Respiratory Physiology
🟢 Lite — Quick Review (1h–1d)
Rapid summary for last-minute revision before your exam.
Respiratory Physiology — Key Facts for NEET PG
- Lung volumes: TV (500 mL), IRV (3 L), ERV (1.2 L), RV (1.5 L); TLC = 6 L
- Dead space: Anatomical (~150 mL) + Physiologic (includes alveolar DS); VD/VT ratio normally ~0.3
- Oxygen transport: 98.5% bound to Hb (HbO₂), 1.5% dissolved in plasma; CO₂ transport: 70% as HCO₃⁻
- Ventilation-Perfusion (V/Q): Normal lung V/Q ≈ 0.8; lung apex has higher V/Q (↑ perfusion than ventilation)
- ⚡ Exam tip: CO has 200× greater affinity for Hb than O₂ → CO poisoning; pulse oximetry cannot distinguish carboxy-Hb
🟡 Standard — Regular Study (2d–2mo)
Standard content for students with a few days to months.
Respiratory Physiology — NEET PG Study Guide
Lung Volumes and Capacities
Primary Lung Volumes:
| Volume | Definition | Normal Value |
|---|---|---|
| Tidal Volume (TV) | Air inhaled/exhaled at rest | ~500 mL |
| Inspiratory Reserve Volume (IRV) | Max inspiration from end-inspiration | ~3.0 L |
| Expiratory Reserve Volume (ERV) | Max expiration from end-expiration | ~1.2 L |
| Residual Volume (RV) | Air remaining after max expiration | ~1.5 L |
Lung Capacities (combinations of volumes):
| Capacity | Components | Normal Value |
|---|---|---|
| IC | TV + IRV | ~3.5 L |
| FRC | ERV + RV | ~2.7 L |
| Vital Capacity (VC) | TV + IRV + ERV | ~4.6 L |
| Total Lung Capacity (TLC) | VC + RV | ~6.0 L |
⚡ Exam tip: FVC (Forced Vital Capacity) and FEV₁ (Forced Expiratory Volume in 1 second) — ratio FEV₁/FVC helps classify obstructive vs restrictive disease
Mechanics of Breathing
Inspiration (active):
- Diaphragm contracts → dome descends → thoracic cavity expands
- External intercostals contract → ribs elevate
- Pleural pressure drops → alveolar pressure drops → air rushes in
- Accessory muscles (scalenes, sternocleidomastoid): Used during forced inspiration
Expiration (passive at rest):
- Diaphragm relaxes → recoil of lungs and chest wall
- Forced expiration: Internal intercostals + abdominal muscles contract
Pressures:
| Pressure | Normal Values |
|---|---|
| Atmospheric (Patm) | 760 mmHg (at sea level) |
| Intrapleural (Ppl) | −5 cmH₂O (rest), −8 cmH₂O (inspiration) |
| Alveolar (Palv) | 0 cmH₂O (rest), −1 cmH₂O (inspiration) |
⚡ Exam tip: Surface tension in alveoli = law of LaPlace (P = 2T/r) — small alveoli have higher pressure; surfactant reduces surface tension disproportionately in small alveoli
Surfactant
Composition: Dipalmitoylphosphatidylcholine (DPPC), other phospholipids, proteins (SP-A, SP-B, SP-C, SP-D)
Functions:
- Reduces surface tension at air-liquid interface
- Prevents alveolar collapse (atelectasis)
- LaPlace’s Law: P = 2γ/r — surfactant decreases γ, preventing high pressure in small alveoli
- Facilitates lung compliance
Clinical Note: Deficiency in premature infants → Hyaline Membrane Disease (NRDS) — treatment with exogenous surfactant + CPAP
⚡ Exam tip: Surfactant is produced by Type II pneumocytes (granular pneumocytes); fetal lungs produce surfactant from ~24 weeks, adequate by ~35 weeks
Gas Exchange
Fick’s Law of Diffusion:
Vgas = (A × D × ΔP) / T
- A: Surface area (↓ in emphysema, fibrosis)
- D: Diffusion coefficient (↓ for CO₂ vs O₂)
