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🫁 RESPIRATORY PHYSIOLOGY - NEET PG / INICET HIGH-YIELD NOTES

Source: Medical Physiology (Boron & Boulpaep), Guyton & Hall, Harrison's 22e, Costanzo Physiology

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MODULE 1: LUNG VOLUMES & CAPACITIES

Standard Spirogram

High-Yield Values Table

MNEMONIC - "TIRE Capacity"

Volumes: TV · IRV · ERV · RV
Capacities (always 2 or more volumes):
  TLC  = TV + IRV + ERV + RV   → Total Lung Capacity
  VC   = TV + IRV + ERV        → Vital Capacity
  IC   = TV + IRV              → Inspiratory Capacity
  FRC  = ERV + RV              → Functional Residual Capacity

MNEMONIC - What CANNOT be measured by spirometry?

"RV Fails To Come" RV, FRC, and TLC Cannot be measured by simple spirometry (Need helium dilution, N2 washout, or body plethysmography)

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PYQs - Lung Volumes

NEET PG: RV is not measured by spirometry because: (A) it cannot be expelled from the lungs Answer: RV is the air remaining after maximal expiration - cannot be measured by spirometry.

INICET/AIIMS: FRC is best measured by: (A) Helium dilution (B) Spirometry (C) Peak flow meter (D) Pulse oximetry Answer: (A) Helium dilution - also body plethysmography (most accurate).

NEET PG: In obstructive lung disease (e.g., COPD, Asthma) - which volumes INCREASE? Answer: RV, FRC, TLC increase (air trapping); FEV1/FVC decreases below 0.70.

NEET PG 2025 Recall: A person develops headache and breathlessness at >3000m altitude. Which is NOT used in treatment? Answer: IV Digoxin (Correct tx: Descent + O2 + Acetazolamide + Dexamethasone + Nifedipine)

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Obstructive vs Restrictive - High-Yield Comparison

                OBSTRUCTIVE         RESTRICTIVE
FEV1             ↓                    ↓
FVC              N or ↓               ↓↓
FEV1/FVC         <0.70 (↓↓)          >0.70 (N or ↑)
TLC              ↑ (air trapping)     ↓
RV               ↑↑                   ↓
FRC              ↑                    ↓

Examples:        Asthma, COPD         Pulmonary fibrosis, 
                 Emphysema            Kyphoscoliosis, IRDS

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MODULE 2: MECHANICS OF BREATHING - COMPLIANCE & SURFACTANT

Compliance

• Definition: Change in volume per unit change in pressure (ΔV/ΔP)
• Normal lung compliance: ~200 mL/cm H2O
• Normal chest wall compliance: ~200 mL/cm H2O
• Combined (total): ~100 mL/cm H2O (they act in series)

COMPLIANCE ↑ (easier to inflate):    Emphysema, old age
COMPLIANCE ↓ (harder to inflate):    Pulmonary fibrosis, ARDS, 
                                      pulmonary edema, IRDS (neonates)

Surfactant - HIGH-YIELD

Pliability (compliance ↑), Prevents alveolar collapse, Prevents fluid accumulation

Surfactant Deficiency Diseases:

• IRDS (Infant Respiratory Distress Syndrome) = prematurity (<35 weeks)
• ARDS (Adult) = destruction of Type II cells by cytokines
• Tx for IRDS: Antenatal steroids (betamethasone/dexamethasone) to accelerate surfactant maturation + postnatal exogenous surfactant

• Antenatal corticosteroids (betamethasone 12mg IM x2 doses) given at 24-34 weeks → stimulate fetal lung maturation (↑ surfactant synthesis)
• Poractant alfa / Beractant = exogenous surfactant used in NICU for IRDS

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PYQs - Mechanics

AIIMS/INICET: In emphysema, lung compliance is: (A) Increased (B) Decreased (C) Normal Answer: (A) Increased - destruction of alveolar walls and elastic tissue.

