Breathing and Exchange of Gases

This article follows NCERT's own map through the chapter:

• Respiratory organs across the animal kingdom, then the human respiratory system, nostrils to alveoli, and its conducting versus exchange parts.
• The mechanism of breathing — how the diaphragm and intercostal muscles change thoracic volume and intra-pulmonary pressure to drive inspiration and expiration.
• Respiratory volumes and capacities — tidal volume, the reserve volumes, residual volume, and the five capacities built from them.
• Exchange of gases — how partial pressures of O2 and CO2 differ across the pathway and drive diffusion.
• Transport of gases — O2 as oxyhaemoglobin, CO2 as bicarbonate, carbaminohaemoglobin and dissolved gas, and the oxygen dissociation curve.
• Regulation of respiration — the medullary rhythm centre, the pneumotaxic centre, and chemosensitive receptors.
• Disorders of the respiratory system — asthma, emphysema and occupational respiratory disorders.

Respiratory organs across the animal kingdom

Mechanisms of breathing vary among animal groups mainly with their level of organisation and habitat. Lower invertebrates such as sponges, coelenterates and flatworms have no dedicated respiratory organ — they exchange O2 and CO2 by simple diffusion over the entire body surface, since every cell lies close to the surface. Earthworms use their moist cuticle. Insects use a network of tracheal tubes that carries atmospheric air directly to tissues, bypassing the blood for gas transport altogether. Vascularised gills (branchial respiration) serve most aquatic arthropods and molluscs, while vascularised lungs (pulmonary respiration) serve terrestrial forms. Among vertebrates, fishes use gills while amphibians, reptiles, birds and mammals use lungs; frogs additionally respire through their moist skin (cutaneous respiration). The common thread is the same physical requirement: a large, thin, moist, richly vascularised surface for diffusion.

The human respiratory system: from nostrils to alveoli

Humans have a pair of external nostrils opening above the upper lip, leading through the nasal passage into a nasal chamber, which opens into the pharynx — part of which is the common passage for food and air. The pharynx opens through the larynx into the trachea. The larynx is a cartilaginous box that also helps in sound production (the sound box); during swallowing its opening (the glottis) is covered by a thin elastic cartilaginous flap, the epiglottis, keeping food out of the larynx. The trachea is a straight tube running to the mid-thoracic cavity, dividing at the level of the 5th thoracic vertebra into a right and a left primary bronchus. Each primary bronchus divides repeatedly into secondary and tertiary bronchi and then bronchioles, ending in very thin terminal bronchioles. The trachea, the bronchi and the initial bronchioles are supported by incomplete cartilaginous rings that keep the airway from collapsing while still letting it flex. Each terminal bronchiole gives rise to many thin, irregular-walled, richly vascularised sac-like alveoli; the branching network of bronchi, bronchioles and alveoli makes up the lungs. Each of the two lungs is covered by a double-layered pleura, with pleural fluid between the layers reducing friction as the lung surface moves. The lungs sit inside the thoracic chamber, an airtight compartment bounded dorsally by the vertebral column, ventrally by the sternum, laterally by the ribs, and below by the dome-shaped diaphragm. Because the pleura couples the lung surface tightly to the thoracic wall, any change in thoracic volume is transmitted to pulmonary volume — essential, since we cannot directly alter pulmonary volume ourselves. It is useful to split the tract into two functional zones. Nostrils to terminal bronchioles form the conducting part, which transports air to the alveoli while clearing it of foreign particles, humidifying it, and warming it to body temperature. The alveoli and their ducts form the respiratory (exchange) part — where O2 and CO2 actually diffuse between blood and air.

The mechanics of breathing: pressure gradients do the work

Breathing has two stages: inspiration, during which atmospheric air is drawn in, and expiration, during which CO2-rich alveolar air is released. Air moves purely because a pressure gradient is created between the lungs and the atmosphere — the lungs have no muscle in their walls to actively pump air. Inspiration occurs only when intra-pulmonary pressure drops below atmospheric pressure; expiration occurs when it rises above atmospheric pressure. The diaphragm and the external and internal intercostal muscles generate these gradients. Inspiration begins with contraction of the diaphragm, increasing thoracic volume along the antero-posterior axis as the dome flattens; simultaneously, contraction of the external intercostals lifts the ribs and sternum, increasing thoracic volume along the dorso-ventral axis. This combined increase is transmitted through the pleura to an equal increase in pulmonary volume, lowering intra-pulmonary pressure below atmospheric and forcing air in. Relaxation of these muscles reduces thoracic and pulmonary volume, raising intra-pulmonary pressure slightly above atmospheric and expelling air — expiration, essentially passive elastic recoil under quiet breathing; additional abdominal muscles can force both phases when needed. A healthy human breathes 12 to 16 times per minute, and a spirometer measures the volumes moved for clinical assessment of lung function.

