Your typical COPD patient on the respiratory ward is a male, older than 40, infective exacerbation of COPD, on oxygen, life time smoker. It’s actually really sad to see. There was this one patient who I was speaking to and I was examining his foot (he had lost sensation and movement in his toes probably due to peripheral nerve damage); he got extremely breathless just reaching down to pull his socks back on. Imagine that- you decide to smoke at the age of 16 and then before you’re even 50, you get breathless putting your socks on. Forget nicotine patches, I think some time seeing COPD patients would be a great addition to smoking cessation programmes.

Chronic Obstructive Pulmonary Disease (COPD)

Definition: common chronic progressive disorder characterised by airway obstruction with little or no reversibility. It includes chronic bronchitis and emphysema. Chronic bronchitis is clinically defined as a productive cough on most days for 3 months of 2 successive years. Emphysema is defined histologically as enlarged air spaces distal to terminal bronchioles, with destruction of alveolar walls.

Aetiology/ risk factors:

-smoking (passive or active) or pollution related

-rarely, α1-antitrypsin deficiency (< 1%)- consider in younger patients or never-smokers


-prevalence: very common, up to 8%

2.5 M deaths/ year worldwide

Age of onset > 35 years

More common in males but likely to chane with increase in female smokers


-Chronic dyspnoea

-Sputum production, chronic cough


-decreased exercise tolerance

-skeletal muscle dysfunction (loss of muscle bulk and strength), weight loss, depression

-minimal diurnal or day-to-day FEV1 variation (unlike asthma’s classic ‘morning dip’)

-symptoms improve if they stop smoking


Image result for decreased cricosternal distance copd-tachypnoea

-use of accessory muscles of respiration

-pursed-lip breathing

-hyperinflation (e.g. barrel chest)

-decreased cricosternal distance (< 3 cm)

-decreased chest expansion

-resonant or hyper-resonant percussion note, loss of liver and cardiac dullness

quite breath sounds (e.g. over bullae- dilated air spaces within the lung parenchyma )


-crepitations- sometimes


-signs of CO2 retention- bounding pulse, warm peripheries, flapping tremor of hands.

-signs of cor pulmonale (pulmonary dysfunction causing right side of the heart to fail)- oedema, hepatomegaly, ↑JVP, right ventricular heave, tachycardia, pan-systolic murmur (TR), loud P2 (part of S2 heart sound)

Pink puffers– increased alveolar ventilation, near normal PaO2, normal or low PaCO2, breathless but not cyanosed- EMPHYSEMA dominant

Blue bloaters– decreased alveolar ventilation, low PaO2, high PaCO2, cyanosed but not breathless. May go on to develop cor pulmonale, rely on hypoxic drive to maintain respiratory effort.- BRONCHITIS dominant

These are ends of a spectrum. In reality, patients will have components of both.


Full blood count- increased haematocrit/ packed cell volume

CXR- hyperinflation ( > 6 anterior ribs seen above diaphragm in mid-clavicular line), flat hemidiaphragms, large central pulmonary arteries, decreased peripheral vascular markings, bullae, elongation of cardiac silhouette


COPD- see the extra ribs and the flattened hemidiaphragm?

ECG: right atrial and ventricular hypertrophy (cor pulmonale)

ABG: decreased PaO2 +/- hypercapnia (from my experience on the Resp ward- I’ve seen lots of COPD ABGs showing Respiratory Acidosis with Full Metabolic Compensation, which gets disturbed during infective exacerbations leading to Partially Compensated Respiratory Acidosis)

Lung function: obstructive picture with air trapping- FEV1 < 80% predicted, FEV1: FVC ratio < 70%, ↑ TLC, ↑ RV, decreased DLCO (diffusing capacity of the lungs for carbon monoxide) in emphysema (determines how much O2 travels from the alveoli of the lungs to the blood stream)

Sputum & blood cultures- in acute exacerbations, for treatment

α1-antitrypsin levels- consider in young patients or minimal smoking history

Severity of COPD (all FEV1/ FVC < 0.7) :

Stage 1 Mild                                       FEV1 ≥ 80% of predicted

Stage 2 Moderate                             FEV1 50-79% of predicted

Stage 3 Severe                                   FEV1 30-49% of predicted

Stage 4 Very Severe                        FEV1 <30 % of predicted


Chronic stable  COPD:


-smoking cessation, encourage exercise

-diet advice +/- supplements as weight often low (or to treat obesity)

-mucolytics (e.g. carbocisteine)

-flu and pneumococcal vaccinations

-screen for and treat depression

-pulmonary rehabilitation/ palliative care

-PRN (when needed) short acting anti-muscarinic (IPRATROPIUM BROMIDE) or β2 agonist (SALBUTAMOL)


inhaled long-acting anti-muscarinic (TIOTROPIUM BROMIDE) or β2 agonist (SALMETEROL, FORMOTEROL)


combination long acting β2 agonist + corticosteroids e.g. SYMBICORT (BUDESONIDE + FORMOTEROL), SERETIDE (FLUTICASONE + SALMETEROL) OR TIOTROPIUM

⇒If remain symptomatic

TIOTROPIUM + inhaled steroid + long acting β2 agonist

-refer to specialist

-consider steroid trial, home nebulisers, theophylline

-Prednisolone (30mg/ 24h PO for 2wks). If FEV1 rises  > 15%, the COPD is ‘steroid responsive’ and may benefit from long-term inhaled corticosteroids.

