PULMONARY DIFFUSING CAPACITY IN NORMAL CHILDREN, AGES 4 TO 13; THE EFFECT OF BODY POSITION AND EXERCISE ON PULMONARY DIFFUSING CAPACITY, LUNG VOLUMES, AND VENTILATORY TESTS.
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The pulmonary diffusing capacity for Carbonmonoxide (DLCO) was measured in 20 normal volunteers of either sex at 9 a.m., 12 noon and 5 p.m. Forced expiratory volume in one second (FEV1) and forced vital capacity (FVC) were also determined after each DLCO measurement. There was a fall in the mean noon value of the diffusing capacity of the lungs which was statistically significant. The value at 5 p.m. was almost same as the noon value. The forced expiratory volume in one second and the forced vital capacity followed a similar trend. The DLCO, FEV1 and FVC appear to exhibit a diurnal rhythm.
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Steady state estimates of the pulmonary diffusing capacity for carbon monoxide require measurement of the uptake and the average partial pressure of CO in the lung. The expired alveolar sample obtained by different experimental methods and/or breathing patterns rarely represents the actural average alveolar partial pressure. This error in choosing the correct alveolar sample arises in the sampling time chosen by the experimental method. The time (TAV) at which the correct alveolar sample (FAV) is obtained occurs one-half of a breathing period after the effective inspiration time. If TAV and the sample time chosen by the experimental method are known then the measured diffusing capacity can be corrected to the actual diffusing capacity.
To test whether orthotopic heart transplant (OHT) patients with low pulmonary diffusion capacity have a greater limitation to exercise than OHT patients with normal pulmonary diffusion capacity, we investigated cardiorespiratory responses and blood gases in two groups of OHT patients, one with low (LdG) and the other with normal pulmonary diffusion capacity (NdG), during a graded exercise test. The results showed 1) significantly reduced peak power (P < 0.05), peak oxygen uptake (VO2, P < 0.001), peak oxygen pulse (VO2/heart rate, P < 0.01), peak minute ventilation (VE, P < 0.05), and delta PaO2 (peak PaO2 - rest PaO2, P < 0.05) in LdG versus NdG; 2) a nonsignificant decrease in peak heart rate in LdG (P < 0.13, P = 24%); and 3) significant increases in peak respiratory equivalent for oxygen (VE/VO2, P < 0.05) and delta P(A-a)O2 (peak P(A-a)O2 - resting P(A-a)O2, P < 0.05) in LdG versus NdG. No significant difference was found for PaO2 and PaCO2 at rest or at peak exercise between the groups. A strong correlation was found between pulmonary diffusion capacity (TLCO/VA) and peak VO2 (r = 0.81, P < 0.01); that is, TLCO/VA explains 66% of the variance in peak VO2. We conclude that OHT patients with decreased pulmonary diffusion capacity have a lower exercise tolerance than patients with normal pulmonary diffusion capacity. However, because of the lack of exercise-induced hypoxemia, diffusion abnormalities are not the main limiting factor for exercise tolerance in the low diffusion group.
Pulmonary diffusing capacity may be determined by rebreathing techniques using various test gases. The errors caused by functional inhomogenities are smaller with the rebreathing method than those found in the single-breath technique. However, until now there have been some disadvantages to the clinical application of the rebreathing technique. In the present paper, a modification of the rebreathing technique suggested by Piiper, Scheid, Meyer and Adaro (1975 and 1976), in which pulmonary diffusing capacity for carbon monoxide, DCO(RB), is measured, has been applied to intubated and anesthetised patients. Measurements were performed in 39 surgical patients with healthy lungs during artificial ventilation and narcosis. Under these conditions all patients had a DCO(RB) greater than or equal to 75 ml/min . kPa (10 ml/min.torr). The coefficient of variation for duplicate measurements was +/- 4.2%. In the same patients DCO-single-breath-measurements, DCO(SB), were also made. There was a significant (p less than 0.0001) correlation between DCO(RB) in artificially ventilated, anaesthetised patients in a supine position and DCO(SB) for spontaneously breathing, awake patients in a sitting position. A linear regression analysis of the data showed the DCO(SB) was related to DCO(RB) in the following manner: DCO(SB) = 1.62DCO(RB) = 4.44 (ml/min.torr) (r = 0.71, n = 39). The mean value of DCO(RB) was 53.4% of the mean value of DCO(SB). This difference may be due to the combination of different techniques used and different conditions during the measurements (reduced FRC, difference in F1O2 etc.). The histogramm of the distribution of DCO(RB) had a similar form to that of DCO(SB). The modified method has a high reproducibility and can easily be performed as a bed-side test without disturbance to patients with an endotracheal tube.