Respiratory volumes and capacities

Spirometry resolves the air moved during breathing into a small set of standard volumes, which are then added together in different combinations to give clinically meaningful capacities.

Tidal volume (TV) is the volume of air inspired or expired during one normal, quiet breath — approximately 500 mL, so a healthy adult moves roughly 6000 to 8000 mL of air per minute at rest. Inspiratory reserve volume (IRV) is the extra air that can be forcibly inspired beyond a normal tidal inspiration, averaging 2500 to 3000 mL. Expiratory reserve volume (ERV) is the extra air that can be forcibly expired beyond a normal tidal expiration, averaging 1000 to 1100 mL. Residual volume (RV) is the air that remains in the lungs even after the most forcible expiration, averaging 1100 to 1200 mL — never exhaled, and it keeps the alveoli from collapsing. Adding volumes together gives the capacities used in clinical diagnosis:

Because residual volume can never be exhaled, RV, FRC and TLC cannot be read directly off a simple spirometer trace — only combinations that exclude RV (TV, IRV, ERV, IC, EC, VC) are directly measurable this way. This is a favourite Board and NEET distinction, and it is developed further in the derivation and worked examples below.

Exchange of gases: partial pressures and the diffusion membrane

The alveoli are the primary site of gas exchange; exchange also occurs between blood and tissues. In both places, O2 and CO2 move by simple diffusion, driven mainly by a pressure or concentration gradient; gas solubility and membrane thickness also affect the rate. The pressure contributed by one gas within a mixture of gases is its partial pressure — written $p_{O_2}$ for oxygen and $p_{CO_2}$ for carbon dioxide. NCERT's Table 14.1 gives these values (in mm Hg) at each site along the pathway:

These numbers show a clear gradient for oxygen from alveoli to blood and blood to tissues, and an equal and opposite gradient for carbon dioxide from tissues to blood and blood to alveoli. Because CO2 is 20 to 25 times more soluble than O2, the amount diffusing per unit of partial-pressure difference is much larger for CO2, compensating for its comparatively small gradient (about 5 mm Hg, against oxygen's 55 to 64 mm Hg). The diffusion membrane has three layers: the thin squamous epithelium of the alveolus, the endothelium of the alveolar capillary, and a shared basement substance sandwiched between them. Even with three layers, total thickness is much less than a millimetre — so every relevant factor favours diffusion of O2 from alveoli toward tissues, and of CO2 from tissues toward alveoli.

Transport of oxygen: haemoglobin and the oxygen dissociation curve

Blood carries both O2 and CO2. About 97 per cent of O2 is transported by red blood cells (RBCs); the remaining 3 per cent stays dissolved in plasma. Haemoglobin (Hb), the red, iron-containing pigment inside RBCs, binds O2 reversibly to form oxyhaemoglobin; each haemoglobin molecule carries up to four molecules of O2. Binding of O2 to haemoglobin depends primarily on $p_{O_2}$, but $p_{CO_2}$, H+ concentration and temperature also interfere. Plotting percentage saturation of haemoglobin against $p_{O_2}$ gives an S-shaped, or sigmoid, curve — the oxygen dissociation curve. In the alveoli, high $p_{O_2}$, low $p_{CO_2}$, low H+ and lower temperature all favour formation of oxyhaemoglobin; in the tissues, low $p_{O_2}$, high $p_{CO_2}$, high H+ and higher temperature all favour dissociation instead. So oxygen binds at the lung surface and is released at the tissues — exactly where needed. Under normal conditions, every 100 mL of oxygenated blood delivers around 5 mL of O2 to the tissues. This rightward shift of the curve under high $p_{CO_2}$, high H+ and high temperature — conditions of actively metabolising tissue — is widely called the Bohr effect: haemoglobin releases more oxygen exactly where tissues are working hardest.

