Breathing and Exchange of Gases

🎯 Key Points

• Inspiration: diaphragm contracts and flattens, external intercostals raise the ribcage, thoracic volume↑, intra-pulmonary pressure↓ below atmospheric, air rushes IN; Expiration is largely the passive reverse
• Lung volumes: Tidal volume ~500mL (normal breath); Vital capacity ~4600mL (max in/out after max in); Total lung capacity ~6000mL (vital capacity + residual volume that never leaves the lungs)
• O₂-Hb dissociation curve is SIGMOID (S-shaped, not linear) due to cooperative binding; it shifts RIGHT (Hb releases O₂ more easily) with ↑CO₂, ↑H⁺, ↑temperature — exactly the conditions found in actively metabolising tissue, which is precisely where more O₂ release is needed (Bohr effect)
• CO₂ transport: ~70% as bicarbonate (via the chloride shift), ~20-23% bound to Hb (as carbaminohaemoglobin), only ~7% simply dissolved in plasma
• Breathing rate is normally controlled by CO₂/pH levels (via central chemoreceptors), NOT by O₂ levels directly — O₂-sensing chemoreceptors (carotid/aortic bodies) only become the dominant driver in severe hypoxia

Mechanism of Breathing

• Inspiration: diaphragm contracts and flattens, external intercostal muscles contract and raise the ribcage; thoracic volume increases, intra-pulmonary pressure falls below atmospheric pressure, and air rushes in
• Expiration: diaphragm and intercostal muscles relax, thoracic volume decreases, intra-pulmonary pressure rises above atmospheric pressure, and air is pushed out
• Quiet expiration is normally a passive process (no muscle contraction needed), but forceful expiration recruits abdominal muscles
• Respiratory centres: the medulla oblongata sets the basic rhythm, while the pons (pneumotaxic centre) fine-tunes and moderates the medulla's signals; chemoreceptors mainly detect rising CO₂ and falling pH to increase breathing rate

Lung Volumes and Capacities

• Tidal volume (~500 mL): air moved in a single normal breath
• Inspiratory/Expiratory reserve volume: extra air that CAN be forcibly inhaled/exhaled beyond a normal tidal breath
• Residual volume: air that always remains in the lungs even after the most forceful exhalation, preventing the lungs from ever fully collapsing
• Vital capacity (~4600 mL): the maximum air that can be exhaled after the deepest possible inhalation (tidal + both reserve volumes)
• Total lung capacity (~6000 mL): vital capacity + residual volume

Gas Transport and the Bohr Effect

• Oxygen transport: ~97% carried bound to haemoglobin (4 O₂ per Hb molecule, cooperative binding produces the sigmoid dissociation curve), only a small fraction dissolved directly in plasma
• Bohr effect: rising CO₂, falling pH, and rising temperature all shift the O₂-Hb dissociation curve to the RIGHT, meaning Hb releases O₂ more readily at any given O₂ partial pressure — this happens automatically in actively respiring tissue (which produces more CO₂/acid/heat), delivering more O₂ exactly where it's needed most
• Fetal haemoglobin (HbF) has a HIGHER O₂ affinity than adult haemoglobin (HbA) — this lets the fetus effectively "pull" oxygen across the placenta from the mother's blood, where O₂ partial pressure is already lower than in the air we breathe
• CO₂ transport: ~70% as bicarbonate ions (CO₂ + H₂O → H₂CO₃ → HCO₃⁻ + H⁺, catalysed by carbonic anhydrase inside RBCs; HCO₃⁻ then exits to plasma in exchange for Cl⁻, the "chloride shift"), ~20-23% bound to Hb as carbaminohaemoglobin, and only ~7% simply dissolved in plasma

Surfactant and Respiratory Disorders

• Surfactant (a phospholipid produced by alveolar cells) reduces surface tension inside alveoli, preventing them from collapsing at the end of each exhalation; premature infants who haven't yet developed sufficient surfactant suffer Respiratory Distress Syndrome
• Chronic disorders like asthma (bronchiole constriction) and emphysema (alveolar wall damage, reduced surface area) both reduce effective gas exchange, though through very different mechanisms
• Occupational respiratory disorders: long-term inhalation of dust or fine particles in certain workplaces damages the lungs — e.g. silicosis (silica/stone dust) and asbestosis (asbestos fibres), which cause inflammation and fibrosis of the upper airways; proper protective equipment is essential

