I now have comprehensive content from Guyton & Hall (the standard textbook that GK Pal closely mirrors). Let me now compile the full, complete, GK Pal-style point-wise and topic-wise BHMS notes.
🫁 RESPIRATORY SYSTEM PHYSIOLOGY
1st Year BHMS - Complete Notes
In the Style of GK Pal | Point-wise & Topic-wise | Simple & Easy to Understand
(Based on Guyton & Hall Textbook of Medical Physiology + Ganong's Review - the standard references aligned with GK Pal's Textbook of Physiology)
TOPIC 1: INTRODUCTION TO RESPIRATORY SYSTEM
What is Respiration?
- Respiration = the process of taking in O₂ and removing CO₂ from the body
- The lungs are the main organ of respiration
Functions of the Respiratory System:
- External respiration - exchange of O₂ and CO₂ between lungs and blood
- Internal/Tissue respiration - exchange of O₂ and CO₂ between blood and tissue cells
- Regulation of blood pH - by controlling CO₂ levels
- Vocalization - speech, voice production
- Defence - filtering dust, microbes from inspired air
- Metabolism of vasoactive substances - e.g., converting Angiotensin I → Angiotensin II
TOPIC 2: FUNCTIONAL ANATOMY OF THE RESPIRATORY SYSTEM
Upper Respiratory Tract:
- Nose, nasal cavity, pharynx, larynx
Lower Respiratory Tract:
- Trachea → 2 main bronchi → lobar bronchi → segmental bronchi → bronchioles → terminal bronchioles → respiratory bronchioles → alveolar ducts → alveoli (site of gas exchange)
Important Points:
- Total number of alveoli in adult lungs = 300-500 million
- Total surface area of alveoli = 70 m² (size of a tennis court)
- Alveolar wall has Type I pneumocytes (flat, for diffusion) and Type II pneumocytes (cuboidal, produce surfactant)
- The alveolar-capillary membrane thickness = 0.5 micrometers (very thin for easy diffusion)
Conducting Zone vs Respiratory Zone:
| Feature | Conducting Zone | Respiratory Zone |
|---|
| Parts | Nose to terminal bronchioles | Respiratory bronchioles to alveoli |
| Function | Conduct air, clean, warm, humidify | Gas exchange |
| Gas exchange? | NO | YES |
TOPIC 3: RESPIRATORY MUSCLES
Muscles of Inspiration (Normal Quiet Breathing):
- Diaphragm - MOST IMPORTANT muscle of inspiration
- Contraction → diaphragm moves down → thoracic cavity length increases
- External intercostal muscles - elevate ribs → increase anteroposterior diameter of chest
Accessory Muscles of Inspiration (during heavy breathing):
- Sternocleidomastoid (SCM) - lifts sternum upward
- Scaleni muscles - elevate first two ribs
- Anterior serratus muscles - lift many ribs
Muscles of Expiration:
- At rest: expiration is PASSIVE (elastic recoil of lungs, no muscle needed)
- During forced/active expiration:
- Abdominal muscles (rectus abdominis) - push diaphragm upward
- Internal intercostal muscles - depress rib cage
Key Point: Normal quiet expiration = passive (no muscle needed). Only forced expiration needs muscles!
TOPIC 4: PRESSURES IN THE RESPIRATORY SYSTEM ⭐⭐
Important Pressures (must know for exam):
| Pressure | Normal Value | Meaning |
|---|
| Atmospheric pressure (Patm) | 760 mmHg | Pressure outside the body |
| Alveolar pressure (Palv) | 0 cmH₂O (relative to atmospheric) | Pressure inside alveoli |
| Intrapleural pressure (Pip) | -5 cmH₂O (at rest) | Pressure in pleural space |
| Transpulmonary pressure | Palv - Pip = +5 cmH₂O | Distending pressure that keeps lungs open |
Why is intrapleural pressure always negative?