- ΔP: Partial pressure gradient
- T: Membrane thickness (↑ in pulmonary fibrosis)
Oxygen Exchange:
- PaO₂ in alveoli = ~100 mmHg
- Blood in pulmonary capillaries → equilibrates with alveolar O₂ in 0.25 sec (one-third of capillary transit time)
Carbon Dioxide Exchange:
- CO₂ diffusion 20× faster than O₂
- PaCO₂ in alveoli = ~40 mmHg
⚡ Exam tip: In exercise, ↓ D (diffusing capacity) → V/Q mismatch → hypoxemia before dyspnea
V/Q Matching
Normal V/Q: ~0.8
| Region | V/Q | Explanation |
|---|---|---|
| Upright lung apex | >0.8 (↑ perfusion) | More perfusion than ventilation |
| Upright lung base | <0.8 (↓ perfusion) | More ventilation than perfusion |
| Normal lung | ~0.8 | Ideal matching |
V/Q Mismatch Types:
| Problem | V/Q | Result |
|---|---|---|
| Shunt | V/Q = 0 | Blood passes without gas exchange (e.g., R-to-L shunt) |
| Dead space | V/Q = ∞ | Ventilated but not perfused (e.g., PE) |
⚡ Exam tip: 100% O₂ challenge test — shunt does NOT improve PaO₂ significantly; V/Q mismatch DOES improve with supplemental O₂
Oxygen and Carbon Dioxide Transport
Oxygen Transport:
| Form | Percentage | Details |
|---|---|---|
| Bound to Hb | 98.5% | 1 g Hb binds 1.34 mL O₂ |
| Dissolved in plasma | 1.5% | Minimal contribution |
Oxyhemoglobin Dissociation Curve:
- Sigmoid shape (cooperative binding)
- Factors shifting curve RIGHT (↓ Hb-O₂ affinity, ↓ SaO₂ at given PaO₂):
- ↑ H⁺ (acidosis)
- ↑ PaCO₂ (hypercapnia)
- ↑ Temperature
- ↑ 2,3-DPG (in RBCs)
- Bohr effect: Shift in curve due to H⁺ and CO₂
⚡ Exam tip: Right shift = helpful in tissues (O₂ unloads more easily); Left shift = helpful in lungs (O₂ loads more easily) — but left shift in pathology is BAD (e.g., CO poisoning, fetal Hb)
Carbon Dioxide Transport:
| Form | Percentage | Mechanism |
|---|---|---|
| As HCO₃⁻ | 70% | CO₂ + H₂O → H₂CO₃ → H⁺ + HCO₃⁻ (CA in RBCs) |
| Bound to Hb | 20% | Carbaminohemoglobin |
| Dissolved | 10% | Physically dissolved |
Haldane Effect: Deoxygenated Hb has higher affinity for CO₂ — explains efficient CO₂ transport from tissues to lungs
Control of Breathing
Respiratory Centers:
| Center | Location | Function |
|---|---|---|
| Medullary respiratory center | Medulla | Inspiratory and expiratory neurons |
| Pneumotaxic center | Pons | Coordinates breathing pattern, inhibits inspiration |
| Apneustic center | Pons | Promotes inspiration |
Chemoreceptors:
| Type | Location | Responds To |
|---|---|---|
| Central chemoreceptors | Medulla | ↑ PaCO₂, ↓ pH in CSF |
| Peripheral chemoreceptors | Carotid bodies, aortic body | ↓ PaO₂, ↑ PaCO₂, ↓ pH |
⚡ Exam tip: Cheyne-Stokes breathing = cyclic breathing (apnea → crescendo-decrescendo) — seen in heart failure, stroke, uremia; Biot’s breathing = irregular groups of breaths with apnea — seen in meningitis, brainstem lesions
Pulmonary Circulation
Special Features:
- Low pressure system: PA pressure ~25/10 mmHg
- Large compliance: Can accommodate increased blood volume
- Hypoxic vasoconstriction: ↓ PaO₂ in alveoli → local vasoconstriction → redirects blood to well-ventilated areas
⚡ Exam tip: High altitude → chronic hypoxemia → pulmonary vasoconstriction → pulmonary hypertension → RV hypertrophy (cor pulmonale)
🔴 Extended — Deep Study (3mo+)
Comprehensive coverage for students on a longer study timeline.
