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Summarise pulmonary ventilation and ventilation perfusion ratio for seminar presentation with all important points and easy to understand for studying

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🫁 Pulmonary Circulation & Ventilation-Perfusion Ratio

Seminar Summary — Chapter 106


PART 1: PULMONARY CIRCULATION

What is Pulmonary Circulation?

  • Blood ejected by the heart into pulmonary circulation = same amount as systemic circulation
  • BUT pulmonary circulation is a low-pressure, low-resistance system
  • Mean pulmonary arterial pressure = 15 mm Hg (vs. ~100 mm Hg in systemic)
  • Total pulmonary vascular resistance = about 1/10th of systemic resistance

Key Special Features (High-Yield)

FeatureDetail
Thin wallsLess smooth muscle; highly compliant
Short, wide vesselsHigh compliance; can hold large volumes
Capillary arrangementForm a lattice (basket) around each alveolus; do NOT form a capillary network like elsewhere
Collapse if alveolar pressure > capillary pressureWalls are very thin
Low resting vasomotor toneVessels are mostly dilated at rest
Memory trick: "Low pressure, thin walls, high compliance, no capillary network."

Functions of Pulmonary Circulation

  1. Gas exchange - bring deoxygenated blood to alveoli; remove CO₂, add O₂
  2. Filter - traps thrombi and emboli from venous blood; endothelial cells release fibrinolytic agents
  3. Metabolic - converts angiotensin I → angiotensin II (via ACE); inactivates bradykinin, serotonin, prostaglandins, norepinephrine
  4. Blood reservoir - ~500 mL at any time (10% of total blood volume)

Pulmonary Blood Flow - Distribution

CompartmentVolume
Pulmonary arteries150 mL
Pulmonary veins270 mL
Pulmonary capillaries80 mL
In upright posture: Blood flow is lowest at the apex and highest at the base due to gravity.

Factors Affecting Pulmonary Blood Flow

4 main factors:
  1. Pulmonary vascular resistance (PVR)
  2. Gravity
  3. Alveolar pressure
  4. Arterio-venous pressure gradient

Pulmonary Vascular Resistance (PVR)

PVR is affected by:
1. Lung Volumes
  • High lung volumes → increased transmural pressure → alveolar vessels compressed → PVR increases
  • Low lung volumes → pleural pressure becomes positive → extra-alveolar vessels compressed → PVR increases
  • PVR is LOWEST at functional residual capacity (FRC)
2. Hormones
  • Vasoconstrictors: Serotonin, norepinephrine, histamine, thromboxane A₂, leukotrienes
  • Vasodilators: Adenosine, acetylcholine, prostacyclin (PG-I₂), isoproterenol
3. Oxygen Tension
  • Low O₂ (hypoxia) → vasoconstriction (unique to pulmonary circulation, opposite of systemic!)
  • Mechanism: hypoxia directly contracts smooth muscle; opens voltage-gated Ca²⁺ channels
  • Accentuated by high CO₂ and low pH

Physiological Significance of Low PVR (Important!)

Low PVR with increased cardiac output has 3 benefits:
  • (a) Decreased velocity → more time for gas exchange
  • (b) Capillary distension → increased surface area for diffusion
  • (c) High capillary pressure is prevented → prevents pulmonary edema
How PVR falls with increased cardiac output (2 mechanisms):
  1. Capillary recruitment - previously closed capillaries at apex open as flow increases
  2. Capillary distension - thin, compliant capillaries expand as pressure increases

Effect of Gravity on Pulmonary Blood Flow (The 3 Zones)

In upright posture, due to hydrostatic differences:
ZoneLocationArterial PressureVenous PressureAlveolar PressureBlood Flow
Zone 1 (Upper)ApexLowVery low> ArterialCapillaries collapse; NO flow (dead space)
Zone 2 (Middle)Mid-lung> Alveolar< AlveolarBetween A & VFlow determined by A-alveolar difference ("waterfall effect")
Zone 3 (Lower)Base> Venous> AlveolarLowestFlow highest; driven by A-V pressure difference
Key numbers: Arterial pressure at apex = 7.4 mm Hg; at base = 17.7 mm Hg. For every 1 cm increase in height, hydrostatic pressure falls by 0.74 mm Hg.

