Breathing and Exchange of Gases

Animals exchange gases in different ways — by simple diffusion across the body surface (sponges, cnidarians), through a network of tracheal tubes (insects), by gills (aquatic animals) or by lungs (terrestrial vertebrates). Humans use a pair of lungs housed in the thoracic cavity. Air follows a fixed pathway, a guaranteed NEET sequence: external nostrils → nasal chamber → pharynx → larynx (the sound box) → trachea → primary, secondary and tertiary bronchi → bronchioles → terminal bronchioles, ending in the thin-walled, balloon-like alveoli where the actual gas exchange occurs.

The trachea and bronchi are held open by C-shaped cartilage rings to prevent collapse. The lungs are enclosed in a double-layered membrane, the pleura, with pleural fluid that reduces friction. Breathing movements are powered by the dome-shaped diaphragm below and the intercostal muscles between the ribs. The whole process of respiration is conveniently broken into five steps: breathing (ventilation), diffusion of gases at the alveoli, transport of gases by blood, diffusion of gases between blood and tissues, and the cellular utilisation of O₂.

Breathing (pulmonary ventilation) moves air in and out by changing the volume — and hence the pressure — of the thoracic cavity. During inspiration, the diaphragm contracts and flattens and the external intercostal muscles contract, lifting the ribs and sternum; this increases the thoracic volume, which lowers the intrapulmonary pressure below the atmospheric pressure, so air rushes into the lungs. The need for a pressure below atmospheric is the key mechanical point.

Expiration is usually a passive process: the diaphragm and external intercostals relax, the thoracic volume decreases, the intrapulmonary pressure rises above atmospheric, and air is pushed out. Forced expiration uses additional (internal intercostal and abdominal) muscles. In short, air always moves down a pressure gradient: inspiration needs intrapulmonary pressure below atmospheric, expiration needs it above. NEET frequently tests the muscle actions and the direction of the pressure change.

The amount of air moved during breathing is measured with a spirometer and described as respiratory volumes and their sums, the capacities. These figures, and especially how the capacities are built from the volumes, are among the most directly examined facts in this chapter.

There are four primary volumes. The tidal volume (TV) is the air inspired or expired in a normal, quiet breath — about 500 mL. The inspiratory reserve volume (IRV) is the extra air that can be forcibly inhaled over a normal inspiration (about 2500–3000 mL). The expiratory reserve volume (ERV) is the extra air that can be forcibly exhaled after a normal expiration (about 1000–1100 mL). The residual volume (RV) is the air that always remains in the lungs even after the most forceful expiration (about 1100–1200 mL).

The capacities are obtained by adding two or more volumes, and you should learn each formula. Inspiratory capacity (IC) = TV + IRV (total air a person can inspire after a normal expiration). Expiratory capacity (EC) = TV + ERV. Functional residual capacity (FRC) = ERV + RV (air left after a normal expiration).

The two most important capacities are the vital capacity and the total lung capacity. Vital capacity (VC) = TV + IRV + ERV — the maximum volume that can be exhaled after a maximum inhalation (it does not include the residual volume, because that air can never be exhaled). Total lung capacity (TLC) = VC + RV, equivalently TV + IRV + ERV + RV — the total volume the lungs can hold. A reliable NEET approach is to memorise VC = TV + IRV + ERV and TLC = VC + RV, and to remember that residual volume is excluded from vital capacity.

Gases are exchanged by simple diffusion along partial-pressure gradients, with the alveoli as the primary site (a second exchange happens between blood and tissues). Oxygen diffuses from the alveolar air (where its partial pressure pO₂ is about 104 mm Hg) into the deoxygenated blood arriving from the body (pO₂ about 40), while carbon dioxide diffuses the other way, from the blood (pCO₂ ~45) into the alveoli (pCO₂ ~40). CO₂ diffuses readily because it is about 20–25 times more soluble than O₂.

Transport of oxygen is dominated by haemoglobin. About 97% of O₂ is carried bound to haemoglobin in the red blood cells as oxyhaemoglobin, and only about 3% is dissolved in the plasma. Each haemoglobin molecule can bind up to four O₂ molecules. The binding depends on conditions, summarised by the oxygen dissociation curve — a sigmoid (S-shaped) plot of percentage saturation of Hb against pO₂.

The position of this curve shifts with the environment, a high-yield NEET concept known as the Bohr effect. In the tissues, where CO₂ is high, pH is low (more H⁺) and temperature is higher, the curve shifts to the right, meaning haemoglobin releases its oxygen more readily — exactly where the tissues need it. In the lungs, the opposite conditions favour loading of O₂ onto haemoglobin. So the curve elegantly matches oxygen delivery to demand.

Transport of carbon dioxide uses three routes, and the proportions are commonly asked. About 70% of CO₂ travels as bicarbonate ions (HCO₃⁻), formed in the red blood cells with the help of the enzyme carbonic anhydrase; about 20–25% is carried as carbamino-haemoglobin (CO₂ bound directly to haemoglobin); and about 7% is dissolved in the plasma. The essentials here are the 97%/3% split for O₂, the four-O₂ capacity of Hb, the right-shift of the dissociation curve in the tissues, and the ~70% bicarbonate route for CO₂.

Breathing must adjust automatically to the body's changing needs, and this is achieved by neural regulation of respiration. The master control is the respiratory rhythm centre in the medulla oblongata of the brain, which sets the basic breathing rhythm. A second centre in the pons, the pneumotaxic centre, can moderate the medullary centre and alter the rate of breathing (mainly by influencing the duration of inspiration).

The strongest chemical signal to change breathing is the level of carbon dioxide. A chemosensitive area near the respiratory centre is highly sensitive to CO₂ and hydrogen ions (H⁺): a rise in CO₂/H⁺ stimulates this area, which signals the respiratory centre to increase the rate and depth of breathing so that the excess CO₂ is removed. By contrast, oxygen plays only a minor role in the moment-to-moment regulation of breathing — an important NEET distinction. Receptors in the aorta and carotid arteries also feed information to the centre.

Several respiratory disorders are part of the syllabus. Asthma is difficulty in breathing, with wheezing, caused by inflammation and spasm of the bronchi and bronchioles, which narrows the airways. Emphysema is a chronic disorder in which the alveolar walls are damaged and broken down, drastically reducing the surface area for gas exchange; its major cause is cigarette smoking.

Finally, occupational respiratory disorders arise in workplaces with a lot of dust. Long exposure to fine particles causes inflammation and fibrosis (scarring) of the lung tissue — for example silicosis (from silica/grinding dust) and asbestosis (from asbestos). Protective measures and proper masks reduce the risk. For NEET, remember: rhythm centre in the medulla; CO₂/H⁺ are the chief stimuli (not O₂); asthma = bronchiolar inflammation; emphysema = alveolar damage from smoking; occupational disorders = dust-induced fibrosis.