⇒Pulmonary hypertension

-assess the need for long term oxygen therapy (LTOT)

-treat oedema with diuretics

⇒More advanced COPD

-pulmonary rehabilitation

-consider LTOT

-consider lung volume reduction surgery or surgery for recurrent pneumothoraces or isolated bullous disease

-non-invasive ventilation may be appropriate if hypercapnic on LTOT (loss of hypoxic ventilatory drive in some patients)

-air travel risky if FEV1 < 50% (Stage 3) or PaO2 < 6.7 kPa

NICE (not the French town) suggests LTOT for:

  1. clinically stable non-smokers with PaO2 < 7.3 kPa despite maximum drugs, stable value 2x > 3 weeks apart
  2. PaO2 7.3-8 kPa AND pulmonary hypertension OR polycythaemia OR peripheral oedema OR nocturnal hypoxia
  3. Terminally ill patients

⇒Acute exacerbation

-nebulised bronchodilators (SALBUTAMOL 5mg/4h and IPRATROPIUM 500μg/6h)

24-28% O2 via non-variable flow Venturi mask (if SaO2 < 88% or PaO2 < 7 kPa)

-increase slowly if no hypercapnia and still hypoxic

-corticosteroids (IV HYDROCORTISONE 200mg & oral PREDNISOLONE 30mg 1/d, for 7-14 days)

-start empirical ABx if evidence of infection (e.g. AMOXICILLIN, CLARITHROMYCIN, DOXYCICLINE)

-respiratory physiotherapy essential to clear sputum

-consider IV AMINOPHYLLINE (bronchodilator- PDE inhibitor) if  no response to nebulisers and steroids

-If not responding, pH falling and PaCO2 rising: non-invasive positive pressure ventilation → intubation and ventilation → respiratory stimulant drug (e.g. DOXAPRAM– short term measure)


-acute exacerbations +/- infection (especially  Strep pneumo and H.influenzae)

-2ry polycythaemia (compensatory increase in RBC content of blood = increased thrombosis risk)

-respiratory failure

-cor pulmonale due to pulmonary arterial hypertension (result of hypoxic pulmonary vasoconstriction, polycythemia, destruction of the pulmonary vascular bed by emphysema, hyperinflation and endothelial dysfunction)

-pneumothorax (ruptured bullae)

-lung carcinoma


-high level of morbidity

-3 year survival rate of 90% if age < 60 years and FEV1 > 50% predicted

                                             75% if age > 60 years and FEV1 40-49% predicted

-there is no excess mortality if lung function is normal

References: Cheese & Onion, Rapid Medicine


4 thoughts on “COPD

    • clumsylostmedicalstudent says:

      🙂 Thank you! It really is like a whole different language. I pick up a new one everyday on the wards. It’s even worse when reading through patient notes: “sorry to bother you, busy junior Dr, but what does ‘patient MFFD?” And they also have really weird symbols- # is fracture…and so on!


      • Odysseus says:

        Well, you have 2/3 years left to master it before getting thrown into your foundation years, so I’m sure you’ll be fine :). By the way, this is something I’ve always wondered whilst trawling the web and I might as well ask you now – what does ‘junior doctor’ mean in the UK health system, and when is it used? It seems to be a little flexible in its usage, at least in television; is it used specifically to refer to those in their foundation years, or does it apply to anyone below the level of consultant/GP/otherwise ‘finished’ with training?

        I hope your time in the wards has been going well for you. Have you moved on to a new assignment now? In any event, I wish you the best of luck and I hope to see more from you soon (the educational aspect of your posts aside, it’s a bit inspiring in a way, to know that when I do finally enter my clinical years I won’t just disappear into a black hole).


      • clumsylostmedicalstudent says:

        Junior doctor really refers to a doctor that has graduated but not yet reached GP/Consultant. Though I think the general UK public think of the term as meaning the really newbie doctors- foundation years. In hospital and med school though, Junior Dr isn’t used. We speak of ‘when you become an F1’- i.e. first year of foundation programme. Funnily enough, the F1s are busy all over the hospital, but I have yet to see an F2. Wonder where they disappear to…

        Wards have been an experience that I have yet to get used to but that I do overall enjoy. I have finished my respiratory firm (placement) and now have a few weeks of lectures. After the Christmas break I start my surgery firm.

        Thanks for the well wishes and all the best with your medical journey 🙂


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