NEET PG: Surfactant is produced by: (A) Type II pneumocytes (B) Type I pneumocytes (C) Clara cells (D) Alveolar macrophages Answer: (A) Type II pneumocytes

NEET PG: DPPC (Dipalmitoyl Phosphatidylcholine) is the main component of: (A) Surfactant - 70% composition

INICET: La Place's law: P = 2T/r - this explains why small alveoli tend to collapse into large ones in the absence of surfactant.

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MODULE 3: GAS EXCHANGE & TRANSPORT

Partial Pressures (Normal Values - MEMORIZE)

                     Inspired air    Alveolar air    Arterial blood    Venous blood
PO2 (mmHg)              159              104              100               40
PCO2 (mmHg)              0.3             40               40               45
PN2 (mmHg)              597              569              569               569
PH2O (mmHg)              ~0              47               47               47

Oxygen Transport

• Dissolved O2: Only 0.3 mL/dL at PO2 = 100 mmHg (only 1.5% of total)
• Hb-bound O2: ~20 mL/dL (98.5% of total)
• Total O2 content = (Hb × 1.34 × SaO2) + (PaO2 × 0.003)
• Normal Hb binds 1.34 mL O2 per gram

         Factors shifting curve RIGHT (↓ affinity, ↑ O2 unloading to tissues):
         ↑ CO2 (Bohr effect), ↑ Temp, ↑ 2,3-DPG, ↑ H+ (acidosis)
         Mnemonic: "CADET face RIGHT"  
         C=CO2, A=Acid, D=2,3-DPG, E=Exercise, T=Temperature

         Factors shifting curve LEFT (↑ affinity, ↓ O2 unloading):
         ↓ CO2, ↓ Temp, ↓ 2,3-DPG, Alkalosis, HbF, COHb, MetHb
         Mnemonic: LEFT = Low Everything (CO2, Temp, DPG) + Fetal Hb

CO2 Transport

• Acetazolamide inhibits carbonic anhydrase → reduces HCO3- formation → metabolic acidosis → stimulates ventilation → used in altitude sickness
• Sildenafil (PDE5 inhibitor) → used in altitude sickness and pulmonary arterial hypertension

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PYQs - Gas Transport

NEET PG: CO2 is transported mainly as: (A) Bicarbonate ions (HCO3-) = 70% of CO2

AIIMS: Which shifts the O2-Hb curve to RIGHT? (A) 2,3-DPG (B) HbF (C) Alkalosis (D) Hypothermia Answer: (A) 2,3-DPG

NEET PG: HbF (Fetal hemoglobin) compared to HbA: (A) Has higher affinity for O2 - shifts curve LEFT, ↓ 2,3-DPG binding

NEET PG 2025 (ARDS recall): PaO2/FiO2 ratio of 100 = severe ARDS → Management: (A) High PEEP + Low tidal volume (lung-protective ventilation, TV 6 mL/kg IBW)

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MODULE 4: VENTILATION-PERFUSION (V/Q) RATIO

Concept Summary

NORMAL V/Q = 0.8 (alveolar ventilation ~4 L/min; pulmonary blood flow ~5 L/min)

V/Q = 0 (NO VENTILATION, perfusion present):
  → Alveolar air = venous blood gases
  → PO2 = 40, PCO2 = 45 mmHg
  → "Pure SHUNT" e.g., atelectasis, lobar pneumonia
  → O2 therapy does NOT correct hypoxia!

V/Q = ∞ (NO PERFUSION, ventilation present):
  → Alveolar air = inspired air
  → PO2 = 149, PCO2 = 0 mmHg  
  → "DEAD SPACE" e.g., pulmonary embolism
  → O2 therapy DOES correct hypoxia

V/Q Flowchart

            LOW V/Q                          HIGH V/Q
         (Shunt-like)                     (Dead space-like)
              ↓                                 ↓
     Hypoxia + Hypercapnia           Hypoxia + Hypocapnia
              ↓                                 ↓
   O2 therapy partially helps       O2 helps (dead space)
              ↓
   Causes: COPD, Asthma,           Causes: PE, Emphysema,
   pneumonia, atelectasis          Low cardiac output

