7.3 Pulmonary Mechanics, Lung Volumes, and Gas Exchange Dynamics

7.3 Pulmonary Mechanics, Lung Volumes, and Gas Exchange Dynamics

The primary function of the respiratory system is gas exchange between atmospheric air and pulmonary capillary blood. This process depends on pulmonary mechanics: the structural properties, pressure gradients, and volume changes that drive ventilation of the alveolar space.

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Standard Lung Volumes and Capacities

Lung volumes are discrete, non-overlapping quantities of gas measured at specific phases of respiration. Lung capacities consist of combinations of two or more lung volumes.

Primary Lung Volumes

• Tidal Volume (TV or $V_T$): Volume of air inspired or expired during normal, quiet breathing (~500 mL).
• Inspiratory Reserve Volume (IRV): Maximum volume of air that can be forcibly inspired above a normal tidal inspiration (~3000 mL).
• Expiratory Reserve Volume (ERV): Maximum volume of air that can be forcibly expired following a normal tidal expiration (~1100 mL).
• Residual Volume (RV): Volume of air remaining in the lungs after maximal forced expiration (~1200 mL). RV cannot be measured by standard spirometry because it cannot be exhaled; it requires gas dilution techniques (e.g., helium dilution) or body plethysmography.

Derived Lung Capacities

• Vital Capacity (VC): Total volume of air that can be expired after maximal inspiration: $VC = TV + IRV + ERV \quad (\sim 4700\text{ mL})$
• Total Lung Capacity (TLC): Total volume of gas contained in the lungs following maximal inspiration: $TLC = VC + RV = TV + IRV + ERV + RV \quad (\sim 5900\text{ mL})$
• Functional Residual Capacity (FRC): Volume of air remaining in the lungs at the end of a normal tidal expiration: $FRC = ERV + RV \quad (\sim 2300\text{ mL})$ FRC represents the mechanical equilibrium point of the respiratory system, where inward elastic recoil of the lungs equals outward chest wall expansion forces.
• Inspiratory Capacity (IC): $IC = TV + IRV$ (~3500 mL).

Dead Space Mechanics

• Anatomical Dead Space ($V_D$): Volume of conducting airways (nose to terminal bronchioles) where no gas exchange occurs (~150 mL, or ~1 mL per lb of body weight).
• Physiological Dead Space: Total volume of air that does not participate in gas exchange, combining anatomical dead space with non-perfused alveolar dead space. Quantified using the Bohr Equation:

$V_D = V_T \times \left( \frac{PaCO_2 - PECO_2}{PaCO_2} \right)$

Where $PaCO_2$ is arterial $\text{CO}_2$ partial pressure and $PECO_2$ is mixed expired $\text{CO}_2$ partial pressure.

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Spirometry: Obstructive vs. Restrictive Lung Disease

Dynamic spirometry measures forced expiratory flow rates, primarily Forced Expiratory Volume in 1 second ($\text{FEV}_1$) and Forced Vital Capacity (FVC).

Spirometry Evaluation:
Check FEV1 / FVC Ratio
  ├── < 0.70 (70%) ──> OBSTRUCTIVE PATTERN (Asthma, COPD, Emphysema)
  └── ≥ 0.70 (70%) ──> Check TLC
                         ├── Low TLC ──> RESTRICTIVE PATTERN (Fibrosis, ARDS)
                         └── Normal TLC ──> NORMAL SPIROMETRY

Comparative Spirometric Profiles

• Obstructive Diseases: Airway resistance during exhalation is elevated due to bronchial lumen narrowing (asthma, chronic bronchitis) or loss of elastic recoil (emphysema). Exhalation is prolonged, trapping gas in lungs and raising RV and TLC.
• Restrictive Diseases: Expansion of lung parenchyma is restricted by interstitial inflammation/fibrosis or neuromuscular weakness. Lung compliance drops; both $\text{FEV}_1$ and FVC decline proportionally, maintaining a normal or elevated ratio.

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Mechanics of Breathing & Pressure Relationships

Ventilation is driven by pressure differentials established between atmospheric pressure ($P_{atm} = 0\text{ cm H}2\text{O}$ baseline), alveolar pressure ($P{alv}$), and intrapleural pressure ($P_{ip}$).

Key Respiratory Pressures

• Intrapleural Pressure ($P_{ip}$): Pressure within the fluid-filled intrapleural space. Under resting baseline conditions at FRC, $P_{ip}$ is always negative ($-4\text{ cm H}_2\text{O}$) because the lungs tend to collapse inward due to elastic recoil, while the chest wall tends to spring outward. During active inspiration, diaphragm contraction enlarges the thoracic cavity, causing $P_{ip}$ to become more negative ($-8\text{ cm H}_2\text{O}$).
• Alveolar Pressure ($P_{alv}$): Pressure within alveoli. At rest (end-expiration), $P_{alv} = 0\text{ cm H}2\text{O}$. During inspiration, expanding lung volume drops $P{alv}$ to $-1\text{ cm H}2\text{O}$, drawing ambient air inward. During expiration, elastic lung recoil raises $P{alv}$ to $+1\text{ cm H}_2\text{O}$, expelling air.
• Transpulmonary Pressure ($P_{tp}$): Distending pressure across the alveolar wall: $P_{tp} = P_{alv} - P_{ip}$ $P_{tp}$ is always positive under normal conditions; a higher $P_{tp}$ maintains greater alveolar expansion.

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Lung Compliance, Elastic Recoil, & Surface Tension

Compliance Mechanics

Lung compliance represents the ease with which the lungs expand per unit change in transpulmonary pressure:

$\text{Compliance } (C) = \frac{\Delta V}{\Delta P_{tp}}$

• Increased Compliance: Observed in emphysema due to destruction of elastic alveolar septa by neutrophil elastase. Lungs expand easily but lose elastic recoil, resulting in dynamic airway collapse during forced expiration.
• Decreased Compliance: Observed in pulmonary fibrosis, pulmonary edema, and Infant Respiratory Distress Syndrome (IRDS). Lungs become stiff, requiring substantial pressure changes to achieve minimal tidal expansion.

Surface Tension & Law of Laplace

Alveoli are lined by a thin fluid film. Liquid molecules attract one another, creating surface tension ($T$) that exerts an inward collapsing pressure ($P$) on the alveolus, as defined by the Law of Laplace for a spherical structure:

$P = \frac{2T}{r}$

Where $P$ is collapsing pressure, $T$ is surface tension, and $r$ is alveolar radius.

Biophysical Implication: Without intervention, smaller alveoli (smaller radius $r$) would experience significantly higher collapsing pressures ($P$) than larger alveoli, causing smaller alveoli to collapse and discharge their air into larger ones (atelectasis).

Physiological Function of Pulmonary Surfactant

• Synthesis: Synthesized and secreted by Type II pneumocytes (stored in intracellular lamellar bodies).
• Composition: Complex mixture of phospholipids, primarily dipalmitoylphosphatidylcholine (DPPC), alongside surfactant proteins (SP-A, SP-B, SP-C, SP-D).
• Mechanism: Intersperses between water molecules at the air-water interface, reducing surface tension ($T$). As an alveolus shrinks during exhalation, surfactant molecules become more tightly packed, reducing surface tension proportionately more in smaller alveoli. This equalizes collapsing pressure across alveoli of varying sizes, preventing alveolar collapse, reducing work of breathing, and increasing overall lung compliance.