Breathing and Exchange of Gases Class 11 Notes

The human respiratory system consists of a pair of lungs and a system of air passages that conduct air from the external environment to the alveoli where gas exchange occurs.

The Air Passage (Conducting Zone)

• External nostrils → nasal cavity (warms, moistens and filters air) → pharynx (common passage for air and food) → larynx (voice box; contains vocal cords) → trachea (C-shaped cartilaginous rings prevent collapse).
• Trachea divides into two primary bronchi (one per lung) → secondary (lobar) bronchi → tertiary (segmental) bronchi → bronchioles → terminal bronchioles → respiratory bronchioles → alveolar ducts → alveolar sacs → alveoli.
• Bronchial tree branching: about 23 generations of branching from trachea to alveoli; the last few generations (respiratory zone) are the site of gas exchange.

Alveoli — The Functional Units

• About 300 million alveoli in two lungs provide a total surface area of about 70–100 m² for gas exchange.
• Type I pneumocytes (simple squamous epithelium) form the thin gas-exchange surface; Type II pneumocytes secrete pulmonary surfactant (dipalmitoylphosphatidylcholine) that reduces surface tension and prevents alveolar collapse.
• Each alveolus is surrounded by a dense network of pulmonary capillaries. The air–blood barrier is only about 0.2 µm thick.

Breathing is a mechanical ventilation process driven by pressure changes between the atmosphere and the intrapulmonary (intra-alveolar) space. Air flows from higher to lower pressure.

Inspiration (Active Process)

• Diaphragm contracts and flattens (increases vertical thoracic diameter).
• External intercostal muscles contract, pulling the ribs upward and outward (increases anteroposterior and lateral diameters).
• Thoracic volume increases → intrapleural pressure drops → lungs expand → intrapulmonary pressure falls below atmospheric pressure → air rushes in.

Expiration (Normally Passive)

• Diaphragm relaxes and returns to dome shape; external intercostals relax; ribs move downward and inward due to elastic recoil of the lungs and thoracic wall.
• Thoracic volume decreases → intrapulmonary pressure rises above atmospheric → air is pushed out.
• Forced expiration additionally uses internal intercostals and abdominal muscles (active process).

Spirometry measures the volumes of air moved during breathing. These volumes and their combinations (capacities) are clinically important for diagnosing respiratory disease.

Volumes

• Tidal volume (TV) — volume of air inspired or expired in a normal breath ≈ 500 mL.
• Inspiratory reserve volume (IRV) — additional volume that can be forcefully inspired after a normal inspiration ≈ 2500–3000 mL.
• Expiratory reserve volume (ERV) — additional volume that can be forcefully expired after a normal expiration ≈ 1000–1100 mL.
• Residual volume (RV) — volume of air remaining in the lungs even after the most forceful expiration ≈ 1100–1200 mL.

Capacities

• Inspiratory capacity (IC) = TV + IRV ≈ 3000–3500 mL.
• Expiratory capacity (EC) = TV + ERV ≈ 1500–1600 mL.
• Functional residual capacity (FRC) = ERV + RV ≈ 2100–2300 mL.
• Vital capacity (VC) = TV + IRV + ERV ≈ 4600 mL (maximum volume that can be breathed out after a maximum inspiration).
• Total lung capacity (TLC) = TV + IRV + ERV + RV ≈ 5800 mL (total volume the lungs can hold).

Gas exchange across the respiratory membrane and at tissue level occurs by simple diffusion along partial pressure gradients. Henry's law governs the amount of gas dissolved in a liquid.

• At the alveoli: PO₂ (alveolar air) = 104 mm Hg > PO₂ (pulmonary capillary blood) = 40 mm Hg → O₂ diffuses into blood. PCO₂ (blood) = 45 mm Hg > PCO₂ (alveolar air) = 40 mm Hg → CO₂ diffuses into alveoli.
• At the tissues: PO₂ (systemic capillary blood) = 95 mm Hg > PO₂ (tissue cells) = 40 mm Hg → O₂ delivered to cells. PCO₂ (tissue cells) = 45 mm Hg > PCO₂ (blood) = 40 mm Hg → CO₂ enters blood.
• CO₂ is about 20–25 times more soluble than O₂ in the respiratory membrane, so CO₂ diffuses faster despite a smaller pressure gradient.

