Doctors Revision

Doctors Revision

Gas Exchange &: Transport

Gas Exchange and Transport

Gas exchange is the process by which oxygen and carbon dioxide move between the lungs and the bloodstream, driven by simple diffusion along partial pressure gradients. This is coupled with the transport of these gases throughout the body via the circulatory system, primarily using hemoglobin in red blood cells. The entire process involves two main stages:

I. External Respiration (in the Lungs)

This is the exchange of gases between the air in the alveoli and the blood in the pulmonary capillaries.

  • Oxygen uptake: Inhaled air has a high partial pressure of oxygen (PO2 ≈ 100 mmHg) in the alveoli, while the deoxygenated blood in the capillaries has a low PO2 ≈ 40 mmHg. This gradient causes oxygen to diffuse rapidly from the alveoli into the blood.
  • Carbon dioxide release: The deoxygenated blood in the capillaries has a higher partial pressure of carbon dioxide (PCO2 ≈ 45 mmHg) compared to the air in the alveoli (PCO2 ≈ 40 mmHg). This causes carbon dioxide to diffuse from the blood into the alveoli to be exhaled.

II. Internal Respiration (in the Tissues)

This is the exchange of gases between the blood in systemic capillaries and the body's tissue cells.

  • Oxygen release: Oxygenated blood arriving at the tissues has a high PO2 ≈ 100 mmHg, while the metabolizing tissue cells have a low PO2 < 40 mmHg due to continuous consumption for cellular respiration. This gradient causes oxygen to dissociate from hemoglobin and diffuse into the cells.
  • Carbon dioxide uptake: Tissue cells produce carbon dioxide as a waste product, resulting in a high PCO2 > 45 mmHg compared to the blood in the capillaries (PCO2 ≈ 40 mmHg). Carbon dioxide diffuses from the cells into the blood.

Objective 1: Describe the partial pressures of oxygen and carbon dioxide in atmospheric air, alveoli, arterial blood, and venous blood.

To understand gas exchange, we first need to grasp the concept of partial pressure.

1. Dalton's Law of Partial Pressures

Dalton's Law states that in a mixture of non-reacting gases, the total pressure exerted is equal to the sum of the partial pressures of the individual gases.

Ptotal = P1 + P2 + P3 + ... Pn

Where Ptotal is the total pressure of the gas mixture and P1, P2, etc. are the partial pressures of each individual gas.

The partial pressure of an individual gas in a mixture is the pressure that gas would exert if it alone occupied the volume. It is directly proportional to its percentage concentration in the mixture.

Partial Pressure of Gas (Px) = % Concentration of Gas x Total Pressure
Example Calculation (Atmospheric Air at Sea Level):

Total Pressure = 760 mmHg. Composition:

  • Nitrogen (N2): ~79%
  • Oxygen (O2): ~21%
  • Carbon Dioxide (CO2): ~0.04%

PO2 = 0.21 x 760 mmHg = ~160 mmHg

2. Partial Pressures in Different Locations

Gases always diffuse down their partial pressure gradients from an area of higher partial pressure to an area of lower partial pressure. This is the driving force for gas exchange.

Let's examine the typical partial pressures of Oxygen (O2) and Carbon Dioxide (CO2) in four key locations:

A. Atmospheric (Inspired) Air (at sea level, dry)

This is the air we breathe in.

PO2 (Atmospheric):
Percentage: ~21%
0.21 x 760 = ~160 mmHg
PCO2 (Atmospheric):
Percentage: ~0.04%
0.0004 x 760 = ~0.3 mmHg
(often rounded to 0 mmHg)

B. Alveolar Air

As atmospheric air enters the lungs, it mixes with the air already present in the dead space and alveoli, and it becomes saturated with water vapor. This significantly alters the partial pressures.

Influencing Factors:
  • Water Vapor: At 37°C, water vapor pressure is 47 mmHg. This dilutes other gases (Effective pressure: 760 - 47 = 713 mmHg).
  • Gas Diffusion: CO2 continuously enters from blood; O2 continuously leaves into blood.
PO2 (Alveolar - PAO2):
~104 mmHg
Lower than atmospheric due to water vapor dilution and O2 diffusion into blood.
PCO2 (Alveolar - PACO2):
~40 mmHg
Higher than atmospheric due to CO2 diffusion from blood.

C. Arterial Blood

This is the blood leaving the pulmonary capillaries (oxygenated blood) and traveling to the systemic tissues.

