Breathing and Exchange of Gases — NEET Notes

Respiratory organs across animals

Every animal has to solve the same problem — get oxygen from the environment to the cells, get carbon dioxide back out — but the engineering solutions differ wildly depending on body size, habitat, and level of organisation. The simplest animals do without dedicated organs altogether. Lower invertebrates such as sponges, coelenterates, and flatworms exchange O₂ and CO₂ by simple diffusion over the entire body surface. The exchange surface and the body wall are one and the same.

As animals get larger, a body-surface solution stops working — interior cells are too far from the outside. Several distinct innovations evolved. Earthworms use their moist cuticle as the exchange surface, with blood capillaries lying just under the skin to ferry gases to and from inner tissues. This is cutaneous respiration. Amphibians like frogs use the same strategy alongside lungs, especially during hibernation when they remain inactive in the cold.

Insects took a radically different route. Cockroaches breathe through a system of internal tubes called tracheae, which open to the outside through paired slit-like apertures called spiracles. The tracheae branch into ever-finer tracheoles that deliver air directly to the cells of the body — no blood is involved in carrying the gas. The ends of the tracheoles are filled with fluid in which O₂ and CO₂ dissolve. The result is extremely efficient gas exchange at the cellular level, but it limits how big an insect can grow.

Aquatic arthropods and molluscs use gills — special vascularised outgrowths through which water is passed (branchial respiration). Fishes use gills too. Terrestrial vertebrates — amphibians, reptiles, birds, and mammals — use vascularised bags called lungs for what is termed pulmonary respiration. Lungs keep the gas-exchange surface internal, where it can be kept moist without losing water to the air.

Human respiratory system — anatomy

Air takes a long, branching journey from the world outside to the thin film of moisture inside an alveolar wall, where it finally meets blood. Trace it once and you have it for life.

A pair of external nostrils opens above the upper lips. They lead into a nasal chamber through the nasal passage, lined with ciliated mucous membrane that filters dust, warms the air, and adds moisture. The nasal chamber empties into the pharynx — a muscular tube that serves as a common passage for both food and air. The pharynx opens through the larynx into the trachea. The larynx is a cartilaginous box that also functions as the sound box, with the vocal cords stretched across it. Above the glottis sits a thin elastic flap called the epiglottis — during swallowing, it covers the glottis so food does not enter the trachea.

The trachea is a straight tube that runs down to the mid-thoracic cavity and divides at the level of the fifth thoracic vertebra into a right and left primary bronchus. Each primary bronchus divides repeatedly to form secondary bronchi, then tertiary bronchi, then bronchioles, ending in very thin terminal bronchioles. The trachea, primary, secondary and tertiary bronchi, and the initial bronchioles are supported by incomplete C-shaped cartilaginous rings — these prevent collapse during pressure swings of inspiration and expiration. Each terminal bronchiole gives rise to many thin, irregular-walled, highly vascularised, balloon-like structures called alveoli. The branching network of bronchi, bronchioles, and alveoli is what we call the lungs.

The two lungs sit within the thoracic chamber, an anatomically air-tight cavity formed dorsally by the vertebral column, ventrally by the sternum, laterally by the ribs, and on the lower side by the dome-shaped diaphragm. Each lung is wrapped in a double-layered pleura with thin pleural fluid between them. The outer pleural membrane is in close contact with the thoracic lining; the inner is fused to the lung surface. The pleural fluid reduces friction between the two layers as the lungs expand and contract. This anatomical setup is essential — because we cannot directly change lung volume, any change in thoracic-cavity volume must instead be transmitted to the lungs through the pleural seal.

NCERT divides the airway into two functional zones. The conducting part — external nostrils through to terminal bronchioles — transports atmospheric air to the alveoli, clears it of foreign particles, humidifies it, and warms it to body temperature. The respiratory or exchange part — alveoli and their ducts — is the site of actual diffusion of O₂ and CO₂ between blood and air.

Mechanism of breathing

You cannot grab your lungs and squeeze them. To move air in and out you have to change the volume of the thoracic chamber, and the pleural seal does the rest. Breathing has two stages — inspiration (drawing air in) and expiration (releasing air out) — and both are driven by pressure gradients created by two muscle groups: the diaphragm and the intercostal muscles between the ribs.

