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As alluded to previously, in order for gas exchange to be efficient, each region of the lung must receive equal amounts of ventilation and pulmonary perfusion to its alveoli. If ventilation and perfusion are not matched, then gas exchange diminishes, particularly in the case of oxygen. The relationship between ventilation and perfusion is referred to as V/Q, which describes the ratio between ventilation (V) and perfusion (Q) for a particular lung region. Because V/Q is critical to gas exchange and as many pulmonary diseases cause ventilation–perfusion mismatches, it is well worth understanding the effect of changing V/Q on arterial gases, and the regional differences in V/Q across the lung and the lung’s responses to maintain V/Q when it deviates from normal.
Let us start with a description of the ideal situation, where ventilation to alveoli is matched with the perfusion, then we will see how the lung does not quite achieve this.
Figure 13.1 shows venous blood approaching and passing two alveoli, becoming oxygenated, and then heading back toward the left heart. The ideal situation is that both alveoli are both ventilated and both perfuse and that the ventilation and perfusion ratio (the V/Q) to each is equal (i.e., 1). If this is the case, then gas exchange is highly efficient, blood PO2 comes into equilibrium with alveolar PO2, and consequently there is no alveolar–arterial PO2 difference.
This is what we would expect if the lung were perfect, with uniform distribution of ventilation and perfusion to all regions and a V/Q of 1 in all regions.
The lung is not a perfect organ, however, and ventilation and perfusion are not equally distributed, and the lung as a whole only achieves an average V/Q of 0.8, which is close to our ideal of 1, but not quite there. Consequently, by the time the blood has passed the alveoli and regrouped in the pulmonary veins, the PO2 of the blood is less than alveolar. This alveolar–arterial PO2 difference is caused by the less-than-perfect matching of V and Q across the lung; but it is not all the lung's fault, as venous blood that has been through the bronchial and a small section of the coronary circulation (and therefore is deoxygenated) is mixed into the vessels returning to the left heart, which brings down arterial saturation as well. The mixing-in of bronchial and coronary circulations and the less-than-ideal V/Q in the lung as a whole is the reason why your saturation monitors do not read 100 percent, but normal oxygen saturation is considered as 96–98 percent.
Partial Pressures and V/Q
When V and Q are matched (V/Q = 1): Atmospheric PO2 is diluted as it descends the airways to give an alveolar PO2 of 100 mmHg, and alveolar PCO2 is 40 mmHg. The blood returning from the tissue has a diminished PO2 of 40 mmHg and a raised PCO2 of 45 mmHg. As this blood passes the alveolus, oxygen moves into the bloodstream down its pressure gradient and CO2 moves into the alveolus down its pressure gradient. As ventilation and perfusion are matched then equilibrium is reached and the blood leaves with arterial gas tensions that are the same as alveolar tensions (figure 13.2).
When V = 0: Now let us look at another and extreme situation, where ventilation (V) is zero so our V/Q is zero (zero divided by anything is zero).
This situation is clinically possible as airways can collapse or become blocked with a mucus plug. Without any ventilation the gas tensions inside the alveolus rapidly equilibrate with the returning venous blood, so alveolar gas tensions end up as a PO2 of 40 mmHg and a PCO2 of 45 mmHg. The venous gas tensions, never having been exposed to a ventilated alveolus, now circulate into the arterial system, and arterial PO2 becomes 40 mmHg and PCO2 becomes 45 mmHg there as well (figure 13.3).
When Q = 0: Now let us go to the other extreme, where perfusion is zero and ventilation is normal (V/Q goes to infinity). Again, this can occur in reality should a pulmonary vessel become blocked by an embolus. In this scenario V/Q becomes infinity—anything divided by zero is infinity. With no perfusion, no gas exchange occurs in this alveolus, and as it is still being ventilated then the alveolar gas tensions equilibrate with the atmosphere (figure 13.4).
So going from these extremes of V/Q as zero, passing through the ideal of V/Q of 1 to a V/Q of infinity, we get a range of alveolar gas tensions going from venous gas tensions when V/Q is zero to atmospheric gas tensions when V/Q is infinite.
This range of alveolar gas tensions is represented by the ventilation–perfusion line (figure 13.5). This graph takes a minute to come to grips with, so let us break it down. The axes of the graph show alveolar PO2 on the X and alveolar PCO2 on the Y. The plot shows the range of V/Q ratios we have just discussed, ranging from zero when there is perfusion but no ventilation, to infinity when there is ventilation but no perfusion. Looking at figure 13.5 more carefully will confirm our numbers. When ventilation and perfusion are present and V/Q is 1, then our alveolar PO2 is 100 mmHg, and the alveolar PCO2 is 40 mmHg—just as we have seen.
If we stop ventilation and go to a V/Q of zero, we again see that the alveolar gas tensions become equal to venous values, with alveolar PO2 at 40 mmHg and PCO2 at 45 mmHg.
And finally, when we stop perfusion and V/Q becomes infinite, then alveolar PO2 becomes 150 mmHg and PCO2 becomes zero (i.e., equilibrates with the atmosphere).
Summary
In summary, the ventilation–perfusion line show the effect of changing V/Q on alveolar gases. Reduce V/Q toward zero and the alveolar gas tensions tend toward venous gas tensions. Increase V/Q toward infinity and the alveolar gas tensions get closer to atmospheric partial pressures.
The importance of understanding this becomes apparent when we see that V/Q changes across the structure of the lung, and if V/Q changes, then alveolar partial pressures change to.
Let us look at the distribution of V/Q across the lung and why it changes from apex to base.
