9.2: Pulmonary Vascular Resistance, Lung Volume, and Gravity

As we have just seen, with little smooth muscle and a compliant wall, the arterioles act more like veins. As pulmonary arterial pressure rises, the resistance of the pulmonary circulation falls, as seen in figure 9.4, and this occurs for several reasons.

Figure 9.4: Pulmonary vascular resistance decreases as pressure increases.

Unlike systemic arterioles there is little autoregulation by the pulmonary arterioles, so the pulmonary arterioles do not actively vasoconstrict when stretched by high pressure. Instead, they passively distend, thereby reducing their resistance with increasing resistance.

A rise in pulmonary pressure not only distends vessels but initiates flow through otherwise unused, or dormant, vessels, particularly those closer to the apex of the lung (we will see why later on). With more vessels recruited, the total cross-sectional area of used vessels increases and total resistance falls.

But there are other and more complex peculiarities of the pulmonary circulation that determine its resistance…

Pulmonary Vascular Resistance and Radial Traction

Another unique characteristic of the pulmonary circulation is that it is exposed to the changing pressures in the airways and alveoli. It is also involved in the fiber network that generates radial traction. Consequently pulmonary vessels can be expanded or compressed in a way no other circulation is.

To explain these phenomena we have to divide the pulmonary circulation into two subdivisions, the alveolar vessels and the extra-alveolar vessels (figure 9.5). These two vessel types behave differently, so we will deal with them separately.

Figure 9.5: Pulmonary vessels can be categorized as alveolar or extra-alveolar.

Alveolar vessels: These are primarily the capillaries and small vessels in close contact with the alveoli. Consequently they are exposed to the alveolar pressures. First, the surface tension within the alveolus that is tending to pull the alveolus closed also pulls on the vessels between alveoli, tending to pull it open as neighboring alveoli pull inward on themselves, and play tug-of-war with the vessel walls in between, extending them and causing a decrease in vascular resistance.

Alternatively, when alveolar pressure increases (e.g., at high lung volumes), the raised alveolar pressure can compress the vessels running over its surface, causing an increase in vascular resistance.

Extra-alveolar vessels: By definition these vessels are not in contact with the alveoli, so they are not exposed to the same alveolar forces. These are exposed to the intrapleural forces, however, so as we saw airways opening during inspiration when intra-pleural pressure falls, these extra-alveolar vessels are also pulled open during inspiration by radial traction, and their resistance consequently falls as lung volume increases.

The summation of these forces (alveolar pressure, surface tension, and radial traction) means that pulmonary vasculature resistance has a complex relationship with lung volume.

Pulmonary Vascular Resistance and Lung Volume

Figure 9.6 shows vascular resistance changing with increasing lung volume. At low and high lung volumes vascular resistance is increased, while it is lower at medium lung volumes. Several forces are at play here, so let us take low lung volumes first.

Figure 9.6: The relationship between lung volume and pulmonary vascular resistance.

Vascular resistance at low lung volumes: At low lung volumes (figure 9.6, gray zone on the left), you should know that intra-pleural pressure is less negative because the lung recoil is less. With less negative pressure to hold open the extra-alveolar vessels via radial traction, these tend to narrow and vasculature resistance becomes relatively high.

Vascular resistance at medium lung volumes: As lung volume increases (figure 9.6, tan zone in the middle), the intrapleural pressure becomes more negative. Radial or parenchymal traction now begins to pull the extra-alveolar vessels open, and as they become wider, vascular resistance falls. Common sense would tell you that this effect would increase with continually larger lung volumes, and one might expect that vascular resistance would continue to decrease as lung volume increased. But this is evidently not the case.

Vascular resistance at high lung volumes: With further increases in lung volume (figure 9.6, pink zone on the right), vascular resistance rises. At high lung volumes the alveoli are enlarging, and this causes the capillaries running around them to stretch. As the capillaries stretch, they narrow—a little like how a piece of latex tubing narrows when it is stretched. This narrowing of a large number of capillaries overcomes the radial traction effect on the extra-alveolar vessels, and there is a net increase in vascular resistance.

So vascular resistance and lung volume are related with an inverted bell-shaped relationship. Now let us look at the forces that determine the distribution of blood flow across the lung structure.

Pulmonary Blood Flow and Gravity

You may recall that gravity affected the distribution of ventilation by generating the gradient of intrapleural pressures down the lung—most negative at the apex, less negative at the base.

We see a similar distribution of blood flow in the lung as well, as figure 9.7 shows with blood flow being greater at the base of the lung than it is at the apex. Again this is simply due to gravity. Gravity pushes against the blood rising from heart level, hence the base is better perfused than the apex. Because of this, gravity is responsible for matching the level of perfusion and ventilation up the lung; both are high at the bottom, and both are low at the apex. This is advantageous, as well ventilated areas need more perfusion for efficient gas exchange, and likewise there is little point in sending large amounts of pulmonary blood to poorly ventilated areas. The relationship between ventilation and perfusion (known as the V/Q ratio) that gravity establishes is not quite ideal, however, and we will see the ramifications of this less-than-perfect relationship later on. There are also other forces affecting the distribution of perfusion as well, and we can look at them now.

Figure 9.7: Perfusion distribution up the lung.