Oxygen Transport

• ~97% of O₂ is transported bound to haemoglobin (Hb) as oxyhaemoglobin (HbO₂). Each Hb molecule has four haem groups, each binding one O₂ molecule — so one Hb carries up to 4 O₂.
• ~3% is dissolved in plasma (Henry's law).
• At the tissues, the lower PO₂, higher PCO₂, lower pH and higher temperature (Bohr effect) reduce Hb's affinity for O₂, promoting O₂ unloading.

Carbon Dioxide Transport

• ~70% as bicarbonate ions (HCO₃⁻) in plasma — CO₂ enters RBCs, carbonic anhydrase catalyses CO₂ + H₂O → H₂CO₃ → H⁺ + HCO₃⁻. HCO₃⁻ is exchanged for Cl⁻ (chloride shift / Hamburger phenomenon).
• ~20–25% as carbaminohaemoglobin (CO₂ bound to the amino groups of Hb, not to the haem group) — forms at tissues, released at lungs.
• ~7% dissolved in plasma.

• Pneumotaxic centre in the pons — modulates the output of the medullary centre; reduces the duration of inspiration and thereby increases the breathing rate.
• Carbon dioxide-sensitive receptors (central and peripheral chemoreceptors) — rising blood CO₂ (and therefore H⁺) stimulates breathing to blow off CO₂. This is the primary drive for breathing under normal conditions.
• Low blood O₂ stimulates peripheral chemoreceptors in the carotid and aortic bodies only when PO₂ falls below about 60 mm Hg.

Common Respiratory Disorders

• Asthma — reversible bronchospasm with wheezing, caused by allergens, cold air or stress. Treatment: bronchodilators (salbutamol).
• Emphysema — chronic destruction of alveolar walls, reducing surface area and elastic recoil. Strongly associated with cigarette smoking. Irreversible.
• Occupational respiratory disorders — prolonged inhalation of industrial dusts causes fibrosis: byssinosis (cotton dust), silicosis (silica), asbestosis (asbestos).

Example: A spirometry test shows: TV = 500 mL, IRV = 3000 mL, ERV = 1100 mL, RV = 1200 mL. Calculate the vital capacity and total lung capacity.

Solution: Vital capacity (VC) = TV + IRV + ERV = 500 + 3000 + 1100 = 4600 mL. Total lung capacity (TLC) = VC + RV = 4600 + 1200 = 5800 mL. These are normal values for a healthy adult male.

Example: Why does a person feel breathless at high altitude (e.g. 4500 m) even though they are breathing normally?

Solution: At high altitude, atmospheric pressure is lower, so the partial pressure of O₂ is reduced. The PO₂ in inspired air falls to about 80 mm Hg (from 159 mm Hg at sea level), which reduces alveolar PO₂ and therefore the O₂ saturation of haemoglobin. Peripheral chemoreceptors detect the low PO₂ and increase the breathing rate, but the reduced ambient PO₂ limits the amount of O₂ that can be loaded — causing breathlessness and fatigue (mountain sickness).

Exercises (NCERT Q1–Q14)

• 1) Define vital capacity. What is its significance?
• 2) State the volume of air remaining in the lungs after a normal breathing.
• 3) Diffusion of gases occurs in the alveolar region only and not in the other parts of respiratory system. Why?
• 4) What are the major transport mechanisms for CO2? Explain.
• 5) What will be the pO2 and pCO2 in the atmospheric air compared to those in the alveolar air ? (i) pO2 lesser, pCO2 higher (ii) pO2 higher, pCO2 lesser (iii) pO2 higher, pCO2 higher (iv) pO2 lesser, pCO2 lesser
• 6) Explain the process of inspiration under normal conditions.
• 7) How is respiration regulated?
• 8) What is the effect of pCO2 on oxygen transport?
• 9) What happens to the respiratory process in a man going up a hill?
• 10) What is the site of gaseous exchange in an insect?
• 11) Define oxygen dissociation curve. Can you suggest any reason for its sigmoidal pattern?
• 12) Have you heard about hypoxia? Try to gather information about it, and discuss with your friends.
• 13) Distinguish between (a) IRV and ERV (b) Inspiratory capacity and Expiratory capacity. (c) Vital capacity and Total lung capacity.
• 14) What is Tidal volume? Find out the Tidal volume (approximate value) for a healthy human in an hour.

