Definition. Vital Capacity (VC) is the maximum volume of air a person can breathe in after a forced expiration. Equivalently, it is the maximum volume of air a person can breathe out after a forced inspiration. It includes ERV, TV and IRV.

Significance.

• It measures the maximum usable volume of the lungs — the air that can actually be moved, as opposed to total lung capacity, which includes the residual volume that can never be exhaled.
• It is of clinical significance: since volumes of air involved in breathing can be estimated with a spirometer, VC is used in the clinical assessment of pulmonary functions and in the diagnosis of lung disease. A reduced VC indicates a restriction on lung expansion or on the ability to empty the lungs.
• A larger vital capacity means a greater volume of fresh air exchanged per breath, and therefore a greater capacity for gas exchange — which is why it is higher in athletes and mountain dwellers and lower in smokers and patients with lung disease.
• Unlike FRC and TLC, VC is made up entirely of volumes that actually move, so it can be measured by a spirometer alone.

The volume remaining after a normal expiration is the Functional Residual Capacity (FRC).

Why FRC and not RV. The question says after normal breathing, not after a forcible expiration. After a normal expiration, the lungs still contain both the expiratory reserve volume (which could still be forced out) and the residual volume (which could not). Only after a forcible expiration would the answer be the residual volume alone, 1100 to 1200 mL. Read the wording carefully — this distinction is exactly what the question tests.

Because only the alveolar region possesses the structural features that diffusion requires. The part starting with the external nostrils up to the terminal bronchioles constitutes the conducting part, whereas the alveoli and their ducts form the respiratory or exchange part.

What the alveolar region has that the rest does not:

• Extremely thin walls. Alveoli are very thin, irregular-walled bag-like structures, and the diffusion membrane's total thickness is much less than a millimetre. The conducting part has thick walls supported by incomplete cartilaginous rings in the trachea, bronchi and initial bronchioles — far too thick for gases to cross.
• Rich vascularisation. Alveoli are vascularised, each wrapped in pulmonary capillaries, so blood is brought within a fraction of a millimetre of the air. The conducting part has no such capillary network applied to its lining.
• The three-layer diffusion membrane. Only here do you find the thin squamous epithelium of alveoli, the endothelium of alveolar capillaries and the basement substance in between. Elsewhere the epithelium is thick, ciliated and mucus-covered.
• Enormous surface area. Each terminal bronchiole gives rise to a number of alveoli, multiplying the exchange surface many times over; the conducting tubes offer only their narrow bore.

And the conducting part has a different job. It transports the atmospheric air to the alveoli, clears it from foreign particles, humidifies it and brings the air to body temperature. Thick, mucus-lined, ciliated walls are exactly what those three tasks need — and exactly what prevents gas exchange. The design is a division of labour, not an accident.

Carbon dioxide is transported in three ways.

1. As bicarbonate — the major route. RBCs contain a very high concentration of the enzyme carbonic anhydrase, and minute quantities of the same is present in the plasma too. This enzyme facilitates the following reaction in both directions:

• At the tissue site, where partial pressure of CO₂ is high due to catabolism, CO₂ diffuses into blood (RBCs and plasma) and forms HCO₃⁻ and H⁺.
• At the alveolar site, where pCO₂ is low, the reaction proceeds in the opposite direction, leading to the formation of CO₂ and H₂O.

Thus CO₂ trapped as bicarbonate at the tissue level and transported to the alveoli is released out as CO₂.

2. As carbamino-haemoglobin. CO₂ is carried by haemoglobin as carbamino-haemoglobin (about 20–25 per cent). This binding is related to the partial pressure of CO₂, and pO₂ is a major factor which could affect this binding. When pCO₂ is high and pO₂ is low, as in the tissues, more binding of carbon dioxide occurs; whereas when pCO₂ is low and pO₂ is high, as in the alveoli, dissociation of CO₂ from carbamino-haemoglobin takes place. So CO₂ which is bound to haemoglobin from the tissues is delivered at the alveoli.

3. Dissolved in plasma. About 7 per cent travels simply dissolved — more than double the 3 per cent managed by oxygen, because the solubility of CO₂ is 20–25 times higher than that of O₂.

The overall figure: every 100 mL of deoxygenated blood delivers approximately 4 mL of CO₂ to the alveoli.

The correct answer is (ii) pO₂ higher, pCO₂ lesser.

Why atmospheric air differs from alveolar air. Inspired air is not a sample of the outside atmosphere by the time it reaches the alveoli, for three reasons:

• It is humidified in the conducting part, and the added water vapour claims its own share of the total pressure, lowering every other partial pressure.
• It mixes with the large volume of air already in the lungs — the functional residual capacity of some 2100 to 2300 mL — which a single 500 mL tidal breath cannot flush out.
• Oxygen is continuously removed into the blood while CO₂ is continuously added, since alveoli are the primary sites of exchange of gases.