Regulation of Pulmonary Blood Flow

Active Factors:
  • Neural: Sympathetic → mild vasoconstriction; parasympathetic → mild vasodilation (resting sympathetic tone is almost absent)
  • Hormonal: Vasoconstrictors (serotonin, norepinephrine, endothelin, angiotensin II, thromboxane A₂, leukotrienes); Vasodilators (adenosine, acetylcholine, prostacyclin, bradykinin, NO)
  • Chemical: Hypoxia → vasoconstriction (hypoxic pulmonary vasoconstriction - HPV)
Passive Factors:
  • Cardiac output, gravity, and lung volumes

Filtration Across Pulmonary Capillaries

Governed by Starling forces. Two additional factors specific to lungs:
  • Alveolar surface tension - favors filtration (pulls fluid toward alveolus)
  • Alveolar pressure - opposes filtration (compresses interstitial space)
Why lungs stay dry (3 protective mechanisms):
  1. Hydrostatic pressure is low (8 mm Hg) - far less than plasma oncotic pressure (25 mm Hg)
  2. Alveolar surface tension favors a small net fluid outflow into interstitium only
  3. Extensive lymphatics near terminal bronchioles drain excess fluid efficiently

Pulmonary Edema

Definition: Excess fluid in interstitial spaces and alveoli
4 Causes (must know):
CauseExample
1. Increased capillary hydrostatic pressureMitral stenosis, left heart failure (most common cause)
2. Increased alveolar surface tensionDecreased surfactant (ARDS)
3. Decreased oncotic pressureHypoproteinemia, starvation
4. Increased capillary permeabilityPulmonary vascular injury, oxidant damage, inflammatory reactions, neurogenic shock
Treatment principles:
  • Diuretics (reduce blood volume)
  • Digitalis (improve left ventricular function)
  • Vasodilators (reduce systemic vascular resistance)

Drowning (Brief)

TypeMechanismDeath
Fresh waterDilutes plasma → hemolysis → hyperkalemia → ventricular fibrillationNOT due to pulmonary edema
Salt waterHypertonic fluid → draws fluid into alveoli → pulmonary edema → asphyxia

PART 2: VENTILATION-PERFUSION (V̇A/Q̇) RATIO

What is V̇A/Q̇ Ratio?

  • It is the ratio of alveolar ventilation to blood flow (perfusion) in the lungs
  • Normal individual at rest:
    • Alveolar ventilation (V̇A) = 4 L/min
    • Pulmonary blood flow (Q̇) = 5 L/min
  • Normal V̇A/Q̇ = 0.8

Regional Differences in V̇A/Q̇ (Very Important!)

RegionBlood FlowVentilationV̇A/Q̇ Ratio
ApexVery low (5-fold less than base)Proportionally greater~3 (high ratio)
BaseHighestAlso high, but less so~0.6 (low ratio)
Average--0.8
Key concept: Blood flow shows a 5-fold difference between apex and base; ventilation shows only a 2-fold difference. So the apex has a HIGHER V̇A/Q̇ and the base has a LOWER V̇A/Q̇.

Physiological Importance of V̇A/Q̇ Ratio

High V̇A/Q̇ (Apex)Low V̇A/Q̇ (Base)
More ventilation relative to perfusionMore perfusion relative to ventilation
PO₂ HIGH, PCO₂ LOWPO₂ LOW, PCO₂ HIGH
Favors growth of TB bacilli (aerobic)Wasted perfusion (venous admixture)
Clinical pearl: Tuberculosis occurs more commonly at the APEX because the high V̇A/Q̇ ratio provides a higher oxygen level that favors growth of Mycobacterium tuberculosis.