Inspiration begins with the contraction of the diaphragm. The dome flattens and pulls downward, increasing thoracic volume along the antero-posterior axis. Simultaneously, the external intercostal muscles contract and lift the ribs and sternum upward and outward, enlarging the chamber in the dorso-ventral axis. The overall increase in thoracic volume is transmitted through the pleural seal to the lungs — pulmonary volume rises, intra-pulmonary pressure drops below atmospheric pressure, and air rushes in. Expiration is the reverse: the diaphragm and external intercostals relax, the chamber shrinks, intra-pulmonary pressure rises above atmospheric, and air is expelled. Under normal conditions inspiration is active (muscles contracting) and expiration is passive (elastic recoil). With effort, abdominal muscles and internal intercostals can drive forced expiration too. A healthy human breathes 12–16 times per minute.

The volume of air involved in breathing can be measured precisely using a spirometer, a clinical instrument that gives sharp diagnostic value — it can flag obstruction, restriction, or muscular weakness long before symptoms appear.

Respiratory volumes and capacities

The textbook splits the air moved by the lungs into four volumes — discrete, non-overlapping fractions — and four capacities, each capacity being a sum of two or more volumes. NEET tests both the numerical values and the addition rules. The numbers below are NCERT's stated ranges.

Exchange of gases at the alveoli

Alveoli are the primary site of gas exchange, and the same kind of exchange happens again between blood and the body tissues. Both transfers are by simple diffusion, driven by partial-pressure gradients. The pressure contributed by an individual gas in a mixture is its partial pressure — written pO₂ for oxygen and pCO₂ for carbon dioxide. NCERT's Table 14.1 gives the values in mm Hg, and NEET has tested them verbatim.

The numbers tell a clean story. Atmospheric air carries pO₂ = 159 and pCO₂ = 0.3. Alveolar air, mixed with residual lung air and saturated with water, sits at pO₂ = 104 and pCO₂ = 40. Deoxygenated blood arriving from the body has pO₂ = 40 and pCO₂ = 45 — so O₂ flows from alveolus into blood, and CO₂ flows from blood into alveolus. After exchange, oxygenated blood leaves with pO₂ = 95 and pCO₂ = 40. At the tissues the gradient flips: tissue pO₂ is around 40 and pCO₂ is around 45, so O₂ unloads to the tissues and CO₂ is picked up.

Two further facts matter. First, the solubility of CO₂ is 20–25 times higher than that of O₂, so per unit of partial-pressure difference, CO₂ moves through the diffusion membrane much faster than O₂. Second, the diffusion membrane is incredibly thin — less than a millimetre in total. It is made of three layers: the squamous epithelium of the alveolus, the endothelium of the alveolar capillary, and the basement substance between them. Thin membrane plus high CO₂ solubility plus steep partial-pressure gradient — all the factors are favourable for diffusion in our bodies.

Transport of oxygen — the oxyhaemoglobin curve

Haemoglobin is a red iron-containing pigment housed inside red blood cells. About 97 per cent of O₂ in blood is bound reversibly to haemoglobin as oxyhaemoglobin; the remaining 3 per cent travels dissolved in plasma. Each haemoglobin molecule carries up to four O₂ molecules, one for each haem group. Binding is determined chiefly by pO₂, but pCO₂, hydrogen-ion concentration, and temperature all influence it.

Plot percentage saturation of haemoglobin with O₂ against pO₂ and you get a characteristic sigmoid (S-shaped) curve — the oxygen dissociation curve. The sigmoid shape arises from cooperative binding: once one O₂ binds, the haemoglobin shifts to a high-affinity conformation, so the next O₂ binds more easily, and so on. The curve is steep in the middle range, meaning a small change in pO₂ causes a large change in saturation — exactly where the tissues operate, exactly where oxygen needs to be released.

In the alveoli — high pO₂, low pCO₂, low H⁺, low temperature — haemoglobin loads oxygen. In the tissues — low pO₂, high pCO₂, high H⁺, high temperature — haemoglobin lets it go.

The oxygen cascade in one sentence

The same four factors that favour loading at the alveoli — high pO₂, low pCO₂, fewer H⁺ ions, cooler temperature — are exactly reversed at the tissues, where unloading is favoured: low pO₂, high pCO₂, more H⁺, warmer temperature. NEET 2021 asked precisely this set of four conditions for oxyhaemoglobin formation at the alveoli.