- The lung has elastic recoil (wants to collapse inward)
- The chest wall has elastic recoil (wants to spring outward)
- They pull against each other → creates a subatmospheric pressure in the pleural space
- This negative pressure keeps the lungs "inflated" against the chest wall
Changes during breathing cycle:
| Phase | Intrapleural Pressure | Alveolar Pressure | Air Flow |
|---|
| At rest (between breaths) | -5 cmH₂O | 0 cmH₂O | No flow |
| Inspiration | -8 cmH₂O | -3 cmH₂O | Air flows IN |
| Expiration | -5 cmH₂O | +3 cmH₂O | Air flows OUT |
Steps of Inspiration:
- Diaphragm contracts → chest cavity expands
- Intrapleural pressure decreases (more negative)
- Lungs expand → alveolar pressure falls below atmospheric
- Pressure gradient created → air flows INTO lungs
Steps of Expiration (passive):
- Diaphragm relaxes
- Lungs recoil (elastic recoil)
- Alveolar pressure rises above atmospheric
- Air flows OUT of lungs
TOPIC 5: COMPLIANCE OF THE LUNGS ⭐
Definition:
- Compliance = change in lung volume per unit change in pressure
- Formula: C = ΔV / ΔP
- Unit: L/cmH₂O
- Normal lung compliance = 0.2 L/cmH₂O
Types of Compliance:
- Lung compliance - ability of lungs alone to expand
- Chest wall compliance - ability of chest wall to expand
- Total (lung + chest wall) compliance - combined = 0.1 L/cmH₂O
Conditions affecting compliance:
| Condition | Compliance | Reason |
|---|
| Emphysema | ↑ Increased | Destruction of elastic tissue |
| Pulmonary fibrosis | ↓ Decreased | Stiff fibrotic tissue |
| Pulmonary oedema | ↓ Decreased | Fluid in lungs |
| Neonatal RDS | ↓ Decreased | No surfactant |
| Ageing | ↓ Decreased | Loss of elastic recoil |
Important: Two forces opposing lung expansion:
- Elastic recoil of lung tissue (due to elastin fibres)
- Surface tension of alveolar lining fluid
TOPIC 6: SURFACTANT ⭐⭐ (Very Important for Exam!)
What is Surfactant?
- A lipoprotein substance lining the alveolar surface
- Produced by Type II alveolar (pneumocyte) cells
- Main component: Dipalmitoyl Phosphatidylcholine (DPPC)
- Also contains: SP-A, SP-B, SP-C, SP-D proteins
Function of Surfactant:
- Reduces surface tension of alveolar fluid → prevents alveolar collapse
- Increases lung compliance → easier to expand lungs
- Equalizes alveolar size → prevents large alveoli from expanding at the expense of small ones
- Prevents pulmonary oedema → reduces fluid transudation into alveoli
Law of Laplace (must know!):
P = 2T / r
- P = pressure needed to keep alveolus open
- T = surface tension
- r = radius of alveolus
Without surfactant: Small alveoli (small r) → very high collapsing pressure → collapse!
With surfactant: T is reduced → collapsing pressure reduced → alveoli stay open
Clinical Importance of Surfactant:
Neonatal Respiratory Distress Syndrome (NRDS) / Hyaline Membrane Disease:
- Occurs in premature babies (< 35 weeks gestation)
- Surfactant production starts at 24 weeks, reliably present by 35 weeks
- Without surfactant:
- Alveoli collapse (atelectasis)
- Hypoxemia (low blood O₂)
- Decreased lung compliance → increased work of breathing
- Ground glass appearance on X-ray
- Treatment: Exogenous surfactant instillation + mechanical ventilation
TOPIC 7: PULMONARY VOLUMES AND CAPACITIES ⭐⭐ (Must Know!)
How are they measured?