Effects of Changes in V̇A/Q̇ Ratio

Decreased V̇A/Q̇ (e.g., airway obstruction):
  • Less O₂ delivery to alveolus → alveolar PO₂ falls
  • Less CO₂ removal → alveolar PCO₂ rises
  • Blood passing through is poorly oxygenated
Increased V̇A/Q̇ (e.g., vascular obstruction):
  • Blood flow reduced relative to ventilation
  • Alveolar CO₂ falls (less CO₂ from blood)
  • Alveolar PO₂ rises (more O₂ being blown in but not taken up)
  • This portion acts like dead space

Venous Admixture and Physiologic Shunt

Wasted perfusion = blood perfuses poorly ventilated areas = blood not fully oxygenated
Venous admixture: Mixing of unoxygenated blood with oxygenated blood. Occurs due to:
  • A shunt, OR
  • Low V̇A/Q̇ ratio areas

Types of Shunts

1. Anatomical Shunt
  • Blood bypasses lungs through an anatomical defect
  • Example: Right-to-left shunt in atrial or ventricular septal defects, or pulmonary artery connecting directly to pulmonary vein
  • In normal individuals: maximum venous admixture (physiological shunt) = only 2% of cardiac output
  • In some bronchial diseases → can increase up to 20%
  • In right-to-left congenital shunts → can reach 50% of cardiac output
2. Physiological Shunt (Bronchial Circulation)
  • Deoxygenated bronchial venous blood drains into oxygenated pulmonary veins
  • Contributes to normally present venous admixture

Low V̇A/Q̇ Ratio (Hypoventilated Lung)

  • Occurs when a fraction of pulmonary capillary blood is not oxygenated due to low alveolar ventilation
  • Normally at the base of the lung
  • Can also occur when an airway is partially obstructed (e.g., hypoventilated portion of lung)
  • Results in venous admixture

PART 3: BRONCHIAL CIRCULATION

  • Supplies blood to walls of conducting airways (trachea down to terminal bronchioles)
  • Does NOT supply respiratory bronchioles or alveoli
  • Features:
    • Receives only 1% of cardiac output (increases to 10% in chronic bronchitis)
    • Bronchial arterial pressure ≈ aortic pressure
    • Venous return via bronchial veins OR pulmonary veins (contributing to physiological shunt)
Physiological Importance:
  • Capable of angiogenesis (formation of new vessels)
  • When pulmonary flow is obstructed (clot/embolus), bronchial circulation provides collaterals to protect lung parenchyma

CHAPTER KEY CONCEPTS (Must-Know Summary)

#Key Concept
1Pulmonary circulation = low pressure, low resistance; resting sympathetic tone is absent
2PVR falls with increased cardiac output via capillary recruitment and distension
3Hypoxia causes pulmonary vasoconstriction (opposite of systemic)
4PVR is lowest at FRC; increases at both high and low lung volumes
5Lung divided into Zone 1 (apex), Zone 2 (middle), Zone 3 (base) based on gravity effects
6Normal V̇A/Q̇ = 0.8; apex ratio = 3, base ratio = 0.6
7High V̇A/Q̇ → high PO₂, low PCO₂ (apex - TB favored here)
8Low V̇A/Q̇ → low PO₂, high PCO₂ (base) → venous admixture
9Pulmonary edema: most common cause = high capillary hydrostatic pressure
10Bronchial circulation does angiogenesis; saves lung when pulmonary artery blocked

VIVA VOICE TIPS (Common Examiner Questions)

  1. What is pulmonary wedge pressure? - Indirect measure of left atrial pressure; measured by Swan-Ganz catheter wedged in small pulmonary artery
  2. Why does TB occur at apex? - High V̇A/Q̇ ratio → high PO₂ → favors aerobic M. tuberculosis
  3. What is waterfall effect? - In Zone 2, flow is determined by arterial-alveolar pressure difference, not A-V gradient; veins are compressed like a waterfall
  4. Why does PVR fall with exercise? - Capillary recruitment + distension → more vessels open
  5. What is hypoxic pulmonary vasoconstriction? - Low alveolar PO₂ directly contracts pulmonary vascular smooth muscle via voltage-gated Ca²⁺ channels; protective - diverts blood away from poorly ventilated areas
  6. Difference between anatomical vs physiological shunt? - Anatomical = structural defect bypassing lungs; Physiological = bronchial venous admixture (normal ~2% of CO)

Source: Chapter 106 - Pulmonary Circulation and Ventilation-Perfusion Ratio (Sembulingam Physiology / Section 10: Respiratory System)
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