Pulmonology

COPD

I. BASIC PRINCIPLES Prevalence: 15% over 40s

A. Group of diseases characterised by airway obstruction – the lungs do
not empty; and air is trapped.
1. Volume of air that can be forcefully expired (FVC) ↓, especially during
1st second of expiration (FEV1) ↓↓.
a. FEV1 < 80%
2. Hence FEV1 : FVC ↓ 
a. FEV1 : FVC < 0.7 with little / no reversibility.
3. Total lung capacity (TLC) ↑, is usually due to air trapping.
B. Hypoxaemia is due to V/Q mismatch.
1. Hypoxia-induced vasoconstriction + media layer hypertrophy over
time  increase load on RV  RVH  eventual RHF (cor pulmonale)
C. BTS/NICE 2010 / GOLD 2015 criteria for Dx: no single Dx test, Dx if
meets ALL the criteria:
1. > 35 years old
a. Consider the possibility of A1AT deficiency if person < 40 years
old or FHx.
2. Risk factor (occupational, smoking) See asthma-COPD overlap
3. Typical Sx: exertional SOB, chronic cough, wheeze, regular sputum
production, recurrent chest infections
4. Other Sx: LoW, low ET, ankle oedema, fatigue
5. Absence of clinical features of asthma
D. Additionally O/E:
1. Cyanosis, raised JVP + peripheral oedema (cor pulmonale), cachexia, Also: tachypnoea, expiration
hyperinflation (barrel chest), accessory muscle usage, reduced phase longer than inspiration.
expansion, pursed lip, wheeze or quiet breath sounds (e.g. over
bullae; subpleural bullae can spontaneously rupture  PTX).
MRC 1: not troubled except
E. Assessment strenuous exercise
1. Assess SOB using MRC dyspnoea scale MRC 2: SOB up a slight hill
2. Assess for anxiety or depression MRC 3: slower than
3. Pack-years contemporaries due to SOB, or
stop for breath when walking own
4. BMI
pace.
5. Overall prognosis – BODE index (BMI, Obstruction, Dyspnoea, MRC 4: SOB ~100 m or few mins
Exercise tolerance) (level ground)
F. Investigations for ALL COPD MRC 5: too breathless to leave
1. FBC house
2. CXR – hyperinflation (> 6 anterior ribs above diaphragm MCL),
flattened diaphragm, large central pulmonary arteries, reduced
peripheral vascular markings. Bullae. Also rule out other path. DDx: asthma, bronchiectasis, HF,
3. Post-bronchodilator spirometry – confirm Dx and assess severity of lung CA, ILD, anaemia, TB.
airflow
Smoking = COPD associated w
a. Performed by trained staff. Carried out 15 – 20 mins after lung CA
person has inhaled 200 mcg salbutamol or 500 mcg terbutaline
via spacer.
b. Obstruction values defined above. Severity:
 Stage 1 FEV1 > 80% (with such values, can only Dx COPD
when there is respiratory Sx)
 Stage 2  FEV1 = 50 – 79% of predicted
 Stage 3  FEV1 = 30 – 49% of predicted

1|Page
Pulmonology

 Stage 4  FEV1 < 30% of predicted

c. Routine reversibility test not recommended unless can’t DDx
asthma or COPD.
d. Repeat spirometry if good response to Tx (steroid trial), and
reconsider Dx if FEV1 : FVC > 0.7 at follow-up.
G. Investigations if appropriate:
1. Sputum culture if sputum is purulent and persistent
2. SpO2 – to assess need for LTOT e.g. if features of cor pulmonale, or if
FEV1 < 50%.
3. ECG and echo – cor pulmonale