PO2 (Arterial - PaO2):
~95-100 mmHg
Slightly lower than alveolar PO2 due to physiological shunts (bronchial circulation).
PCO2 (Arterial - PaCO2):
~40 mmHg
Same as alveolar PCO2; high solubility allows rapid equilibration.

D. Venous Blood (Mixed Venous Blood)

This is the blood returning to the lungs from the systemic tissues, carrying metabolic waste products.

PO2 (Mixed Venous - PvO2):
~40 mmHg
Lower than arterial because O2 was delivered to tissues.
PCO2 (Mixed Venous - PvCO2):
~45 mmHg
Higher than arterial because CO2 was picked up from tissues.

Summary of Partial Pressures (Approximate Values at Sea Level)

Location PO2 (mmHg) PCO2 (mmHg)
Atmospheric Air 160 0.3
Alveolar Air 104 40
Arterial Blood 95-100 40
Mixed Venous Blood 40 45

Key Gradients for Gas Exchange

  • O2 gradient for diffusion (Alveoli to Pulmonary Capillaries):
    104 mmHg (alveolar) - 40 mmHg (venous) = 64 mmHg
  • CO2 gradient for diffusion (Pulmonary Capillaries to Alveoli):
    45 mmHg (venous) - 40 mmHg (alveolar) = 5 mmHg

Note: Notice the much larger gradient for O2 compared to CO2. This is important because CO2 is much more soluble than O2, allowing it to diffuse efficiently even with a smaller pressure gradient.

Checkpoint Question:

Why is the partial pressure of oxygen in the alveoli (PAO2) significantly lower than the partial pressure of oxygen in atmospheric air (PO2)?

Objective 2: Explain the principles governing gas exchange across the alveolar-capillary membrane (e.g., Dalton's Law, Henry's Law, Fick's Law of Diffusion).

Gas exchange, both between the alveoli and pulmonary capillaries, and between systemic capillaries and tissues, is driven by fundamental physical laws. We've already touched upon Dalton's Law of Partial Pressures, which establishes the pressure gradient for individual gases. Now let's integrate Henry's Law and Fick's Law of Diffusion to understand how these gases actually move and dissolve.

1. Dalton's Law of Partial Pressures (Recap)

  • Principle: The total pressure exerted by a mixture of gases is the sum of the partial pressures of the individual gases. The partial pressure of a specific gas is proportional to its concentration in the mixture.
  • Relevance to Gas Exchange: This law explains why gases move. Gases diffuse from an area where their partial pressure is higher to an area where it is lower. This partial pressure gradient is the primary driving force for gas exchange.
    • O2: High PO2 in alveoli, low PO2 in venous blood → O2 moves into blood.
    • CO2: High PCO2 in venous blood, low PCO2 in alveoli → CO2 moves into alveoli.

2. Henry's Law

Principle:

When a gas is in contact with a liquid, the amount of gas that dissolves in the liquid is directly proportional to its partial pressure above the liquid, and its solubility coefficient in that liquid, at a given temperature.

  • The higher the partial pressure of a gas above a liquid, the more of that gas will dissolve into the liquid.
  • The higher the solubility of a gas in a specific liquid, the more of that gas will dissolve at a given partial pressure.
Amount of dissolved gas = Px * Solubility Coefficient

Where Px is the partial pressure of the gas.

Relevance to Gas Exchange:

  • Loading and Unloading: Henry's Law explains how O2 and CO2 move between the gaseous phase (alveoli) and the liquid phase (blood plasma) and vice versa.
  • Solubility Differences: It highlights a critical difference between O2 and CO2:

    CO2 is about 20-24 times more soluble in plasma than O2. This is extremely important because even though the partial pressure gradient for CO2 across the alveolar-capillary membrane (typically 5 mmHg) is much smaller than for O2 (typically 64 mmHg), CO2 can still diffuse across the membrane very rapidly and efficiently due to its high solubility. This ensures efficient CO2 elimination despite the small gradient.

3. Fick's Law of Diffusion

Fick's Law quantifies the rate at which a gas diffuses across a membrane.

V gas = (A * D * ΔP) / T
V gas: Rate of gas diffusion.
A (Area): Surface area of the membrane. (Larger area = faster diffusion).
D (Diffusion Coefficient): Depends on solubility/molecular weight. (D ∝ Solubility / √MW).
ΔP (Pressure Gradient): Difference in partial pressure. (Larger gradient = faster diffusion).
T (Thickness): Membrane thickness. (Thicker membrane = slower diffusion).