Answers at a glance

1. 1
   Q1 → Vital capacity is the maximum volume of air a person can breathe in after a forced expiration, equivalently the maximum volume of air that can be breathed out after a forced inspiration. It is a derived value: it includes the expiratory reserve volume, the tidal volume and the inspiratory reserve volume, so VC = ERV + TV + IRV. Its significance is that the pulmonary capacities obtained by adding up respiratory volumes can be used in clinical diagnosis, and the volume of air involved in breathing movements is estimated with a spirometer, which assists clinical assessment of pulmonary function. Vital capacity matters because it is the largest volume of air that can actually be moved in and out of the lungs, and because it is only half the story of lung volume: adding the residual volume to it gives the total lung capacity, TLC = VC + RV. So vital capacity measures how much air the lungs can handle, while the residual volume measures how much air remains trapped and can never be expelled.
2. 2
   Q2 → The volume of air remaining in the lungs after a normal breathing is the functional residual capacity, which is the volume left after a normal expiration. It includes the expiratory reserve volume plus the residual volume, FRC = ERV + RV. With the expiratory reserve volume averaging 1000 to 1100 mL and the residual volume averaging 1100 to 1200 mL, the functional residual capacity is about 2100 to 2300 mL. The point to be careful about is that this is not the residual volume alone. Residual volume, 1100 to 1200 mL, is the air that stays in the lungs even after a forcible expiration, whereas the question specifies a normal breathing, so the air of the expiratory reserve must be added to it.
3. 3
   Q3 → Diffusion of gases occurs in the alveolar region only because that is the only part of the respiratory system built as an exchange surface. The chapter divides the system into a conducting part, running from the external nostrils up to the terminal bronchioles, and an exchange part formed by the alveoli and their ducts. The conducting part merely transports atmospheric air to the alveoli and conditions it by clearing foreign particles, humidifying it and bringing it to body temperature; it performs no exchange. The exchange part is the site of the actual diffusion of O2 and CO2 between blood and atmospheric air, and the alveoli are the primary sites of exchange of gases. The alveoli alone provide the required physical set-up: each terminal bronchiole gives rise to very thin, irregular-walled, vascularised bag-like alveoli, and the diffusion membrane of thin squamous epithelium, basement substance and capillary endothelium is much less than a millimetre thick, spread over a very large surface and closely backed by capillaries. The conducting passages, held open by incomplete cartilaginous rings, are rigid air conduits and have neither this surface nor this blood supply, so gases are delivered there but not exchanged.
4. 4
   Q4 → Carbon dioxide is transported by the blood in three major forms. The first is as carbamino-haemoglobin, carried by the RBCs and accounting for nearly 20 to 25 per cent of the CO2. This binding is related to the partial pressure of CO2, and pO2 is a major factor affecting it: where pCO2 is high and pO2 is low, as in the tissues, more binding of carbon dioxide occurs, whereas where pCO2 is low and pO2 is high, as in the alveoli, dissociation takes place, so the CO2 bound to haemoglobin at the tissues is delivered at the alveoli. The second and largest mechanism is carriage as bicarbonate, which carries 70 per cent of the CO2. This is done by the enzyme carbonic anhydrase, present in very high concentration in RBCs and in minute quantities in the plasma, which catalyses CO2 plus H2O reversibly forming H2CO3 and then HCO3- plus H+. At the tissue site the partial pressure of CO2 is high because of catabolism, so CO2 diffuses into the blood and forms HCO3- and H+; at the alveolar site the pCO2 is low, so the reaction proceeds in the opposite direction and CO2 and H2O are formed, so the CO2 trapped as bicarbonate at the tissue level is released out as CO2 in the alveoli. The third form is simple solution, with about 7 per cent of the CO2 carried in a dissolved state through the plasma. Altogether, every 100 ml of deoxygenated blood delivers approximately 4 ml of CO2 to the alveoli.
5. 5
   Q5 → The correct option is (ii), pO2 higher, pCO2 lesser. The table of partial pressures in mm Hg gives atmospheric air as pO2 159 and pCO2 0.3, and the alveoli as pO2 104 and pCO2 40. Atmospheric air therefore has the higher partial pressure of oxygen, 159 against 104, and the lower partial pressure of carbon dioxide, 0.3 against 40. Option (i) has both figures reversed, option (iii) is wrong in claiming that atmospheric pCO2 is higher, and option (iv) is wrong in claiming that atmospheric pO2 is lower, so only option (ii) agrees with the values. The underlying reason is that air has been depleted of its oxygen and loaded with carbon dioxide on its way to the alveoli.
6. 6
   Q6 → Inspiration is the drawing in of atmospheric air, and it occurs when the intra-pulmonary pressure is less than the atmospheric pressure, that is when there is a negative pressure in the lungs with respect to the atmosphere. It is brought about by two muscular actions acting together. Inspiration is initiated by the contraction of the diaphragm, which increases the volume of the thoracic chamber in the antero-posterior axis, and at the same time the contraction of the external intercostal muscles lifts up the ribs and the sternum, increasing the volume of the thoracic chamber in the dorso-ventral axis. The overall increase in thoracic volume causes a similar increase in pulmonary volume, an effect that follows from the lungs lying in the anatomically air-tight thoracic chamber, so that any change in the volume of the thoracic cavity is reflected in the lung cavity, since the pulmonary volume cannot be altered directly. The increase in pulmonary volume in turn decreases the intra-pulmonary pressure to less than the atmospheric pressure, and this pressure difference forces air from outside to move into the lungs, which is inspiration. On an average a healthy human breathes 12 to 16 times per minute, and the volume of air involved in these breathing movements can be estimated using a spirometer, which assists clinical assessment of pulmonary function.
