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Crucial MedPrep

From Traditional Study To Digital Mastery – Respiratory Revision

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Study Notes

Comprehensive revision notes covering every topic from all four past papers – expanded with Guyton & Ganong knowledge.

📚 20+ topics · 400 questions covered
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Paper 1

20 topics · 100 questions

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Paper 2

20 topics · 100 questions

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Paper 3

20 topics · 100 questions

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Paper 4

20 topics · 100 questions

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Word Search Puzzle

Find 10 respiratory terms, then test your knowledge with a quiz.

🧠 10 terms · 120 questions

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📚 Study Notes

📚 Respiratory Physiology – Complete Revision Notes

Guyton & Ganong‑oriented – covers every topic from Papers 1–4.

1. Overview & General Principles

Main Function: To extract O₂ from the atmosphere, deliver it to tissues, and remove CO₂ from the body.

  • External Respiration: Absorption of O₂ and removal of CO₂ from the body as a whole.
  • Internal Respiration: Utilisation of O₂ and production of CO₂ by cells, and gas exchange between cells and their fluid medium.

Weibel's Lung Model (Tracheobronchial Tree)

Introduced by E.R. Weibel (1963). The air passage divides 23 times from the trachea (generation 0) to the alveolar sacs (generation 23).

  • Conducting Zone (Generations 0–16): No alveoli present. No gas exchange occurs. This area forms the anatomical dead space. The 16th generation are the terminal bronchioles.
  • Respiratory Zone (Generations 17–23): Alveoli begin to appear. Gas exchange takes place here; these are the respiratory bronchioles.
  • Advantage: The multiple divisions dramatically increase the total cross‑sectional area (from 2.5 cm² to ~11,800 cm²), greatly reducing airflow velocity and allowing better gaseous exchange.

The Respiratory Membrane

Separates alveolar air from pulmonary capillary blood. It consists of six layers:

  1. Surfactant layer lining the alveolus.
  2. Alveolar epithelium.
  3. Basal lamina of alveolar epithelium.
  4. Thin interstitial space.
  5. Basal membrane of capillary endothelium.
  6. Capillary endothelial membrane.

Despite these layers, the total thickness is only 0.2–0.6 μm (average). The total surface area is about 70 m² in an adult male, with roughly 300 million alveoli.

Factors Affecting Gas Diffusion (Fick's Law)

Vgas = (A × D × ΔP) / T

  • T (Thickness): Increases in pulmonary oedema and fibrosis → reduces diffusion.
  • A (Surface Area): Decreases in pneumonectomy and emphysema → reduces diffusion.
  • D (Diffusion Coefficient): ∝ Solubility / √(Molecular Weight).
  • ΔP (Partial Pressure Gradient): The driving force for gas exchange.

Airway Resistance

Normal value: 1.5 – 2 cm H₂O/L/sec.

  • Formula: R = (Patm – Palv) / Airflow.
  • Poiseuille-Hagen: R = 8ηL / πr⁴ → R ∝ 1/r⁴ (if radius halves, resistance increases 16‑fold).
  • Cross‑sectional area: Inversely related. High in conducting zone, low in respiratory zone.
  • Flow type: Turbulent flow (rapid breathing) has higher resistance than laminar (quiet breathing).

Incentive Spirometer

  • Purpose: Therapeutic tool to encourage sustained maximal inspiration. Used post‑operatively to prevent atelectasis.
  • Does NOT measure vital capacity – that requires diagnostic spirometry.
  • Cannot distinguish obstructive vs restrictive – requires formal FEV₁/FVC testing.

N₂ Washout Curve (Fowler's Method)

  • Phase I: Dead space washout (pure O₂, 0% N₂).
  • Phase II: Transition zone – mixing of dead space and alveolar gas.
  • Phase III: Pure alveolar gas plateau.
  • Phase IV: Closing volume – due to airway closure at the base.
  • Anatomical dead space is estimated using the equal‑area vertical line across Phase II.