The rise of pCO₂ from 0.3 to 40 mm Hg is therefore not a defect but the very proof that CO₂ is being excreted.

The principle. The movement of air into and out of the lungs is carried out by creating a pressure gradient between the lungs and the atmosphere. Inspiration can occur if the pressure within the lungs (intra-pulmonary pressure) is less than the atmospheric pressure — i.e., there is a negative pressure in the lungs with respect to atmospheric pressure.

The steps, in order:

1. Inspiration is initiated by the contraction of the diaphragm, which increases the volume of the thoracic chamber in the antero-posterior axis. The dome-shaped diaphragm flattens as it contracts, deepening the chest.
2. The contraction of the external inter-costal muscles lifts up the ribs and the sternum, causing an increase in the volume of the thoracic chamber in the dorso-ventral axis.
3. The overall increase in the thoracic volume causes a similar increase in pulmonary volume. This follows because the thoracic chamber is anatomically an air-tight chamber and any change in the volume of the thoracic cavity will be reflected in the lung (pulmonary) cavity — the two being coupled by the double layered pleura with pleural fluid between them. Such an arrangement is essential, as we cannot directly alter the pulmonary volume.
4. An increase in pulmonary volume decreases the intra-pulmonary pressure to less than the atmospheric pressure, which forces the air from outside to move into the lungs — that is, inspiration.

Two points that earn marks. First, air is not pulled in: the body enlarges a sealed chamber and the atmosphere pushes air down the gradient. Second, the two muscle groups act on different axes — diaphragm antero-posteriorly, external intercostals dorso-ventrally — so the chest expands in three dimensions. We have the ability to increase the strength of inspiration with the help of additional muscles in the abdomen, and on average a healthy human breathes 12–16 times per minute.

Human beings have a significant ability to maintain and moderate the respiratory rhythm to suit the demands of the body tissues, and this is done by the neural system. Four structures are involved.

• Respiratory rhythm centre. A specialised centre present in the medulla region of the brain, primarily responsible for this regulation.
• Pneumotaxic centre. Another centre present in the pons region of the brain, which can moderate the functions of the respiratory rhythm centre. Neural signal from this centre can reduce the duration of inspiration and thereby alter the respiratory rate.
• Chemosensitive area. Situated adjacent to the rhythm centre, it is highly sensitive to CO₂ and hydrogen ions. Increase in these substances can activate this centre, which in turn can signal the rhythm centre to make necessary adjustments in the respiratory process by which these substances can be eliminated.
• Peripheral receptors. Receptors associated with the aortic arch and carotid artery also can recognise changes in CO₂ and H⁺ concentration and send necessary signals to the rhythm centre for remedial actions.

A high pCO₂ promotes the dissociation of oxygen from oxyhaemoglobin, and a low pCO₂ promotes its formation. So pCO₂ is one of the factors that determines where haemoglobin gives up its oxygen.

The reasoning. Binding of oxygen with haemoglobin is primarily related to partial pressure of O₂, but partial pressure of CO₂, hydrogen ion concentration and temperature are the other factors which can interfere with this binding.

Why this is useful, not incidental. A tissue that is respiring hard produces more CO₂ by that very fact. The rise in pCO₂ then makes haemoglobin release more oxygen precisely where the demand is greatest. The effect is visible on the oxygen dissociation curve as a shift to the right, so that at any given pO₂ the percentage saturation is lower — more oxygen has been handed over. No nerve, hormone or enzyme is involved; the regulation is built into the chemistry of haemoglobin itself.

A related effect worth adding. The relationship runs both ways: pO₂ is a major factor which could affect the binding of CO₂ as carbamino-haemoglobin — high pCO₂ with low pO₂ in the tissues favours CO₂ loading, and the reverse at the alveoli. Each gas assists the other's exchange.

Two separate things happen, and a good answer separates them: one from the exertion of climbing, and one from the fall in atmospheric pressure with altitude.

Because of the exertion

• Muscles respire faster, so pCO₂ and H⁺ concentration in the blood rise. The chemosensitive area, highly sensitive to CO₂ and hydrogen ions, is activated and signals the rhythm centre to make necessary adjustments by which these substances can be eliminated. Receptors of the aortic arch and carotid artery do the same.
• The rate and depth of breathing therefore increase — well above the resting 12–16 per minute — so more air is moved per minute.
• In the working muscles, low pO₂, high pCO₂, high H⁺ concentration and higher temperature all make conditions favourable for dissociation of oxygen from oxyhaemoglobin, so more than the usual 5 mL of O₂ per 100 mL of blood is delivered.

