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Objectives/possible exam questions:
Understand the pathophysiology of COPD
Be able to explain the pathology responsible for the common symptoms and signs of
COPD
Understand that COPD treatment needs a stepwise approach
Scenario:
60 yr old man
1 yr history of cough
Wheeze and SOB on exertion
Ex-smoker (20 cigs/day for 30yrs)
Possible diagnoses:
Asthma or COPD
COPD --> narrow airways and emphysema
Definition
Group of conditions characterised by airway obstruction that is not completely reversible
BTS definition:
Slowly progressive disorder characterised by airways obstruction (reduced FEV1 and
FEV1/FVC ratio), which does not change markedly over several months
Alpha1-anti-trypsin deficiency can cause COPD
Coal miners can get COPD
COPD severity
Age, height and ethnicity taken into account
Mild
FEV1, 50-80% predicted
Moderate
FEV1, 30-50% predicted
Severe
FEV1, <30% predicted
Background
COPD is the 6th comment cause of death (will be 3rd by 2020)
95% of cases are smoking related (typically >20 pack years) (20 cigarettes a day for 20
years)
Only 10-20% of smokers are affected

If you stop smoking your risk wont return to never smoked but goes back to the same rate
of decline

There is a spectrum between Asthma and COPD
Asthma - reversible airway obstruction
COPD - irreversible airway obstruction
Asthma vs COPD
Asthma
Airway inflammation and hyper responsiveness
Leads to Bronchial muscle contraction
Airway narrowing
REVERSIBLE
COPD
Alveolar destruction and airway inflammation
Airway narrowing (not just due to mucus) and decreased gas transfer
IRREVERSIBLE
COPD and smoking
Increase in alveolar macrophages due to tar
Release of proteases
Leads to destruction of collagen and elastase
Leads to damage to the alveolar wall
Lead to emphysema --> larger airlocks --> harder for O2 to get into blood vessel
Paralysis of cilia and direct mucosal toxicity
Leads to airway inflammation and mucus gland hyperplasia
Leads to airway oedema and mucus hyper secretion
Leads to chronic bronchitis

COPD
Group of conditions
Chronic bronchitis --> coughing up mucus
Emphysema
Airways obstruction
Alveolar walls pulling open airways are absent (small vessels have no SM)
Alveolar 'springs' help keep airways open when breathing out, therefore removal of
this can lead to alveoli collapse
COPD: Chronic Bronchitis
Definition:
Cough productive sputum on most days for at least 3 months for 2 consecutive years
Largely affects large/proximal airways
Pathologically:
Increase in Goblet cells
Gland hypertrophy
Presence of mucus glands in smaller
airways
Bronchial wall inflammation
Activated T-cells, macrophages,
eosinophils, neutrophils
Mucosal thickening
Symptoms:
Cough
Sputum production
Dyspnoea (esp
...
7 indicates obstructive disease
Air stays in lungs in COPD
Measuring whether changes are reversible
Repeat FEV1 after salbutamol
Measurement of FEV1 pre and post bronchodilator
Significant reversibility if >15% improvement (airways getting bigger)
Dyspnoea
Abnormal/uncomfortable awareness of breathing
Sensation of increased drive to breath
Increased respiratory rate
Increase in tidal volume
Sensation of inability to breath in or out
COPD patients and dyspnoea
Airflow obstruction
Impaired alveolar ventilation
Air-trapping
Impaired gas transfer
Due to decreased surface area for gas exchange
Hyperinflation
Impaired alveolar ventilation
Impaired O2 and CO2 exchange
Decreased PaO2 and increase PaCO2
O2:
Peripheral receptor
Monitors O2 concentration of blood
Decreased O2 concentration = increased rate and depth of breathing
CO2:
Central Receptor
Monitors CO2 concentration in CSF
Increased CO2 concentration = increased rate and depth of breathing
Strongest stimulator in respiration

COPD: Hyperinflammation and Barrel chest
Emphysema + small airway narrowing (loss of elastic recoil, loss of traction on airways by
alveolar structure)
Leads to airway collapse during expiration (loss of alveolar pressure exceeds airway
pressure)
Leads to Gas Trapping
Leads to increase in Antero-Posterior chest diameter
COPD: Hypoxaemia
Caused by decreased surface area for gas exchange
Consequences of Hypoxaemia:
Pulmonary vasoconstriction (trying to redirect blood elsewhere)
Pulmonary hypertension
Right heart strain and failure (narrow vessels) (leg oedema)
Increased erythropoietin production (Increase O2 carrying capacity)
Increased red cells (polycythaemia)
Increased haematocrit and viscosity
Increased risk of stroke etc
...
25 (low)
PaCO2: 9
...
2 (normal) - but on pure O2!

Respiratory acidosis
Type 2 respiratory failure
Hypoventilation due to lack of respiratory drive (CO2)
COPD: Respiratory failure
Type 1 - Hypoxic
PaO2 < 8kPa
PaCO2 - normal or low (< 6
...
5k Pa) (high)

Control of Respiration
O2:
Peripheral receptor
Monitors O2 concentration of blood
Decreased O2 concentration = increased rate and depth of breathing
CO2:
Central Receptor
Monitors CO2 concentration in CSF
Increased CO2 concentration = increased rate and depth of breathing
Strongest stimulator in respiration
Hydrogen ion (pH):
Peripheral and central
Sensitive to pH of blood and CSF
Increased hydrogen ion = increased rate and depth of breathing
Renal excretion of HCO3- = metabolic acidosis
Single most important driver of ventilation is CO2
Some patients with COPD chronically retain CO2
Chemoreceptors become insensitive
Hence they rely upon hypoxia to drive ventilation
Giving high flow oxygen removes hypoxic drive to breath
Leads to hypoventilation
Leads to increase in PaCO2
Stable COPD: Management
Corticosteroids:
Inhaled:
For all patients with FEV1 <50% pred or 2 or more exacerbations
Oral:
For those with disease unresponsive to other measures

Oxygen:
Short Burst - symptomatic
Long term O2 therapy - 16 hrs/day if PaO2 <7

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