Transport of carbon dioxide: bicarbonate, carbamino compounds, and dissolved gas

CO2 is transported by blood through three parallel routes. About 20 to 25 per cent is carried by haemoglobin as carbaminohaemoglobin, a binding related to $p_{CO_2}$ (pO2 is a major factor too). When $p_{CO_2}$ is high and $p_{O_2}$ is low, as in the tissues, more CO2 binds haemoglobin; when $p_{CO_2}$ is low and $p_{O_2}$ is high, as in the alveoli, CO2 dissociates and is released. The great majority, nearly 70 per cent, is carried as bicarbonate (HCO3-). RBCs contain a very high concentration of the enzyme carbonic anhydrase (a smaller amount is in plasma too), which catalyses the reaction in both directions:

At the tissues, high $p_{CO_2}$ drives CO2 into blood and pushes this reaction forward, producing HCO3- and H+. At the alveoli, low $p_{CO_2}$ reverses it, regenerating CO2 and H2O so CO2 diffuses out into alveolar air — CO2 trapped as bicarbonate at the tissue level is thus carried to the lungs and released as gas. The remaining roughly 7 per cent stays dissolved in plasma. Every 100 mL of deoxygenated blood delivers approximately 4 mL of CO2 to the alveoli.

Regulation of respiration: the neural control loop

The body maintains and adjusts respiratory rhythm neurally, without conscious effort. A specialised respiratory rhythm centre in the medulla is primarily responsible. A second centre, the pneumotaxic centre, sits in the pons and moderates the rhythm centre's output; its signal can reduce the duration of inspiration and thereby alter respiratory rate. A chemosensitive area next to the rhythm centre is highly sensitive to CO2 and hydrogen ions; a rise in either activates it, signalling the rhythm centre to adjust breathing until the excess is eliminated. Receptors in the aortic arch and carotid artery also sense CO2 and H+ changes and signal the rhythm centre. Oxygen's own role in regulating respiratory rhythm under normal conditions is quite insignificant — the system is tuned to CO2 and H+, not O2, which is why breathing stays comfortable until oxygen is severely depleted, as at very high altitude.

Disorders of the respiratory system

Asthma is difficulty in breathing with wheezing, from inflammation of the bronchi and bronchioles. Emphysema is a chronic disorder in which alveolar walls are damaged, reducing the exchange surface; cigarette smoking is a major cause. Occupational respiratory disorders arise in industries such as grinding or stone-breaking, where dust overwhelms the body's defences; long exposure causes inflammation leading to fibrosis and serious lung damage, so workers should wear protective masks.

Board level - Respiratory volumes and capacities from spirometer data

A healthy adult's spirometer trace gives tidal volume (TV) = 500 mL, inspiratory reserve volume (IRV) = 3000 mL, expiratory reserve volume (ERV) = 1100 mL, and residual volume (RV) = 1200 mL. Find the inspiratory capacity, expiratory capacity, functional residual capacity, vital capacity and total lung capacity.

Step 1. Inspiratory capacity: $IC = TV + IRV = 500 + 3000 = 3500$ mL.

Step 2. Expiratory capacity: $EC = TV + ERV = 500 + 1100 = 1600$ mL.

Step 3. Functional residual capacity: $FRC = ERV + RV = 1100 + 1200 = 2300$ mL.

Step 4. Vital capacity: $VC = ERV + TV + IRV = 1100 + 500 + 3000 = 4600$ mL.

Step 5. Total lung capacity: $TLC = VC + RV = 4600 + 1200 = 5800$ mL. Answer: IC = 3500 mL, EC = 1600 mL, FRC = 2300 mL, VC = 4600 mL, TLC = 5800 mL.

Competitive level (NEET) - Oxygen delivery to resting and exercising tissues

Using NCERT's figure that every 100 mL of oxygenated blood delivers about 5 mL of O2 to the tissues, find the rate of oxygen delivery (in mL per minute) when cardiac output is 5000 mL/min at rest, and again when cardiac output rises to 20,000 mL/min during vigorous exercise, assuming the same 5 mL per 100 mL extraction in both cases.

Step 1. At rest, the blood delivered per minute is 5000 mL, so the number of 100 mL units is $5000/100 = 50$.

Step 2. Oxygen delivered at rest $= 50 \times 5\ \text{mL} = 250$ mL O2 per minute.

Step 3. During exercise, cardiac output is 20,000 mL/min, so the number of 100 mL units is $20000/100 = 200$.