Regional V/Q Variation in Upright Lung

APEX:   V/Q = 3.3  (more ventilation, little perfusion → "wasted ventilation")
BASE:   V/Q = 0.6  (more perfusion, relatively less ventilation)
OVERALL: V/Q = 0.8

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Dead Space

VD/VT = (PaCO2 - PECO2) / PaCO2 Where PECO2 = CO2 in mixed expired air

• Normal: (500 - 150) × 14 = 4900 mL/min ≈ 5 L/min

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PYQs - V/Q

NEET PG 2025 (Recall): In pulmonary embolism, V/Q graph shows complete obstruction of blood flow - which point? (D) = V/Q = ∞ (dead space point - no perfusion)

INICET: In lobar pneumonia, hypoxia is due to: (A) V/Q mismatch (low V/Q / shunt) - alveoli filled with exudate, no ventilation

NEET PG: Anatomical dead space is measured by: (A) Fowler's method (single breath N2 washout) Physiological dead space = Bohr's method

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MODULE 5: CONTROL OF RESPIRATION

Respiratory Control Centers

MEDULLA (primary):
  - Dorsal Respiratory Group (DRG) → inspiration (basic rhythm)
  - Ventral Respiratory Group (VRG) → expiration (active) + forced breathing

PONS:
  - Pneumotaxic center (Pontine Respiratory Group) → LIMITS inspiration, ↑ RR
  - Apneustic center → PROLONGS inspiration (held in check by pneumotaxic)

• If pneumotaxic center is damaged → apneustic breathing (prolonged gasping inspiration)
• If BOTH pons lesions → Biot's breathing (irregular)

Chemoreceptors

CENTRAL CHEMORECEPTORS (Medulla, ventral surface):
  → Respond to: ↑ PCO2 (via ↑ CSF H+ → most potent stimulus)
  → Do NOT respond directly to O2
  → Blood-brain barrier is permeable to CO2 but NOT to H+ directly
  → CO2 crosses → forms H2CO3 → H+ in CSF → stimulates receptors
  
PERIPHERAL CHEMORECEPTORS (Carotid body >> Aortic body):
  → Respond to: ↓ PO2 (primary), ↑ PCO2, ↓ pH
  → Carotid body: via CN IX (Hering's nerve) → NTS (medulla)
  → Aortic body: via CN X → NTS
  → Only source of hypoxic drive
  → Also respond to ↓ blood flow (e.g., cyanide → ↑ firing despite normal PO2)

MNEMONIC - Chemoreceptors: "Central CO2, Peripheral O2"

Central = CO2 sensitive Peripheral = PO2 sensitive (+ CO2 & pH)

Hering-Breuer Reflex

• Lung stretch receptors (slowly adapting, myelinated) → via vagus
• Triggered by lung inflation → inhibits inspiration → prevents over-inflation
• Active when TV > 1.5 L (minimal role in quiet breathing in adults)
• Important in neonates (active at normal TV)

• Opioids (morphine, fentanyl) → directly depress respiratory centers → ↓ RR, respiratory acidosis → Rx: Naloxone
• Benzodiazepines → potentiate GABA → respiratory depression (less severe than opioids)
• Doxapram → stimulates peripheral chemoreceptors → used as respiratory stimulant
• Almitrine → peripheral chemoreceptor stimulant
• Nikethamide / Ethamivan → central respiratory stimulants (obsolete)

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PYQs - Control of Respiration

NEET PG: Primary stimulus for central chemoreceptors: (A) Increased PCO2 / increased H+ in CSF

NEET PG: Peripheral chemoreceptors are stimulated by: (A) Decrease in PO2 (primary), not just decrease in O2 content (anemia alone doesn't stimulate unless PO2 also drops)

AIIMS: CO2 stimulates central chemoreceptors by crossing BBB and forming: (A) H+ ions in CSF - H+ is the actual stimulus (not CO2 directly)

INICET: Apneustic breathing occurs due to lesion at: (A) Pneumotaxic center (pontine respiratory group - upper pons)

NEET PG: Hering-Breuer reflex - receptor type: (A) Slowly adapting pulmonary stretch receptors via vagus nerve

NEET PG (Altitude sickness): IV Digoxin is NOT used in acute mountain sickness - correct treatment uses: Descent, O2, Acetazolamide, Dexamethasone, Nifedipine.

