Spirometry. FEV1 vs FEF25-75 percent.
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Biomedical subjects
Publications and source records attributed to A F Gelb.
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The purpose of the present clinical research was to establish the major site of resistance and obstruction in patients with severe, symptomatic chronic obstructive pulmonary disease. We used a noninvasive technique by measuring airflow in a plethysmograph after patients breathed air and after breathing a mixture of 80 percent helium and 20 percent oxygen. In group 1 were 14 patients (mean age, 63 +/- 7 years [+/- 1 SD]) with bronchitis. The ratio of their forced expiratory volume in one second over the vital capacity (FEV1/VC) was 43 +/- 10 percent (mean +/- 1 SD), and their single-breath carbon monoxide diffusing capacity (Dsb) was normal (125 +/- 41 percent of the predicted value). In group 2 were 13 patients with emphysema (mean age, 60 +/- 10 years), whose FEV1/VC was 33 +/- 11 percent and Dsb was 55 +/- 14 percent of predicted. All patients had abnormally low increases in the maximum expiratory flow at midvital capacity after breathing the helium-oxygen mixture. The range in group 1 was -11 percent to +14 percent and in group 2 was -10 percent to +15 percent. Normal subjects in our laboratory show increases of at least +24 percent. This indicates that the limitation of airflow occurs primarily in the small (less than 2 mm in internal diameter) and not the large airways.
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We studied 129 patients during acute, severe asthmatic attacks. Electrocardiograms showed P pulmonale in 49% of patients who had an arterial carbon dioxide tension (PaCo2) greater than or equal to 45 mm Hg and an arterial pH less than or equal to 7.37, whereas P pulmonale was present in only 2.5% of asthmatics who had a PaCO2 less than or equal to 44 mm Hg and a pH greater than or equal to 7.38 (p less than 0.001). P wave and QRS axes were 79 +/- 8 degrees and 80 +/- 20 degrees, respectively, in the presence of P pulmonale. When P pulmonale disappeared, the P wave and QRS axes shifted significantly to the left (p less than 0.001). Electrocardiographic P pulmonale persisted 12 to 60 hr after correction of hypoxemia, hypercapnia, and acidosis. In 7 patients with P pulmonale and respiratory acidosis, cardiac catheterization demonstrated normal artery pressures (PAPs) measured relative to atmospheric pressure. In 12 of these peak inspiratory pulmonary artery transmural pressures (PATPs) were increased. Since increased right heart transumural pressures could result in chamber distention, these data are consistent with the hypothesis that reversible P pulmonale in status asthmaticus is explainable on the basis of markedly negative tidal pleural pressures and increased right heart transmural pressures.
We measured pulmonary functions in 10 nonsmoking asymptomatic subjects, ages 40.5 years +/- 9.2 years, with alpha1 antitrypsin heterozygous deficiency (phenotype MZ). The subjects were longstanding residents of the greater Los Angeles area. The range of physiologic studies and per cent of normal predicted values were forced vital capacity (FVC), 2.8 to 7.0 liters (86 to 124 per cent predicted); ratio of the forced expiratory volume in 1 second to the FVC, 70 to 86 per cent (86 to 104 per cent predicted); the ratio of the residual volume to total lung capacity, 28 to 44 per cent (94 to 119 per cent predicted); total lung capacity, 4.8 to 9.8 liters (80 to 119 per cent predicted); flow at 50 per cent FVC, 3.1 to 7.8 liters per second (69 to 140 per cent); and volume of isoflow, 7.3 to 26 per cent of forced vital capacity (38 to 137 per cent predicted). In eight patients studied, static deflation pressure volume curves were normal, and at respiratory rate of 60 breaths/min the ratio of dynamic compliance to static compliance did not fall below 84 per cent. We have found that these nonsmoking heterozygotes with alpha1 antitrypsin deficiency have normal pulmonary functions (within 1.67 SD of predicted mean).
We measured hypercapnic ventilatory responses using the rebreathing technique and ventilatory drive using mouth occlusion pressure in 15 normal subjects (6 with added external inspiratory resistance), 11 asthmatics, and 17 patients with chronic obstructive pulmonary disease (9 with chronic CO2 retention and 8 with normal values for arterial pco2). normal subjects, obstructed normal subjects, asthmatics, and patients with chronic obstructive pulmonary disease without CO2 retention had overlapping ventilatory responses. Ventilatory drive was increased in asthmatics and obstructed normal subject. Patients with chronic obstructive pulmonary disease without CO2 retention maintained a ventilatory drive similar to that of normal subjects, whereas patients with chronic obstructive pulmonary disease with chronic CO2 retention demonstrated blunted ventilatory drives as a group, even though 5 of 9 had normal drives. Patients with CO2 retention also had the greatest obstruction when compared to other groups. In some patients, chronic CO2 retention is primarily a consequence of mechanical end-organ limitation rather than a blunted neurorespiratory center output. Acute airway obstruction is associated with an increased drive, which may become reduced with chronic obstruction.