Relevance to Gas Exchange:

This law combines the key anatomical and physiological factors that determine how effectively gas moves between the alveoli and blood.

  • Surface Area (A): The human lungs have an enormous alveolar surface area (estimated 50-100 m², about the size of a tennis court). Diseases like emphysema reduce this area, impairing diffusion.
  • Diffusion Coefficient (D): As mentioned with Henry's Law, CO2 has a much higher diffusion coefficient than O2 due to its greater solubility, meaning it diffuses much faster than O2 for a given partial pressure gradient.
  • Partial Pressure Gradient (ΔP): This is the driving force from Dalton's Law. Maintaining appropriate partial pressure differences is crucial.
  • Thickness (T): The alveolar-capillary membrane is incredibly thin (0.2-0.6 µm). Diseases like pulmonary fibrosis or pulmonary edema increase this thickness, significantly impairing gas diffusion.

In Summary:

  • Dalton's Law explains the direction and driving force (gradients).
  • Henry's Law explains solubility and dissolving into liquid.
  • Fick's Law describes the rate of diffusion integrating area, thickness, gradients, and solubility.
Checkpoint Question:

Given that the partial pressure gradient for O2 across the alveolar-capillary membrane is much larger (64 mmHg) than for CO2 (5 mmHg), why do O2 and CO2 still diffuse across the membrane at roughly equal rates under normal physiological conditions?

Objective 3: Discuss the factors affecting the efficiency of gas exchange at the alveolar-capillary membrane.

The efficiency of gas exchange across the delicate alveolar-capillary membrane is paramount for maintaining proper blood gas levels. Several interconnected factors, derived directly from the laws we just discussed (especially Fick's Law), determine this efficiency.

1. Partial Pressure Gradients of O2 and CO2

How it affects efficiency: This is the most fundamental driving force (Dalton's Law). The steeper the gradient for a gas, the faster it will diffuse.

  • For O2: PO2 alveoli (~104 mmHg) >> PO2 venous blood (~40 mmHg). Large gradient ensures rapid uptake.
  • For CO2: PCO2 venous blood (~45 mmHg) >> PCO2 alveoli (~40 mmHg). Smaller gradient sufficient due to high solubility.
Factors influencing gradients:
  • Alveolar ventilation: Maintains PAO2 and PACO2. Hypoventilation reduces gradients.
  • Perfusion: Brings deoxygenated blood to maintain gradients.
  • Altitude: Low atmospheric PO2 reduces alveolar PO2 and the gradient.

2. Thickness of the Respiratory Membrane

How it affects efficiency: Per Fick's Law, diffusion is inversely proportional to thickness. A thicker membrane slows down diffusion.

Normal state: Extremely thin (0.2-0.6 µm).

Pathological conditions causing increased thickness:
  • Pulmonary Edema: Fluid accumulation in interstitial space.
  • Pulmonary Fibrosis: Scarring/thickening of tissue.
  • Pneumonia: Inflammatory exudates.

These conditions primarily impair O2 diffusion (less soluble) more than CO2.

3. Surface Area of the Respiratory Membrane

How it affects efficiency: Rate of diffusion is directly proportional to surface area.

Normal state: Immense surface area (50-100 m²).

Pathological conditions causing decreased surface area:
  • Emphysema: Destruction of alveolar walls, merging alveoli.
  • Lung Resection: Surgical removal.
  • Tumors/Atelectasis: Reduced functional area.

4. Ventilation-Perfusion (V/Q) Matching

How it affects efficiency: Requires a close match between ventilation (V) and perfusion (Q).

Ideal V/Q ratio: Around 0.8-1.0.

High V/Q Ratio ("Dead Space")

Ventilation exceeds perfusion (e.g., pulmonary embolism). Ventilated air doesn't exchange gas effectively.

Low V/Q Ratio ("Shunt")

Perfusion exceeds ventilation (e.g., pneumonia, atelectasis). Blood remains poorly oxygenated, reducing arterial PO2.

5. Diffusion Coefficient of Gases

How it affects efficiency: Depends on solubility and molecular weight.

  • CO2 vs. O2: CO2 is ~20-24 times more soluble. Its diffusion coefficient is ~20 times greater than O2.
  • Result: CO2 diffuses much more rapidly despite the smaller gradient.
Clinical Relevance:

When diffusion capacity is impaired (e.g., thick membrane), O2 diffusion is affected much more severely than CO2. A patient may present with hypoxemia (low O2) but a relatively normal PCO2.