H. When to refer? See asthma.

1. Haemoptysis + red flags: to R/O lung cancers
2. Dx uncertainty (COPD-asthma overlap): for confirmation of Dx
3. Very severe (stage 4) or worsening COPD: for Dx & optimise Tx Also be suspicious of A1AT, if < 10
pack years (packs/day x years of
4. Suspicion of cor pulmonale: for Dx & optimise Tx smoking; 1 pack = 15 cig).
5. Age < 40, FHx of A1ATD: for Dx, family screening, and Tx access
6. Frequent infections: R/O bronchiectasis
7. Pattern of Sx disproportionate to spirometry: R/O other path
Surgery rarely indicated. Other
8. For O2 therapy (LTOT)
surgery = lung TXP (single-lung
9. For NEBs therapy or LT PO steroids MCC).
10. For lung surgery (e.g. bullous lung disease who still Sx on max Tx)
11. Refer to pulmonary rehabilitation if: Rehab sessions last 2-3 / wk for 6-
a. MRC grade > 3 = functionally disabled 12 wks.
b. Recent hospitalisation for acute exacerbation
c. DO NOT refer if can’t walk, or unstable angina, or recent MI.
12. MDT
a. Dietician (obese), OT (ADLs affected), PT (PEEP masks and active
cycle of breathing), psych (anx/dep)
b. Cease smoking.
Regardless of initial FEV1, if so
I. Management in adults with STABLE COPD (> 16). severe – always end up with triple
1. May be started even before Dx confirmed, provided spirometry therapy of LAMA + LABA + ICS.
performed and other assessments R/O asthma.
2. Steroid trial – look for increase in FEV1 > 15%.

FEV1 > 50%

General SOB  See MDT.
 NIPPV may be life-saving in T2RF (when PaCO2 > 6, pH LABA monotherapy may increase
< 7.3). exacerbation rates (but not excess
 PRN SAMA (ipratropium) or SABA. mortality / hospitalisation) c.f.
asthma. ICS can increase risk
Persistence of  Either: inhaled LAMA (tiotropium); discontinue SAMA PNA. But dual therapy beneficial.
SOB or QDS.
exacerbations  Or LABA
Step-up for  LABA yet remains breathless  LABA + ICS
LABA only combination inhaler e.g. Symbicort (formoterol +
budesonide)
Persistence of  LAMA + LABA + ICS
exacerbations  Specialist referral. Consider steroid trial, home NEBs.
or SOB
N.B. the SABA is continued at all stages (PRN).

2|Page
Pulmonology

FEV1 < 50%

General SOB  SABA or SAMA PRN
Exacerbations/  Symbicort or Remember that in more severe
persistence of  If ICS not tolerated/ declined: LABA + LAMA. COPD, pulmonary rehab is greatly
valued by patients
SOB
Persistence of  LAMA + LABA + ICS
exacerbations  Specialist referral.
or SOB
N.B. the SABA is continued at all stages (PRN).

3. Add-on Tx:
a. Mucolytics – if chronic productive cough (continue if Sx improve;
should not be routinely Rx)
b. Theophylline or aminophylline PO – still Sx after short and long-
acting bronchodilators + ICS, or can’t use inhaler devices
successfully… but S/E: arrhythmias
c. Anxiolytic/antidepressants
d. Diuretics for cor pulmonale’s oedema.

4. DO NOT START PO steroids in primary care. This is a specialist

decision.

J. Types of O2 therapy
1. LTOT if person have: SpO2 < 92%, very severe obstruction (FEV1 <
30%), cyanosis (PaO2 < 7.3), 2o polycythaemia, peripheral oedema, or
raised JVP (cor pulmonale and PaCO2: 7.3 – 8).
a. Improve 3Y survival by 50% if PaO2 > 8, for 15 h / day.
2. Ambulatory (portable) O2T: if wish to be out of home.
3. Short-burst O2T: PRN use for 10-20 mins to relieve SOB (referral may
not be necessary if used for palliation). Also used for people who are
not elibigle for LTOT but SOB can’t be relieved by other Tx.
4. Don’t smoke (explosions/fire)
Immunosuppressed: HIV, DM,
K. Vaccinations hypo- or a-splenic, on chemo, or
1. Flu vaccine  high risk groups (DM, COPD, asthmatic that are not on steroids, post-TXP.
mild, heart/renal/liver failure, immunosuppressed, Hbpathy, HCW,
Sickle-cell or asplenic  high risk
the elderly: > 65 y – esp. in institutions). fatal pneumococcal infections 
2. Pneumoccocal vaccine  high-risk groups as above. C/I in re-vaccinate every 6 y.
pregnancy/lactation/high To.
a. See pneumonia for schedules.

L. Management in COPD exacerbation.

1. Common in Winter. May be ppt. by infections.
2. Increasing cough, SOB, wheeze; decreasing ET.
3. Very brief Hx – if able to talk (A clear), mainly to risk-assess @start 
influence the threshold to send to ITU or to ventilate
a. Usual or recent Tx esp. home O2
b. ET
c. Have you been to ED, or ICU, or intubated before? How
frequent?