Because of the altitude

• Atmospheric pressure falls, so atmospheric pO₂ falls below its sea-level value of 159 mm Hg, and alveolar pO₂ falls below 104.
• The partial pressure gradient driving O₂ from alveoli into blood becomes shallower, so haemoglobin is loaded less completely. If the altitude is high enough, this produces hypoxia — an inadequate oxygen supply to the tissues — with breathlessness, headache, fatigue and dizziness, the condition known as altitude sickness.
• Breathing becomes faster and deeper as a compensation, and over days of stay the body acclimatises: the number of RBCs and the haemoglobin content of the blood increase, and the rate of breathing stays raised, so that more oxygen can be carried despite the shallower gradient.

Insects have a network of tubes called tracheal tubes to transport atmospheric air within the body. Gaseous exchange takes place at the fine terminal endings of these tracheal tubes, where they lie in direct contact with the tissues.

The arrangement in full. Air enters through paired openings on the body surface called spiracles, passes into the tracheae, which branch repeatedly into finer and finer tracheoles, whose moist tips end among the body cells. Oxygen diffuses from the air in the tracheole directly into the cells, and CO₂ diffuses out the same way.

Definition. A sigmoid curve is obtained when percentage saturation of haemoglobin with O₂ is plotted against the pO₂. This curve is called the Oxygen dissociation curve, and it is highly useful in studying the effect of factors like pCO₂, H⁺ concentration, etc., on binding of O₂ with haemoglobin.

Why it is sigmoidal

The reason lies in a fact stated earlier in the chapter: each haemoglobin molecule can carry a maximum of four molecules of O₂. Those four binding sites do not act independently.

• Cooperative binding. When the first O₂ molecule binds to one of the four haem groups, the haemoglobin molecule changes its shape slightly, which makes it easier for the second O₂ to bind, and easier still for the third and fourth. The affinity of haemoglobin for oxygen therefore increases as it loads.
• The shallow start. At very low pO₂ the first molecule binds with difficulty, so the curve rises slowly.
• The steep middle. Once binding has begun, cooperativity takes over and saturation rises sharply for a small rise in pO₂.
• The flat plateau. Near full saturation, almost all sites are occupied, so further increases in pO₂ can add very little — the curve levels off.

Why that shape is physiologically valuable

• The plateau gives safety in loading. At the alveolar pO₂ of 104 mm Hg haemoglobin is about 97 per cent saturated, and it remains nearly fully saturated even if alveolar pO₂ falls appreciably — at altitude, or in mild lung disease. Loading is therefore robust.
• The steep portion gives sensitivity in unloading. Tissue pO₂ of 40 mm Hg sits on the steep part, so a small further fall in tissue pO₂ releases a large quantity of oxygen exactly where demand has risen.
• A straight-line relationship could not do both — it would either load poorly or unload poorly.

One more use of the curve. Because pCO₂, H⁺ concentration and temperature interfere with the binding, the whole curve shifts to the right under tissue conditions, so that at the same pO₂ still more oxygen is released.

Hypoxia is a condition in which the supply of oxygen to the tissues is inadequate for their normal functioning. (If oxygen is absent altogether, the term is anoxia.)

Why it arises — read against the five steps of respiration

Hypoxia can result from a failure at any step of the pathway studied in this chapter:

Symptoms

Breathlessness, headache, dizziness, fatigue, poor concentration and impaired judgement; in severe cases a bluish tinge of the skin and lips, confusion, and eventually unconsciousness. The brain is affected first because it is the tissue least tolerant of oxygen shortage.

High-altitude hypoxia and acclimatisation

This is the form most students meet. As altitude rises, atmospheric pO₂ falls below 159 mm Hg, alveolar pO₂ falls below 104, and the gradient driving oxygen into the blood becomes shallower, so haemoglobin loads less completely. The body compensates over days by increasing the rate and depth of breathing and by raising the number of RBCs and the haemoglobin content of the blood — which is why climbers ascend in stages and why athletes sometimes train at altitude.

(a) IRV and ERV

(b) Inspiratory capacity and Expiratory capacity

(c) Vital capacity and Total lung capacity

Relationship to remember: TLC = VC + RV, so TLC always exceeds VC by exactly the residual volume.

Definition. Tidal Volume (TV) is the volume of air inspired or expired during a normal respiration. It is approximately 500 mL.

The calculation for one hour

Using the chapter's figures: tidal volume ≈ 500 mL and a healthy human breathes 12–16 times per minute.

A check on the answer. The chapter states independently that a healthy man can inspire or expire approximately 6000 to 8000 mL of air per minute — which is exactly the per-minute figure calculated above, confirming both the tidal volume and the breathing rate used. Multiplying by 60 gives the hourly value.

If a single value is wanted, take the midpoint: about 14 breaths per minute × 500 mL × 60 = 4,20,000 mL, or roughly 420 litres per hour.