Chronic Bronchitis

24/05/2013 by admin | Respiratory

Chronic Bronchitis (‘blue bloater’):

  1. p/c: obese, chronic mucus production and cough (=impaired mucociliary), course rhonci and wheezing, RHF (=oedema/cyanosis), reduced PEFR.
  2. Pathology:
    1. o Arteriovenous anastomoses (‘shunts’)hypoxaemiapulmonary vasoconstriction (to reduce deoxygenated blood flow in lungs)PAHCPRVHRHFsystemic symptoms (oedema/cyanosis) = blue bloater.
    2. o Pt may be hypercapnic = bounding pulse, papilloedema (RICP).
    3. o Hyperplasia of mucus producing glands
    4. o Undamaged pulmonary capillary beds.
    5. o Body compensates by reducing ventilation = inc CO (to inc perfusion through poorly oxygenated lungs)

Epidemiology

  1. Incidence: 10-20% of heavy smokers develop COPD
  2. Prevalence: 7-9/1000
  3. Mortality: 30,000/y

 

Severity of COPD FEV1 % predicted
Mild 80
Moderate 50–79
Severe 30–49
Very severe <30 or Chronic respiratory failure symptoms

 

If FEV1 <80% and FEV1/FVC <70% = COPD!

Diagnostic/Investigation:

  1. Lung function tests (=spirometry)
  2. Show airflow limitation
  3. FEV1:FVC is reduced (FEV1 reduced, FVC normal or raised)
  4. PEFR is low and fixed

 

  1. CXR
  2. Often Normal
  3. Classical features:
  4. Bullae pneumonthorax!
  5. Severe overinflation of lungs with low, flattened diaphragms
  6. Large retrosternal air space on lateral film
  7. Deficiency of blood vessel in periphery of the lung fields

 

  1. Haemoglobin level and PCV
  2. Elevated Hb and packed cell volume (PCV) as a result of persistent hypoxaemia

 

  1. Blood gases
  2. Often normal.
  3. May be some evidence of hypoxemia and hypercapnia (=RF T2)

 

  1. Electrocardiogram
  2. In advanced cor pulmonale (RHF secondary to RF) the P wave is taller, and there may be right bundle branch block.

 

Aetiology – cause, risk factors

In developed countries – smoking in 90% of cases.

Cigarette smoking

  1. o Neutrophil granulocytes in lumen of bronchial tree which infiltrate airways.
  2. o Release elastases and proteases = break down lung parenchyma = centri-acinar emphysema (Common, Cigarettes, Centri-acinar)!!

 

Infections

  1. o Precipitation cause of acute exacerbations

 

Alpha-1-antitrypsin deficiency (autosomal recessive condition)

  1. o Antiproteinase inhibitor produced by the liver
  2. o Secreted into blood
  3. o Diffuses into lung
  4. o Inhibits neutrophil elastase
  1. o If deficient (A1AT <20%) then elastase CAN break down alveolar cell walls! = pan-acinar emphysema.

 

Pathophysiology

Hypertrophy and increase in number of mucus-secreting goblet cells, mucus hypersecretion, ciliary dysfunction, airflow limitation, hyperinflation, PAH and cor pulmonale, RHF).

Microscopically:

  1. Infiltration of the walls of the bronchi and bronchioles with acute and chronic inflammatory cells and lymphoid follicles in severe disease.
  2. CD8+ lymphocytes – mediated by LTB4, IL-8, TNF-alpha.
  3. Columnar epithelial layer may become ulcerated and when ulcer heals, squamous epithelium may replace the columnar cells.

 

Small airways particularly affected.

Further progression of disease leads to progressive squamous cell metaplasia and fibrosis of the bronchial walls. Airway narrowing. Causes airflow limitation. = CHRONIC BRONCHITIS

If also get loss of elastic recoil of the lung with collapse of small airways during expiration = EMPHYSEMA

Normal pCO2 = Pink Puffers (=EMPHYSEMA)!

  1. Maintain normal blood gases by increasing their respiratory effort.

 

Increase pCO2 = Blue Bloater (=CHRONIC BRONCHITIS)!

  1. Fail to increase respiratory effort, carbon dioxide levels increase.
  2. In long term become insensitive to CO2 and depend on hypoxaemia to drive their ventilation.
  3. Retain fluid.
  4. Stimulate production of erythrocytes: Hypoxia = HIF = EPO = inc RBCs

 

  1. Carbon dioxide is the major stimulant of the respiratory centre.

 

  1. Loss of 50ml per year in FEV1 in COPD patients

 

Treatment/management

Stop smoking

Pneumococcal and influenza vaccinations

1: Single short acting inhaled bronchodilator

Eg. Salbutamol

2: Long acting bronchodilator (salmeterol)

Eg. Antimuscarinics: Tiotropium

Ipratropium

Oxitropium

3: Combination of muscarinic and beta agonist bronchodilator

4: Combination of inhaled then oral corticosteroid and long acting beta agonist

Eg. Prednisolone

Eg. Salmeterol

5: Theophylline

Further management at home

Oxygen (long term oxygen therapy = LTOT)

Benefit patients who have:

  1. PaO2 of <7.2kPa (55mmHg) when breathing air
  2. PaO2 7.3-8kPa with secondary polycythaemia, nocturnal hypoxemia, peripheral oedema, or evidence of pulmonary hypertension.
  3. Carboxyhaemoglobin of less than 3%
  4. Process: 16hr/d, inc QoL, reduce admissions, no effect on lung function.

 

Surgery

Some patients with large emphysematous bullae (which reduce lung capacity) can benefit from bullectomy.

FEV1<1L offered lung volume reduction surgery.

Prognosis

50% patients with severe breathlessness die within one year

Complications

Respiratory failure

  1. Normal ABG = PaO2 >10.5kPa and PaCO2 4.5-6.0kPa
  2. Type 1 RF: PaO2 < 8kPa (60mmHg) and PaCO2 > 7kPa (55mmHg)
  3. Type 2 RF: Persistence of chronic alveolar hypoxia and hypercapnia leads to constriction of the pulmonary arterioles and subsequent pulmonary arterial hypertension.

 

Cor pulmonale (RHF secondary to RF)

Heart disease secondary to disease of the lung.

Characterised by:

  1. PAH
  2. RVH
  3. RHF
  4. Central cyanosis
  5. Breathless
  6. Ankle oedema 
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