Gas Exchange

Core Concepts

Dalton's law: partial pressures

Air is a mixture. Dalton's law says the total pressure of a mixture equals the sum of the pressures each gas would exert alone, and each gas's partial pressure is proportional to its fraction of the mixture. Atmospheric air at sea level (about 760 mmHg total) is roughly 21% oxygen and 78% nitrogen, so PO₂ ≈ 0.21 × 760 ≈ 160 mmHg and PN₂ ≈ 0.78 × 760 ≈ 593 mmHg. Gases behave independently: the PO₂ gradient, not the total pressure, is what drives oxygen movement. In the alveoli the numbers differ because inspired air is warmed, humidified (water vapor adds ~47 mmHg of its own partial pressure), and mixed with CO₂ added by the blood: alveolar PO₂ is about 100 mmHg and alveolar PCO₂ about 40 mmHg (commonly taught reference values). These are the gradients' "starting points."

Henry's law: getting gas into solution

Henry's law states that the amount of a gas that dissolves in a liquid is directly proportional to its partial pressure in contact with the liquid — and depends on the gas's solubility. At body temperature, CO₂ is roughly 20–24 times more soluble in plasma than O₂ — which is why very little oxygen (about 1.5% of the total) travels dissolved while a much larger fraction of CO₂ does. Dissolved gas follows the same rule as the gas phase: it diffuses from higher to lower partial pressure. Henry's law also explains the bubbles divers experience under pressure changes — covered in "Modifications in Respiratory Functions" later in this chapter.

The respiratory membrane and the diffusion gradient

Gas must cross the respiratory membrane — alveolar fluid, alveolar epithelium (type I cells), fused basement membranes, and capillary endothelium, often under a micrometer of total thickness. Diffusion across it follows Fick's law: rate ∝ (surface area × partial-pressure difference) ÷ membrane thickness. Anything that thickens the membrane (fluid, fibrosis), reduces surface area (emphysema destroys alveoli), or shrinks the gradient (low inspired oxygen) slows exchange. Normal capillary transit time is under a second — plenty for equilibrium if the membrane is healthy.

External respiration: exchange at the lungs

In the pulmonary capillaries, venous blood arrives with a PO₂ of about 40 mmHg and a PCO₂ of about 45 mmHg. Alveolar air has a PO₂ of about 100 mmHg and a PCO₂ of about 40 mmHg. Oxygen therefore diffuses into the blood (40 → 100 mmHg gradient) and carbon dioxide diffuses out (45 → 40 mmHg gradient) until partial pressures equilibrate. Because diffusion is so fast, blood leaving the lungs normally has a PO₂ near 100 mmHg — nearly equilibrated with alveolar air. Anything that prevents equilibration (thickened membrane, shunt, low alveolar PO₂) leaves arterial PO₂ below 100 mmHg.

Internal respiration: exchange at the tissues

At the tissue capillaries, the gradient flips. Metabolizing cells consume oxygen, dropping the interstitial PO₂ to about 40 mmHg, while producing CO₂ and raising the interstitial PCO₂ to about 45 mmHg. Arterial blood arrives at about 100/40; oxygen diffuses out to the cells and CO₂ diffuses in, so venous blood leaving the tissues carries about 40 mmHg PO₂ and 45 mmHg PCO₂. The "internal respiration" step is thus the mirror image of the external one, and both obey the same physics: diffusion down partial-pressure gradients across a thin membrane. (Note: these values are commonly taught textbook references for resting conditions; actual tissue values vary with metabolic activity.)

Ventilation-perfusion (V/Q) matching

For external respiration to work well, alveoli must be both ventilated (fresh air reaching them) and perfused (blood flowing past them). In an upright person, both ventilation and blood flow are greater at the lung bases than at the apices, but blood flow changes more steeply — so the apex has a higher V/Q ratio (over-ventilated relative to perfusion) and the base a lower one. The lungs compensate with local matching: if an alveolus is underventilated, its PO₂ falls and PCO₂ rises; the low PO₂ constricts nearby arterioles (hypoxic vasoconstriction), shunting blood away; high CO₂ relaxes nearby bronchioles, redirecting airflow toward it. These local reflexes steer ventilation and perfusion toward each other. When matching fails — a pulmonary embolism blocks blood flow to ventilated regions (dead-space effect), or pneumonia fills perfused alveoli (shunt effect) — arterial oxygen falls. A shunt is harder to fix with oxygen therapy, because blood bypassing ventilated alveoli never sees the higher inspired oxygen.

Common Confusions