2. Non‑Respiratory Functions of the Lungs

Defence Mechanisms

  • Humidification & temperature control: Inspired air is warmed and moistened to body temperature by the time it reaches the alveoli.
  • Immunological: Bronchial secretions contain secretory IgA. Pulmonary alveolar macrophages (PAMs) are highly phagocytic.
  • Particle filtration:
    • >10 μm: Trapped by nasal hairs and mucus.
    • 2–10 μm: Settle in bronchi → removed by reflex bronchoconstriction, coughing, and ciliary escalator.
    • <2 μm: Reach alveoli → ingested by macrophages.
  • Protease‑activated receptors (PARs): Trigger release of PGE₂ to protect epithelial cells.

Pulmonary Circulation Functions

  • Blood reservoir: Stores ~500 mL of blood for the left ventricle.
  • Filter: Traps fibrin clots, fat cells, cancer cells, and agglutinated RBCs.
  • Fluid exchange & drug absorption: Low hydrostatic pressure keeps alveoli dry. Anaesthetic gases and aerosols diffuse rapidly into the systemic circulation.

Metabolic & Endocrine Functions

  • Surfactant: Manufactured by Type II pneumocytes for local use.
  • Prostaglandins: Synthesised and released (e.g., PGE₂, PGF₂α).
  • Fibrinolytic system: Lyses clots in pulmonary vessels.
  • Angiotensin conversion: ACE converts Angiotensin I → Angiotensin II (a potent vasopressor). Also inactivates bradykinin.
  • Removal of vasoactive substances: Removes serotonin and norepinephrine; epinephrine, dopamine, and oxytocin pass through unchanged.
📌 Clinical Pearls:
  • Kartagener's Syndrome: Immotile cilia (congenital absence of axonemal dynein) → recurrent infections, infertility.
  • Alveolar Cells: Type I (flat, structural) and Type II (granular, produce surfactant).

3. Mechanism of Breathing (Ventilation)

Eupnea: Rhythmic breathing at rest, consisting of inspiration and expiration.

Inspiration (Active Process)

  • Diaphragm: Accounts for 75% of the change in intrathoracic volume. It descends, increasing vertical diameter.
  • External Intercostals: Elevate ribs.
  • Rib Movements:
    • Pump Handle: 2nd–6th ribs move upward and forward → increases anteroposterior (AP) diameter.
    • Bucket Handle: 7th–10th ribs swing outward → increases transverse diameter.
  • Accessory Muscles: Scalene and sternocleidomastoid (active during deep or forced inspiration).
  • Intrinsic Laryngeal: Posterior cricoarytenoid abducts vocal cords to open the glottis.

Expiration

  • Quiet breathing: Passive process (elastic recoil of lungs and thoracic cage).
  • Forced expiration: Active contraction of abdominal muscles (rectus abdominis, transversus abdominis, obliques) and internal intercostals. Accessory muscles include adductors of the vocal cords.

Work of Breathing

  • ~65% of the work is to overcome elastic resistance (compliance work).
  • ~35% is to overcome non‑elastic resistance (airway resistance and tissue viscosity).
  • The diaphragm performs the majority (~75%) of the inspiratory work during quiet breathing.

Intrapulmonary (Alveolar) Pressure

  • At end‑inspiration/end‑expiration (no airflow): Equals atmospheric pressure (0 cmH₂O relative).
  • During inspiration: Drops to approximately −3 cmH₂O.
  • During expiration: Rises to approximately +3 cmH₂O.
  • Valsalva Maneuver: Forced expiration against a closed glottis → pressure can reach +100 cmH₂O.
  • Müller's Maneuver: Forced inspiration against a closed glottis → pressure can drop to −80 cmH₂O.

Intrapleural (Intrathoracic) Pressure

  • Always subatmospheric (negative).
  • Non‑uniform due to gravity: −2 cmH₂O at the base, −7 cmH₂O at the apex.
  • Deep inspiration can decrease it to as low as −30 mm Hg.

Transpulmonary Pressure

Defined as the difference between alveolar pressure (Palv) and pleural pressure (Ppl). It represents the recoil pressure – the elastic forces in the lungs that tend to collapse them at each instant.

