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Discussion of the impact of lung physiology in respiratory diseases.
Describe the comparative similarities and differences in the respiratory systems of mammals.
Understand how the respiratory system adapts to high altitude and diving.

Depth review will occur in Human Pathology.
Insight into physiology through abnormal cases.
Dyspnoea: Clinical term for distress due to difficulty in breathing.
Ventilatory capacity: Ability of the lungs to provide enough air to meet the body's respiratory needs.
Three main classes of respiratory disorders:
- Obstructive
- Restrictive
- Muscle weakening

Triggers: Environmental allergens leading to sudden dyspnoea.
Physiological changes during an asthma attack:
- Functional Residual Capacity (FRC): Increased
- Residual Volume (RV): Increased
- Vital Capacity (VC): Normal
- Forced Expiratory Volume in 1 second (FEV1): Reduced by more than half
- Peak flow: Reduced significantly.
Chronic inflammation leads to thickening and obstruction of airways.
Key point: Airways must remain free from inflammation for normal expiratory capacity.

Causes: Most commonly smoking, but not exclusive.
Pathophysiology:
- Neutrophils invade alveoli and secrete enzymes, enhancing lung resistance.
- Alveoli enlarge, while cilia are immobilized by smoke leading to increased mucus secretion and chronic inflammation/infection.
Resulting symptoms: Reduced diffusing capacity due to alveoli destruction and narrower airways.
FEV1 and peak flow: Both reduced.

Most prevalent respiratory condition and leading cause of death.
Affected population: Approximately 5%.
Composition of COPD: Combination of emphysema (limits airflow) and chronic bronchitis (inflammation of bronchi).
Key metrics: Peak flow and FEV1 under 70%.
Key point: Impaired diffusion and reduced airway diameter exacerbate lung function reduction, with chronic inflammation worsening physiology.

Excess fibrous tissue replacement in lungs leading to loss of parenchyma functionality.
Etiology: Mostly idiopathic, but associated with environmental pollutants (e.g., dust, silica from farming).
Possible causes: Asbestos, smoking, radiation therapy.
Specific condition: Asbestosis, a type of pulmonary fibrosis due to asbestos exposure.
Mechanism: Overactive immune response secretes harmful products damaging lung tissue.
Key point: Balance exists between healthy immune reaction and ongoing fibrosis development.

Apnoea defined: Temporary cessation of breathing during sleep.
Causes: Physical obstruction of airways, often due to relaxed muscles causing pharyngeal collapse.
Physiological effects:
- Decreased PO2 and increased PCO2 during obstruction.
- Stimulation for breath increases intrathoracic pressure to overcome airway blockage.
Episodes can last for 2 minutes, frequently occurring throughout the night.
Key point: Muscle tone is essential in maintaining open airways; collapse leads to obstruction.

Normal vs. Apnoea: Typical breathing is regulated by central respiratory centres; in central sleep apnoea, these centres fail to initiate breathing.
Duration of apnoea: 10-30 seconds.
Breathing pattern: Cheyne-Stokes breathing characterized by progressively deeper and shallower breaths before apnoea.
Can occur post-brain damage or in healthy individuals at high altitude.
Key point: The central respiratory centre is critical for initiating breaths.

Need for adaptation: Cardiac and respiratory adjustments are necessary due to increased oxygen demand during exercise.
Oxygen consumption: Increases from 75 mL to 3000 mL, indicating a 40-fold increase in demand.
Response time: Oxygen consumption rises gradually over several minutes, meeting exercise needs.

Resting pulmonary ventilation: Approximately 5-8 L/min.
Maximum during heavy exercise: Pulmonary ventilation can exceed 100 L/min.
Adjustments during exercise: Ventilation increases until meeting steady state where oxygen delivery matches demand.
Post-exercise: Ventilation decreases rapidly but does not immediately return to resting levels, taking several hours.

Training results:
- Increase in vital capacity: 5-15% increase observed.
- Increase in Total Lung Capacity (TLC), enhancing minute ventilation capacity.
- Enhanced pulmonary diffusion efficiency via capillary growth and size increase.
- Alveoli changes: Number of alveoli—unclear; existing alveoli may enlarge to boost lung capacity.
- Notably, elite swimmers may show an increase in alveoli number.

Acute hypoxia: Short-term exposure (minutes to hours) manifesting as “mountain sickness”.
Symptoms include: Nausea, gastrointestinal disturbance, headache, psychological disturbances.
More severe risks: Sleep apnoea and potentially fatal pulmonary oedema.

Chronic hypoxia: Adaptation process for individuals living at high altitudes or mountaineers.
Physiological adaptations:
- Increased respiratory minute volume.
- Increased red blood cell (RBC) count and hemoglobin content.
- Increased cardiac output.
- Enhanced vascularisation of tissues.

Mechanism: A reflex in humans (and other mammals) upon facial immersion in cold water.
Typical responses: Bradycardia, reallocation of blood flow towards the brain, and reduced heart rate.
Common mistake: Hyperventilating before a dive to “store” oxygen is inadvisable; it may lead to cerebral hypoxia and drowning.

Obstructive diseases (e.g., asthma, COPD) and restrictive diseases (e.g., pulmonary fibrosis) disrupt standard lung physiology causing breathing difficulties.
Cold water submersion triggers a diving response, resulting in peripheral vasoconstriction and bradycardia to conserve oxygen.
High altitude exposure leads to both acute and chronic effects; acclimatization involves increased minute volume and RBC count helping alleviate symptoms.