Step 4. Oxygen delivered during exercise $= 200 \times 5\ \text{mL} = 1000$ mL O2 per minute. Answer: 250 mL O2/min at rest, rising to 1000 mL O2/min during exercise — a fourfold increase driven entirely by the fourfold rise in cardiac output, since extraction per 100 mL is held constant. Timing note: well under a minute — divide cardiac output by 100 and multiply by 5 mL. The trap is forgetting that real exercising muscle also widens its extraction beyond 5 mL per 100 mL; this question's constant-extraction assumption is a simplification, so do not invent extraction changes unless the question supplies a new figure.

Competitive level (NEET) - Partitioning carbon dioxide transport in the blood

Tissues load 200 mL of CO2 into the blood every minute. Using NCERT's transport percentages (about 70 per cent as bicarbonate, about 20 to 25 per cent as carbaminohaemoglobin, and about 7 per cent dissolved in plasma), estimate how many mL of CO2 travel by each route. Take the carbaminohaemoglobin share as 23 per cent for this calculation.

Step 1. Check the percentages sum to 100: $70 + 23 + 7 = 100$, so the three routes are exhaustive and there is no leftover CO2 unaccounted for.

Step 2. CO2 as bicarbonate: $70\% \times 200\ \text{mL} = 140$ mL, generated via the carbonic-anhydrase reaction inside the RBC and carried mostly in plasma.

Step 3. CO2 as carbaminohaemoglobin: $23\% \times 200\ \text{mL} = 46$ mL, bound directly to haemoglobin.

Step 4. CO2 dissolved in plasma: $7\% \times 200\ \text{mL} = 14$ mL. Answer: 140 mL as bicarbonate, 46 mL as carbaminohaemoglobin, 14 mL dissolved in plasma — summing back to the full 200 mL. Timing note: about 30 seconds — convert each percentage to a decimal and multiply once, and always check the fractions sum to 100 per cent first, since NEET distractors sometimes quietly supply percentages that sum to 95 or 105.

Treating "breathing" and "respiration" as identical. NCERT calls gas exchange with the atmosphere "breathing, commonly known as respiration," but breathing (pulmonary ventilation) is only step (i) of a five-step process; cellular respiration, the oxidation of glucose inside mitochondria, is a separate topic in Chapter 12.

Confusing which volumes a simple spirometer can measure. TV, IRV, ERV and capacities built only from those three (IC, EC, VC) can be read directly off a spirometer trace. RV, and anything containing RV (FRC, TLC), cannot be, because residual air is never expired.

Assuming O2 drives breathing rate the way CO2 does. The chemosensitive area and aortic/carotid receptors are tuned mainly to CO2 and H+; O2's own role in normal regulation is quite insignificant, so rate does not rise sharply until oxygen is severely depleted.

Mixing up the diffusion membrane's layers. It is three layers — alveolar squamous epithelium, a shared basement substance, and capillary endothelium — not one, though combined thickness is still under a millimetre.

• List the respiratory organs of sponges, earthworms, insects, aquatic arthropods and molluscs, fishes, and terrestrial vertebrates, and explain why each suits its habitat.
• Trace the human respiratory pathway from external nostrils to alveoli, naming every structure along the way.
• Distinguish the conducting part of the respiratory tract from the respiratory (exchange) part.
• Explain, in terms of thoracic volume and intra-pulmonary pressure, how the diaphragm and intercostal muscles cause inspiration and expiration.
• Define TV, IRV, ERV and RV, and correctly build IC, EC, FRC, VC and TLC from them.
• State the partial pressures of O2 and CO2 at each site along the pathway and explain the resulting diffusion gradients.
• Describe O2 transport (97% oxyhaemoglobin, 3% dissolved) and the shape and meaning of the oxygen dissociation curve.
• Describe CO2 transport (about 70% bicarbonate via carbonic anhydrase, 20 to 25% carbaminohaemoglobin, about 7% dissolved) and write the carbonic anhydrase reaction both ways.
• Explain the roles of the medullary rhythm centre, the pneumotaxic centre and the chemosensitive area (plus aortic/carotid receptors) in regulating breathing.
• Describe asthma, emphysema and occupational respiratory disorders, including their causes.

Ask the tutor: want to work through a few more spirometer or oxygen-dissociation-curve NEET problems together, or trace how this chapter's oxygenated blood becomes the subject of the next chapter, Body Fluids and Circulation?