- By Spirometry using a Spirometer
- Subject breathes into the spirometer; the displacement of a bell is recorded
Lung VOLUMES (4 volumes)
| Volume | Abbreviation | Normal Value | Definition |
|---|
| Tidal Volume | TV or Vt | 500 mL | Air inspired or expired in one normal quiet breath |
| Inspiratory Reserve Volume | IRV | 3000 mL | Extra air that can be inspired after normal inspiration |
| Expiratory Reserve Volume | ERV | 1200 mL | Extra air that can be expired after normal expiration |
| Residual Volume | RV | 1200 mL | Air remaining in lungs after maximum forced expiration; CANNOT be measured by spirometry |
Memory trick for volumes: TIRE → Tidal, IRV, RV, ERV
Lung CAPACITIES (4 capacities - each = 2 or more volumes added together)
| Capacity | Abbreviation | Normal Value | Formula |
|---|
| Inspiratory Capacity | IC | 3500 mL | TV + IRV |
| Functional Residual Capacity | FRC | 2400 mL | ERV + RV (cannot be measured by spirometry) |
| Vital Capacity | VC | 4700 mL | IRV + TV + ERV = TLC - RV |
| Total Lung Capacity | TLC | 5900 mL | VC + RV = All 4 volumes added (cannot be measured by spirometry) |
Important Points:
- RV, FRC, and TLC cannot be measured by spirometry (they all include RV)
- FRC and RV are measured by helium dilution method or body plethysmograph
- FRC = equilibrium/resting volume of lungs (lung volume after a normal quiet expiration)
Factors affecting Vital Capacity:
- ↑ VC in: males, tall people, athletes, deep breathing
- ↓ VC in: females, old age, short stature, obstructive/restrictive lung diseases
Minute Respiratory Volume:
MRV = Respiratory Rate × Tidal Volume = 12-15 × 500 = 6000-7500 mL/min (~6-7.5 L/min)
Alveolar Ventilation:
VA = (TV - Dead Space) × Respiratory Rate = (500 - 150) × 12 = 4200 mL/min
TOPIC 8: DEAD SPACE ⭐
Definition: Volume of the respiratory tract where NO gas exchange takes place
Types:
| Type | Normal Value | Description |
|---|
| Anatomical dead space | ~150 mL | Volume of conducting airways (nose to terminal bronchioles) |
| Alveolar dead space | ~0 mL (in health) | Ventilated alveoli NOT perfused with blood |
| Physiological dead space | ~150 mL (in health) | Anatomical + Alveolar dead space |
Important: In disease (e.g., pulmonary embolism), alveolar dead space increases → physiological dead space > anatomical dead space
TOPIC 9: AIRWAY RESISTANCE AND AIRFLOW
Ohm's Law applied to airways:
Q = ΔP / R
- Q = Airflow (L/min)
- ΔP = Pressure difference between mouth and alveoli
- R = Airway resistance (cmH₂O/L/sec)
Poiseuille's Law (for resistance):
R = 8ηL / πr⁴
- Radius (r) is the MOST important factor
- Doubling radius → decreases resistance 16 times!
Factors increasing airway resistance:
- Bronchoconstriction (asthma, histamine, parasympathetic stimulation)
- Mucus secretion (bronchitis)
- Foreign body
- Decreased lung volume (airways narrow)
Factors decreasing airway resistance:
- Bronchodilation (sympathetic, adrenaline, β₂ agonists)
- Deep inspiration (airways pulled open)
- Normal surfactant
Neural Control of Airway Diameter:
- Parasympathetic (vagus nerve): Bronchoconstriction (via ACh → M₃ receptors)
- Sympathetic: Bronchodilation (via adrenaline → β₂ receptors)
- This is why adrenaline is used in acute asthma!
TOPIC 10: GAS LAWS (Applied to Respiration)
| Gas Law | Statement | Application |
|---|
| Dalton's Law | Total pressure = sum of partial pressures of all gases | Partial pressures of O₂, CO₂, N₂ in air |
| Henry's Law | Amount of gas dissolved ∝ partial pressure | O₂ dissolved in blood |
| Boyle's Law | P × V = constant (at constant temperature) | Breathing mechanics |
| Fick's Law | Diffusion rate ∝ (area × diff. coeff. × ΔP) / thickness | Gas exchange across alveolar membrane |
| Laplace's Law | P = 2T/r | Alveolar stability, surfactant |
TOPIC 11: PARTIAL PRESSURES OF GASES ⭐⭐
Composition of Inspired Air:
- O₂ = 21%, N₂ = 79%, CO₂ = 0.04%
Partial Pressures (in mmHg) at different locations:
| Gas | Dry Air | Humidified Air | Alveolar Air | Arterial Blood | Venous Blood |
