13.2: Distribution of V/Q (2024)

As you should understand, ventilation increases down the lung so is greatest at the base, and perfusion follows the same pattern—all due to the effects of gravity. But the increase in ventilation down the lung structure is not equal to the increase in perfusion, as can be seen in figure 13.6. You can see here that perfusion is higher than ventilation at the base; it falls off much more rapidly as the lung is ascended, so it ends up being lower than ventilation at the apex.

This means there is a range of ventilation–perfusion ratios up the height of the lung (figure 13.6, maroon plot). At the base perfusion is higher than ventilation, so V/Q is less than 1, while toward the apex V/Q rises and becomes greater than 1. At about the level of the third rib, V/Q is perfect (yay!) as ventilation and perfusion are matched, seen here at the points the lines cross. This range of V/Q results in the previously mentioned whole lung average of 0.8.

As you should appreciate from understanding the ventilation–perfusion line, this range of V/Q across the lung results in a range of alveolar gas partial pressures across the lung. The apical alveoli, being relatively overventilated (or underperfused, whichever way you would like to think about it), have a high V/Q and consequently have partial pressures closer to atmospheric partial pressures. On the other extreme, the basal alveoli are relatively underventilated (or overperfused, your choice) and so have a low V/Q, tending toward zero; thus their partial pressures are closer to venous values (figure 13.7).

In between these two extremes is a progressive range, so what we see is that alveolar PO₂ declines down the lung while alveolar PCO₂ rises. As you might imagine, having a range of alveolar gas tensions down the lung has ramifications for gas exchange and particularly for oxygen saturation. This inequality in V/Q resulting in differences in alveolar PO₂ is substantial enough to suppress arterial oxygen saturation—and contribute to your oxygen saturation meter never reading 100 percent. Let us see why.

The difference in alveolar PO₂ from apex to base is as high as 40 mmHg, as is reflected in this figure. The apical alveoli have a high PO₂ (shown in figure 13.8 as 132 mmHg), primarily due to their poor perfusion and relatively high ventilation and thus high V/Q. This produces a high diffusion gradient from 132 mmHg in the apical alveoli, to 40 mmHg in the apical blood. Consequently, what blood does go to the apex becomes fully saturated before it heads back toward the left heart.

Down at the base, however, V/Q is low because of the high perfusion and relatively low ventilation. Consequently the PO₂ in basal alveoli tend toward venous values, shown in figure 13.8 as 89 mmHg. This lower alveolar PO₂ means a diminished diffusion gradient (from 89 in the alveoli to 40 mmHg in the blood), and combined with a shift down the hemoglobin saturation curve (more on this later), this means blood leaving the basal alveoli may not be completely saturated with oxygen.

When the blood from the apex and base mix on their journey back to the left heart, the outcome is that the combined oxygen saturation is less than 100 percent, about 97 percent. It is worth making perhaps an obvious but critical point here. The blood from the apex is exposed to a substantially higher PO₂ and becomes 100 percent saturated (i.e., it cannot take on any more O₂ as it is at its full oxygen carrying capacity). There is no way that it can pick up extra to compensate for the blood coming from basal alveoli, which are not at capacity.

The same is not true for CO₂ though. Because of its high solubility, CO₂ transport does not rely on a transporter protein like hemoglobin; the transfer of CO₂ is really dependent on the diffusion gradient present. So at the apex the lower alveolar PCO₂ (slightly less than 30 mmHg looking at our V/Q line) generates a larger diffusion gradient with venous blood, and more CO₂ is transferred out the blood, meaning that it can compensate for the low diffusion gradient (perhaps only a few mmHg) that occurs between the alveoli and blood at the lung’s base.

As a study exercise it may be worthwhile for you to go back to the ventilation–perfusion line and calculate the diffusion gradients for oxygen and carbon dioxide between the alveoli and venous blood at different heights in the lung. I urge you to come to grips with this concept as it is highly pertinent to respiratory disease and can explain clinical-related changes in blood gases.

The take-home message, however, is that even the normal lung is not perfect and has an average V/Q ratio of 0.8, rather than the ideal of 1, and this slight matching of ventilation and perfusion contributes to the arterial saturation being slightly less than 100 percent, but has little effect on arterial CO₂. If respiratory disease increases the mismatch, this effect on oxygen saturation can become more pronounced, but the lung has a defense mechanism for this.

Correcting V/Q Mismatches

In an attempt to maintain V/Q close to 1 and prevent V/Q mismatching, the pulmonary vasculature has an unusual response to hypoxia. While the systemic vasculature responds to local hypoxia with a vasodilation to bring more blood to the area, the pulmonary vasculature constricts in the presence of low oxygen to shunt blood away from hypoxic regions.

Let us look at a common scenario that might occur in a patient with chronic bronchitis. Figure 13.9 represents two regions of the lung. One region becomes blocked by a mucus plug, and ventilation to that region goes to zero.

The alveolar partial pressures will rapidly equilibrate to venous pressures, and desaturated blood goes back to the left heart from this region while the local region around this area becomes mildly hypoxic. The pulmonary vasculature responds to the hypoxia by vasoconstricting, reducing the perfusion to the unventilated region and helping to rematch the V/Q ratio in this region (i.e., low ventilation is matched with low perfusion). In common sense terms, there is no point sending pulmonary blood to an unventilated region, so the hypoxia-driven vasoconstriction prevents this from happening.

The distensibility of the pulmonary vasculature means that the blood is shunted to unconstricted vessels (i.e., those supplying ventilated regions). Thus the lung has its own inherent mechanism to optimize V/Q and promote the most effective gas exchange possible.

The unusual response of the pulmonary vasculature is demonstrated in figure 13.10, showing how as alveolar PO₂ falls (as occurs with a decline in alveolar ventilation) then blood flow falls—and likewise, the more oxygen in the alveolus, the more pulmonary perfusion it receives.

This effect is driven by a hypoxia-sensitive potassium channel found on the albeit sparse smooth muscle of the pulmonary arterioles. This channel is normally open and allows the exit of potassium, which in turn keeps the inside of the muscle cell polarized. When exposed to hypoxia the channel closes, and the outward potassium current stops, allowing the muscle cell’s membrane potential to rise and consequently depolarize to cause a contraction.