The purpose of this report is to review the role of helium in the early detection of obstructive pulmonary disease. The underlying physiologic mechanisms of the volume of isoflow (the volume at which flow was the same with the subject breathing air and breathing a mixture of 80 percent helium and 20 percent oxygen) and increases in maximal flow at 50 percent of vital capacity (Vmax50) after breathing helium are reviewed. These tests are able to detect physiologic abnormalities in asymptomatic subjects when the results of other tests are normal; and following cessation of smoking, abnormal results may be reversible. The volume of isoflow is increased when maximal flow is reduced because of loss of elastic recoil or increase in upstream resistance. The increase in Vmax50 after breathing helium appears to be relatively specific for the caliber of the small airways, being uninfluenced by loss of elastic recoil; it can further help to localize the major site of obstruction to either small or large airways. At present, random screening for early unsuspected disease is not warranted, and these tests remain an investigative tool.
Hemodynamic data were obtained within 15 hours of admission in 11 previously healthy patients (20 to 51 years of age, 7 men and 4 women) who had developed transient, reversible pulmonary edema without cardiac dilation in association with near-death from freshwater drowning (2 cases), pentobarbital overdose, heroin overdose (2 cases), smoke inhalation, chest trauma, sepsis (2 cases), pancreatitis, or prolonged abdominal surgery with suspected sepsis. Using a balloon-tipped flow-directed catheter, the pulmonary artery systolic/diastolic pressures (in mm Hg) were 25/12, 22/9, 31/11, 26/15, 20/10, 35/15, 40/15, 32/18, 20/10, 24/10, and 20/7; the corresponding pulmonary capillary wedge pressures (in mm Hg) were 8, 9, 6, 14, 6, 6, 15, 15, 10, 10, and 5, respectively. Plasma colloidal osmotic pressures measured in the latter 5 cases were 26, 18, 18, 18, and 15 mm Hg, respectively. In addition, the protein content of the alveolar fluid was 5.1, 3.4, 4.0, and 7.1 g per 100 ml in 4 patients. The concentration and distribution of the protein in plasma and alveolar fluid were very similar. These findings provide strong efidence that altered capillary permeability is responsible for the pulmonary edema.
The relative sensitivity of volume of isoflow test for detecting obstruction was compared to that of other tests, including flow at 60 per cent of total lung capacity, closing volumes, and frequency dependence of dynamic lung compliance. The volume of isoflow was measured in a waterless spirometer after 3 vital capacity inspirations of a mixture of 80 per cent oxygen. We studied 22 asymptomatic, healthy smokers (18 men and 4 women, 32.5 +/- 7.2 years of age, who smoked 5 to 20 pack-years). Thirteen smokers had an abnormal volume of isoflow, yet only 4 had an abnormal flow at 60 per cent of total lung capacity and 2 had an abnormal closing volume. Abnormal frequency dependence of dynamic lung compliance was demonstrated in 3 of 7 smokers tested with an abnormal volume of isoflow; none was detected in 7 smokers tested with normal volume of isoflow. Static pressure-volume curves and diffusing capacity were normal in all smokers with an abnormal volume of isoflow, and after bronchodilator inhalation, volume of isoflow improved in one half of the subjects. These results suggest reversible, intrinsic airway obstruction in the presence of normal flow at 60 per cent of total lung capacity and closing volume. Furthermore, volume of isoflow was a more sensitive test that flow at 60 per cent total lung capacity, closing volume, or frequency dependence of dynamic lung compliance.
The purpose of the present investigation was to determine the effects of aging on air flow limitation. In 22 healthy nonsmoking subjects, we constructed maximum expiratory flow-static recoil pressure curves. Analysis indicates that with aging there was a progressive increase in the critical transmural pressure. The conductance of the S segment was not dependent on age, with the exception of a significant increase in the oldest group. This is probably due to a more peripheral location of the equal pressure point secondary to a loss of lung recoil or to increased resistance, or both.
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