COPD

Question 1

COPD: What is it?

Answer 1

COPD= the collective term for a group of chronic inflammatory airway diseases that causes non-reversible airway obstruction.

The two most common conditions are:
- Chronic bronchitis- chronic inflammation of trachea, bronchi, and bronchioles the lining leading to bronchoconstriction and thick mucous accumulation and stagnation, making it hard to breathe.
- Emphysema- dilation and damage of the lung alveoli, decreasing the surface area for gas exchange. Destroyed alveoli makes it harder to move air out of the body, leading to CO2 retention.
- smoking causes centrilobular emphysema, where destruction begins at the centre of the lobule. Smoking stimulates inflammatory products which breaks down elastic tissue and inhibits alpha1-antitrypsin (AAT) anti-elastase activity
- AAT deficiency causes panlobular emphysema, where alveolar destruction occurs in all alveoli within the lobule simultaneously.

Infective exaccerbation of COPD= acute worsening of COPD symptoms and lung function due to infection. The damaged lungs are more susceptible to infection.

Question 2

COPD: Aetiology

Answer 2

• mostly caused by smoking
• can be caused by chronic airway disease
  GOOGLE

Question 3

COPD: Symptoms

Answer 3

• dysponea (MRC Dysponea and FEV1 to determine severity)
• wheeze
• cough + sputum (NOT BLOOD)
• recurrent LRT infections, particularly in winter
• Fatigue
• Headache (due to CO2 retention)

NO HAEMOPTYSIS, CHEST PAIN, CLUBBING

Question 4

COPD= Examination Signs

Answer 4

Most common findings
Tachypnoea: due to an increased neural respiratory drive to breathe
Wheeze on auscultation: due to inflammatory airway oedema and mucous obstructing the airway
Pursed lips breathing: to increase airway resistance and therefore reduce expiratory flow limitation
Less common findings
Barrel chest (Figure 1): due to gas trapping
Peripheral cyanosis (Figure 2)
Cor pulmonale (signs of right heart failure, such as peripheral oedema and hepatomegaly): due to pulmonary hypertension, which results from chronic hypoxic pulmonary vasoconstriction
CO2 retention flap: while the exact mechanism is unknown, some hypothesise that it is due to abnormal function of the diencephalon (which acts as a relay centre for sensory and motor impulses)

Question 5

COPD= Investigations

Answer 5

• clinical presentastion
• spirometry will show obstructive pathology (FEV1:FVC < 70%) with little to no BDR

Theseveritycan be graded using theforced expiratory volumein 1 second(FEV1):
- Stage 1 (mild): FEV1 more than 80% of predicted
- Stage 2 (moderate): FEV1 50-79% of predicted
- Stage 3 (severe): FEV1 30-49% of predicted
- Stage 4 (very severe): FEV1 less than 30% of predicted

Question 6

COPD: Investigations

Answer 6

• O2 sats
• Body mass index(BMI) at baseline (weight loss occurs in severe disease)
• Full blood countforpolycythaemia(raised haemoglobin due to chronic hypoxia),anaemiaandinfection
• CRP
• U&Eto check electrolytes, which can be affected by infections and medications
• • Sputum cultureto assess for chronic infections, such as pseudomonas
• Blood culturesin patients with signs of sepsis (e.g., fever)
• ABGs: respiratory acidosis
• Serum alpha-1 antitrypsinto look for alpha-1 antitrypsin deficiency
• Transfer factor for carbon monoxide(TLCO) tests the diffusion of inhaled gas into the blood (reduced in COPD)
• • Chest x-rayto exclude other pathology, such as lung cancer
• CT thoraxfor alternative diagnoses such as fibrosis, cancer or bronchiectasis
• ECGandechocardiogramto assess for heart failure and cor pulmonale. look for arrhythmias or evidence of heart strain

Question 7

COPD: Treatment

Answer 7

• Smoking cessation services
• Pneumococcalandannual fluvaccine.
• Pulmonary rehabilitationinvolves a MDT to help improve function and quality of life, including physical training and education.

1. SABA + SAMA Short-acting muscarinic antagonists(e.g., ipratropium bromide)
2. LABA + LAMA unless they have asthma or are irresponsive to steroids. Combination inhaler.
   LABA + ICS if they are asthmatic or steroid- responsive. Combintation inhaler
3. Triple therapy LABA + LAMA + ICS combination inhaler

More severe cases:
- Nebulisers (e.g., salbutamol or ipratropium)
- Oral theophylline
- Prophylactic antibiotics (e.g., azithromycin - needECGandliver functionmonitoring before and during treatment)
- Oral corticosteroids (e.g., prednisolone)
- Oral mucolytic therapy to break down sputum (e.g., carbocisteine)
- Oral phosphodiesterase-4 inhibitors (e.g., roflumilast)
- Long-term oxygen therapy (LTOT) at home - severe COPD withchronic hypoxia(sats < 92%),polycythaemia,cyanosisorcor pulmonale. Smoking is a contraindication due to the fire risk. Target oxygen saturations of 88-92%are used for patients with COPD at risk of retaining CO2. These may be adjusted to 94-98% when confident they do not retain CO2.
- Lung volume reduction surgery (removing damaged lung tissue to improve the function of healthier tissue)
- Palliative care (opiates and other drugs may be used to help breathlessness)

Question 8

COPD: Acute Exaccerbation

Answer 8

Management of an Acute Exacerbation

First-line medical treatment of an acute exacerbation of COPD involves:

• Regularinhalersornebulisers(e.g., salbutamol and ipratropium)
• Steroids(e.g., prednisolone 30 mg once daily for 5 days)
• Antibioticsif there is evidence of infection

Respiratory physiotherapycan be used to help clear sputum.

Additional options in severe cases include:

• IV aminophylline
• Non-invasive ventilation(NIV)
• Intubationandventilationwith admission to intensive care

Doxaprammay be used as arespiratory stimulantwhere NIV or intubation is not appropriate.

Non-Invasive Ventilation

Non-invasive ventilation (NIV) involves using afull face mask,hood(covering the entire head) or a tight-fittingnasal maskto blow air forcefully into the lungs and ventilate them. It is not pleasant for the patient but is much less invasive than intubation and ventilation. It is a valuable middle point between basic oxygen therapy and mechanical ventilation.

NIVinvolves a cycle of high and low pressure to correspond to the patient’s inspiration and expiration:

• IPAP(inspiratory positive airway pressure) is the pressure duringinspiration– where air is forced into the lungs
• EPAP(expiratory positive airway pressure) is the pressure duringexpiration– stopping the airways from collapsing

NIV is considered when the following inclusion criteria are met:

• Persistentrespiratory acidosis(pH < 7.35 and PaCO> 6)despitemaximal medical treatment2
• Potential to recover
• Acceptable to the patient

The decision to initiate it would be made by a registrar or above. The maincontraindicationsare anuntreatedpneumothoraxor any structural abnormality or pathology affecting the face, airway or gastrointestinal tract. Patients should have a chest x-ray before NIV to exclude pneumothorax. A plan should be in place if the NIV fails so that everyone agrees on whether the patient should proceed to intubation, ventilation, and ICU or whether palliative care is more appropriate.

The initial pressures are estimated based on the patient’s body mass. Pressures are measured in cm of water. Potential pressures for an average patient might be:

• IPAP 16-20cm HO (usually starting at 12 and increasing every 2-5 minutes until the target pressure is reached)2
• EPAP 4-6cm HO2

ABGs are monitored closely whilst on NIV (e.g., 1 hour after every change, then 4 hourly until stable). The IPAP is increased by 2-5 cm increments until the acidosis resolves.