  • Clinical Significance:
    • Pneumothorax: Injury to the thorax allows air into the pleural space, equalising Ppl with atmospheric pressure. Transpulmonary pressure drops to zero, causing lung collapse.
    • Emphysema: Loss of lung elasticity increases intrapleural pressure, leading to a barrel‑shaped chest.
    • Because transmural pressure is lower at the bases, those lung regions are normally less expanded than the apices.

4. Spirometry & Lung Volumes

Spirometry records the volume movement of air into and out of the lungs. A classic spirometer consists of an inverted drum over a water chamber, counterbalanced by a weight. As the subject breathes, the drum rises and falls, tracing a spirogram.

What Spirometry CAN Measure

  • Tidal Volume (TV) – air breathed in/out during normal quiet respiration.
  • Inspiratory Reserve Volume (IRV) – maximal air inspired after a normal tidal inspiration.
  • Expiratory Reserve Volume (ERV) – maximal air expired by active effort after a normal tidal expiration.
  • Inspiratory Capacity (IC) – TV + IRV.
  • Expiratory Capacity (EC) – TV + ERV.
  • Vital Capacity (VC) – TV + IRV + ERV (the largest volume that can be forcefully expired after a maximal inspiration).
  • Forced Vital Capacity (FVC) – maximal volume exhaled as forcefully and rapidly as possible.
  • FEV₁, FEV₂, FEV₃ – volumes expired in the 1st, 2nd, and 3rd seconds of a forced expiration.
  • Minute Ventilation (RMV) – TV × respiratory rate.
  • Maximal Voluntary Ventilation (MVV) – with voluntary effort (maximal breathing over 12–15 seconds).

What Spirometry CANNOT Measure

Spirometry cannot measure any volume that remains in the lungs after a maximal expiration.

  • Residual Volume (RV) – the air left in the lungs after maximal expiration.
  • Functional Residual Capacity (FRC) – ERV + RV (volume at the end of a normal expiration).
  • Total Lung Capacity (TLC) – VC + RV (volume after maximal inspiration).

Why? These volumes contain air that cannot be exhaled. They require gas dilution techniques (helium dilution) or body plethysmography to measure.

Static Lung Volumes (Time‑Independent) – Measurable by Spirometry

  • TV: 500 ml.
  • IRV: 3.3 L (men), 1.9 L (women).
  • ERV: 1.0 L (men), 0.7 L (women).
  • RV: NOT measurable by spirometry (requires plethysmography).

Lung Capacities

  • IC = TV + IRV (measurable).
  • EC = TV + ERV (measurable).
  • VC = TV + IRV + ERV (measurable).
  • FRC = ERV + RV (NOT measurable by spirometry alone).
  • TLC = VC + RV (NOT measurable by spirometry alone).

Dynamic Lung Volumes – Forced Vital Capacity (FVC)

  • FEV₁: 80% of FVC (normal).
  • FEV₂: 95% of FVC.
  • FEV₃: 98–100% of FVC.
  • Clinical Differentiation:
    • Restrictive: VC ↓, FEV₁ normal or ↓ proportionally (FEV₁/FVC normal or ↑).
    • Obstructive: VC normal, FEV₁ ↓↓ (FEV₁/FVC < 70%).

5. Surfactant

Surfactant is a lipid‑protein complex that lines the alveoli and lowers surface tension.

Composition

Component% Composition
Dipalmitoylphosphatidylcholine (DPPC)62%
Phosphatidylglycerol5%
Other phospholipids10%
Neutral lipids13%
Proteins (SP‑A, SP‑B, SP‑C, SP‑D)8%
Carbohydrates2%

Synthesis

Produced by Type II alveolar epithelial cells. Lamellar bodies containing phospholipids are secreted into the alveolar lumen by exocytosis, forming tubular myelin. The lipids are then converted into the surfactant film. Surfactant is recycled by alveolar macrophages and re‑uptaken by Type II cells. SP‑B and SP‑C enhance the formation of the phospholipid film.

