Alveolar Ventilation-Perfusion-Ratio

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Alveolar Ventilation-Perfusion-Ratio
HR Ahmad*

The dynamic cardio-respiratory control of equilibrium between alveolar ventilation and perfusion as a marker of gas exchange determines the alveolar and arterial PO2 and PCO2. When an alveolus is ventilated but not perfused, it approximates to the inspired air. In the reverse order, it would be equal to the mixed venous capillary blood gas content. This concept shows that the O2 and CO2 pressure values in the lung capillary surrounding an alveolus is the result of the matching between alveolar ventilation and perfusion. It means the alveolar ventilation–perfusion ratio [AVPR] is a limiting factor for a gas exchange. For an effective gas exchange in lungs, the matching of alveolar ventilation and perfusion more precisely the alveolar diffusion capacity to perfusion ratio [ADPR], is a prerequisite.


Prof. HR Ahmad

Indeed the alveolar ventilation – perfusion inhomogeneity is observed under normal physiological condition. The arterial blood sampling from the apical lung shows higher PO2 than the base of lung in the erect standing position. This is due to a steep apical-base gradient of perfusion. This affects the hydrostatic pressure in alveoli to be higher than the pulmonary capillary pressure. It means the apical lungs can be perfused only during systole in the erect standing position. Contrastingly, there is a continuous flow at the base of lungs during a cardiac cycle. It is because the hydrostatic pressure is higher in the capillary than in alveolus at the base of lungs.

The lung compliance is higher at the base than the apical lungs. It means ventilation experiences also an apical-base gradient. This gradient, however, is less pronounced than the perfusion gradient. In sum it means that despite the fact the apical lungs are poorly ventilated than the basal ones, the alveolar ventilation is relatively higher than the perfusion. Consequently, the alveolar PO2 at the apex is higher than the base of lungs. The AVPR is 3.3 at apex and 0.6 at the base of lungs in standing position. The alveolar-arterial-difference for oxygen is 10 mmHg and for CO2 1 mmHg due to the perfusion gradient.

The application of this concept favors the growth of tubercle bacteria as the first residence at the apex of lungs in the body. This high PO2 growth dependence is the basis of high altitude therapy for TB patients. Hypoxic vasoconstriction blocks further the spread using the Euler – Liljestrand reflex. It operates through oxygen sensitive potassium channels of vascular smooth muscles to a drop in alveolar PO2.This divert the flow to the ventilated part of lung but with a drop in AVPR.

An increase in the alveolar-arterial PO2 difference is a marker of AVPR disorder. This can be well observed in patients with central and peripheral cyanosis. Oxygen saturation is reduced in former but remains normal in later. The skin and the tongue are cyanotic in central one due to the shunt admixing. Blue lips but normal tongue is the finding in the peripheral cyanosis. It is caused by shock, heart failure and cold exposure. This synopsis is adapted from the work, on the cell-capillary gas diffusion model underlying mechanisms of AVPR, of laureate scientists Gerhard Thews and Peter Vaupel from University of Mainz Germany.

This is dedicated to memories of Irfan Zubair, an enlightened teacher of Waldorf Schule in Germany, who passed away in Duisburg on 7th January, 2021.

*The author is a professor of physiology at SIUT and AKU Karachi – Pakistan.

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