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INTEGRATION: MEDICINE + PHARMACOLOGY

COPD (Medicine + Physiology Integration)

Pathophysiology:
  Airway inflammation + mucus → ↑ airway resistance
  Alveolar wall destruction → ↑ compliance, ↓ elastic recoil
  Air trapping → ↑ RV, ↑ FRC, ↑ TLC → barrel chest
  Ventilation-Perfusion mismatch → hypoxia ± hypercapnia

"Blue Bloater" (Chronic Bronchitis): V/Q mismatch, cyanosis, cor pulmonale
"Pink Puffer" (Emphysema): increased dead space, V/Q high, hyperventilates

Drug Targets:
  SABA (Salbutamol/Albuterol)     → β2 agonist → bronchodilation
  LABA (Salmeterol, Formoterol)   → long-acting β2 agonist
  SAMA (Ipratropium)              → M3 antagonist → bronchodilation
  LAMA (Tiotropium)               → long-acting M3 antagonist
  ICS (Fluticasone, Budesonide)   → anti-inflammatory
  Theophylline                    → PDE inhibitor → bronchodilation + respiratory stimulant
  Roflumilast                     → PDE4 inhibitor → anti-inflammatory in COPD

Asthma (Medicine + Physiology Integration)

Pathophysiology:
  Airway hyperresponsiveness → bronchoconstriction → ↑ Raw
  Mucus plugging → V/Q mismatch (low V/Q)
  Air trapping → ↑ RV, ↑ FRC
  FEV1/FVC < 0.70, reversible with bronchodilators

Pharmacology:
  Acute:  SABA (Salbutamol 200-400 mcg inhaled) + O2 + steroids IV
  Chronic:ICS (first-line controller), LABA add-on, Montelukast (LTD4 antagonist)
  Severe: Omalizumab (anti-IgE), Mepolizumab (anti-IL-5), Dupilumab (anti-IL-4/13)
  Mast cell stabilizer: Sodium cromoglicate (prophylaxis, not treatment)
  Avoid: Beta-blockers (cause bronchoconstriction), NSAIDs in aspirin-sensitive asthma

Pulmonary Embolism (Medicine + Physiology Integration)

Physiology: V/Q = ∞ (dead space) → hypoxia + hypocapnia (↑ RR initially)
  → A-a gradient ↑
  → Pulmonary hypertension → RV strain → RV failure

ABG: ↓ PaO2, ↓ PaCO2 (hyperventilation), respiratory alkalosis
ECG: S1Q3T3, sinus tachycardia, RBBB
CXR: Hampton's hump, Westermark sign, Fleischner lines

ARDS (Medicine + Physiology Integration)

Pathophysiology: 
  Diffuse alveolar damage → ↓ surfactant (Type II cell damage)
  → ↓ compliance, ↑ shunt (V/Q = 0)
  → Refractory hypoxia (doesn't respond to O2)

Berlin Criteria: PaO2/FiO2 ratio:
  Mild:     200-300 mmHg
  Moderate: 100-200 mmHg
  Severe:   <100 mmHg

Management: 
  Lung-protective ventilation: TV 6 mL/kg IBW + High PEEP
  Prone positioning for severe ARDS
  Dexamethasone (COVID-ARDS - RECOVERY trial)

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MASTER MNEMONIC SUMMARY

All Lung Volumes and Capacities

"IRV TEC" for Volumes: IRV · TV · ERV · RV (top to bottom in spirogram)
"VITAL CAPACITY" = TV + IRV + ERV (vital = alive, doesn't include RV)
"TOTAL = ALL" = TLC includes everything
"FRC = ERV + RV" → Remember: FRC is where the lung rests at end-expiration