  • Hormonal influences: Thyroid hormone and glucocorticoids ↑ production; Insulin ↓ synthesis; Smoking reduces surfactant.

Functions (Laplace's Law & Stability)

Laplace's Law: P = 2T / r (P = distending pressure, T = surface tension, r = radius).

  • Reduces surface tension: Surfactant molecules become concentrated during expiration (as radius decreases), preventing alveolar collapse. Surface tension with surfactant is 7‑14 times lower than without.
  • Stabilises alveoli: Prevents air from moving from smaller (higher pressure) to larger (lower pressure) alveoli, maintaining uniform size.
  • Prevents pulmonary oedema: Low surface tension keeps alveoli dry and facilitates gas exchange.

Clinical Significance: Infant Respiratory Distress Syndrome (IRDS)

IRDS (Hyaline Membrane Disease) occurs in premature infants (especially those born before 28 weeks, or to diabetic mothers due to hyperinsulinemia). Surfactant normally appears by 28 weeks and matures around 36 weeks.

  • Pathophysiology: Surfactant deficiency → high surface tension → alveolar collapse (atelectasis) and pulmonary oedema.
  • Contributing factors: Low levels of thyroid/glucocorticoids, immaturity of epithelial Na⁺ channels (ENaCs) causing fluid retention.
  • Patchy atelectasis is also seen after cardiac surgery where pulmonary circulation is interrupted (bypass pump).

6. Compliance

Compliance (C) is the change in lung volume per unit change in pressure: C = ΔV / ΔP (expressed as L/cm H₂O). It measures the "stretchability" of the lungs and chest wall.

Lung Compliance (alone)

Expansion per unit increase in transpulmonary pressure. Normal: 0.2 L/cm H₂O.

  • Influenced by elastic forces (elastin/collagen – ~1/3) and surface tension of alveolar fluid (~2/3).
  • Compliance is slightly higher during expiration than inspiration (hysteresis).

Compliance of the Total Pulmonary System (Lungs + Thorax)

Measured in a paralysed/relaxed individual. It requires nearly twice the pressure to inflate the lungs inside the chest compared to outside. Normal: 0.11 L/cm H₂O.

Factors Affecting Compliance

  • Emphysema: Loss of elastic fibres → increased compliance (curve shifts up and left).
  • Fibrosis / Congestion: Stiffening/scarring → decreased compliance (curve shifts down and right).
  • Other factors: lumen size, blood supply, interdependence, chest wall deformities.

Specific Compliance

Compliance divided by the lung volume at which it is measured (usually FRC). Specific Compliance = Compliance / FRC. This standardises measurements for different lung sizes (e.g., comparing a child with one lung to an adult). It remains relatively constant despite changes in lung volume.

7. Dead Space

Dead space is the volume of air in the respiratory passages that does not participate in gas exchange.

  • Anatomical Dead Space: Volume of the conducting zone (nose to terminal bronchioles). Normal: 150 ml (approximately equal to body weight in pounds).
  • Physiological Dead Space: Anatomical dead space + alveolar dead space (alveoli that are ventilated but not perfused). In healthy individuals, physiological dead space is essentially equal to anatomical dead space because alveolar dead space is negligible.
  • Significance: Only (TV − VD) × Respiratory Rate equals alveolar ventilation – the air that actually reaches the respiratory membrane.

8. Dead Space – Variations & Clinical Significance

In healthy subjects, anatomical and physiological dead spaces are essentially the same. They differ only when ventilation and perfusion are not in equilibrium.

Physiological Variations

  • Sex: Dead space is greater in males (larger airways).
  • Age: Increases with age as lungs become more compliant and airways are pulled open, increasing diameter.
  • Body height: Directly proportional – taller individuals have larger dead space volumes.

Pathological Variations

  • Emphysema: Loss of elastic recoil leads to hyperinflation of the lungs, which increases dead space.
  • Bronchiectasis: Dilated bronchi increase the volume of the conducting airways, raising dead space.

