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Pulmonary Function Testing

Page history last edited by PBworks 14 years, 8 months ago

Pulmonary Function Testing.

Charles e. McCormack, Ph.D.

(Read Chapt. 10 of Respiratory Physiology-the essentials, by J. B. West.)


  • I. Forced vital capacity: If you could only run a single pulmonary function test on a patient, your choice would probably be to determine the patient's forced vital capacity (FVC). In this test, the patient inspires maximally, and then exhales forcibly and rapidly. The volume of air the patient exhales is measured as a function of time. The volume of air a patient exhales during the first second is called the forced expiratory volume in 1 second (FEV-1) and in 3 seconds, the FEV-3. When coupled with the patient's clinical history and physical examination, FVC, FEV-1, and FEV-3 provide valuable information on the nature of the pulmonary problem. Representative values from a normal subject, a patient with obstructive lung disease, and a patient with restrictive lung disease will be inserted on the graph and table on the following page. Major points to remember are:
  1. Even in subjects with normal lungs, the airways are subjected to negative transmural pressures during a forced expiration (dynamic compression), and therefore airways tend to collapse.
  2. In obstructive lung disease, because lung tissue is lost, the airways are even more likely to collapse during a forced expiration, thus greatly increasing resistance to air flow. As a result, FVC, FEV-1, and FEV-3 are below normal.
  3. In restrictive lung disease, the airways do not have an increased tendency to collapse during expiration, but the expansion of the lungs during inspiration is restricted. As a result, FVC and FEV-1 are below normal.
  4. The ratio, FEV1/FVC, is below normal in patients with obstructive lung disease, but is normal or above normal in patients with restrictive lung disease.
  5. Maximum flow rates during forced expiration are below normal whether patients have obstructive or restrictive lung disease. (Patients with obstructive lung disease get the air into their lungs satisfactorily, but cant get it out. Patients with restrictive lung disease can't get the air into their lungs, and they can't get out what they didn't get in.)
  6. Residual volume (RV), functional residual capacity (FRC), and total lung capacity (TLC) are increased in obstructive lung disease, and decreased in restrictive lung disease.
  7. Examples of obstructive lung disease include emphysema, chronic bronchitis, and asthma. Examples of restrictive lung disease include interstitial fibrosis, scoliosis, and loss of surfactant (respiratory distress syndrome).

Flow-Volume curves: If during a forced expiration, flow is plotted as a function of lung volume, the differences in flow rate between normal subjects and those with obstructive or restrictive lung disease become apparent (See figure 10.2 from West below).

II. Time constant: West p. 115-116 uses the term "time constant" in his text to reflect the time it takes for a given volume of air to move in the airways. In the lung, the time constant is directly proportional to resistance to air flow, and to lung-compliance. When the units of resistance are multiplied by the units of compliance (see below) , the resulting unit is time. In essence, flow slows if either resistance or compliance increases. Some obstructive lung diseases (asthma) primarily increase resistance; other obstructive lung diseases (emphysema) increase resistance and compliance.

III. Tests for abnormal V/Q ratios: Most all lung diseases produce hypoxemia by virtue of creating abnormal V/Q ratios. The first two tests given below for the presence of abnormal V/Q ratios have been described in earlier lectures. The third and fourth tests will be described in more detail here.

  1. Measurement of physiologic dead air space, VDAS. An abnormally large VDAS is an indication of an abnormal V/Q ratio.
  2. Determination of the alveolar-arterial (A-a) difference in PO2: A larger than normal A-a PO2 difference is usually a sign of abnormal V/Q ratios. However, right to left shunts also produce a larger than normal A-a PO2 difference. (How can right to left shunt be eliminated as a cause of an abnormally large A-a PO2 difference?)
  3. "Single breath nitrogen washout test": This test was covered earlier in the lectures on mechanics of the lung. An increase in the slope of the increase in nitrogen percentage during the plateau (alveolar-emptying) stage indicates unevenness of alveolar ventilation, and thus abnormal V/Q ratios. This is because well-ventilated alveoli, which receive more of the inhaled oxygen, empty first thus lowering the initial plateau-nitrogen concentration; poorly-ventilated alveoli, which receive less of the inhaled oxygen, empty last thus raising the final plateau-nitrogen concentration. In practice, the slope of the plateau is measured and comparisons with normal values are made between 750 and 1250 ml of exhaled air. The normal increase in percentage of nitrogen in exhaled air between these volumes is less than 1.5 %. This test is illustrated in Figure 1.10 of Pulmonary Pathophysiology by J.B.West 6th edition and in figure 18 from page 62 of Comroe, The Lung, 2nd ed., 1962 (shown on the next page of these notes).
  4. Closing volume: When, as a result of dynamic compression, mid-size airways in the base of the lungs collapse during the "single breath nitrogen washout test," the percentage of nitrogen in mixed exhaled air markedly increases. (See figure 1.11 from West on the next page.) This is because once the basal airways close, only the apical airways remain open and continue to empty. Because of their low compliance, the apical alveoli receive less of the inhaled oxygen, thus when they alone are emptying, the percentage of nitrogen in the mixed exhaled air markedly increases. The volume at which this occurs is called the closing volume. Closing volume is increased in obstructive lung disease. It also increases with age and by 65 years-of-age is nearly equal to the FRC. The increased closing volume is a sign of "loss of interdependence" due to loss of lung tissue.

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