Bohr/Haldane Effects (Frequently Confused in PYQs)

BOHR Effect:   ↑ CO2/H+ → Hb releases O2 (RIGHT shift) → tissues get O2
               "BOHR = Blood Offloads O2 in tissues when CO2 Rises"

HALDANE Effect:↓ O2 → Hb picks up MORE CO2 (deoxygenated Hb carries more CO2)
               "HALDANE = Hypoxia Allows Lots of Dissolved AND new CO2 to bind Hb"

Shunt vs Dead Space

SHUNT (V/Q = 0):    No ventilation → O2 therapy FAILS → PaO2 doesn't rise
DEAD SPACE (V/Q=∞): No perfusion  → O2 therapy WORKS → PaO2 rises
MNEMONIC: "SHUNT = Stubborn, O2 doesn't help"

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PREVIOUS YEAR THEMES (NEET PG / INICET / AIIMS)

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QUICK REVISION FLOWCHART

RESPIRATORY PHYSIOLOGY - MASTER FLOWCHART

Breathing Mechanics
    ├── Compliance = ΔV/ΔP
    │     ↑ in Emphysema, ↓ in Fibrosis/ARDS
    └── Surfactant (DPPC, Type II cells)
          → ↓ surface tension, La Place's law

Lung Volumes (Spirometry)
    ├── Measured:  TV, IRV, ERV, VC, IC
    └── NOT measured: RV, FRC, TLC → need He dilution / plethysmography

Gas Exchange
    ├── Diffusion: PO2 alveoli 104 → capillary 40 mmHg
    ├── O2 Transport: 98.5% as OxyHb (1.34 mL/g Hb)
    ├── CO2 Transport: 70% HCO3- | 23% carbamino | 7% dissolved
    └── Hb Curves: RIGHT = CADET (↑ CO2, acid, DPG, exercise, temp)
                   LEFT  = HbF, COHb, alkalosis

V/Q Matching
    ├── Normal = 0.8
    ├── Shunt (V/Q=0): alveoli filled, no ventilation, O2 therapy fails
    └── Dead space (V/Q=∞): no perfusion, O2 therapy works

Respiratory Control
    ├── Central (medulla): CO2/H+ via CSF
    └── Peripheral (carotid/aortic body): ↓PO2, ↑PCO2, ↓pH
          └── Only source of hypoxic drive

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What's covered in this guide:

• Standard spirogram with actual textbook image
• Exact values table with which volumes CANNOT be measured by spirometry
• Obstructive vs Restrictive comparison table
• Mnemonics: "TIRE Capacity," "RV Fails To Come"

• Compliance definitions, normal values, disease changes
• Surfactant (DPPC, Type II cells) with textbook diagram showing braking action
• La Place's Law application
• Pharma: Antenatal betamethasone, Poractant alfa

• Complete partial pressure values table (inspired → venous blood)
• O2-Hb dissociation curve factors - CADET mnemonic for right shift
• CO2 transport: 70-23-7 (Bicarbonate-Carbamino-Dissolved)
• Bohr Effect vs Haldane Effect (frequently confused in PYQs)
• Pharma: Acetazolamide, Sildenafil in altitude sickness

• V/Q = 0 (shunt) vs V/Q = ∞ (dead space) with gas values
• Why O2 therapy fails in shunt but works in dead space
• Regional V/Q variation: Apex vs Base
• Bohr vs Fowler methods for dead space

• Medullary + Pontine centers with Harrison's 22e diagram
• Central vs Peripheral chemoreceptors comparison table
• Hering-Breuer reflex
• Pharma: Opioid respiratory depression + Naloxone, Doxapram, Theophylline

• COPD (Blue Bloater vs Pink Puffer), Asthma drug targets, PE physiology (V/Q = ∞), ARDS Berlin criteria + lung-protective ventilation