7. 7
   Q7 → Respiration is regulated by the neural system, which allows us to maintain and moderate the respiratory rhythm to suit the demands of the body tissues. A specialised centre in the medulla region of the brain, the respiratory rhythm centre, is primarily responsible for this regulation. Its functions are moderated by another centre, the pneumotaxic centre, in the pons region of the brain, whose neural signal can reduce the duration of inspiration and thereby alter the respiratory rate. The chemical input comes from a chemosensitive area situated adjacent to the rhythm centre, which is highly sensitive to CO2 and hydrogen ions; an increase in these substances activates this centre, which in turn signals the rhythm centre to make the necessary adjustments in the respiratory process so that these substances can be eliminated. Peripheral receptors associated with the aortic arch and carotid artery also recognise changes in CO2 and H+ concentration and send signals to the rhythm centre for remedial actions. An important qualification is that the role of oxygen in the regulation of respiratory rhythm is quite insignificant, so the system is driven mainly by carbon dioxide and hydrogen ions.
8. 8
   Q8 → The effect of pCO2 on oxygen transport is to control where haemoglobin loads and unloads. Binding of oxygen with haemoglobin is primarily related to the partial pressure of O2, and pCO2, the hydrogen ion concentration and the temperature are the other factors which can interfere with this binding. In the alveoli, where there is high pO2, low pCO2, lesser H+ concentration and lower temperature, the factors are all favourable for the formation of oxyhaemoglobin. In the tissues, where there is low pO2, high pCO2, high H+ concentration and higher temperature, the conditions are favourable for the dissociation of oxygen from the oxyhaemoglobin. Thus a high pCO2 causes haemoglobin to release oxygen, and since the high pCO2 occurs precisely in the tissues that are consuming oxygen, pCO2 acts as the local signal that makes haemoglobin unload exactly where it is needed. In terms of the oxygen dissociation curve, the raised pCO2 at the tissues, together with the raised H+ and temperature, shifts the curve to the right, lowering the percentage saturation of haemoglobin at a given pO2. The overall result is that O2 gets bound to haemoglobin at the lung surface and gets dissociated at the tissues, and every 100 ml of oxygenated blood can deliver around 5 ml of O2 to the tissues under normal physiological conditions.
9. 9
   Q9 → When a man goes up a hill, his respiratory process increases in rate and depth. The reason is that climbing is muscular work, so the muscles consume oxygen at a higher rate and produce more carbon dioxide, raising both the oxygen demand of the tissues and the CO2 and hydrogen ion concentration in the blood. The rise in these substances is what is detected: a chemosensitive area situated adjacent to the respiratory rhythm centre is highly sensitive to CO2 and hydrogen ions, and an increase in them activates this centre. The activated centre signals the respiratory rhythm centre in the medulla to make the necessary adjustments in the respiratory process so that these substances can be eliminated, which makes breathing faster and deeper. Receptors associated with the aortic arch and carotid artery reinforce the signal by recognising the same changes. The net effect is that more fresh air is inspired, alveolar pO2 is raised and more CO2 is expired, so the extra oxygen needed by the working muscles is supplied and the CO2 load is brought back down. Two details are worth holding on to. The pneumotaxic centre in the pons can moderate the rhythm centre, reducing the duration of inspiration and altering the rate. And since the role of oxygen in the regulation of respiratory rhythm is quite insignificant, the breathlessness a climber feels is driven mainly by the accumulating CO2 and H+ rather than by any direct sensing of the thin air.
10. 10
    Q10 → The site of gaseous exchange in an insect is its network of tracheal tubes, the tracheal system. The chapter groups insects separately because the mechanisms of breathing vary among different groups of animals depending mainly on their habitats and levels of organisation: lower invertebrates such as sponges, coelenterates and flatworms exchange O2 with CO2 by simple diffusion over their entire body surface, earthworms use their moist cuticle, and insects have a network of tubes, the tracheal tubes, to transport atmospheric air within the body. In insects this network delivers atmospheric air through the branching tubes to the tissues, so the air is brought to the cells directly and no lung and no blood-borne carriage of the gas is involved. This distinguishes the insect from the terrestrial vertebrates, among which amphibians, reptiles, birds and mammals respire through lungs, that is through vascularised bags used for pulmonary respiration; fishes use gills, and special vascularised structures called gills are used by most of the aquatic arthropods and molluscs. So although an insect is a terrestrial animal, it does not breathe by a lung, and the site of gaseous exchange is the tracheal tube network.
11. 11
