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The role of diffusion in producing abnormalities in gas exchange is of little importance and for practical purposes can be ignored under resting conditions. Limitation of diffusion consists of an oxygen gradient between alveolar and end-capillary oxygen tensions. This value is normally zero. Only if cardiac output is increased and the fraction of inspired oxygen is decreased does
Figure 26-16
Schematic representation of multiple-breath nitrogen
washout curves in a young, healthy nonsmoker (Normal) and in an asymptomatic smoker
(Abnormal). Expired nitrogen concentration is plotted on a logarithmic scale against
cumulative expired volume during pure oxygen breathing.
Diffusing capacity of the lungs (DL) is defined as the rate at which a gas enters the blood divided by its driving pressure. The latter term is the gradient between alveolar and end-capillary tensions. DL is expressed in units of milliliters per minute per millimeter of mercury.
In addition to driving pressure, DL is determined by the thickness of the alveolar-capillary membrane. DL is influenced by the number of capillaries in the alveolar wall, which determines the area of the alveolar-capillary membrane surface. Measurement of DL provides information about the amount of functioning capillaries in contact with ventilated air spaces. The number of functioning capillaries may be reduced in certain pulmonary vascular and parenchymal disease states. The brief inhalation of nontoxic low concentrations of carbon monoxide (CO) has become standard in most pulmonary function laboratories for this purpose.
CO has several features that make the gas useful for measuring DL. It has 200 times the affinity for hemoglobin as oxygen does and therefore does not build up rapidly in plasma. CO concentration is low in the blood under normal conditions, and pulmonary capillary tension can be assumed to be zero. Of the techniques using CO, the rebreathing method is least influenced by changes in V̇/ distributions.
To measure the CO diffusing capacity of the lungs (DLCO),
three values must be obtained: the milliliters of CO transferred from alveoli to
blood per minute, the mean alveolar CO tension (PACO),
and the pulmonary capillary CO tension (PCCO):
Of the several techniques for estimating DLCO, the most widely employed is the single-breath test. In the single-breath method, the patient inspires a dilute mixture of CO and holds the breath for 10 seconds. During this period, CO leaves alveolar gas to enter the blood in proportion to the diffusing capacity. The number of milliliters of CO transferred is calculated from the percentage of CO in alveolar gas at the beginning and at the end of the breath-hold by infrared analysis. To do this, the FRC must be calculated from the helium dilution and then added to the inspiratory volume. The PCCO is essentially zero and can be ignored.
The single-breath method requires very little patient cooperation and is relatively simple to perform because it requires no blood samples. It is relatively insensitive to the backpressure of CO in the blood and is only mildly affected by V̇/ inequalities. Disadvantages include the extensive mathematical computations and the requirement for 1.3 L or greater inspired volume with a breathhold. The latter may not be feasible in the dyspneic patient or in the exercising subject.
Normal values of DLCO range from 20 to 30 mL/min/mm Hg and depend on lung size. The use of helium enables determination of total alveolar volume (VA). Dividing DLCO by VA normalizes for lung volume. Decreases in DLCO are caused by emphysema, lung resection, pulmonary emboli, and anemia, all of which effectively decrease surface area by reducing capillary blood volume. Other diseases, such as pulmonary fibrosis, sarcoidosis, and alveolar proteinosis, increase alveolar wall thickness, which also decreases DLCO. Increased DLCO is rarely of much clinical concern. Many conditions that increase pulmonary blood volume result in an increased DLCO, including the supine position, exercise, obesity, and left-to-right intracardiac shunts.
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