Chapter 14: Breathing and Exchange of Gases (Human Physiology)

Vital capacity is the maximum volume of air a person can breathe in after a forced expiration (or breathe out after a forced inspiration): VC = ERV + TV + IRV (about 3500–4600 mL). Significance: it measures the maximum exchange of air in one breath and the strength of the respiratory muscles; it is higher in athletes and lower in lung diseases (asthma, emphysema, fibrosis), so it is used in the clinical assessment of lung function.

After a normal expiration the lungs still hold the functional residual capacity: FRC = ERV + RV = (1000–1100) + (1100–1200) = about 2100–2300 mL.

Only the alveoli have the features needed for diffusion: an extremely thin diffusion membrane (squamous alveolar epithelium, capillary endothelium and a thin basement substance; much less than a millimetre), a huge surface area, a rich network of blood capillaries, and a partial-pressure gradient between alveolar air and blood. The other parts (nose to terminal bronchioles) form the conducting part: their walls are thick, often supported by cartilage, and have no such capillary network; they only conduct, clean, warm and humidify the air.

(i) About 70% as bicarbonate: in tissues, where pCO₂ is high, CO₂ diffuses into RBCs and plasma; carbonic anhydrase (very high in RBCs) catalyses CO₂ + H₂O → H₂CO₃ → HCO₃⁻ + H⁺; at the alveoli, where pCO₂ is low, the reaction reverses and CO₂ is released. (ii) 20–25% bound to haemoglobin as carbamino-haemoglobin: binding is favoured by high pCO₂ and low pO₂ (tissues) and release by low pCO₂ and high pO₂ (alveoli). (iii) About 7% dissolved in plasma. Each 100 mL of deoxygenated blood delivers about 4 mL of CO₂ to the alveoli.

(ii): atmospheric pO₂ 159 mm Hg vs. 104 in alveoli (higher); pCO₂ 0.3 vs. 40 (lesser).

Inspiration occurs when the pressure inside the lungs falls below atmospheric pressure. (i) The diaphragm contracts and flattens, increasing the volume of the thoracic chamber in the antero-posterior axis. (ii) The external intercostal muscles contract, lifting the ribs and sternum and increasing the volume in the dorso-ventral axis. (iii) Because the thorax is air-tight, the increase in thoracic volume increases the pulmonary volume. (iv) This lowers the intra-pulmonary pressure below atmospheric pressure, so air from outside rushes into the lungs.

By the neural system. The respiratory rhythm centre in the medulla sets the rhythm. The pneumotaxic centre in the pons moderates it, shortening inspiration and so changing the rate. A chemosensitive area beside the rhythm centre is very sensitive to CO₂ and H⁺; when they rise it signals the rhythm centre to increase breathing so they are removed. Receptors in the aortic arch and carotid artery also detect CO₂ and H⁺ and signal the rhythm centre. The role of O₂ is insignificant.

High pCO₂ (with high H⁺ and temperature) lowers the affinity of haemoglobin for O₂, shifting the oxygen dissociation curve to the right, so oxyhaemoglobin releases O₂ more easily: this happens in the tissues. Low pCO₂ in the alveoli favours the binding of O₂ to haemoglobin. So pCO₂ helps load O₂ in the lungs and unload it in the tissues.

At high altitude the atmospheric pressure and hence pO₂ are low, so less O₂ diffuses into the blood and haemoglobin is less saturated: the person feels breathless and the body gets less O₂ (hypoxia). In addition, climbing is exercise, raising CO₂ production. So the breathing rate and depth increase, and heart rate rises. On staying for some time the body acclimatises: more RBCs and haemoglobin are made (erythropoietin), helping to carry more O₂.

Insects have a tracheal system: air enters through spiracles and is carried by branching tracheal tubes to fine tracheoles, which reach the tissues; gas exchange takes place directly between the tracheoles and the body cells (blood does not carry O₂).

The oxygen dissociation curve is the graph of the percentage saturation of haemoglobin with O₂ against the partial pressure of O₂. It is sigmoid because of cooperative binding: haemoglobin has four haem groups; binding of the first O₂ is difficult, but it changes the shape of the molecule so that the next O₂ molecules bind much more easily (steep middle part); when nearly all sites are filled, saturation levels off (plateau). This lets haemoglobin load O₂ fully in the lungs and release a lot at the lower pO₂ of tissues.

Hypoxia is a shortage of O₂ reaching the tissues. Types: (i) hypoxic (low pO₂ in air, e.g. high altitude: altitude sickness with breathlessness, headache, nausea); (ii) anaemic (too little haemoglobin, e.g. anaemia, or CO poisoning, which blocks haemoglobin); (iii) stagnant (poor blood flow, e.g. heart failure); (iv) histotoxic (cells cannot use O₂, e.g. cyanide poisoning). Prevention and treatment: gradual ascent and acclimatisation, oxygen cylinders for mountaineers and pilots, treating anaemia, avoiding smoke and CO.

(a) IRV: additional air inspired by forcible inspiration (2500–3000 mL); ERV: additional air expired by forcible expiration (1000–1100 mL). (b) IC = TV + IRV: total air inspired after a normal expiration; EC = TV + ERV: total air expired after a normal inspiration. (c) VC = ERV + TV + IRV: maximum air breathed in after forced expiration; TLC = VC + RV: total air the lungs hold at the end of forced inspiration (includes the residual volume).

Tidal volume is the volume of air inspired or expired in a normal breath: about 500 mL. At 12–16 breaths per minute: 500 × 12 = 6000 to 500 × 16 = 8000 mL per minute; in an hour, 6000 × 60 = 3,60,000 mL to 8000 × 60 = 4,80,000 mL, i.e. about 360–480 litres per hour.