Look for 
- nicotine staining on fingers
- CO2 retention flap and bounding pulse
- central cyanosis
- pursed lips
- use of accessory muscles of respiration
- hyper-expanded chest
- expiratory wheeze
- crackles if infection present

For bonus points, look for signs of cor pulmonale (= right heart failure caused by pulmonary hypertension):
- loud P2
- right ventricular heave
- raised JVP
- peripheral oedema

Recap of Part 1 and 2 COPD notes here

Possible questions:

What is COPD?
Chronic obstructive pulmonary disease is a chronic respiratory condition characterised by airflow obstruction which is not fully reversible.  It combines chronic bronchitis, which is a clinical diagnosis of cough productive of sputum on most days for 3 months of 2 consecutive years, with emphysema, which is a pathological diagnosis of destruction of alveolar walls.  Patients with COPD will have a FEV1/FVC of <0.7.

How would you investigate a patient with possible COPD?
You would arrange spirometry after bronchodilators, expecting to see a FEV1/FVC of <0.7.  Other investigations would include CXR looking for hyperinflation and also to exclude other causes of breathlessness, FBC looking for polycythaemia and anaemia, ABG looking for type 2 respiratory failure and ECG looking for evidence of right heart failure.  In a young patient you would additionally look for alpha 1 antitrypsin deficiency.

What treatment would you offer to a patient with COPD?
Firstly you would encourage smoking cessation, offering nicotine replacement therapy, supportive talking therapies and bupropion. You would start a 'reliever' inhaler of a short-acting beta 2 agonist, for example salbutamol.  A 'preventor' inhaler should also be started.  If the FEV1 >50% predicted this can be a long-acting beta 2 agonist such as salmeterol (serevent) or a long-acting antimuscarinic such as tiotropium (spiriva).  If the FEV1 is <50% predicted either spiriva or a combination inhaler of LABA and steroid should be used, such as seretide (fluticasone and salmeterol).  Amiophylline can be considered in patients who cannot use inhalers or who do not achieve adequate control with them.
Pulmomary rehabilitation should also be offered to all patients.  Some patients may also require long-term oxygen therapy or surgery.

What are the indications for LTOT in COPD?
LTOT should be considered in patients with FEV1 <30% predicted, peripheral oedema, raised JVP, cyanosis, polycythaemia or sats 92% or less on RA.  2 ABGs need to be performed at least 3 weeks apart.  If the Pa02 is <7.3kPa in stable COPD this is an indication for LTOT.  If the PaO2 is <8kPa in stable COPD and one of 4 criteria are met this is also an indication for LTOT.  The 4 criteria are nocturnal hypoxaemia, pulmonary hypertension, peripheral oedema or secondary polycythaemia.

How long does LTOT need to be used for?
At least 15 hours per day.

How would you manage an exacerbation of COPD?
Controlled O2 via a venturi mask, salbutamol and ipratropium nebulisers, oral prednisolone and IV amiophylline if inadequate response to nebulisers.  If the exacerbation is infective also give antibiotics.  NIV may be required.

How and why would you initiate NIV?
If after an hour of medical management the patient remained acidotic and in type 2 respiratory failure NIV should be considered, but you should always have an 'exit strategy' in terms of whether you plan to escalate if this fails.  Initially NIV should be started on an IPAP of around 10cm H2O and a PEEP of  5, with the IPAP increased in response to blood gases.

Are there any risks associated with amiophylline?
Amiophylline has a fairly narrow therapeutic window.  Toxicity can manifest as nausea and vomiting, diarrhoea, agitation, dilated pupils or more seriously arrhythmias or convulsions.  It can cause low potassium.  It is therefore important to dose amiophylline appropriately (a loading dose of 5mg/kg ideal body weight over 30 minutes then an infusion of 0.5mg/kg/hr continuously) and to check levels 24 hours after starting the infusion and then daily afterwards.

What is alpha 1 antitrypsin deficiency?
Alpha-1 antitrypsin is a protease inhibitor produced in the liver. In the lungs this protects alveolar tissue from damage by neutrophil elastase. Deficiency makes it likely COPD will develop in the third or fourth decade in smokers or fifth or sixth decade in non-smokers. The classical pattern of lung damage is panlobular emphysema in the lower lobes

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