Gas exchange in the lungs, blood and tissues

Gas exchange is the physical process by which gases move passively, meaning that no energy is required to power the transport, by diffusion across a surface.

External respiration is another term for gas exchange.

It describes both the bulk flow of air into and out of the lungs and the transfer of oxygen and carbon dioxide into the bloodstream through diffusion.

Internal respiration, on the other hand, describes the capillary gas exchange in body tissues.

While the flow of air from the external environment happens due to pressure changes in the lungs, the mechanisms of alveolar gas exchange are more complex.

The primary three components of gas exchange are the surface area of the alveolo-capillary membrane, the partial pressure gradients of the gasses, and the matching of ventilation and perfusion.

So, if we were to draw a path for the oxygen molecules entering the body, it would start from the nose or mouth and end up in the lungs, where it reaches the alveoli which are wrapped in an intricate network of tiny blood vessels called pulmonary capillaries.

So, from the alveoli, the gas molecules will go into the blood in the capillaries.

Carbon dioxide follows the same path, but in the opposite direction, moving from the blood in the capillaries to the air in the alveoli and then getting exhaled.

Now, the important role in this process belongs to the alveolo–capillary membrane where the layer of alveolar cells lining the alveoli meets the endothelial cells that make up the pulmonary capillary, and is where gas exchange happens.

With that in mind, let’s just say that when it comes to the surface area of the alveolo-capillary membrane, bigger is better because a respiratory membrane with a large surface area has more gas to diffuse across it in a given period of time leading to a more efficient gas exchange.

With emphysema, for example, which is a condition where the alveoli are gradually destroyed, the total surface area that allows gas exchange is reduced.

If there’s less surface area for gas exchange to occur, the rate of diffusion decreases.

Another aspect related to the alveolo-capillary membrane which influences gas exchange is its thickness.

So, in healthy lungs, respiratory membrane is 0.5–1 micrometer thick.

In lung fibrosis, on the other hand, the alveolar-capillary wall thickens and a thicker alveolo-capillary membrane reduces the rate of diffusion.

Now, the gas exchange across the alveolo-capillary membrane happens according to what is known as Fick’s law.

Fick’s law states that the net rate of diffusion - V of any particular gas across the alveolar-capillary membrane, is proportional to the driving force, which is the difference between the partial pressure of the gas in the alveolar sacs, or PA, and the partial pressure of the gas in the blood, or Pa, and also proportional to the surface area of the membrane, or A, but inversely proportional to the wall’s thickness - T.

And this is all times the diffusion coefficient - D, which varies from gas to gas. Therefore,

V=(PA-Pa)ADT

Specifically, the driving force for diffusion is the partial pressure difference of the gas across the membrane, and NOT the concentration difference.

So, the diffusion of oxygen and carbon dioxide are driven across the respiratory membrane by their partial pressure gradients.

Therefore, if the oxygen partial pressure in alveolar air is 100mm Hg and the one of mixed venous blood entering the pulmonary capillary is 40mm Hg, then we have a driving force for oxygen across the alveolar-capillary barrier of 60mm Hg.

Basically, a steep oxygen partial pressure gradient occurs through the alveolo-capillary membrane because the partial pressure of oxygen in the alveolar air is greater than the partial pressure of oxygen in the pulmonary arteries, causing oxygen to rapidly cross the respiratory membrane from the alveoli into the blood.

The partial pressure of carbon dioxide is also different between the alveolar air and the blood of the capillary.

However, the partial pressure difference is less than that of oxygen, about 5 mm Hg.

The partial pressure of carbon dioxide in the blood of the capillary is about 45 mm Hg, whereas its partial pressure in the alveoli is about 40 mm Hg.

Now, the partial pressures of inhaled air and alveolar air determine why oxygen goes into the alveoli, and why carbon dioxide leaves the alveoli.

This brings us to what is called Dalton’s law, which states that the sum of partial pressures of all the gases in a mixture equals the total pressure of that mixture.

Thus, for dry gas, the partial pressure is the total pressure multiplied by the fractional concentration of dry gas, while the relationship for humidified gas is determined by correcting the barometric pressure for the water vapor pressure.

Therefore:
For dry gas -> Px=Pb x F For humidified gas -> Px = (Pb - PH2O) x F, where Px is the partial pressure of a gas, Pb is the barometric pressure, PH2O is the water vapor pressure at 37°C/98.6°F having a value of 47mmHg.

F is the fractional concentration of a gas.

To exemplify this, in dry inspired air, the PO2 is approximately 160 mm Hg, which is computed by multiplying the barometric pressure of oxygen, which is 760mmHg, by the fractional concentration of O2, 21% (760 mm Hg x 0.21 = 160 mm Hg).

For practical purposes, there is no CO2 in dry inspired air and PCO2 is zero.

In humidified tracheal air, it is assumed that the air becomes fully saturated with water vapor.

At 37°C, PH2O is 47 mm Hg.

Thus in comparison to dry inspired air, humidified tracheal air has a lower PO2 because the O2 is “diluted” by water vapor.

Again, recall that partial pressures in humidified air are calculated by correcting the barometric pressure for water vapor pressure, then multiplying by the fractional concentration of the gas.

Thus the PO2 of humidified tracheal air is 150 mm Hg ([760 mm Hg − 47 mm Hg] × 0.21 = 150 mm Hg).

Because there is no CO2 in inspired air, the PCO2 of humidified tracheal air also is zero.

The humidified air enters the alveoli, where gas exchange occurs.

In alveolar air, the values for PO2 and PCO2 are changed substantially when compared with inspired air.

PAO2 is 100 mm Hg, which is less than the PO2 in inspired air, which is 160mm Hg, and PACO2 is 40 mm Hg, which is greater than the PCO2 in inspired air, which is close to 0mm Hg.

So, according to Dalton’s law, these partial pressure values influence the moving of these gases, meaning they will move from an area of high concentration to an area of low concentration.

Now, within the lungs, oxygen and carbon dioxide diffuse between the air in the alveoli and the blood, that is between a gas and a liquid.

This movement is governed by Henry's Law which states that at a constant temperature, the amount of a gas that dissolves in a liquid is directly proportional to the partial pressure of that gas in equilibrium with that liquid.

Basically, according to this law, gases can be forced to dissolve into a liquid, let’s say blood, if there is enough pressure applied and a controlled volume.

It also says that once that pressure is released, gases can come out of solution.

The concentration of a gas in solution is expressed as volume percent (%), or volume of gas per 100 mL of blood (mL gas/100 mL blood).

Thus for blood:

Cx = Px X Solubility, where Cx is the concentration of dissolved gas(mL gas/100mL blood), Px is the partial pressure of gas (mm Hg) and Solubility refers to the solubility of gas in blood (mL gas/100mL blood per mm Hg)

So, to test this relationship, let’s consider the PO2 of arterial blood is 100 mm Hg and given that the solubility of O2 is 0.003 mL O2/100 mL blood per mm Hg, we should be able to know what is the concentration of dissolved O2 in blood, right?

Well, yes, because O2 = PO2 X solubility, so the concentration of dissolved O2 is 0.3 mL/100mL blood.

Actually, this law interconnects with Boyle’s law during breathing cycle and gas exchange.

Boyle’s Law states that for a fixed amount of a gas kept at a fixed temperature, pressure and volume are inversely proportional.