|---|
| PO₂ | 159 | 150 | 100 | 100 | 40 |
| PCO₂ | 0.3 | 0.3 | 40 | 40 | 46 |
| PN₂ | 600 | 563 | 573 | 573 | 573 |
| PH₂O | 0 | 47 | 47 | 47 | 47 |
Water vapour pressure at body temperature (37°C) = 47 mmHg (always subtract when calculating)
Humidified inspired air PO₂ = 0.21 × (760 - 47) = 0.21 × 713 = 150 mmHg
TOPIC 12: DIFFUSION OF GASES (GAS EXCHANGE) ⭐
Fick's Law of Diffusion:
Rate of diffusion = (A × D × ΔP) / T
- A = Surface area of membrane
- D = Diffusion coefficient = solubility / √molecular weight
- ΔP = Partial pressure difference
- T = Thickness of membrane
Normal Alveolar-capillary membrane properties:
- Thickness = 0.5 micrometers (very thin)
- Surface area = 70 m²
Diffusion capacity of lungs:
- For O₂ at rest = 21 mL/mmHg/min (can increase 3× during exercise)
- CO₂ diffuses 20 times faster than O₂ despite a smaller gradient (because CO₂ is much more soluble)
Conditions that decrease diffusion:
- ↑ Membrane thickness (pulmonary fibrosis, oedema)
- ↓ Surface area (emphysema, pneumonia, surgical removal of lung)
- ↓ Pressure gradient (high altitude, hypoventilation)
TOPIC 13: OXYGEN TRANSPORT IN BLOOD ⭐⭐⭐
O₂ is carried in blood in TWO forms:
Form 1: Dissolved O₂ (~2-3%)
- Dissolved directly in plasma
- Amount = PaO₂ × 0.003 = 100 × 0.003 = 0.3 mL O₂/100 mL blood
- Very small amount - insufficient alone to sustain life
Form 2: Bound to Haemoglobin (~97-98%)
- O₂ + Haemoglobin → Oxyhaemoglobin (HbO₂)
- 1 gram Hb can carry 1.34 mL O₂ (Hüfner's constant)
- Normal Hb = 15 g/dL
- O₂ carrying capacity = 15 × 1.34 = 20.1 mL O₂/100 mL blood
Total O₂ content of arterial blood = 20.1 + 0.3 = ~20.4 mL/100 mL blood
Structure of Haemoglobin:
- 4 subunits: each has a globin chain + haem group
- Haem = iron-containing porphyrin ring
- Iron in ferrous state (Fe²⁺) to bind O₂
- Adult Hb (HbA) = α₂β₂
- Fetal Hb (HbF) = α₂γ₂ → higher affinity for O₂ than HbA
- 1 molecule of Hb can carry 4 molecules of O₂
Types of Haemoglobin:
| Type | Structure | Feature |
|---|
| HbA (Adult) | α₂β₂ | Normal adult |
| HbF (Fetal) | α₂γ₂ | Higher O₂ affinity, present in fetus |
| HbS (Sickle) | Abnormal β | Sickle cell disease |
| Methaemoglobin | Fe³⁺ (oxidized) | Cannot carry O₂ |
| Carboxyhaemoglobin | CO attached | CO has 250× greater affinity than O₂ |
TOPIC 14: OXYHAEMOGLOBIN DISSOCIATION CURVE ⭐⭐⭐ (MOST IMPORTANT!)
What is it?
- A graph showing the relationship between PO₂ (x-axis) and % Hb saturation (y-axis)
- S-shaped (sigmoid) curve due to cooperative binding of O₂ to Hb
Key Points on the curve:
- At PO₂ = 100 mmHg (lungs): Hb is 97-98% saturated ← Loading O₂ in lungs
- At PO₂ = 40 mmHg (tissues): Hb is 75% saturated ← Unloading O₂ to tissues
- P50 = 26 mmHg = PO₂ at which Hb is 50% saturated
BOHR EFFECT: ⭐⭐
CO₂/H⁺ shift the curve to the RIGHT → reduced O₂ affinity → more O₂ unloaded at tissues
Right Shift of Curve (↓ O₂ affinity, more O₂ released to tissues):
- ↑ CO₂ (Bohr effect)
- ↑ H⁺ (acidosis, ↓ pH)
- ↑ Temperature
- ↑ 2,3-Diphosphoglycerate (2,3-DPG)
- Memory tip: "CADET face RIGHT" = CO₂, Acidity, 2,3-DPG, Exercise, Temperature
Left Shift of Curve (↑ O₂ affinity, Hb holds O₂ more tightly):
- ↓ CO₂
- ↓ H⁺ (alkalosis, ↑ pH)
- ↓ Temperature
- ↓ 2,3-DPG
- Fetal Hb (HbF)
- CO poisoning
- Methemoglobin
Right shift = Good at tissues (releases O₂ more easily)
Left shift = Good at lungs (loads O₂ more easily)
Significance of Sigmoid Shape:
- Flat upper part = Loading zone in lungs (Hb stays saturated even if PO₂ drops slightly)
- Steep lower part = Unloading zone at tissues (small drop in PO₂ → large O₂ release)
TOPIC 15: CARBON DIOXIDE TRANSPORT ⭐⭐
CO₂ is carried in blood in THREE forms:
| Form | Amount (%) | Details |
|---|
| As Bicarbonate (HCO₃⁻) | 70% | Major form |
| Carbaminohaemoglobin | 20-23% | CO₂ bound to Hb protein (not to Fe²⁺) |
| Dissolved in plasma | 7-10% | Minor form |
Bicarbonate Formation (most important reaction):
Inside RBC:
CO₂ + H₂O ⇌ H₂CO₃ ⇌ H⁺ + HCO₃⁻
(catalyzed by Carbonic Anhydrase enzyme - speeds reaction 5000 times!)
