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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)
| Feature | Detail |
|---|
| Thin walls | Less smooth muscle; highly compliant |
| Short, wide vessels | High compliance; can hold large volumes |
| Capillary arrangement | Form a lattice (basket) around each alveolus; do NOT form a capillary network like elsewhere |
| Collapse if alveolar pressure > capillary pressure | Walls are very thin |
| Low resting vasomotor tone | Vessels are mostly dilated at rest |
Memory trick: "Low pressure, thin walls, high compliance, no capillary network."
Functions of Pulmonary Circulation
- Gas exchange - bring deoxygenated blood to alveoli; remove CO₂, add O₂
- Filter - traps thrombi and emboli from venous blood; endothelial cells release fibrinolytic agents
- Metabolic - converts angiotensin I → angiotensin II (via ACE); inactivates bradykinin, serotonin, prostaglandins, norepinephrine
- Blood reservoir - ~500 mL at any time (10% of total blood volume)
Pulmonary Blood Flow - Distribution
| Compartment | Volume |
|---|
| Pulmonary arteries | 150 mL |
| Pulmonary veins | 270 mL |
| Pulmonary capillaries | 80 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:
- Pulmonary vascular resistance (PVR)
- Gravity
- Alveolar pressure
- 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):
- Capillary recruitment - previously closed capillaries at apex open as flow increases
- 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:
| Zone | Location | Arterial Pressure | Venous Pressure | Alveolar Pressure | Blood Flow |
|---|
| Zone 1 (Upper) | Apex | Low | Very low | > Arterial | Capillaries collapse; NO flow (dead space) |
| Zone 2 (Middle) | Mid-lung | > Alveolar | < Alveolar | Between A & V | Flow determined by A-alveolar difference ("waterfall effect") |
| Zone 3 (Lower) | Base | > Venous | > Alveolar | Lowest | Flow 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):
- Hydrostatic pressure is low (8 mm Hg) - far less than plasma oncotic pressure (25 mm Hg)
- Alveolar surface tension favors a small net fluid outflow into interstitium only
- Extensive lymphatics near terminal bronchioles drain excess fluid efficiently
Pulmonary Edema
Definition: Excess fluid in interstitial spaces and alveoli
4 Causes (must know):
| Cause | Example |
|---|
| 1. Increased capillary hydrostatic pressure | Mitral stenosis, left heart failure (most common cause) |
| 2. Increased alveolar surface tension | Decreased surfactant (ARDS) |
| 3. Decreased oncotic pressure | Hypoproteinemia, starvation |
| 4. Increased capillary permeability | Pulmonary 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)
| Type | Mechanism | Death |
|---|
| Fresh water | Dilutes plasma → hemolysis → hyperkalemia → ventricular fibrillation | NOT due to pulmonary edema |
| Salt water | Hypertonic 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!)
| Region | Blood Flow | Ventilation | V̇A/Q̇ Ratio |
|---|
| Apex | Very low (5-fold less than base) | Proportionally greater | ~3 (high ratio) |
| Base | Highest | Also 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 perfusion | More perfusion relative to ventilation |
| PO₂ HIGH, PCO₂ LOW | PO₂ 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 |
|---|
| 1 | Pulmonary circulation = low pressure, low resistance; resting sympathetic tone is absent |
| 2 | PVR falls with increased cardiac output via capillary recruitment and distension |
| 3 | Hypoxia causes pulmonary vasoconstriction (opposite of systemic) |
| 4 | PVR is lowest at FRC; increases at both high and low lung volumes |
| 5 | Lung divided into Zone 1 (apex), Zone 2 (middle), Zone 3 (base) based on gravity effects |
| 6 | Normal V̇A/Q̇ = 0.8; apex ratio = 3, base ratio = 0.6 |
| 7 | High V̇A/Q̇ → high PO₂, low PCO₂ (apex - TB favored here) |
| 8 | Low V̇A/Q̇ → low PO₂, high PCO₂ (base) → venous admixture |
| 9 | Pulmonary edema: most common cause = high capillary hydrostatic pressure |
| 10 | Bronchial circulation does angiogenesis; saves lung when pulmonary artery blocked |
VIVA VOICE TIPS (Common Examiner Questions)
- What is pulmonary wedge pressure? - Indirect measure of left atrial pressure; measured by Swan-Ganz catheter wedged in small pulmonary artery
- Why does TB occur at apex? - High V̇A/Q̇ ratio → high PO₂ → favors aerobic M. tuberculosis
- 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
- Why does PVR fall with exercise? - Capillary recruitment + distension → more vessels open
- 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
- 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)