9. Alveolar Ventilation

V̇A = (Tidal Volume – Dead Space) × Respiratory Rate

Normal: (500 ml – 150 ml) × 12 breaths/min = 4.2 L/min

  • Tachypnoea (rapid, shallow breathing): Alveolar ventilation decreases despite normal minute ventilation.
  • Slow, deep breathing: Both alveolar and total ventilation are optimal.

10. Ventilation‑Perfusion (V/Q) Ratio

V/Q = Alveolar Ventilation / Pulmonary Blood Flow = 4.2 / 5.5 = 0.8

  • Physiological (Gravity): V/Q is higher at the apices (~3.0) than at the bases (~0.6).
  • Pathological: Uneven ventilation (asthma, pneumothorax) or uneven perfusion (embolism) alters V/Q.
  • Clinical Insight: High apical V/Q favours TB growth due to high alveolar pO₂.

Physiological Shunt

  • Low V/Q areas (base) cause incomplete oxygenation – "shunted" blood.
  • Normal shunts: bronchial veins and coronary blood flow.
  • Net effect: arterial pO₂ is ~2 mm Hg lower than alveolar pO₂.

11. Oxygen Transport

  • Dissolved: 0.3 ml O₂ / 100 ml blood per 100 mm Hg pO₂.
  • Bound to Hb: 1 g Hb binds 1.34 ml O₂. With 15 g% Hb, O₂ capacity = 20.1 ml%. Normal saturation = 97.5%.
  • Utilisation coefficient: ~25% at rest, up to 80% during exercise.

O₂‑Hb Dissociation Curve

  • Sigmoid shape due to haem‑haem interaction (T → R configuration).
  • Right shift (↓affinity): ↑CO₂, ↓pH, ↑temperature, ↑2,3‑BPG. (Bohr effect – promotes unloading).
  • Left shift (↑affinity): ↓CO₂, ↑pH, ↓temperature, HbF, CO.
  • P50 = 26.8 mm Hg (normal); higher P50 = lower affinity.

12. Carbon Dioxide Transport

FormArterialVenous%
Dissolved2.4 ml%2.7 ml%~7%
Carbamino3.0 ml%3.7 ml%~23%
Bicarbonate42.6 ml%45.6 ml%~70%
  • Chloride Shift: HCO₃⁻ exits RBCs, Cl⁻ enters (Band 3 protein). Venous haematocrit is ~3% higher.
  • Haldane Effect: O₂ loading in lungs reduces Hb affinity for CO₂, doubling CO₂ release.

13. Regulation of Respiration – Overview

Respiration is regulated mainly by:

  • Neural control (voluntary and involuntary)
  • Chemical control (central and peripheral chemoreceptors)
📌 Exam Pearl: Neural and chemical mechanisms are the major regulators of respiration.

14. Neural Control of Respiration

A. Voluntary Control

  • Location: Cerebral cortex
  • Pathway: Corticospinal tract → motor neurons → respiratory muscles
  • Functions: Breath holding, speaking, singing, blowing, voluntary hyperventilation

B. Involuntary (Automatic) Control

  • Location: Brainstem – pons and medulla oblongata
  • Maintains breathing automatically during sleep, unconsciousness, and normal quiet breathing.

15. Respiratory Centers – Detailed Deep Dive

A. Pre-Bötzinger Complex

  • Location: Ventrolateral medulla, near the nucleus ambiguus
  • Function: Respiratory pacemaker – generates the basic respiratory rhythm

B. Dorsal Respiratory Group (DRG)

  • Location: Medulla (nucleus tractus solitarius)
  • Function: Controls inspiration during quiet breathing
  • Contains mainly inspiratory (I) neurons; receives input from CN IX and X

C. Ventral Respiratory Group (VRG)

  • Location: Medulla (nucleus ambiguus and retroambiguus)
  • Function: Contains both inspiratory and expiratory neurons; active during forced breathing