- HCO₃⁻ moves out of RBC into plasma
- Cl⁻ moves into RBC to maintain electrical balance
- This is called the CHLORIDE SHIFT (Hamburger's shift)
HALDANE EFFECT: ⭐
Deoxygenated Hb (at tissues) binds MORE CO₂ and H⁺ than oxygenated Hb
- Helps load CO₂ in tissues and unload CO₂ in lungs
- Opposite of Bohr effect - both work together to facilitate gas exchange!
TOPIC 16: VENTILATION-PERFUSION RATIO (V/Q RATIO) ⭐⭐
Definition:
- V = Ventilation (VA) = 4.2 L/min
- Q = Perfusion (cardiac output to lungs) = 5 L/min
- Normal V/Q = 0.8
Regional V/Q variations (in standing person - due to gravity):
| Region | V/Q Ratio | Explanation |
|---|
| Apex (top) | > 0.8 (high) | Under-perfused, relatively over-ventilated |
| Base (bottom) | < 0.8 (low) | Over-perfused, relatively under-ventilated |
Extreme V/Q values:
| V/Q Value | Condition | Example |
|---|
| V/Q = 0 | Pure shunt | Airway blocked, alveolus perfused but NOT ventilated |
| V/Q = ∞ | Pure dead space | Pulmonary embolism, alveolus ventilated but NOT perfused |
| V/Q = 0.8 | Normal | Healthy lung |
Hypoxic Vasoconstriction: ⭐
- When alveolar PO₂ is low → pulmonary arterioles constrict
- Blood diverted away from poorly ventilated alveoli
- Purpose: Improves V/Q matching, reduces hypoxemia
- This is the OPPOSITE of what happens in systemic circulation!
- At high altitude: widespread hypoxic vasoconstriction → pulmonary hypertension
TOPIC 17: THREE ZONES OF THE LUNG (West's Zones) ⭐
In a standing person, blood pressure in pulmonary vessels varies with height due to gravity.
| Zone | Location | Pressure Relationship | Blood Flow |
|---|
| Zone 1 | Apex | PA > Pa > Pv | Very low / zero |
| Zone 2 | Middle | Pa > PA > Pv | Moderate |
| Zone 3 | Base | Pa > Pv > PA | Maximum |
Where: PA = Alveolar pressure, Pa = Pulmonary arterial pressure, Pv = Pulmonary venous pressure
In supine position, there is no Zone 1 - blood flow is nearly uniform throughout the lung.
TOPIC 18: CONTROL OF RESPIRATION ⭐⭐⭐
18A: Respiratory Control Centres (in Brainstem)
Located in the Medulla and Pons
| Centre | Location | Function |
|---|
| Dorsal Respiratory Group (DRG) | Medulla | Controls INSPIRATION; sets basic rhythm; sends signals via phrenic nerve to diaphragm |
| Ventral Respiratory Group (VRG) | Medulla | Controls EXPIRATION (active during forced breathing) |
| Pneumotaxic Centre | Upper Pons | Inhibits DRG → switches off inspiration → prevents lung over-inflation; controls rate and depth |
| Apneustic Centre | Lower Pons | Prolongs inspiration (apneusis = prolonged inspiratory gasps); opposed by pneumotaxic centre |
Important Points:
- Basic breathing rhythm is generated in the Medulla (even if pons is cut, breathing continues)
- Cortex can voluntarily override the brainstem (e.g., breath-holding, singing)
18B: Chemoreceptors ⭐⭐⭐ (Most Important!)
