Chapter Review

Gaseous Exchange

Human Respiratory System and Gas Exchange · Smoking and Respiratory Health

Air Passageway Structure

The respiratory tract conducts air from the nostrils through the nasal cavity, pharynx, larynx, trachea, bronchi, and bronchioles to the alveolar sacs, warming, moistening, and filtering it along the way.

Key Points

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    Nasal cavity is lined with ciliated mucous epithelium that filters, warms, and humidifies incoming air
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    Epiglottis is forced horizontal by the backward tongue during swallowing, while the larynx moves up under it — food is diverted to the oesophagus
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    Trachea has C-shaped cartilage rings (open side facing the oesophagus) to maintain an open airway
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    Bronchi progressively lose cartilage plates; bronchioles (≤1 mm) have no cartilage, only circular smooth muscle that can constrict or dilate

Lungs, Pleura, and Alveoli

Lungs are spongy organs in the thoracic cavity, covered by a double-layered pleura. Approximately 300 million alveoli provide ~70 m² surface area for gas exchange across a diffusion barrier only two cells thick.

Key Points

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    Diaphragm is a dome-shaped skeletal muscle separating the thoracic and abdominal cavities; its contraction drives inhalation
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    Visceral pleura adheres to the lung surface; parietal pleura lines the thoracic wall; the pleural cavity between them contains lubricating fluid
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    Each alveolus is a single-cell-thick (simple squamous epithelium) air sac surrounded by dense blood capillaries
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    The alveolar-capillary diffusion barrier is ~0.5 μm thick, allowing rapid passive diffusion of gases

Gas Exchange by Partial Pressure Gradients

Oxygen and carbon dioxide diffuse passively across the alveolar-capillary membrane, each driven by its own partial pressure gradient. No energy is required — diffusion rate depends on the pressure difference, surface area, and barrier thickness.

Key Points

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    Partial pressure of a gas = its fractional concentration × total pressure of the mixture
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    Alveolar PO₂ (~100 mmHg) > venous blood PO₂ (~40 mmHg) → O₂ diffuses into blood
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    Venous blood PCO₂ (~45 mmHg) > alveolar PCO₂ (~40 mmHg) → CO₂ diffuses out of blood
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    Inhaled air: ~21% O₂, 0.04% CO₂; Exhaled air: ~16% O₂, ~4% CO₂; nitrogen stays at 79%
Formula

Oxygen Transport — Haemoglobin

Oxygen is carried mainly bound to haemoglobin in red blood cells, forming reversible oxyhaemoglobin. Only ~1.5% dissolves directly in plasma. Fully oxygenated blood carries ~20 ml O₂ per 100 ml; normally ~19.6 ml at 98% saturation.

Key Points

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    In lungs (high PO₂): Hb binds O₂ → HbO₂ (oxyhaemoglobin, bright red)
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    In tissues (low PO₂ < 60 mmHg): HbO₂ dissociates sharply, releasing oxygen where demand is high
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    Bohr effect: Higher PCO₂, higher temperature, and lower pH all shift the dissociation curve rightward — haemoglobin releases more O₂ at the same PO₂
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    These three factors work together in active tissues: muscles produce CO₂ and heat, lowering local pH, all enhancing O₂ delivery
Formula

Carbon Dioxide Transport

CO₂ is transported in four forms, with bicarbonate ions (HCO₃⁻) accounting for ~70%. The conversion is catalysed by carbonic anhydrase in red blood cells and is fully reversible between tissues and lungs.

Key Points

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    Bicarbonate ions (HCO₃⁻) — 70%: CO₂ + H₂O → H₂CO₃ → H⁺ + HCO₃⁻ (carbonic anhydrase catalysed); HCO₃⁻ combines with Na⁺ in plasma
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    Carboxyhaemoglobin — 20%: CO₂ binds to amino groups of haemoglobin (distinct from O₂ binding to haem iron)
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    Plasma proteins — 5%: carry a small fraction of CO₂
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    Arterial blood: ~50 ml CO₂/100 ml; Venous blood: ~54 ml CO₂/100 ml — a net exchange of ~4 ml per cycle
Formula

Lung Capacities and Breathing Rate

An adult's total lung capacity is ~5 L. At rest, only ~0.5 L (tidal volume) is exchanged per breath at 15–20 breaths/min. During exercise, both rate and depth increase to meet higher oxygen demand.

