Pulmonary ventilation and perfusion function as a vital unit that supports life and promotes health. Knowledge of pertinent and key basic concepts is of value to those that provide health care as well as to those that receive it.
Alveolar ventilation is the volume of air that reaches the gas exchange units of the lungs per minute. It is a fraction of the pulmonary ventilation; calculated as the tidal volume minus the physiologic dead space times the breathing rate. The formula for calculating it is as follows:
Alveolar ventilation rate =
(Tidal Volume –Dead Space) x Respiratory Rate
Pulmonary ventilation on the other hand, is the total volume of gas inhaled or exhaled per minute. It includes the volume that enters the anatomical and alveolar dead spaces. The lion’s share of the air spaces where gas exchange does not occur is anatomic dead space in the normal state.
Regional differences in pulmonary ventilation
In upright lungs the movement of air to and from alveoli is greatest in the base (the bottom); least in the apex (the top); and intermediate in the points in between. To understand this it is important to first know some basic mechanics of breathing.
Mechanics of breathing
The flow of air into the lungs is the result of a pressure gradient between the pleural space and the atmosphere. Contraction of the diaphragm and muscles of the chest wall causes the pleural space and chest cavity to expand. This creates negative pressure in both areas. That negative pressure transmits to the lung units. The gradient between the positive pressure in the atmosphere and the negative pressure in the lungs results in the flow of air into the lungs.
During expiration the diaphragm and other breathing muscles relax. This causes the chest cavity to decrease in size as the thorax recoils. That change causes pressure in the chest cavity and pleural space to increase. The resulting positive pressure gradient from the inside out along with the elastic recoil of the lungs causes air to flow out of the lungs.
Reasons for regional differences in pulmonary ventilation
There are two commonly held beliefs to explain the differences in pulmonary ventilation between the lower and upper portions of the lungs while sitting or standing. They have to do with the effects of gravity and the same end result.
First of all there is a pleural space pressure gradient which increases vertically from the bottom to the top of the lungs. The commonly held notion is that the weight of the lungs and the difference in the shape of the lungs and pleural space from top to bottom is responsible. Consequently, at the end of a normal expiration the alveoli in the lower regions of the lungs contain less air; thus they can expand to a greater degree and receive more air during inhalation.
Secondly, the weight of the lungs which is greater in the lower portions causes the alveoli in those areas to be less air-filled at FCR. This is another reason they can expand more during inspiration.
Despite the time honored above explanations, recent research has called them into question. Studies using more refined methods of evaluating ventilation not only suggest that other mechanisms are involved. They also imply that the effects of gravity might not be the main factor.
Pulmonary perfusion and regional differences
In relation to ventilation, pulmonary perfusion refers to the flow of blood that reaches alveoli by means of capillaries. It is also greatest in the base and least in the apex of the lungs in the upright position. Gravity and resulting hydrostatic pressure is also the commonly expressed reason. But recent research also casts some doubt on this notion as the sole or main explanation.
Ventilation/perfusion matching and mismatching
Pulmonary ventilation (V) and perfusion (Q) function in tandem. Air moves in and out of gas exchange units of the lungs as blood flows to and from and around and around them. The abbreviation for the ratio of the two functions is V/Q. V/Q = 1 means there is absolute matching of the two processes, but it is unrealistic.
The average V/Q in the resting state is 0.8 as opposed to 1. The reason is, even though both ventilation and perfusion decrease from the base to the apex and increase from the apex to the base in upright lungs, there is a differential between the two at the various levels and a greater change in perfusion than ventilation in either direction. Therefore, V/Q tends to be higher for the gas exchange units in the upper portions of the lungs than those in the lower parts. At the base of the lungs the average V/Q is 0.6. In the apex it is 3.
Thus, ventilation/perfusion mismatch (V/Q mismatch) – this nonuniformity of V/Q in different areas of the lungs – is normal to a degree. But when it increases beyond a certain point it causes a problem. That problem is hypoxemia, of which V/Q mismatch is the most common cause. Conditions associated with it include: 1) pneumonia; 2) pulmonary embolism; 3) COPD; 4) asthma; 5) interstitial lung disease; 6) pulmonary edema; (7) etc.
Low V/Q and oxygenation
There are two reasons for low V/Q. They are deficient alveolar airflow relative to capillary blood flow; or excessive capillary blood flow relative to alveolar airflow. In either case, the result is decreased oxygenation and O2 saturation.
Oxygen saturation (O2 sat) is the amount of oxygen in blood, expressed as a percentage of the maximal quantity the blood can hold; that amount is a function of the concentration of hemoglobin to which most of the O2 is bound. If blood is 100% saturated it contains the full amount of O2 it can hold. Venous blood is typically around 70% saturated. Blood oxygenated by healthy lungs is around 98% saturated.
Intrapulmonary shunt is the extreme of a low V/Q state. It is an area of the lung in which perfusion is normal or near normal but there is no gas exchange. It might be due to destroyed, fluid-filled, or collapsed alveoli. It differs from other V/Q mismatch situations in that the administration of 100% oxygen does not improve the O2 sat when a shunt is present.
High V/Q and oxygenation
There are two reasons for high V/Q. They are greater alveolar airflow than capillary blood flow; or lower capillary blood flow than alveolar airflow. For obvious reasons, high V/Q does not cause hypoxemia in and of itself. The alveoli in these areas saturate the blood with O2.
High V/Q indirectly causes hypoxemia though, if the high ratio is due to reduced or blocked blood flow. The blood flow problem in one area(s) causes greater flow to other areas of the lung. The alveoli in those areas can’t match the increased blood flow with their set ventilation. Oxygenation drops. Hypoxemia is the result. Pulmonary embolism and pulmonary hypertension are the best examples of diseases that can cause this type of V/Q mismatch.
Alveolar dead space is the high V/Q extreme. It is the volume of air in alveoli that does not participate in gas exchange because of the lack of adequate perfusion. It is similar to the trachea and other parts of the respiratory tract where gas exchange does not occur. The difference though is that it is not normal and is usually the result of a disease.