Central Chemoreceptors:
- Location: Ventral surface of Medulla (not in respiratory centre itself)
- Stimulus: CO₂ and H⁺ ions (mainly CO₂)
- Mechanism: CO₂ crosses blood-brain barrier → combines with H₂O → H₂CO₃ → H⁺ → stimulates receptors
- Most important for minute-to-minute regulation of breathing
- Do NOT respond directly to hypoxia (low O₂)
Peripheral Chemoreceptors:
- Location: Carotid bodies (at bifurcation of common carotid artery) + Aortic bodies (in aortic arch)
- Nerve supply: Carotid body → CN IX (Glossopharyngeal); Aortic body → CN X (Vagus)
- Stimuli: ↓ PaO₂, ↑ PaCO₂, ↑ H⁺, ↓ arterial pressure
- Carotid bodies are more important in humans
- ONLY receptors that respond to hypoxemia (low PO₂)
- Stimulated when PaO₂ falls below 60 mmHg
Summary: What stimulates breathing?
| Stimulus | Main Receptor | Effect on Breathing |
|---|
| ↑ CO₂ (hypercapnia) | Central chemoreceptors (mainly) | ↑↑ Ventilation (most powerful stimulus) |
| ↓ pH (acidosis) | Both central and peripheral | ↑ Ventilation |
| ↓ O₂ (hypoxemia) | Peripheral chemoreceptors only | ↑ Ventilation (only when PaO₂ < 60 mmHg) |
CO₂ is the most powerful stimulus for breathing!
18C: Pulmonary Reflexes
1. Hering-Breuer Inflation Reflex:
- Stretch receptors in bronchial walls activated by lung inflation
- Send signals via vagus nerve → inhibit inspiratory centre → stops further inspiration
- Prevents over-distension of lungs
- Active mainly at large tidal volumes (> 1.5 L); not very active in normal quiet breathing in adults
2. Cough Reflex:
- Stimulus: Dust, mucus, foreign body, chemical irritants in trachea, bronchi, carina
- Afferents via vagus nerve to medulla
- Steps:
- Deep inspiration (~2.5 L)
- Vocal cords close tightly; glottis closes
- Forceful contraction of expiratory muscles → intrapulmonary pressure rises to 100 mmHg
- Glottis suddenly opens → explosive outflow of air at 75-100 miles/hr
- Mucus and foreign material expelled
3. Sneeze Reflex:
- Similar to cough but receptors in nasal mucosa
- Afferents via trigeminal nerve (CN V)
- Uvula depresses → air expelled mainly through nose
TOPIC 19: PULMONARY CIRCULATION
Special features:
- Low pressure system: Pulmonary artery pressure = 25/8 mmHg (mean = 15 mmHg)
- Compare with systemic: 120/80 mmHg
- Low resistance (vessels are thin-walled, distensible)
- Large compliance (acts as blood reservoir)
Hypoxic Pulmonary Vasoconstriction: ⭐
- Low alveolar PO₂ → pulmonary arteriole constriction
- Opposite of systemic circulation (where hypoxia causes vasodilation)
- Purpose: Diverts blood to better-ventilated alveoli
- Clinical: At high altitude → widespread pulmonary vasoconstriction → pulmonary hypertension → cor pulmonale (right heart failure)
Distribution of pulmonary blood flow:
- In standing: Maximum at BASE, Minimum at APEX (gravity effect)
- In supine: Nearly uniform (no gravitational effect)
TOPIC 20: MUCUS AND CILIA - RESPIRATORY DEFENCE
- All respiratory passages lined with ciliated epithelium with ~200 cilia per cell
- Cilia beat at 10-20 times/sec toward pharynx (mucociliary escalator)
- Mucus traps dust particles, bacteria, allergens
- Trapped particles → swept upward → swallowed or coughed out
- This is called the Mucociliary Clearance Mechanism
Goblet cells and submucosal glands secrete mucus
- Cigarette smoke damages cilia → impairs clearance → chronic bronchitis
TOPIC 21: HYPOXIA AND HYPOXEMIA ⭐
Definitions:
- Hypoxemia = low PaO₂ (↓ O₂ in arterial blood)
- Hypoxia = low O₂ supply to tissues (or inability to use O₂)
