Chronic bronchitis

 

Aetiology

Irritation of airways leads to inflammation

Tobacco smoke

Smoke

Pollution

Climate

Mucosal inflammation

 

Pathophysiology

Chronic bronchitis larger airways

Chronic bronchiolitis smaller airways

Exposure to smoke inflammatory response

Increased mucous production

Mucous gland hypertrophy and hyperplasia

More mucous glands in submucosa

Increased number of goblet cells

Increased mucus

Insufficient clearance of viscid mucus

Mucus stasis and plugging

Thicker layer of mucus and inflammatory oedema reduces bronchial lumen

Thicker submucosa reduces bronchial lumen

Obstructive airflow limitation

Inflammation leads to metaplasia

Ciliated columnar changes to squamous

Early disease reversible

Loss of cilia therefore loss of mucociliary clearance system

Fibrosis in smaller airways

Stasis leads to superimposed infection, acute on chronic effect

Acute exacerbations of chronic

 

Features

Cough for 3 months over 2 years

Cough increases gradually over years

Large amounts of expectorated mucus

Possible haemoptysis

Morning cough

Dyspnoea

Deoxyhaemoglobin causes cyanosis (blue)

Hypercarbia can cause morning headaches

Loss of hypercarbic drive therefore not SOB

Depend on hypoxaemic drive

Non fighters but SOBE

Polycythaemia

 

Pulmonary heart disease

Cor pulmonale

Reduced levels of O2 with increased CO2 and carbonic acid in lungs

Global pulmonary arterial vasoconstriction

Pulmonary hypertension

Right heart failure leads to systemic oedema (bloated)

 

Management

Improve health, stop smoking is known to improve lung function and reduce symptoms

Encourage expectoration

Prevent / treat infections

Bronchodilators

Inhaled corticosteroids

Mucolytic therapy

Pulmonary rehabilitation - exercise

LTOT, reduces polycythaemia, prevents progress of pulmonary hypertension, improves survival

Influenza vaccination

NIV

 

Emphysema

 

Loss of elasticity in the alveoli with permanent enlargement of the air spaces

 

 

 

 

Aetiology

 

Smoke

 

Alpha antitrypsin deficiency

 

 

 

 

Pathophysiology

 

Smoke particles in alveoli

 

Inflammation

 

Neutrophils and monocytes x 6

 

Phagocyctosis

 

Proteases, collagenase and elastase

 

Cells in wall of alveoli are partly digested

 

Loss of respiratory surface area

 

Loss of elastic tissues means loss of elastic recoil of alveoli

 

As expiration begins, reduced air pressure allows collapse of bronchioles

 

Closure of bronchioles made worse by pressure from adjacent hyperinflated alveoli

 

Airway obstruction

 

Lung hyperinflation

 

 

 

 

Features

 

Preserved hypercarbia drive

 

Fighters pink and puffing

 

Dyspnoea

 

Difficulty breathing out - pursed lip expiration to increase back pressure

 

Normal levels of O2 and CO2 in lungs

 

No pulmonary heart disease, so no systemic oedema

 

Lung hyperinflation leads to barrel chest

 

 

Management in COPD

 

Eliminate pulmonary irritants

 

Observe level of dyspnoea / cyanosis / mental state

 

Influenza vaccination

 

Sputum, green, yellow, clear

 

T P R BP SpO2

 

Peak flow measurements, before and after, observations for side effects.

 

Regular weight

 

Oxygen therapy, NIV

 

Type I or type II respiratory failure

 

Oxygen in carbon dioxide retainers

 

Avoid narcotics and sedatives

 

Nurse sitting up

 

Encourage expectoration

 

Encourage deep breathing

 

Keep secretions liquid, avoid dehydration

 

Postural drainage - percussion

 

Cough - something to spit into.

 

Prevent / treat infection

 

Early detection of any infection

 

Sputum C&S

 

Prevent cross infection

 

ADL, mouth care

 

Nutrition but counter obesity

 

Regular small meals - reduce pressure on diaphragm

 

Keep patients fit

 

Psychological support

 

Antibiotics

 

Bronchodilators

 

Corticosteroids e.g. prednisolone 30 mg/day for 2 weeks

 

Possible maintenance with inhaled corticosteroids

 

Diuretics for oedema