D. Pneumotaxic Center (Pontine Respiratory Group)

  • Location: Upper pons (nucleus parabrachialis and Kölliker‑Fuse nuclei)
  • Function: Limits / inhibits inspiration; shortens inspiratory time, increases rate
  • Lesion: Loss of inhibition causes apneusis (prolonged inspiration)

E. Apneustic Center

  • Location: Lower pons
  • Function: Stimulates / prolongs inspiration (excitatory)
  • Normally balanced by the pneumotaxic center and vagal stretch receptor input

F. Ondine's Curse (Congenital Central Hypoventilation Syndrome)

  • Feature: Loss of automatic respiratory control
  • Patient breathes voluntarily while awake but stops breathing during sleep
  • Requires mechanical ventilation during sleep

16. Chemical Control of Respiration

A. Central Chemoreceptors

  • Location: Ventral surface of the medulla
  • Stimulated by: ↑ arterial PCO₂ (via CSF H⁺), CSF acidosis
  • NOT stimulated by: Hypoxia, serum metabolic acidosis (H⁺ cannot cross BBB)
  • Contribution: ~60% of the ventilatory response to hypercapnia

B. Peripheral Chemoreceptors

  • Location: Carotid bodies (bifurcation of common carotid) and Aortic bodies (near aortic arch)
  • Memory aid: Bodies = chemoreceptors; Sinuses = baroreceptors
  • Stimulated by: Hypoxia (↓PaO₂ < 60 mmHg), Hypercapnia (↑PaCO₂), Metabolic acidosis (↓pH)
  • Also stimulated by: Nicotine, lobeline, K⁺
  • Contribution: ~35–40% of the ventilatory response to hypercapnia

Blood Supply of Carotid Bodies

Among the most highly vascularised tissues. Blood flow: ≈ 2000 mL/100 g tissue/min.

Glomus Cells

  • Type I (Chief Cells): Sensory cells; detect hypoxia; contain O₂‑sensitive K⁺ channels; release dopamine
  • Type II Cells: Supporting (sustentacular) / glial‑like cells

Mechanism of Hypoxia Detection

Normoxia: O₂‑sensitive K⁺ channels open → K⁺ leaves → cell polarised.

Hypoxia:

  1. O₂‑sensitive K⁺ channels close
  2. K⁺ accumulates → depolarisation
  3. L‑type Ca²⁺ channels open → Ca²⁺ enters
  4. Dopamine is released
  5. Afferent nerves (CN IX and X) stimulated
  6. Respiratory centre increases ventilation

Carotid Bodies vs Aortic Bodies

  • Carotid Bodies: More sensitive; increase both rate and depth
  • Aortic Bodies: Less sensitive; mainly increase rate

Conditions That Do NOT Stimulate Peripheral Chemoreceptors

  • Anaemia: PaO₂ is normal (only O₂ content is reduced)
  • Carbon Monoxide Poisoning: PaO₂ remains normal (only O₂ carriage by Hb is impaired)

Peripheral chemoreceptors respond to PaO₂ (dissolved O₂), not O₂ content.

High‑Yield Comparison Table: Central vs Peripheral Chemoreceptors

FeatureCentral ChemoreceptorsPeripheral Chemoreceptors
LocationVentral medullaCarotid & aortic bodies
Respond to hypoxia❌ No✅ Yes (PaO₂ < 60)
Respond to serum acidosis❌ No✅ Yes
Respond to increased CO₂✅ Yes (via CSF H⁺)✅ Yes
Respond to CSF acidosis✅ Yes❌ No
Hypercapnic response~60%35–40%

17. Clinical Correlates – Lesions & Reflexes

Lesions at Different Levels

  • Lesion A (Cortex): Voluntary control lost; automatic breathing preserved.
  • Lesion B (Upper pons): Loss of pneumotaxic inhibition → apneusis.
  • Lesion C (Between pons and medulla): Irregular, poorly coordinated breathing.
  • Lesion D (Below medulla): Respiratory arrest → death unless ventilated.

