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Chronic bronchitis is a chronic progressive condition where airflow is limited.

It is not reversible.

Characterised by inflammation of the lining of the bronchial tubes and hypersecretion of mucus in airways.
Patients have a chronic productive cough that continues for at least 2 consecutive years.

Risk factors that increase prevalence of disease are:

smoking

antibiotic use

preterm birth

air pollution

Predicted to become the 4th leading cause of death world- wide!!!

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2. Is it obstructive or restrictive? Why?

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2. Is it obstructive or restrictive? Why?

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Obstructive disease

The constant inflammation in the lining of the bronchial tubes causes excessive amounts of sticky mucus to build up in the airways.
This restricts the amount of airflow going into and out of the lungs.

The blockage in airflow gets worse over time, resulting in breathing difficulties and increased mucus production in the lungs.

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3. How does the condition effect lung compliance and/or airway resistance?

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3. How does the condition effect lung compliance and/or airway resistance?

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Increased air resistance due to mucus plugs and narrowed airways. This causes air trapping and hyperinflation of lungs on expiration.

During inspiration the airways are pulled open, allowing gas to flow past the obstruction.

During expiration decreased elastic recoil of the bronchial walls results in collapse of the airways and prevents normal expiratory airflow hence airway resistance increases

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4. Explain the role of V/Q mismatch in this condition.

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4. Explain the role of V/Q mismatch in this condition.

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Decrease in ventilation with normal perfusion present
Decreased V/Q ratio therefore wasted perfusion with shunting due to thick mucus in airways

Airway obstruction results in decreased alveolar ventilation and hypercapnia leading to V̇/Q̇ mismatch with hypoxemia.

Chronic bronchitis affects the oxygen and carbon dioxide exchange because the airway swelling as well as increase in mucus production can also narrow the airways and reduce the flow of oxygen-rich air into the lung and carbon dioxide out of the lung.

The damage to the alveoli and airways makes it harder to exchange carbon dioxide and oxygen during each breath. Decreased levels of oxygen in the blood and increased levels of carbon dioxide cause the breathing muscles to contract harder and faster.

The nerves in the muscles and lungs sense this increased activity and report it to the brain. As a result, you feel short of breath.

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5. How is oxygenation and ventilation affected? Eg. consider O2 content, O2 delivery, alveolar ventilation 

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5. How is oxygenation and ventilation affected? Eg. consider O2 content, O2 delivery, alveolar ventilation 

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Due to thick mucus around alveoli there is reduced O2 available for diffusion across membrane

COPD patients who chronically retain carbon dioxide lose their carbon dioxide drive and rely only on hypoxia. Therefore with low levels PC02 the respiratory drive decreases with high levels of 02 therapy.

COPD effects the normal hypoxic drive which uses oxygen chemoreceptors to regulate breathing and normally becomes active when the oxygen levels in the arteries are low.

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Patient normally presents with:

expiratory wheeze

chest tightness

persistent cough

dyspnoea - inability to speak in full sentences

inability to lay flat and require an upright postition

Patients may also have:

altered LOC,

diminished breath sounds

central cyanosis

> use of accessory muscles

tachypnoea

tachycardia

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6. What type of respiratory failure would this condition lead to?

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6. What type of respiratory failure would this condition lead to?

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Type 2 Respiratory failure due to gas trapping caused by difficulty of the obstructed airway. Difficulty in expelling C02 leading to hypercapnia.

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Respiratory acidosis due to high PCO2 due to unable to excrete CO2

pH: <7.35
CO2: >45mmHg
HCO3: >26 and most likely chronically alkalotic to compensate acidosis
SaO2: can be less than 60mmHg due to poor ventilation
PO2: should not exceed 92% but should aim above 88%