Respiratory Physiology

🟢 Lite — Quick Review (1h–1d)

Rapid summary for last-minute revision before your exam.

Respiratory Physiology — Key Facts for FMGE Core concept: Pulmonary ventilation brings air to alveoli where gas exchange occurs; diffusion gradients drive O₂ uptake and CO₂ removal High-yield point: Boyle’s law explains how negative intrapleural pressure (created by chest wall expansion) creates airflow into lungs; understand surfactant’s role in preventing atelectasis ⚡ Exam tip: Remember ventilation-perfusion matching - areas with low V/Q act like shunts, high V/Q act like dead space

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🟡 Standard — Regular Study (2d–2mo)

Standard content for students with a few days to months.

Respiratory Physiology — FMGE Study Guide

Lung Volumes and Capacities

Primary Lung Volumes

Tidal Volume (TV): Air inhaled/exhaled during normal breathing (500 mL) Inspiratory Reserve Volume (IRV): Max air that can be inhaled after normal inspiration (3000 mL) Expiratory Reserve Volume (ERV): Max air that can be exhaled after normal expiration (1200 mL) Residual Volume (RV): Air remaining in lungs after maximal expiration (1200 mL) - cannot be measured by spirometry

Lung Capacities (combinations of volumes)

Total Lung Capacity (TLC): Sum of all volumes (6000 mL) Vital Capacity (VC): TV + IRV + ERV (4500 mL) - maximum amount that can be exhaled after maximal inhalation Inspiratory Capacity (IC): TV + IRV (3500 mL) Functional Residual Capacity (FRC): ERV + RV (2400 mL) - air remaining after normal expiration

Spirometry

FVC (Forced Vital Capacity): Max volume exhaled with maximal force after maximal inspiration FEV1 (Forced Expiratory Volume in 1 second): Volume exhaled in first second of FVC FEV1/FVC ratio:

• Normal: >0.75-0.80
• Obstructive (asthma, COPD): <0.70 (air trapping, slow exhalation)
• Restrictive (fibrosis): Normal or even >0.80 (all volumes reduced proportionally)

Mechanics of Breathing

Inspiration

• Active process requiring muscle contraction
• Diaphragm: Primary muscle; descends ~1-2 cm during quiet breathing
• External intercostals: Elevate ribs, expand chest
• Accessory muscles: Scalenes, sternocleidomastoid (used in heavy breathing)
• Intrapleural pressure: Always negative (subatmospheric) - keeps lungs inflated
  • At rest: -5 cmH₂O (during quiet breathing)
  • Max inspiration: -30 cmH₂O
• Alveolar pressure: Falls below atmospheric during inspiration (-1 cmH₂O) → air flows in
• Transpulmonary pressure (alveolar - pleural) keeps lungs inflated

Expiration

• Quiet breathing: Passive; elastic recoil of lungs and chest wall
• Forced expiration: Active; internal intercostals, abdominal muscles compress lungs

Compliance

Compliance = ΔV / ΔP (change in volume per change in pressure)

• Normal: 200 mL/cmH₂O
• Decreased (stiff lungs): Pulmonary fibrosis, ARDS, pneumonia - hard to inflate
• Increased (floppy lungs): Emphysema - too easy to inflate but hard to exhale
• Hysteresis: Different inflation vs deflation curves (due to surfactant)

Surfactant

• Secreted by Type II pneumocytes (alveolar cells)
• Composition: Dipalmitoylphosphatidylcholine (DPPC), other lipids, proteins
• Function: Reduces surface tension (water molecules at air-liquid interface attract each other); prevents alveolar collapse
• Effect of surfactant: ↓surface tension proportional to area (smaller alveoli = less surfactant = higher surface tension = equalizes pressure between small and large alveoli)
• Surfactant deficiency: Hyaline membrane disease/respiratory distress syndrome (RDS) in premature infants; treated with exogenous surfactant

Airway Resistance

• Location: 50% in upper airway, 40% in medium-sized bronchi, 10% in terminal airways
• Bronchoconstriction increases resistance (asthma, COPD)
• Bronchodilation decreases resistance (sympathetic, drugs)

Work of Breathing

• Elastic work: Overcome lung compliance (60% of work in quiet breathing)
• Flow-resistive work: Overcome airway resistance (40%)
• Increases with: Obesity, pulmonary fibrosis, asthma, COPD

Gas Exchange

Diffusion

• Fick’s law of diffusion: Rate ∝ (A × D × (P1-P2)) / (T × √MW)
• A = surface area; D = diffusion coefficient; P1-P2 = pressure gradient; T = thickness
• Thickness: 0.5 μm for gas exchange (O₂, CO₂)
• Diffusion-limited: Some diseases (fibrosis) slow gas transfer
• Perfusion-limited: Normal lung - blood moves through capillary too fast for full equilibration (but adequate)