Checkpoint Question:

A patient with severe pulmonary edema (fluid in the interstitial space) is likely to experience more significant problems with oxygenation (hypoxemia) than with carbon dioxide elimination (hypercapnia) in the initial stages. Explain why, using the factors discussed above.

Objective 4: Explain the mechanisms of oxygen transport in the blood, including the role of hemoglobin and the oxyhemoglobin dissociation curve.

Once oxygen diffuses from the alveoli into the blood, it needs to be transported efficiently to the metabolically active tissues. Oxygen is transported in two main forms:

1. Oxygen Dissolved in Plasma (Small Amount)

  • Mechanism: A small percentage of oxygen (~1.5%) dissolves directly into the blood plasma.
  • Amount: For every mmHg of PO2, about 0.003 mL of O2 dissolves in 100 mL of blood.
Significance:

While small in quantity (at an arterial PO2 of 100 mmHg, only ~0.3 mL O2/100 mL blood), this fraction is critically important because:

  • It's the only form of oxygen that exerts a partial pressure.
  • It creates the partial pressure gradient for diffusion into the tissues.
  • It serves as the "gateway" for O2 to bind to hemoglobin.

2. Oxygen Bound to Hemoglobin (Major Amount)

Mechanism: The vast majority of oxygen (~98.5%) is transported bound reversibly to the iron atoms within the heme groups of hemoglobin (Hb) inside red blood cells.

Hemoglobin Structure

  • Composed of four subunits (2 alpha, 2 beta).
  • Each subunit contains a heme group with an iron atom (Fe2+).
  • Each iron atom binds one O2 molecule (Max 4 O2 per Hb).

Definitions & Capacity

  • Oxyhemoglobin (HbO2): Hb with bound oxygen.
  • Deoxyhemoglobin (HHb): Hb without bound oxygen.
  • Capacity: Each gram of Hb carries ~1.34 mL O2. (Normal 15 g/dL = ~20 mL O2/100 mL blood).

3. The Oxyhemoglobin Dissociation Curve

This S-shaped (sigmoidal) curve represents the relationship between partial pressure of oxygen (PO2) and hemoglobin saturation (%).

Plateau (High PO2 - Lungs)

At Lung PO2 (100 mmHg): Hb is ~97-98% saturated.

Significance: The flat upper part provides a "safety margin." Large drops in PO2 (e.g., to 60 mmHg) result in only small decreases in saturation, ensuring loading.

Steep Slope (Low PO2 - Tissues)

At Tissue PO2 (40 mmHg): Saturation drops to ~75%.

Significance: Small drops in tissue PO2 cause large unloading of O2. Crucial for active tissues (PO2 < 20 mmHg) to receive massive O2 release.

4. Factors Shifting the Curve

Releases O2

Right Shift (Decreased Affinity)

"Bohr Effect" - Favors unloading to tissues.

  • PCO2
  • Acidity (H+) / Low pH
  • Temperature
  • 2,3-BPG
Holds O2

Left Shift (Increased Affinity)

Favors loading in lungs.

  • PCO2
  • Acidity / High pH
  • Temperature
  • 2,3-BPG
  • HbF (Fetal Hemoglobin)
Checkpoint Question:

During intense exercise, a person's muscle tissue produces more CO2 and generates more heat. How do these changes affect the oxyhemoglobin dissociation curve, and what is the physiological advantage of this shift?

Objective 5: Explain the mechanisms of carbon dioxide transport in the blood.

Carbon dioxide (CO2) is a metabolic waste product constantly produced by body cells. It is transported in the blood in three main forms:

Form Percentage
Dissolved in Plasma 7-10%
Carbaminohemoglobin 20-23%
Bicarbonate Ions (HCO3-) 70%

1. Dissolved in Plasma

Creates the PCO2 gradient for diffusion. It is the only form that can diffuse across membranes.

2. Carbaminohemoglobin

CO2 binds to protein (globin), not heme. Favored by deoxygenated Hb (Haldane Effect).

3. As Bicarbonate Ions (HCO3-) (Major Amount)

This is the most significant mechanism (70%) and is crucial for buffering blood pH.

A. Process in Systemic Capillaries (Loading)

  1. CO2 Entry: Diffuses from tissues into RBCs.
  2. Conversion: CO2 + H2O ↔ H2CO3 (Catalyzed by Carbonic Anhydrase).
  3. Dissociation: H2CO3 ↔ H+ + HCO3-.
  4. Buffering: H+ is buffered by hemoglobin (H+ + Hb → HHb).
  5. Chloride Shift: HCO3- diffuses out to plasma; Cl- enters RBC to maintain electrical neutrality.