Respiratory Physiology — Comprehensive NEET PG Notes
Detailed Pulmonary Function Tests
Obstructive Patterns (↓ FEV₁/FVC):
- Asthma: Reversible obstruction, ↓ FEV₁ > ↓ FVC
- COPD: Irreversible, barrel chest, emphysema (↑ RV, ↑ TLC)
- Chronic bronchitis: “Blue bloater,” cyanosis, productive cough
Restrictive Patterns (proportional ↓ FEV₁ and FVC, FEV₁/FVC normal or ↑):
- Pulmonary fibrosis: ↓ TLC, ↓ FRC, ↓ RV
- Neuromuscular diseases: Weakness of respiratory muscles
- Chest wall deformities: Kyphoscoliosis
DLCO (Diffusing Capacity):
- Measures gas transfer across alveolar membrane
- ↓ in: Emphysema (↓ surface area), Pulmonary fibrosis (↓ membrane area), Anemia (↓ Hb)
Ventilation Mechanics
Compliance:
Compliance = ΔV / ΔP (volume change per pressure change)
- Normal: ~200 mL/cmH₂O
- ↓ compliance: Stiff lungs (pulmonary fibrosis, atelectasis, ARDS)
- ↑ compliance: Floppy lungs (emphysema)
Work of Breathing:
- Elastic work (overcoming lung/chest wall recoil)
- Resistive work (overcoming airway resistance)
- Total work = ∫ (pressure × volume change)
Gas Exchange — Detailed
Oxygen Cascade: Atmospheric O₂ (760 mmHg) → Tracheal (713 mmHg) → Alveolar (100 mmHg) → Arterial (95 mmHg) → Mitochondria (~5 mmHg)
Anatomical Dead Space: ~150 mL — air in conducting airways (nose to terminal bronchioles)
Physiological Dead Space: Sum of anatomical + alveolar dead space (ventilated alveoli not perfused)
Alveolar Gas Equation:
PAO₂ = FiO₂ × (Patm − PH₂O) − (PaCO₂ /RQ)
- PAO₂ = Alveolar O₂ partial pressure
- FiO₂ = Fraction of inspired O₂ (0.21 on room air)
- RQ = Respiratory quotient (CO₂/O₂, normally 0.8)
⚡ Exam tip: A-a gradient (PAO₂ − PaO₂) increases when there is V/Q mismatch, shunt, or diffusion impairment; Normal A-a gradient increases with age and at high altitude
Oxygen-Hemoglobin Interactions
Hemoglobin Structure: 2 α + 2 β chains; 4 heme groups; Each heme binds 1 O₂
O₂-Hb Dissociation Curve:
- Flat portion (80–100 mmHg): Large drop in PaO₂ produces minimal change in SaO₂
- Steep portion (20–40 mmHg): Small changes in PaO₂ cause large changes in SaO₂ — facilitates O₂ unloading in tissues
Factors Affecting O₂-Hb Affinity:
| Factor | Effect | Mechanism |
|---|---|---|
| ↑ Temperature | Right shift | Denatures Hb structure |
| ↑ H⁺ (acidosis) | Right shift | Bohr effect |
| ↑ PaCO₂ | Right shift | Carbamino-Hb formation |
| ↑ 2,3-DPG | Right shift | Stabilizes deoxy-Hb |
| ↑ CO | Left shift | Blocks O₂ binding |
| Fetal Hb (HbF) | Left shift | γ chains vs β chains |
CO Transport on Hb:
- 20% of CO₂ transported as carbaminohemoglobin
- CO has 200× greater affinity than O₂
- CO poisoning: SaO₂ appears normal on pulse oximetry (measures light absorption not specific to HbO₂ vs CO-Hb)
