So I have two sources and they seem to be saying two opposite things. When V/Q is high, is the PaO2 highest or lowest? thanks
The question you're asking is very general. Are you inquiring as to where in the lung Pa is greatest, or are you asking about whether a perfusion vs ventilation defect results in a greater ebb of arterial oxygen content?
In terms of lung location (
physiological):
V/Q is ~3.0 at the lung apex and ~0.6 at the lung base when
upright. It's
not that ventilation (PA) is greatest at the apex; perfusion (Pa) is merely lesser at that location due to gravity. Therefore, arterial pressure is lesser than alveolar pressure, and PA > Pa > Pv. As you move inferiorly in the lung (mid-lung zone), when
upright, arterial pressure surpasses alveolar pressure and Pa > PA > Pv. At the lung base, perfusion is greatest such that even venous pressure can surprass alveolar pressure (Pa > Pv > PA). Furthermore,
physiologically, when considering the higher V/Q at the lung apex vs the lower V/Q at the lung base, Pa is greatest at the lung base where V/Q is low.
In terms of ventilation vs perfusion defect (
pathological):
If V/Q is elevated, a perfusion defect is present. If V/Q is low, a ventilation defect is present. PaO2 may decrease with both perfusion and ventilation defects, but it classically decreases
more with a ventilation defect (PaO2 is lower with low V/Q). This is because under-ventilated regions have a substantially decreased P
AO2 such that properly ventilated regions, even if hyper-ventilated, cannot fully compensate (i.e. if net PAO2 should be ~100mm Hg, if one area of under-ventilated region can only yield PAO2 = 40mm Hg, it doesn't matter whether other hyper-ventilated regions yield PAO2 = 120mm Hg, because shunting of blood from high O2 to low occurs, and the net result is PAO2 < 100mm Hg). Therefore, since the hyper-ventilated regions cannot compensate in a ventilation defect, putting the patient on 100% O2 won't change his or her PaO2 because any additional O2 merely enters a decompensated shunt. In a perfusion defect, blood not reaching one area of lung is transferred to other areas of lung.
Since healthy lung is perfusion-limited, augmented perfusion in areas
not affected by the perfusion defect results in sufficient compensation. Therefore, giving O2 to a patient with a perfusion defect
does increase his or her PaO2.
The take away message: Pathologically, PaO2 decreases with both high and low V/Q, however it classically decreases more with low V/Q. Low V/Q is
not subject to PaO2 augmentation with 100% O2 administration, whereas high V/Q is. Physiologically, Pa is greater at the lung bases than at the lung apices due to greater longitudinal distance below the level of the left atrium, when upright, resulting in higher proximal vascular pressures and lesser vasoconstrictive effects. Healthy lung is perfusion-limited.