8.1 Pulmonary Ventilation, Gas Exchange & Pulmonary Circulation/Edema

Pulmonary Ventilation, Gas Exchange & Pulmonary Circulation

Quick Answer: Air moves into and out of the lungs because of pressure gradients generated by the respiratory muscles. Gas exchange occurs at the alveolar-capillary membrane and is governed by partial pressures (Dalton's and Henry's laws). The pulmonary circulation is a low-pressure, low-resistance bed that can become engorged when left-sided cardiac function fails, producing pulmonary edema.

Mechanics of Breathing

Pulmonary ventilation is the bulk flow of air between the atmosphere and the alveoli. At end-expiration the diaphragm and external intercostals are relaxed, alveolar pressure (PA) equals atmospheric pressure (Patm), and no air flows. During inspiration, the diaphragm contracts downward and the external intercostals elevate the ribs, increasing thoracic volume. The intrapleural pressure (normally about −5 cm H₂O at rest) becomes more negative (≈ −8 cm H₂O), the lungs expand, alveolar pressure drops below Patm, and air flows in. Expiration at rest is passive: elastic recoil of the lung and chest wall returns the system to its equilibrium volume, alveolar pressure briefly exceeds Patm, and air flows out.

Accessory muscles (scalenes, sternocleidomastoid, pectoralis minor) recruit during exercise or distress; the abdominal muscles and internal intercostals force active expiration.

Lung Compliance and Surfactant

Compliance (C = ΔV/ΔP) is the ease with which the lung expands. A low-compliance lung (pulmonary fibrosis, restrictive disease) requires greater pressure for a given volume change. A high-compliance lung (emphysema) inflates easily but loses elastic recoil, so it collapses poorly and traps air.

Surfactant, a phospholipid-rich mixture secreted by Type II pneumocytes, reduces alveolar surface tension (Laplace's law: P = 2T/r). Without surfactant, small alveoli would collapse into large ones. Premature infants deficient in surfactant develop neonatal respiratory distress syndrome. Surfactant also pulls fluid back into the capillaries and lowers the work of breathing.

Ventilation-Perfusion Relationships

The lung is not homogeneous. Both ventilation (V) and perfusion (Q) increase from apex to base, but perfusion increases more steeply than ventilation, so the V/Q ratio is high (~3) at the apex and low (~0.6) at the base. A normal overall V/Q ratio is about 0.8.

Hypoxic pulmonary vasoconstriction redirects blood from poorly ventilated alveoli to better-ventilated ones, optimizing V/Q matching. Chronic generalized hypoxia (e.g., high altitude) can raise pulmonary arterial pressure.

Gas Exchange: Dalton's and Henry's Laws

Dalton's law states that the total pressure of a gas mixture equals the sum of the partial pressures of its individual gases. At sea level, dry inspired air at Patm = 760 mmHg contains roughly 21% O₂, so the partial pressure of inspired O₂ (PIO₂) ≈ 760 × 0.21 = 160 mmHg. After humidification in the airways, water vapor pressure (47 mmHg at 37 °C) reduces the dry-gas pressure, and by the time gas reaches the alveolus, CO₂ is also present, so PAO₂ ≈ 100 mmHg.

Henry's law states that the amount of a gas dissolved in a liquid is proportional to its partial pressure at the gas-liquid interface. This governs how much O₂ and CO₂ dissolve in plasma (a small fraction of total O₂ transport; most O₂ is bound to hemoglobin). The alveolar gas equation, PAO₂ = PIO₂ − PaCO₂/R, where R is the respiratory quotient (~0.8 on a mixed diet), lets you compute the A-a gradient.

Gas exchange at the alveolar-capillary membrane depends on the diffusion distance (≈0.5 µm), the surface area (~70 m²), and the partial pressure gradient. O₂ moves from alveolus (PAO₂ ≈ 100) to mixed venous blood (PvO₂ ≈ 40); CO₂ moves from venous blood (PvCO₂ ≈ 46) to alveolus (PACO₂ ≈ 40).

Pulmonary Circulation and Edema

The pulmonary circulation is a low-pressure, low-resistance, high-flow system. Mean pulmonary artery pressure is about 15 mmHg versus ~100 mmHg systemic. Pulmonary capillary hydrostatic pressure is normally ~7–10 mmHg, well below plasma oncotic pressure (~25 mmHg), so the net Starling force keeps alveoli dry.

Pulmonary edema appears when fluid overwhelms the alveolar-capillary barrier:

• Cardiogenic (hydrostatic) — left ventricular failure, mitral stenosis: pulmonary venous pressure rises, capillary hydrostatic pressure exceeds oncotic pressure, fluid transudates. Pink frothy sputum, bilateral crackles, orthopnea.
• Non-cardiogenic (permeability) — ARDS, sepsis, aspiration, smoke inhalation: capillary endothelial and alveolar epithelial injury allow protein-rich fluid to flood alveoli. Stiff, low-compliance lungs, severe refractory hypoxemia from shunt.

Kerley B lines, perihilar bat-wing infiltrates, and cephalization on imaging suggest cardiogenic edema; normal heart size with diffuse bilateral opacities favor non-cardiogenic.

This respiratory physiology is testable in the PA-CAT Physiology section (Bulletin Table 4) — expect items pairing a clinical scenario (PE, pulmonary edema, infant RDS) with the underlying V/Q, compliance, or surfactant mechanism.