B. Process in Pulmonary Capillaries (Unloading)

  1. Reversal of Chloride Shift: HCO3- re-enters RBC; Cl- moves out.
  2. Reformation: HCO3- + H+ (released from Hb as O2 binds) → H2CO3.
  3. Conversion: H2CO3 → CO2 + H2O (Catalyzed by CA).
  4. Diffusion: CO2 diffuses into plasma and then into alveoli for exhalation.
The Haldane Effect

Describes the relationship between O2 binding and CO2 transport.

  • Principle: Deoxygenated Hb (systemic) has greater affinity for CO2 and H+. Oxygenated Hb (pulmonary) has reduced affinity.
  • Significance: Enhances CO2 loading in tissues (where Hb is deoxygenated) and CO2 unloading in lungs (where Hb becomes oxygenated).
Checkpoint Question:

A person is experiencing severe metabolic acidosis (excess H+ in the blood). How might the body's mechanisms for CO2 transport respond to help compensate for this acidosis?

Objective 6: Describe the concept of ventilation-perfusion (V/Q) matching and its importance for efficient gas exchange.

For optimal gas exchange, it is not enough to simply ventilate the lungs and perfuse them with blood. The amount of air delivered to the alveoli (ventilation, V) must be appropriately matched with the amount of blood flowing through the pulmonary capillaries (perfusion, Q). This relationship is known as Ventilation-Perfusion (V/Q) Matching.

1. Defining Ventilation (V) and Perfusion (Q)

Ventilation (V)

The volume of fresh air reaching the alveoli per minute.

Normal ≈ 4-5 L/min
Perfusion (Q)

The volume of blood flowing through the pulmonary capillaries per minute (Cardiac Output).

Normal ≈ 5 L/min

2. The Ideal V/Q Ratio

  • Ideal: In a perfectly ideal lung, every alveolus would be perfectly ventilated and perfectly perfused, resulting in a V/Q ratio of 1.0.
  • Healthy/Actual: However, in a healthy lung, the overall V/Q ratio is approximately 0.8 (e.g., 4 L/min ventilation / 5 L/min perfusion). This slight mismatch is normal and due to physiological differences in ventilation and perfusion throughout the lung.

3. Physiological Variations in V/Q Ratio

Due to gravity, both ventilation and perfusion are not uniform throughout the lung, especially in an upright person.

Apex (Top) of Lung

  • Ventilation: Lower than at the base (alveoli are stretched/less compliant).
  • Perfusion: Significantly lower than at the base (harder to flow against gravity).
  • V/Q Ratio: High (> 1.0)
  • Note: Ventilation is relatively better than perfusion. Referred to as having "physiological dead space".

Base (Bottom) of Lung

  • Ventilation: Higher than at the apex (alveoli less stretched/more compliant).
  • Perfusion: Significantly higher than at the apex (gravity assists flow).
  • V/Q Ratio: Low (< 1.0, approx 0.6)
  • Note: Perfusion is relatively better than ventilation. Referred to as having "physiological shunt".

Despite these regional differences, the overall V/Q matching is remarkably efficient in a healthy lung.

4. Consequences of V/Q Mismatch

V/Q mismatch is the most common cause of hypoxemia (low arterial PO2) in many lung diseases.

Low V/Q Ratio (Perfusion > Ventilation)

"Shunt-like" effect

  • Definition: Alveoli are well-perfused but poorly ventilated (e.g., airway obstruction, fluid).
  • Result: Blood passes without picking up O2. "Venous admixture" lowers arterial PO2.
  • Examples: Pneumonia, atelectasis, pulmonary edema, asthma.
  • Effect on Blood Gases: Low PO2, normal/elevated PCO2.

High V/Q Ratio (Ventilation > Perfusion)

"Dead Space-like" effect

  • Definition: Alveoli are well-ventilated but poorly perfused (e.g., reduced blood flow).
  • Result: Ventilated air does not contact enough blood. Increases "physiological dead space".
  • Examples: Pulmonary embolism, emphysema (capillary destruction), low cardiac output.
  • Effect on Blood Gases: Increased PCO2 (if severe), normal PO2 or mild hypoxemia.