The shift in haemoglobin's affinity for O₂ in response to pCO₂ and H⁺ is called the Bohr effect. When pCO₂ or [H⁺] rises — as in working muscles producing CO₂ and lactate — the dissociation curve shifts to the right, meaning haemoglobin holds O₂ less tightly and releases more of it. Higher temperature does the same. The result is a beautifully tuned delivery system: oxygen is released most aggressively in exactly the tissues that are working hardest. Under normal physiological conditions, every 100 mL of oxygenated blood delivers about 5 mL of O₂ to the tissues — a number NEET 2022 tested directly.

Transport of carbon dioxide

Carbon dioxide leaves the tissues and reaches the alveoli by three parallel routes — and NEET tests the percentages.

The biggest fraction relies on a single enzyme: carbonic anhydrase, present in very high concentration inside RBCs and in trace amounts in plasma. It catalyses a reaction that runs both ways:

CO₂ + H₂O  ⇌  H₂CO₃  ⇌  HCO₃⁻ + H⁺

Carbonic anhydrase, working in both directions

At the tissue site, pCO₂ is high. CO₂ diffuses into RBCs and plasma, the reaction runs forward, and HCO₃⁻ and H⁺ are produced — the bicarbonate dissolves freely in plasma and is carried back to the lungs. At the alveolar site, pCO₂ is low. The reaction reverses: HCO₃⁻ and H⁺ recombine to form H₂CO₃, then split back into CO₂ and H₂O. The newly liberated CO₂ diffuses out into the alveolar air and is exhaled. Every 100 mL of deoxygenated blood delivers about 4 mL of CO₂ to the alveoli.

The carbamino route is the other major path: CO₂ binds directly to amino groups on haemoglobin to form carbamino-haemoglobin. This binding is favoured by high pCO₂ and low pO₂ — exactly the tissue conditions — and reverses at the alveoli where pCO₂ is low and pO₂ is high. The smallest route, dissolved CO₂, is a thin band that simply rides in plasma because CO₂ is 20–25 times more soluble than O₂.

Regulation of respiration

Breathing has to adjust to demand without conscious effort. You speed up when you climb stairs, hold steady when you sleep, and never have to think about it. The nervous system does the regulation, and it operates through three coordinating centres.

The primary controller is the respiratory rhythm centre in the medulla oblongata. It generates the basic in–out cycle by alternately stimulating and silencing the diaphragm and external intercostal muscles. A second centre, the pneumotaxic centre, sits in the pons region of the brain and can shorten the duration of inspiration, raising the respiratory rate when the body demands faster breathing. The third controller is a chemosensitive area adjacent to the rhythm centre — highly sensitive to CO₂ and H⁺. When CO₂ or H⁺ levels rise, this area activates and signals the rhythm centre to speed breathing so the excess can be blown off. Receptors in the aortic arch and carotid artery also monitor CO₂ and H⁺ and feed signals back to the medulla.

The role of O₂ in setting respiratory rhythm is, surprisingly, quite insignificant under normal conditions. The body uses CO₂ as its primary signal because rising CO₂ is the most reliable early sign of inadequate ventilation. Only when O₂ falls dramatically — as at extreme altitude — do the chemoreceptors start to respond strongly to hypoxia. That is why altitude sickness shows up as breathing difficulty and palpitations: atmospheric pressure drops, alveolar pO₂ falls below the threshold, and the body cannot extract enough oxygen no matter how fast it breathes.

Disorders of the respiratory system

Three textbook disorders cover the bulk of NEET questions on the disease section.

Asthma is a difficulty in breathing characterised by wheezing, caused by inflammation of the bronchi and bronchioles. It is most often an allergic reaction — mast cells in the lungs release histamine and other mediators in response to allergens, narrowing the airways. Increasing urban air pollution and rising airborne allergens have made asthma far more common. Treatment focuses on bronchodilators and anti-inflammatory drugs.

Emphysema is a chronic disorder in which the walls of the alveoli are damaged, reducing the respiratory surface area. Fewer functional alveoli means less surface for diffusion, which means a chronic shortness of breath that worsens over time. Cigarette smoking is the major cause — emphysema is often called "smoker's disease." Where asthma narrows the airways, emphysema destroys the exchange surface itself.

Occupational respiratory disorders arise in industries that produce heavy airborne dust — grinding, stone-breaking, asbestos handling. Long-term inhalation overwhelms the body's defences and leads to chronic inflammation, fibrosis (proliferation of fibrous tissue in the lung), and serious permanent lung damage. Silicosis, caused by silica dust in stone grinders, and asbestosis, caused by asbestos fibres, are the textbook examples. Workers in such industries should wear protective masks; NEET 2018 tested silicosis directly as an occupational respiratory disease.