Human Respiratory System

• Air passes through the external nostrils → nasal chamber → pharynx → larynx (the sound box, its opening guarded by the epiglottis) → trachea → two primary bronchi → bronchioles → terminal bronchioles → alveoli
• The trachea, bronchi and initial bronchioles form the conducting part — it transports, warms, moistens and filters the incoming air but performs no gas exchange
• The alveoli and their ducts form the respiratory (exchange) part — thin-walled, richly vascularised sacs where the actual exchange of gases occurs
• Each lung is enclosed by a double-layered pleura with pleural fluid in between that reduces friction; the lungs sit in the air-tight thoracic chamber bounded by the diaphragm below and the ribs and intercostal muscles around

Exchange of Gases: Partial Pressures and Diffusion

• Gases move by simple diffusion down their partial-pressure gradients; the direction and rate depend on the partial pressures (pO₂ and pCO₂), the solubility of the gas, and the thickness of the diffusion membrane
• At the alveoli, pO₂ is high (~104 mm Hg) and pCO₂ low (~40 mm Hg), while the deoxygenated blood arriving has low pO₂ (~40) and high pCO₂ (~45) — so O₂ diffuses INTO the blood and CO₂ diffuses OUT into the alveoli
• At the tissues the gradients reverse (tissue pO₂ ~40, pCO₂ ~45), so O₂ leaves the blood for the cells and CO₂ enters the blood
• The diffusion membrane is made of three thin layers — the alveolar squamous epithelium, the capillary endothelium, and the basement substance between them — so the total diffusion distance is very small
• CO₂ is about 20-25 times more soluble than O₂, so it diffuses far more readily across the membrane despite its smaller pressure gradient

Regulation of Respiration

• The respiratory rhythm centre in the medulla oblongata generates and maintains the basic rhythm of breathing
• The pneumotaxic centre in the pons can moderate the rhythm centre's activity, shortening the duration of inspiration and thereby altering the breathing rate
• A chemosensitive area adjacent to the rhythm centre is highly sensitive to CO₂ and H⁺; a rise in these signals the rhythm centre to increase breathing so the excess is expelled
• Peripheral receptors in the carotid and aortic bodies also detect changes in CO₂ and H⁺ and signal the rhythm centre to make the necessary adjustments; the role of oxygen in this moment-to-moment regulation is quite insignificant under normal conditions

🚀 NEET Advanced Edge

Why CO₂/pH, not O₂, is the primary trigger for breathing rate under normal conditions: Central chemoreceptors in the medulla are highly sensitive to even small rises in CO₂ (or the resulting fall in pH), making CO₂ the primary moment-to-moment regulator of breathing rate; peripheral chemoreceptors (carotid and aortic bodies) DO sense O₂ directly, but only kick in strongly once O₂ falls to quite low levels — explaining why hyperventilating (blowing off CO₂) can delay the urge to breathe even as O₂ stores are simultaneously being used up, a genuinely dangerous combination in breath-holding scenarios.

Why the sigmoid shape of the O₂-Hb dissociation curve matters physiologically: The steep middle portion of the curve means a relatively small drop in tissue O₂ partial pressure causes Hb to release a disproportionately large amount of O₂ — this cooperative-binding behaviour (each O₂ that binds makes the next one bind more easily, and vice versa for release) makes haemoglobin a far more efficient O₂ delivery system than a hypothetical non-cooperative carrier would be.

Worked reasoning: During intense exercise, a muscle's local CO₂ and temperature both rise, and its pH falls. Predict the net effect on O₂ delivery to that specific muscle. Answer: All three changes shift the local O₂-Hb dissociation curve to the right (Bohr effect), causing haemoglobin passing through that tissue to release MORE oxygen than it would under resting conditions — a built-in mechanism that automatically routes extra oxygen to exactly the tissue working hardest.