Cough Reflex

  1. Deep inspiration
  2. Glottis closes
  3. Expiratory muscles contract forcefully → intrathoracic pressure rises
  4. Glottis suddenly opens → air expelled explosively

Purpose: Removes mucus, foreign bodies, and secretions.

Sneezing

  • Stimulus from nasal mucosa
  • Afferent nerve: Trigeminal nerve (CN V)
  • Purpose: Clears nasal passages

Yawning

  • Mechanism not completely understood.
  • Current hypotheses: brain state transitions, social/contagious mechanisms, brain temperature regulation.
  • Older theories (low O₂ / high CO₂) are not well supported.

18. Acid‑Base Balance & Blood Buffers

Major Blood Buffers

  • Bicarbonate (HCO₃⁻): Main ECF buffer. Henderson‑Hasselbalch: pH = 6.1 + log([HCO₃⁻]/(0.03 × PaCO₂)).
  • Haemoglobin: Primary intracellular buffer. Histidine residues (imidazole groups) provide powerful buffering in the physiological pH range.
  • Plasma proteins: Amphoteric – can buffer both acids and bases.
  • Phosphate: Effective intracellular and renal tubular buffer.

Compensation

  • Lungs: Rapid (minutes) – alter ventilation to change PaCO₂.
  • Kidneys: Final defence (hours–days) – excrete H⁺, reabsorb HCO₃⁻, generate new bicarbonate.
  • Metabolic acidosis → hyperventilation (↓PaCO₂).
  • Metabolic alkalosis → hypoventilation (↑PaCO₂).

19. Cystic Fibrosis

  • Mutation: Defective CFTR (Cystic Fibrosis Transmembrane Conductance Regulator) – a Cl⁻ channel.
  • Pathophysiology: Loss of Cl⁻ secretion coupled with hyperabsorption of Na⁺ via ENaC → dehydrated, thick mucus.
  • Consequences: Impaired mucociliary clearance → recurrent infections, bronchiectasis, pancreatic insufficiency.

20. Asthma

  • Chronic inflammatory disease of the airways.
  • Reversible airway obstruction – bronchoconstriction, mucus, oedema.
  • FEV₁/FVC < 70% (obstructive pattern).
  • Treatment: Bronchodilators (β₂‑agonists) and inhaled corticosteroids.

21. Surfactant & COVID‑19

  • SARS‑CoV‑2 binds to ACE2 receptors on Type II pneumocytes.
  • Cytokine storm can destroy Type II cells → ↓surfactant → ↑surface tension → alveolar collapse and oedema.
  • This contributes to ARDS (Acute Respiratory Distress Syndrome) in severe COVID‑19.

22. Non‑Chemical Stimuli (Reflex Control)

  • Pulmonary stretch receptors (Hering‑Breuer) – prevent overinflation.
  • J‑receptors (Juxtacapillary): Stimulated by oedema/embolism → rapid shallow breathing.
  • Irritant receptors: Cough/sneeze (protective).
  • Baroreceptors: ↑BP → reflex inhibition of inspiration.
  • Proprioceptors: Exercise → ↑ventilation.

23. Respiratory Quotient (RQ) & Gas Exchange

  • RQ = VCO₂ / VO₂.
  • Carbohydrates: 1.0; Fats: 0.7; Proteins: 0.8.
  • Gas exchange is driven by partial pressure gradients, not concentration.
  • CO₂ diffuses 20× faster than O₂ due to higher solubility.

24. Hypoxia – Types & Effects

TypeExamplePaO₂O₂ ContentA‑V O₂ diff
HypoxicHigh altitude, pneumonia↓↓Normal/↑
AnemicAnaemia, CO poisoningNormal↓↓
StagnantHeart failure, shockNormalNormal↑
HistotoxicCyanide poisoningNormalNormal↓
  • Effects: ↑erythropoietin, ↑HR, ↑ventilation, CNS depression.
  • O₂ therapy: Highly effective in hypoxic hypoxia; less effective in anemic, stagnant, or histotoxic.