Alveolar Gas Equation

PAO₂ = PIO₂ - (PaCO₂ / R)

• PIO₂ = FiO₂ × (Patm - PH₂O) = 0.21 × (760 - 47) ≈ 150 mmHg at sea level
• R (respiratory quotient) = CO₂ produced / O₂ consumed = 0.8
• Normal PAO₂: ~100 mmHg
• A-a gradient: PAO₂ - PaO₂; normal = 5-15 mmHg (increases with age)
• Increased A-a gradient: V/Q mismatch, diffusion impairment, shunt (always pathological)

Ventilation-Perfusion Matching

V/Q = ventilation / perfusion

• V/Q = 0: Perfusion without ventilation → shunt (blood leaves without gas exchange)
• V/Q = ∞: Ventilation without perfusion → dead space
• V/Q = 0.8: Normal (approximately matched)

Regions:

• West zone 1 (top of lung): V/Q > 1 (alveolar pressure > arterial pressure → capillary compression → poor perfusion) - rare in normal standing person
• West zone 2 (mid lung): Greatest blood flow - arterial pressure > alveolar pressure > venous pressure (turbulent flow)
• West zone 3 (bottom of lung): V/Q < 1 (highest perfusion; lowest ventilation due to压迫effect on alveoli)

Shunt

• Anatomic shunt: Blood bypasses alveoli (Thebesian veins, bronchial veins)
• Physiologic shunt: V/Q = 0 (perfused but not ventilated)
• Right-to-left shunt: Congenital heart defects with R→L flow, ARDS, pneumonia
• Effect: Hypoxemia that doesn’t respond well to O₂ (shunt blood mixes with oxygenated blood)

Oxygen Transport

Forms

• Dissolved in plasma: 1.5% (minimal, PaO₂ determines this)
• Bound to hemoglobin (Hb): 98.5% (carries most O₂)

Hemoglobin

• Structure: 4 polypeptide chains (2α, 2β); each binds 1 O₂ molecule
• O₂ carrying capacity: 1.34 mL O₂/g Hb × Hb (g/dL) × 100
• Normal Hb: 15 g/dL → O₂ content = ~20 mL O₂/dL blood
• Saturation: % of Hb binding sites occupied by O₂

Oxygen-Hemoglobin Dissociation Curve

• Sigmoidal shape (cooperativity - heme molecules facilitate each other’s O₂ binding)
• P50: O₂ partial pressure at which Hb is 50% saturated; normal = 26.6 mmHg
• Right shift (↓affinity = ↑P50): ↑Temperature, ↑[H⁺], ↑2,3-DPG, ↑CO₂ (Bohr effect) - tissues get more O₂
• Left shift (↑affinity = ↓P50): ↓Temperature, ↓[H⁺], ↓2,3-DPG, ↓CO₂, fetal Hb (HbF has γ chains instead of β) - seen in fetal blood, hypothermia, alkalosis

CO₂ Transport

• Dissolved: 5%
• As bicarbonate: 70% (CO₂ + H₂O ↔ H₂CO₃ ↔ H⁺ + HCO₃⁻; enzyme = carbonic anhydrase)
• As carbaminohemoglobin: 25% (CO₂ binds to Hb amino groups)

Control of Breathing

Respiratory Center

• Medulla: Inspiratory/expiratory neurons (controls automatic breathing)
• Pons: Pneumotaxic and apneustic centers (adjust rhythm)
• Dorsal respiratory group (DRG): Inspiratory; receives input from peripheral chemoreceptors and mechanoreceptors
• Ventral respiratory group (VRG): Both inspiratory and expiratory; activated during increased demand

Chemical Control

• Central chemoreceptors (medulla): Sensitive to pH in CSF (reflects PaCO₂); ↑CO₂ → ↑H⁺ in CSF → ↑ventilation
• Peripheral chemoreceptors (carotid and aortic bodies): Respond to ↓PaO₂ (<60), ↑H⁺, ↑PaCO₂
• Primary drive: PaCO₂ (not PaO₂!) - even small changes in PaCO₂ cause large ventilatory changes

Other Inputs

• Stretch receptors: Hering-Breuer reflex (inhibit inspiration when lungs over-expanded)
• J receptors: Respond to pulmonary congestion; cause shallow breathing
• Joint and muscle receptors: Increased ventilation during exercise
• Temperature: ↑temp → ↑ventilation

Respiratory Adaptations to Altitude

• Acute: Hyperventilation (↓PaCO₂), ↑HR, ↑CO
• Subacute: ↑2,3-DPG (shifts O₂-Hb curve right → ↑O₂ unloading)
• Chronic: Polycythemia (↑RBC mass), ↑ventilation, ↑capillary density

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