3|Page
Pulmonology

d. Smoking status
e. Consider DDx from Hx: asthma, HF, URT obstruction, PE,
anaphylaxis.
4. ABCDE approach (management – diagram).
5. Sepsis-6 if pyrexia.
6. Further assessment: CXR (R/O PTX, infection); FBC + U&Es + CRP;
ABGs. Theophylline blood levels if on that drug (low TI). ECG (rarely
find much).
7. Prior to discharge: safety net + signpost
a. Liaise with GP to consider O2, reduction of steroid dose
(infection risk), smoking cessation advice, and vaccination
b. Rescue medications.

In real life, you still give 100% O2.

NEBs driven by air, not O2

Monitor closely if administer O2.

Amox covers pneumococcal

infection, clarithromycin & doxy
covers atypicals.

Ceiling-of-care & MCA 2005

4|Page
 Pulmonology

II. CHRONIC BRONCHITIS

A. A type of COPD that is clinically Dx as chronic productive lasting, on
C.f. acute bronchitis
most days, for at least 3 months, over a minimum of 2 successive years.
B. Highly associated with smoking. Sx improves if cease smoking. No excess mortality if PFT normal.
C. Path: hypertrophy (and hyperplasia) of bronchial mucinous glands 
excessive mucus.
1. Oedema and inflammation within bronchial mucosa Also goblet cell metaplasia = more
2. Peribronchiolar fibrosis develops chronically = narrow airways mucus secreted.
D. Histo: thickened mucus glands relative to bronchial wall (Reid index >
50%; normal < 40%). Not the same as bronchiolitis =
E. Clinical features: another obstructive but acute
respiratory disorder, in which
1. Productive cough due to excessive mucus production acute inflammation destroys
2. Cyanosis (blue bloaters) – mucus plugs trap CO2  ↑ PaCO2, ↓ small airways. E.g. RSV, HSV,
PaO2 (T2RF)  can progress into cor pulmonale. toxins, ARDS.
a. Respiratory centres may be insensitive to CO2 = may rely on
hypoxic drive to maintain respiratory effort. Careful w O 2.
3. Increased risk of infection (exacerbations)
4. 2o polycythaemia

III. EMPHYSEMA
A. A type of COPD that is histologically defined as enlarged air spaces distal
to terminal bronchioles, with destruction of alveolar air sacs.
B. Path:
1. Due to imbalance between proteases (neutrophil elastase) and
antiproteases (1-antitrypsin, A1AT).
2. Predominant activity by the formal  destruction of alveoli.
3. Loss of elastic recoil and collapse of airways during exhalation 
obstruction and air trapping.
C. Two subtypes:
1. Centriacinar emphysema
a. Due to smoking or air pollutants
b. Activates neutrophils  protease-mediated damage
c. Most severe in upper lobes (smoke rises)
2. Panacinar emphysema
a. A1AT deficiency (rare AD condition, < 10 % of all COPDs) 
imbalance = protease over-activity. Disease severity depends
on degree of severity:
 PiM (normal allele)  PiMM is normal.
 PiS (slow electrophoresis motility) = reduced A1AT (60%). See GI.
 PiZ (most common clinically relevant mutation; very slow Dx: A1AT serum levels, isoelectric
motility) = low circulating A1AT (15%). focusing, liver Bx with PAS+ stain,
 High-risk is PiZZ, low-risk PiSZ. pre-natal (CV DNA sample at 11-
13 weeks).
 Panacinar emphysema is most severe in lower lobes
 Also causes liver cirrhosis  due to accumulation of
mutated A1AT in the ER of hepatocytes PiS = osition 264 single amino acid
b. Could also develop eventually from smoking. sub
PiZ = Position 342 “”
D. Clinical features of emphysema.
Both lead to misfolded protein.
1. SOB with minimal sputum
2. Prolonged expiration with pursed lips (creates PEEP)  Pink puffers
(strong hypercapnic drive)
3. Weight loss (from work of breathing)

5|Page
 Pulmonology

4. Increased A/P diameter of chest (barrel chest)

5. Tripoding
6. Late complications: hypoxaemia (destruction of alveoli = V/Q
mismatch) + cor pulmonale

IV. CYSTIC FIBROSIS

A. AR mucoviscidosis disorder where CFTR is mutated
B. Path: obstructive; tubes plugged up with mucus  leads to neonatal
bowel obstruction, pancreatic insufficiency (and so malabsorption),
recurrent bronchial infections (esp. Pseudomonas) = leading into an
eventual bronchiectasis.
C. Can be obstructive or restrictive in nature.
D. Sweat test is Dx.

6|Page