5. Body's Compensatory Mechanisms

The body has local regulatory mechanisms to optimize V/Q matching:

Hypoxic Pulmonary Vasoconstriction
  • Mechanism: If an alveolus is poorly ventilated (low PAO2), the pulmonary arterioles supplying it constrict.
  • Purpose: Diverts blood flow away from poorly ventilated areas to better-ventilated areas.
  • Unique to pulmonary circulation; systemic hypoxia causes vasodilation.
Bronchoconstriction (Low PCO2)
  • Mechanism: If an area is poorly perfused (high V/Q), leading to low local PCO2, bronchioles constrict.
  • Purpose: Reduces ventilation to poorly perfused areas, redirecting air to better-perfused areas.

6. Importance of V/Q Matching

  • Efficient Gas Exchange: Ensures O2 is loaded and CO2 is removed effectively.
  • Homeostasis: Critical for maintaining arterial PO2 and PCO2 within limits.
  • Clinical Relevance: Hallmark of many respiratory diseases.

Conclusion of Module 7, Section III

We have now covered the complete journey of oxygen from the atmosphere to the blood, and carbon dioxide from the blood to the atmosphere, detailing the physical laws, anatomical features, and physiological mechanisms that govern this vital process.

Final Review Question:

Consider a patient who has experienced a severe acute asthma attack, leading to widespread bronchoconstriction. How would this primarily affect their V/Q ratio, and what would be the immediate impact on their blood gas levels (PO2 and PCO2)? How would the body attempt to compensate?

How V/Q Ratios are Determined and Why They Vary

The V/Q ratio represents the ratio of alveolar ventilation (V̇A) to pulmonary blood flow (Q̇c).

V/Q =
Alveolar Ventilation (L/min)
Pulmonary Blood Flow (L/min)
Formula used to calculate the efficiency of matching air to blood.

1. Overall V/Q Ratio (Typically ~0.8)

Measured Values at Rest:
  • Total Alveolar Ventilation (V̇A): Approximately 4-5 L/min.
    Calculated from minute ventilation (tidal volume x respiratory rate) minus anatomical dead space ventilation.
  • Total Pulmonary Blood Flow (Q̇c): Approximately 5 L/min.
    Equal to the cardiac output of the right ventricle.
Calculation:
V/Q = 4 L/min / 5 L/min = 0.8
V/Q = 5 L/min / 5 L/min = 1.0

So, the overall V/Q ratio of 0.8-1.0 is simply a division of the average measured total alveolar ventilation by the average measured total pulmonary blood flow.

2. Regional V/Q Variations (Apex vs. Base)

This is where it gets more complex and is based on experimental observations, primarily due to the effects of gravity in an upright lung.

Perfusion (Q) Gradient

  • Gravity: Significantly affects blood flow. In an upright person, blood tends to pool at the bottom (base).
  • Hydrostatic Pressure: The pressure of the blood column is highest at the base and lowest at the apex. This means pulmonary arterial pressure is highest at the base, leading to greater distension of capillaries and more blood flow.
  • Result: Blood flow (Q) is much higher at the base than at the apex.
    • Apex: Perfusion can be almost zero (Zone 1 of West's Lung Zones).
    • Base: Perfusion is highest (Zone 3).
  • Quantification: Perfusion at the base might be 5-10 times higher than at the apex.

Ventilation (V) Gradient

  • Pleural Pressure: Gravity makes pleural pressure more negative at the apex and less negative (or more positive) at the base.
  • Alveolar Size & Compliance:
    • At Apex: The more negative pressure stretches alveoli more at rest. They are larger but less compliant (stiffer). They are "full" at the start, so they expand less with each breath.
    • At Base: The less negative pressure means alveoli are smaller and less stretched at rest. They are more compliant. They expand more with each breath.
  • Result: Ventilation (V) is higher at the base than at the apex, though the gradient is less steep than for perfusion.
  • Quantification: Ventilation at the base might be 2-3 times higher than at the apex.

3. Calculating Regional V/Q (Conceptual)

The Apex

High Ratio

Since V is relatively low and Q is very low (even lower than V):

Low V
Very Low Q
= High V/Q (> 1.0)
Hypothetical Example:

V_apex = 0.2 L/min
Q_apex = 0.05 L/min
Ratio = 4.0

The Base

Low Ratio

Since V is relatively high and Q is very high (even higher than V):

High V
Very High Q
= Low V/Q (< 1.0)
Hypothetical Example:

V_base = 0.8 L/min
Q_base = 1.2 L/min
Ratio = 0.67

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