    Q11 → The oxygen dissociation curve is the curve obtained when the percentage saturation of haemoglobin with oxygen is plotted against the partial pressure of oxygen. It is highly useful in studying the effect of factors like pCO2 and H+ concentration on the binding of O2 with haemoglobin. The sigmoidal, or S-shaped, pattern has its reason in the structure of the carrier: each haemoglobin molecule can carry a maximum of four molecules of O2, and the binding of the four is cooperative rather than independent, so the first oxygen molecule is bound only slowly, once it is bound haemoglobin becomes more willing to take the next, binding then accelerates through the steep middle portion of the curve, and finally haemoglobin approaches saturation and the curve flattens out. That staged, four-step binding is what gives the curve its S shape. The shape is also physiologically apt, because the steep middle region corresponds to the pO2 range found in the tissues, so a small fall in tissue pO2 there releases a large quantity of oxygen, while the flat upper part ensures efficient loading in the alveoli. Finally, the curve is not fixed in position: in the tissues, where there is low pO2, high pCO2, high H+ concentration and higher temperature, the curve shifts to the right and the conditions favour dissociation of oxygen from the oxyhaemoglobin, whereas in the alveoli, with high pO2, low pCO2, lesser H+ concentration and lower temperature, the conditions favour the formation of oxyhaemoglobin, so O2 gets bound to haemoglobin at the lung surface and gets dissociated at the tissues.
12. 12
    Q12 → Hypoxia is the condition in which the tissues do not receive enough oxygen to meet their metabolic needs, that is when oxygen supply falls short of oxygen demand, and it is best understood in this chapter as a failure of the oxygen supply side of the transport story. Its cause follows from the transport mechanism. About 97 per cent of O2 is transported by RBCs, and the percentage saturation of haemoglobin depends on the partial pressure of O2, so wherever pO2 is low, haemoglobin cannot be fully saturated and less oxygen reaches the tissues even though the mechanism itself is working normally. A familiar setting is altitude. Atmospheric air has a pO2 of 159 mm Hg, and at height this is lower, so on going up a hill the alveolar pO2 falls below its value of 104 mm Hg, the percentage saturation of haemoglobin falls with it, and each 100 ml of blood delivers correspondingly less than the usual around 5 ml of O2 to the tissues. The feature worth discussing is that the body is poorly placed to notice this directly. The chemosensitive area adjacent to the respiratory rhythm centre is sensitive to CO2 and to hydrogen ions, and the role of oxygen in the regulation of respiratory rhythm is quite insignificant, so there is no strong direct signal from the falling oxygen itself. What is felt is therefore second-hand: the breathlessness, rapid breathing, headache and fatigue of a climber are driven by the CO2 and H+ produced by the increased muscular work acting on the chemosensitive area, and by the general metabolic shortfall, which is why a person can be markedly hypoxic without a proportionate feeling of breathlessness. The remedy follows the same logic. Because the deficiency is in alveolar pO2 and not in the haemoglobin, breathing more air to raise alveolar pO2 restores the loading of haemoglobin, and because the control loop is tuned to CO2 and H+, those substances provide the reliable signal to increase ventilation. Finally, hypoxia has a second context within the same framework: where the carrier itself is prevented from carrying oxygen, as with carbon monoxide, haemoglobin is present and pO2 may be adequate, yet the same shortage of oxygen at the tissue is produced, so hypoxia can result either from a failing gradient or from a failing carrier.
13. 13
    Q13 → The three distinctions are as follows. First, between IRV and ERV: inspiratory reserve volume is the extra volume of air a person can inspire by a forcible inspiration beyond the tidal volume, averaging 2500 to 3000 mL, whereas expiratory reserve volume is the extra volume of air a person can expire by a forcible expiration beyond the tidal volume, averaging 1000 to 1100 mL. The first is the extra air held back on inspiration, the second is the extra air pushed out on expiration, and the inspiratory reserve is the larger of the two. Second, between inspiratory capacity and expiratory capacity: both begin from a normal breath, and inspiratory capacity is the total volume of air a person can inspire after a normal expiration, equal to TV + IRV, whereas expiratory capacity is the total volume of air a person can expire after a normal inspiration, equal to TV + ERV. They are mirror images taken from opposite starting points, they both include the tidal volume, and because IRV exceeds ERV, the inspiratory capacity is the larger. Third, between vital capacity and total lung capacity: vital capacity is the maximum volume of air a person can breathe in after a forced expiration, equal to ERV + TV + IRV, equivalently the maximum volume that can be breathed out after a forced inspiration, whereas total lung capacity is the total volume of air accommodated in the lungs at the end of a forced inspiration, equal to RV + ERV + TV + IRV, that is vital capacity plus residual volume, TLC = VC + RV. The decisive difference is that every component of the vital capacity can actually be breathed in or out, whereas the total lung capacity includes the residual volume, the 1100 to 1200 mL of air left in the lungs even after a forcible expiration which can never be expelled, so the total lung capacity is always the larger and the two differ by exactly the residual volume.
14. 14
    Q14 → Tidal volume, TV, is the volume of air inspired or expired during a normal respiration, and it is approximately 500 mL. On an average a healthy human breathes 12 to 16 times per minute, which is 720 to 960 breaths in an hour, and the tidal volume per breath is a further 500 mL. The chapter's own per-minute figure confirms the arithmetic, since 500 mL multiplied by 12 to 16 gives 6000 to 8000 mL of air per minute, matching the statement that a healthy man can inspire or expire approximately 6000 to 8000 mL of air per minute. Over one hour this becomes 6000 to 8000 mL multiplied by 60 minutes, that is 360000 to 480000 mL. Expressed in litres, a healthy human moves approximately 360 to 480 litres of tidal air in an hour, so the tidal volume in an hour is about 360 to 480 litres.