- Hypoxemia can cause hypoxia, but not always (e.g., cyanide poisoning = hypoxia without hypoxemia)
Types of Hypoxia:
| Type | Cause | PaO₂ | Hb | Cardiac Output | O₂ Utilization |
|---|
| Hypoxic hypoxia | Low PaO₂ (lung disease, high altitude) | ↓ Low | Normal | Normal | Normal |
| Anaemic hypoxia | Low Hb (anaemia, metHb, CO poisoning) | Normal | ↓ Low | Normal | Normal |
| Stagnant/Ischaemic hypoxia | Poor blood flow (heart failure, shock) | Normal | Normal | ↓ Low | Normal |
| Histotoxic hypoxia | Cells can't use O₂ (cyanide poisoning) | Normal | Normal | Normal | ↓ Impaired |
Signs of Hypoxia:
- Cyanosis (bluish discoloration), headache, restlessness, confusion, tachycardia, tachypnoea
TOPIC 22: NON-RESPIRATORY FUNCTIONS OF THE LUNGS
- ACE action: Angiotensin I → Angiotensin II (by ACE in pulmonary capillaries)
- Inactivation: Bradykinin, serotonin, norepinephrine inactivated in lungs
- Synthesis: Prostacyclin (PGI₂ = vasodilator) synthesized
- Prostaglandin metabolism: PGE₁, PGF₂α removed
- Thromboxane A₂ synthesis (vasoconstrictor)
- Blood reservoir for left heart
- Vocalization (speech, singing)
- pH regulation (rapid, by adjusting ventilation → changes PaCO₂ → changes pH)
- Filtration of microemboli and clots from venous blood
QUICK REFERENCE: IMPORTANT NUMBERS TO MEMORIZE ⭐⭐
| Parameter | Value |
|---|
| Respiratory rate (normal) | 12-20 breaths/min |
| Tidal Volume | 500 mL |
| IRV | 3000 mL |
| ERV | 1200 mL |
| RV | 1200 mL |
| IC | 3500 mL |
| FRC | 2400 mL |
| VC | 4700 mL |
| TLC | 5900 mL |
| Dead space | 150 mL |
| Minute ventilation | 6-7.5 L/min |
| Alveolar ventilation | 4.2 L/min |
| PaO₂ (arterial) | 100 mmHg |
| PaCO₂ (arterial) | 40 mmHg |
| PvO₂ (venous) | 40 mmHg |
| PvCO₂ (venous) | 46 mmHg |
| Water vapour pressure (37°C) | 47 mmHg |
| Normal V/Q ratio | 0.8 |
| P50 | 26 mmHg |
| Pulmonary artery pressure | 25/8 mmHg |
| Arterial pH | 7.35-7.45 |
| Normal HCO₃⁻ | 22-26 mEq/L |
| Hüfner's constant | 1.34 mL O₂/g Hb |
| O₂ carrying capacity of blood | 20 mL/100 mL |
| CO₂ diffuses faster than O₂ by | 20 times |
| Alveolar surface area | 70 m² |
| Alveolar-capillary membrane thickness | 0.5 micrometers |
| Cilia beat rate | 10-20/sec |
IMPORTANT EXAM QUESTIONS FROM EACH TOPIC
Short Answer Questions (SAQ - 5-10 marks):
- Define tidal volume. List all lung volumes and capacities with normal values.
- What is surfactant? Name its type and functions.
- Describe the oxyhaemoglobin dissociation curve and factors causing shifts.
- What is Bohr effect? What is Haldane effect?
- Explain the mechanics of inspiration.
- What is FRC? How is it measured?
- Define dead space. What are its types?
- What is V/Q ratio? What are its regional variations?
- Classify types of hypoxia with examples.
- Describe the cough reflex.
Long Answer Questions (LAQ - 10-15 marks):
- Describe the regulation/control of respiration with a neat diagram of respiratory centres.
- Discuss the transport of O₂ in blood. Draw and explain the oxyhaemoglobin dissociation curve.
- Discuss the transport of CO₂ in blood.
- Describe lung volumes and capacities with a spirogram diagram.
- Describe the mechanics of breathing - inspiration and expiration.
- What is surfactant? Describe its production, composition and clinical significance.
Sources: Guyton and Hall Textbook of Medical Physiology (14th Ed.), Ganong's Review of Medical Physiology (26th Ed.) - the standard reference texts aligned with GK Pal's Textbook of Medical Physiology for 1st BHMS/MBBS.