Memory tricks for breathing, gas exchange, and O₂ transport

Breathing follows Boyle's Law: pressure and volume are inversely proportional (at constant temperature). Inspiration (active): diaphragm contracts (flattens) + external intercostals contract → thoracic volume increases → intrapulmonary pressure drops below atmospheric (~758 mmHg) → air flows in. Forced inspiration adds scalene and sternocleidomastoid muscles. Expiration (passive at rest): diaphragm and intercostals relax → thoracic volume decreases → intrapulmonary pressure rises above atmospheric → air flows out. Forced expiration: internal intercostals + abdominal muscles contract. Intrapleural pressure: always slightly negative (−4 to −8 mmHg) — keeps lungs expanded against thoracic wall. Pneumothorax: air enters pleural space → lungs collapse.

Conducting zone: nose → nasal cavity → pharynx → larynx → trachea → primary bronchi → secondary (lobar) bronchi → tertiary (segmental) bronchi → bronchioles → terminal bronchioles. Functions: warm, humidify, filter air. No gas exchange. Respiratory zone: respiratory bronchioles → alveolar ducts → alveolar sacs → alveoli. Gas exchange occurs here. ~300 million alveoli in adult lungs — massive surface area (~70 m²). Alveolar walls: Type I pneumocytes (thin, gas exchange), Type II pneumocytes (produce surfactant). Surfactant: reduces surface tension — prevents alveolar collapse on expiration. Respiratory distress syndrome in premature infants = surfactant deficiency.

Tidal volume (TV): ~500 mL — air moved in one normal breath. Inspiratory reserve volume (IRV): ~3000 mL — extra air inhaled beyond TV with max effort. Expiratory reserve volume (ERV): ~1200 mL — extra air exhaled beyond TV with max effort. Residual volume (RV): ~1200 mL — air left after max exhalation — cannot be expelled. Capacities (sum of volumes): Vital capacity (VC) = TV + IRV + ERV = ~4700 mL — maximum usable range. Total lung capacity (TLC) = VC + RV = ~5900 mL. Functional residual capacity (FRC) = ERV + RV. Inspiratory capacity = TV + IRV. RV cannot be measured by spirometry — requires body plethysmography or helium dilution.

Gas exchange follows Dalton's Law (partial pressures) and Fick's Law (diffusion rate). Atmospheric air: PO₂ = 159 mmHg, PCO₂ = 0.3 mmHg. Alveolar air: PO₂ = 104 mmHg, PCO₂ = 40 mmHg. Pulmonary capillary blood arriving: PO₂ = 40 mmHg, PCO₂ = 45 mmHg. Result: O₂ diffuses from alveoli (104) into blood (40). CO₂ diffuses from blood (45) into alveoli (40). Blood leaving lungs: PO₂ = 100 mmHg, PCO₂ = 40 mmHg. Tissue gas exchange (opposite): tissues have low PO₂ (~40) and high PCO₂ (~45) → O₂ leaves blood → CO₂ enters blood. Fick's law: rate ∝ surface area × concentration difference ÷ membrane thickness.

Oxygen transport: 98.5% bound to hemoglobin (oxyhemoglobin), 1.5% dissolved in plasma. Each Hb molecule has 4 heme groups → binds 4 O₂. Cooperative binding: first O₂ makes subsequent binding easier → sigmoid (S-shaped) dissociation curve. Oxygen saturation (SpO₂): measured by pulse oximeter. Normal >95%. Right shift (decreased O₂ affinity — releases O₂ more readily at tissues): ↑ temperature, ↑ CO₂, ↑ H+ (↓ pH), ↑ 2,3-DPG (Bohr effect). Exercise shifts right → more O₂ delivered to muscles. Left shift (increased O₂ affinity — holds O₂ more tightly): ↓ temperature, ↓ CO₂, ↓ H+, fetal Hb (HbF). CO poisoning: CO binds Hb 200× tighter than O₂ → shifts curve left → tissues can't get O₂.

CO₂ is transported three ways: 70% as bicarbonate (HCO₃⁻): CO₂ enters RBC → carbonic anhydrase (CA) converts CO₂ + H₂O → H₂CO₃ → H⁺ + HCO₃⁻. H⁺ buffered by Hb. HCO₃⁻ exits RBC → Cl⁻ enters (chloride shift = Hamburger phenomenon — maintains electroneutrality). 23% as carbaminohemoglobin: CO₂ binds to amino groups of Hb (not heme). 7% dissolved in plasma. At lungs: process reverses — bicarbonate re-enters RBC → CA converts back to CO₂ → exhaled. H⁺ released → picked up by Hb → Bohr effect promotes O₂ release at tissues. Haldane effect: oxygenation of Hb reduces its CO₂-carrying capacity — promotes CO₂ unloading at lungs.

Respiratory centers in medulla oblongata: dorsal respiratory group (DRG) — rhythmic inspiration, ventral respiratory group (VRG) — forced breathing. Pontine centers: pneumotaxic (limits inspiration duration) and apneustic centers. Chemoreceptors control breathing: Central chemoreceptors (medulla): respond to H⁺ in CSF — CO₂ crosses BBB → reacts with water → H⁺ → stimulates breathing. Most powerful drive for breathing. Peripheral chemoreceptors (carotid and aortic bodies): respond to ↓ PO₂ (<60 mmHg), ↑ PCO₂, ↑ H⁺. O₂ drive only kicks in when PO₂ drops severely. COPD hypoxic drive: some COPD patients rely on low O₂ as breathing stimulus — giving high-flow O₂ can suppress breathing.

CO₂ + H₂O ↔ H₂CO₃ ↔ H⁺ + HCO₃⁻. CO₂ is the respiratory acid — lungs control it. HCO₃⁻ is the metabolic base — kidneys control it. Respiratory acidosis: ↑ CO₂ (hypoventilation, COPD, pneumonia) → ↓ pH. Kidneys compensate: retain HCO₃⁻. Respiratory alkalosis: ↓ CO₂ (hyperventilation, anxiety, altitude) → ↑ pH. Kidneys compensate: excrete HCO₃⁻. Metabolic acidosis: ↓ HCO₃⁻ (diabetic ketoacidosis, renal failure) → ↓ pH. Lungs compensate: hyperventilate (Kussmaul breathing) → blow off CO₂. Metabolic alkalosis: ↑ HCO₃⁻ (vomiting, antacid overuse) → ↑ pH. Lungs compensate: hypoventilate → retain CO₂.

Obstructive lung diseases: airflow OUT is obstructed — airways narrow. FEV1 markedly reduced, FVC relatively preserved → FEV1/FVC ratio less than 70%. TLC increased (air trapping). Examples: asthma (reversible bronchospasm — treat with bronchodilators), COPD/emphysema (irreversible — alveolar destruction, loss of elastic recoil), chronic bronchitis (hypersecretion, Blue Bloater), cystic fibrosis. Restrictive lung diseases: lungs cannot fully expand — small volumes. FVC and TLC reduced, but FEV1/FVC ratio normal or increased. Examples: pulmonary fibrosis (stiff lungs), sarcoidosis, obesity, neuromuscular disease (can't generate force), pleural effusion, pneumothorax. Pink Puffer (emphysema) vs Blue Bloater (chronic bronchitis) distinction.