Ventilation:perfusion Equality

Ordinarily, ventilation and perfusion of blood within the alveolus are optimally balanced.  Note that among the many things that can interfere with this balance, factors that we tend to overlook are hypo- and hypertension!  Note that perfusion is greater in the inferior parts of the lung than in the superior parts and mean pulmonary arterial pressure (approximately 15 mmHg) is just enough to get blood to the superior portion of the lungs.  If pulmonary arterial pressure is decreased (eg. under anesthesia), there may not be sufficient pressure to get blood to the entire lung.  The figures below will probably seem fairly remedial... however, they demonstrate in a very simple way a very important concept!

A = very, very good - balanced ventilation and perfusion

In the normal lung in the perfect state, alveolar gases and pulmonary venous  blood gases (on the way back to the heart) are the same.  Again, recognize that there will be a slight drop in pO₂ due to mixing of bronchiolar venous blood with pulmonary venous blood and that blood in the left side of the heart will receive some de-oxygenated blood from the myocardium via the Thebesian veins.  This means that the pO₂ of blood leaving the left ventricle and entering the systemic circulation will be approximately 95 mmHg.  This is the value used in the diagram, here, as it more closely reflects pO₂ in systemic arterial blood gases.   In addition, we do not get absolutely perfect O₂ diffusion across the alveolar wall!  CO₂ diffusion is more perfect over the time and distance alloted as CO₂ is far more diffusible in aqueous solution than is O₂.

B = a decrease in ventilation

This situation is very bad, indeed!  Gas tensions in the alveoli approximate gas tensions in the "deoxygenated" blood returning to the alveoli.  Certain parts of the lung are being uselessly perfused as there is no oxygenation of the blood going on there.  Some of the blood will be diverted away from the poorly ventilated area of the lung by local hypoxic vasoconstriction of arterioles entering the hypoxic portion of the lung!  Any condition or symptom that occludes or otherwise blocks any of the airways will result in impaired ventilation!

An example of a severe ventilation problem would be atelactasis resulting from pneumothorax!  You get some diffusion from the lung and blood to the tissue but it is obviously impossible to achieve sufficient ventilation in a collapsed lung.  Alveolar gas exchange would be minimal in the affected lung!  You are essentially fighting a losing battle against the effect of air rushing in and out of the intrapleural space with the breathing movements of the thorax.

C = decrease in perfusion (and increased alveolar dead space!)

This situation is also very bad.  Certain parts of the lungs are being uselessly ventilated as there is no blood perfusion there and therefore no oxygenation going on there.

While this situation may occur with vascular damage in the pulmonary circulation, the outcome is analogous to that which would be seen in a pathological "shunt."  The term shunt refers to any blood that reaches the systemic arterioles without being oxygenated (we know there are some physiological shunts).  A pathological shunt would be a right to left shunt in the heart through a right to left deviation in the ventricular septum (a potentially very serious pathological shunt).  When you dump deoxygenated blood into the systemic arteries, it mixes with normally oxygenated blood to decrease the PO₂ in the systemic circulation.  The greater the amount of "shunting," the worse off you are!

Local Myogenic Mechanisms that Help Match Ventilation and Perfusion

When there is a localized buildup of CO₂ anywhere in the lung, the smooth muscle of the bronchioles in that region will respond to the increased CO₂ by relaxing, reducing resistance to airflow and increasing ventilation of that region of the lung.  Decreased CO₂ levels will cause bronchiolar smooth muscle to constrict, reducing air flow back to normal.

Smooth muscle of the pulmonary arterioles responds to changes in O₂ levels.  When there is a reduction of O₂ in a localized region of the lung, vascular smooth muscle will constrict, increasing resistance to blood flow, reducing blood flow to the hypoxic region, and shunting blood away to areas of the lung where the blood can be more effectively oxygenated.  This local myogenic redistribution of blood only becomes problematic when there is insufficient O₂ available throughout the lung, leading to increased pulmonary vascular resistance throughout the entire pulmonary circuit... possibly leading to cor pulmonale if a reasonable oxygen supply is not established.  An increase in O₂ levels will cause pulmonary vascular smooth muscle to relax, allowing blood to flow into well oxygenated regions of the lung.

Note finally that the effect of decreased O₂ on pulmonary vascular smooth muscle is opposite to that seen in the systemic circulation.  To review... in the pulmonary circuit, blood vessels respond to low O₂ levels by constricting in order to direct blood away from poorly oxygenated areas of the lung... whereas in the systemic circuit... low O₂ levels promote vasodilation to direct blood into poorly oxygenated areas of organs.