Acid-Base and Respiratory System
Primary Respiratory Disturbances:
| Disorder | PaCO₂ | pH | Compensation |
|---|---|---|---|
| Respiratory acidosis | ↑ | ↓ | ↑ HCO₃⁻ (renal, 6–8 hr to start) |
| Respiratory alkalosis | ↓ | ↑ | ↓ HCO₃⁻ (renal, 6–8 hr to start) |
Primary Metabolic Disturbances:
| Disorder | HCO₃⁻ | pH | Compensation |
|---|---|---|---|
| Metabolic acidosis | ↓ | ↓ | ↑ PaCO₂ (hyperventilation) |
| Metabolic alkalosis | ↑ | ↑ | ↓ PaCO₂ (hypoventilation) |
⚡ Exam tip: Winter’s formula for expected respiratory compensation in metabolic acidosis: PaCO₂ = (1.5 × HCO₃⁻) + 8 ± 2
Respiratory Adjustments
Acute Mountain Sickness (AMS):
- Headache, nausea, fatigue, dizziness
- Usually resolves in 1–2 days
- Preventive: Acetazolamide (CA inhibitor → metabolic acidosis → stimulates ventilation)
High Altitude Pulmonary Edema (HAPE):
- Non-cardiogenic pulmonary edema
- Due to hypoxic pulmonary vasoconstriction → elevated PA pressure → capillary leak
- Treatment: Descent, supplemental O₂, nifedipine
High Altitude Cerebral Edema (HACE):
- Cerebral edema (vasogenic)
- Ataxia, confusion, altered consciousness
- Treatment: Immediate descent, dexamethasone
Respiratory Failure
Type I (Hypoxemic):
- PaO₂ <60 mmHg
- Causes: V/Q mismatch, shunt, diffusion impairment
- Responds to supplemental O₂ (except shunt)
Type II (Hypercapnic):
- PaCO₂ >50 mmHg
- Causes: Hypoventilation, COPD
- May also have hypoxemia
⚡ Exam tip: Acute Respiratory Distress Syndrome (ARDS) = non-cardiogenic pulmonary edema, bilateral infiltrates, PaO₂/FiO₂ <300; Causes: sepsis, aspiration, trauma, pancreatitis
Defense Mechanisms
Upper Airway Defenses:
- Nasal hair and turbinates: Filter particles
- Sneezing: Expels irritants
- Cough: Clears lower airways
- Mucociliary escalator: Cilia propel mucus
Lower Airway Defenses:
- Alveolar macrophages: Phagocytose particles, bacteria
- IgA: Immune defense
- Surfactant proteins (SP-A, SP-D): Collectins — opsonization
Cystic Fibrosis:
- CFTR mutation → thick, viscous secretions
- Impaired mucociliary clearance → recurrent infections
- Pancreatic insufficiency (digestive enzymes can’t reach duodenum)
Practice Questions for NEET PG
- Draw and label a spirogram showing lung volumes and capacities.
- Explain the mechanism of surfactant and its role in preventing atelectasis.
- Compare oxygen transport in blood with carbon dioxide transport.
- Describe the factors that shift the oxygen-hemoglobin dissociation curve.
- A patient with COPD has an FEV₁/FVC ratio of 0.55. Explain the classification and pathophysiology.
- Explain the respiratory compensation for metabolic acidosis.
- What is hypoxic pulmonary vasoconstriction? Why is it important?
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