Acute infective exacerbation of COPD
 Pneumonia
 Cor pulmonale
 Bronchiectasis
 Pathophysiology
 Define COPD clinically
 Histopathology?
 Pathophysiology?
Definitions
 COPD: Umbrella term encompassing chronic
bronchitis (chronic cough and sputum production on
most days for at least 3 months per year for 2 years)
and emphysema (pathological diagnosis of
permanent destructive enlargement of distal air
spaces)
 Chronic bronchitis: airway narrowing due to
bronchiole inflammation, mucosal oedema and
mucus hypersecretion
 Emphysema: Destruction and enlargement of
alveoli that reduces elastic recoil and results in
bullae.
Investigations
 What investigations would you like to do?
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Bedside: ECG, sputum culture
Bloods: ABG, FBC, U&E, CRP, blood cultures
Imaging: CXR
Special tests: ECHO, α1-antitrypsin levels
 ABG: assess the oxygenation
 Checking for respiratory failure- failure to fully oxygenate the
blood passing through the lungs giving rise to hypoxia +/hypercapnea.
 ABG
 pH 7.29
 pCO2 6.8
 pO2 7.9
 HCO3 25
Respiratory failure
 Type 1- hypoxia with low or normal pCO2 – anything
that impairs gas exchange
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Atelectasis, pulmonary oedema, pneumonia, pneumothorax
 Type 2 – hypoxia with hypercapnea – alveolar
hypoventilation
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Same causes for a respiratory acidosis
COPD, neuromuscular disorders (GBS, MND), CNS depression
(drugs, brainstem injuries)
Initial management – infective exacerbation of
COPD
 How would you like to manage this patient?
 Immediate
 A to E
 Maintain sats 88-92% (titrate to ABG)
 Corticosteroids (oral/IV)
 Empirical antibiotics
 Salbutamol 5mg and Ipratropium via O2 driven nebulisers
 Consider need for NIV – if desaturating/decompensating
 Admit, chest physiotherapy
Flow volume loops - Spirometry
FEV1/FVC
 Determines the severity of COPD
 Describes the proportion of a person’s vital capacity
(maximum air expelled after maximum inhalation) that can be
expired in the first second.
 Normal ~ 70%
 Mild 50-70%
 Moderate 30-50%
 Severe <30%
Management
 Long term
 Conservative – smoking cessation, pulmonary rehabilitation,
flu vaccination, Spirometry
 Medical – LTOT (only if not smoking), bronchodilators,
steroids (can consider if more than 2 infective
exacerbations/year), prophylactic antibiotics
 Surgical – Transplant, lobectomy, bullectomy
 LTOT criteria
 PaO2 <7.3 kPa on air during period of clinical stability
 PaO2 7.3-8.0 kPa and signs of secondary polycythaemia,
nocturnal hypoxaemia, peripheral oedema or pulmonary
hypertension
Drugs 1
 Bronchodilators:
 Beta-2 agonists – Short acting/Long acting
(Salbutamol/Salmeterol)
 MOA: increases cAMP production in the lung which decreases
calcium concentration
 Effect: Smooth muscle relaxation, bronchial dilatation
 S/e: tachycardia, sweating, tremor
 Anticholinergics:
 Ipratropium (Atrovent), Tiotropium (Spiriva)
 MOA: Anti-muscarinic. Ipratropium is non-selective,
Tiotropium is selective (M3)
 s/e: dry mouth, sedation, skin flushing, tachycardia
Drugs 2
 Methyxanthines
 Theophylline, Aminophylline
 MOA: Phosphodiesterase antagonists – raise intracellular cAMP levels.
Works well with beta-2 agonists
 s/e: narrow therapeutic window
 Leukotriene receptor antagonists
 Montelukast, Zafirlukast
 s/e: GI upset, drowsiness
 Corticosteroids
 Prednisolone, Beclamethosone
 MOA: upregulates intracellular proteins after binding with receptor and
causes expression of anti-inflammatory agents
 s/e: weight gain, immunosuppression, skin thinning, bruising,
osteoporosis, cataracts
Pretest
 Define asthma
 What constitutes COPD?
 Briefly outline the pathophysiology of asthma
 Describe 4 differences in the airways of acute and





chronic asthmatics.
How can you categorise severity of acute asthma attacks?
List 4 classes of drug used to treat Asthma/COPD
What are their mechanisms of action?
How can you determine severity of COPD?
Compare type 1 and type 2 respiratory failure
Take home message
 33-92 CHEST
 Focussed history taking: Symptoms, red flags,
complications
 Structure your answers
 Questions?