Key Points

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    Total lung capacity: ~5 litres when fully inflated
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    Tidal volume (rest): ~0.5 litres per normal breath
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    Exercise volume: rises to ~3.5 litres per breath; breathing rate increases to ~30 breaths/min
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    Residual volume: ~1.5 litres — air that cannot be expelled, keeping alveoli partially inflated for continuous gas exchange

Smoking Damage to the Airways

Cigarette smoke contains over 4000 chemicals (tar, CO, nicotine, carcinogens) that overwhelm respiratory defences at every level. The mucociliary escalator is progressively destroyed, leading to chronic mucus accumulation and smoker's cough.

Key Points

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    Tar: coats airway lining and introduces carcinogens; CO: binds Hb with 240× affinity of O₂; Nicotine: addictive, raises heart rate and blood pressure
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    Smoke paralyses cilia, then causes metaplasia — replacement of ciliated columnar epithelium with non-ciliated stratified squamous epithelium
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    Goblet cells produce excess mucus that cannot be cleared without functional cilia, causing persistent smoker's cough
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    Bronchioles are especially vulnerable — no cartilage, so irritant-induced smooth muscle constriction severely narrows them

Emphysema and Chronic Bronchitis

The two main smoking-related obstructive lung diseases (COPD). Emphysema destroys alveolar walls via elastase–antitrypsin imbalance; chronic bronchitis inflames airways with mucus hypersecretion. Most smokers with COPD have features of both.

Key Points

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    Emphysema: elastase destroys alveolar elastin; smoking increases elastase release AND inactivates alpha-1 antitrypsin → alveolar walls merge into fewer, larger sacs with less surface area
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    Chronic bronchitis: productive cough ≥3 months/year for 2 consecutive years; airway inflammation + mucus gland hypertrophy + ciliary loss
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    Emphysema dominant symptom: dyspnoea (breathlessness); chronic bronchitis dominant symptom: productive cough
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    Lung cancer progression in smokers: normal epithelium → metaplasia → dysplasia → carcinoma (dose-dependent on pack-years)

Carbon Monoxide and Gas Exchange Impairment

CO from smoke reduces oxygen delivery both by occupying haemoglobin binding sites and by promoting alveolar damage. Combined with mucus plugging and airway narrowing, the net effect is significantly reduced oxygen delivery to tissues.

Key Points

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    CO forms stable carboxyhaemoglobin (COHb) — each percent COHb directly equals lost oxygen-carrying capacity
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    Tar deposits and chronic inflammation destroy alveolar walls, reducing the gas exchange surface area
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    Mucus plugs and narrowed bronchioles create ventilation-perfusion mismatch — blood flows past unventilated alveoli
  • •
    Chronic hypoxia forces cardiovascular compensation: increased heart rate, elevated blood pressure, polycythaemia
Formula

Formulas

Oxyhaemoglobin Dissociation

Haemoglobin binds O₂ in lungs (high PO₂) and releases it in tissues (low PO₂). Fully oxygenated blood carries 20 ml O₂ per 100 ml; normally ~19.6 ml at 98% saturation.

CO₂ to Bicarbonate Conversion

CO₂ reacts with water (carbonic anhydrase catalysed) to form H₂CO₃, which dissociates into H⁺ + HCO₃⁻. This accounts for ~70% of CO₂ transport and is reversible between tissues and lungs.

Partial Pressure of a Gas

Partial pressure equals the fractional concentration of the gas multiplied by the total pressure of the mixture. Drives diffusion of O₂ and CO₂ across the alveolar membrane.

Carboxyhaemoglobin Percentage

Percentage of haemoglobin bound to CO. Each percent COHb equals that percent of oxygen-carrying capacity lost. >10% causes reduced exercise tolerance; >50% is potentially fatal.

Elastase–Antitrypsin Balance

Ratio of protective alpha-1 antitrypsin to destructive elastase. Smoking increases elastase and inactivates antitrypsin. Ratio < 1 means unchecked alveolar wall destruction (emphysema).