MCQ Questions

1 Mark Questions

1. 1
   From which part of the lungs does O₂ diffuse into the blood? (Ans: the alveoli)
2. 2
   What is the function of the epiglottis? (Ans: covers the glottis during swallowing so food does not enter the trachea)
3. 3
   Name the volume of air inspired or expired with each normal breath. (Ans: tidal volume, ~500 mL)
4. 4
   What is the regulatory centre of breathing in the brain? (Ans: the respiratory rhythm centre in the medulla oblongata)

2 Mark Questions

1. 1
   Differentiate between inspiration and expiration on the role of the diaphragm.
2. 2
   What are compliance and surfactant of lungs? (Ans: ability to stretch; the detergent-like substance that lowers surface tension and prevents alveoli collapse)
3. 3
   State the value of vital capacity and give its formula (TV + IRV + ERV).

3 Mark Questions

1. 1
   Describe how carbon dioxide is transported in human blood. (Ans: ~70% as bicarbonate, 20–25% as carbamino-haemoglobin, dissolved CO₂)
2. 2
   Explain the neural and chemical regulation of respiration. (Ans: medulla rhythm centre; pneumotaxic centre; chemoreceptors respond to CO₂/H⁺/O₂)
3. 3
   What are the respiratory volumes and capacities? Write the normal value of each. (Ans: TLC ~5800 mL, VC ~4500 mL, IRV, ERV, TV, residual volume)

5 Mark Questions

1. 1
   Describe the mechanism of breathing (inspiration and expiration), the exchange at alveolar level, and the transport of oxygen by haemoglobin with the factors affecting its affinity.
2. 2
   Give a detailed account of respiratory disorders — asthma, emphysema, occupational respiratory diseases — and the exchange of gases across the alveolar membrane (diffusion gradients of PO₂ and PCO₂).