25. Dyspnea, Orthopnea, Hypercapnia, Hypocapnia

  • Dyspnea: Laboured breathing. Dyspneic Index = (MVV – RMV)/MVV × 100. Normal >90%, dyspnoea <70%.
  • Orthopnea: Dyspnoea on lying down (cardiac failure).
  • Hypercapnia: CO₂ retention. PaCO₂ >60 → rapid breathing; >80 → CNS depression; >120 → death.
  • Hypocapnia: Low CO₂ (hyperventilation) → vasoconstriction, dizziness, tetany.

26. Asphyxia & Cyanosis

  • Asphyxia: Airway occlusion → hypoxia + hypercapnia. Stages: exaggerated breathing → convulsions → collapse.
  • Cyanosis: Bluish skin when >5 g/dL reduced Hb. Central (warm, tongue/lips) vs Peripheral (cold, nail beds).

27. Special Breathing Patterns

  • Cheyne‑Stokes: Waxing/waning tidal volume (heart failure, brain damage).
  • Biot's: Abrupt apnoea and return (meningitis).
  • Kussmaul: Rapid, deep (metabolic acidosis).

28. Artificial Respiration & Mechanical Ventilation

  • Mouth‑to‑mouth: Extend neck, seal mouth, blow ~12/min.
  • Mechanical: PEEP prevents atelectasis; barotrauma risk.

29. Acclimatization & Dysbarism

  • Acclimatisation: ↑ventilation, ↑2,3‑BPG (right shift), ↑Hb, ↑capillaries.
  • Dysbarism (Caisson's): N₂ bubbles from rapid ascent → joint pain, chokes, paralysis. Treatment: recompression.

30. Hiccup & Respiratory Changes in Exercise

  • Hiccup: Spasmodic diaphragm + glottic closure.
  • Exercise: Ventilation ↑ to 100 L/min, O₂ consumption ↑ 15‑20×, O₂ debt repaid after exercise.

🚀 One‑Minute Revision – Must‑Know Facts

  • ✅ Incentive spirometer = therapeutic, not diagnostic.
  • ✅ N₂ washout: Phase I = dead space; Phase III = alveolar plateau.
  • ✅ Spirometry CAN measure TV, IRV, ERV, IC, EC, VC, FVC, FEV₁, MVV.
  • ✅ Spirometry CANNOT measure RV, FRC, TLC (need gas dilution/plethysmography).
  • ✅ Work of breathing: 65% elastic, 35% non‑elastic.
  • ✅ ACE converts Ang I → Ang II in lungs.
  • ✅ FEV₁/FVC normal ~80%; <70% = obstructive.
  • ✅ Surfactant = DPPC 62%, lowers surface tension, prevents atelectasis.
  • ✅ Compliance = ΔV/ΔP; ↑ in emphysema, ↓ in fibrosis.
  • ✅ Alveolar ventilation = (TV – VD) × f.
  • ✅ V/Q = 0.8; apex ~3.0, base ~0.6.
  • ✅ O₂‑Hb curve: Right shift (Bohr) = ↓affinity; Left shift = ↑affinity.
  • ✅ CO₂ transport: 70% bicarbonate, 23% carbamino, 7% dissolved.
  • ✅ Pre‑Bötzinger = pacemaker; DRG = inspiration; VRG = forced.
  • ✅ Pneumotaxic limits inspiration; lesion = apneusis.
  • ✅ Central chemoreceptors respond to CSF H⁺; Peripheral respond to ↓PaO₂ (<60).
  • ✅ CFTR defect = cystic fibrosis.
  • ✅ Asthma = reversible obstruction, FEV₁/FVC <70%.
  • ✅ Hypoxia types: Hypoxic, Anemic, Stagnant, Histotoxic.
  • ✅ Cyanosis = >5 g/dL reduced Hb.
  • ✅ Acclimatisation = ↑2,3‑BPG (right shift).
📚 References: Guyton & Hall (14th Ed), Ganong's Review of Medical Physiology, West's Respiratory Physiology, and lecture notes.

BMS112 – Paper 1

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🧩 RESPIRATORY PHYSIOLOGY EXAM

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