Pulmonary diffusing capacity has been noted by many investigators to be higher in championship swimmers than in average swimmers and in the non-swimming population. We measured pulmonary diffusing capacity (DLCO) and other parameters in 22 members of a collegiate swimming team and studied the relationship between pulmonary diffusing capacity and swimming performance. We also investigated change in lung function over a season of training and racing. Results suggested that while most good swimmers had above average diffusing capacities, there was no statistically significant difference in performance between those swimmers with high DLCO (greater than or equal to 110% predicted value) and those with a low DLCO (less than 100% predicted value). It was also determined that there was not a good correlation between performance (measured by either "best time" or "average time") and lung function (DLCO or VC).
Steady state estimates of the pulmonary diffusing capacity for carbon monoxide (DLCO) require measurement of the uptake and the average alveolar partial pressure of carbon monoxide (PACO). The expired alveolar sample obtained by different experimental methods and/or breathing patterns rarely represents the actual PACO. It is widely accepted that nonuniform distribution of ventilation, diffusion and perfusion causes discrepancies in the measurement of diffusing capacity. tan additional source of error in choosing PACO arises in the sampling time chosen by the experimental method. A theoretical study of a ramp-with-pause and a square breathing pattern demonstrates that the sample-time error exists even in the homogeneous lung. The study shows for the homogeneous lung that the correct fractional concentration of alveolar carbon monoxide (FAV) occurs at a time (TAV), one-half of a breathing period after the effective inspiration time (TI) for the two very different breathing patterns. TI is well-defined in relation to any breathing pattern which can be approximated by ramps and pauses. If TAV and the sample time chosen by the experimental method are known, then the measured DLCO can be corrected to the actual diffusing capacity (DL). The theory agrees with experimental results and computer simulations of inhomogeneous lungs from the literature. This agreement suggests that the theory for the homogeneous lung is also relevant to the inhomogeneous lung.
Pulmonary diffusion capacity for carbon monoxide (DLCO), regional electrical impedance (Z0), and the distribution of technetium-99m-labeled erythrocytes together with concentration of plasma atrial natriuretic peptide (ANP) were determined before and after a 6-min "all-out" row in nine oarsmen and in six control subjects. Two and one-half hours after exercise in the upright seated position, DLCO was reduced by 6 (-2 to 21; median and range) %, the thoracic-to-thigh electrical impedance ratio (Z0 thorax/Z0 thigh) rose by 14 (-1 to 29) %, paralleled by a 7 (-3 to 11) % decrease and a 3 (-5 to 12) % increase in the thoracic and thigh blood volume, respectively. These responses were associated with a decrease in the plasma ANP concentration from 15 (13-31) to 12 (9-27) pmol/l (P < 0.05). Similarly, in the supine position, Z0 thorax/Z0 thigh increased by 10 (-5 to 28) % when DLCO was reduced 12 (6-26) % (P < 0.05), whereas DLCO remained stable in the control group. The increase in Z0 thorax/Z0 thigh and the corresponding redistribution of the blood volume in both body positions show that approximately one-half of the postexercise reduction of DLCO is explained by a decrease in the pulmonary blood volume. The role of a reduced postexercise central blood volume is underscored by the lower plasma ANP, which aids in upregulating the blood volume after exercise in athletes.
Determination of pulmonary diffusing capacity is a routine method in pulmonary function laboratories for spontaneous breathing patients. However, it is not used in intensive care medicine for controlled ventilated patients with severe respiratory failure. We describe a rebreathing method for determination of pulmonary diffusing capacity for carbon monoxide (DCO) during mechanical ventilation based on an improved mathematical approach by Piiper and coworkers. The theoretical two-compartment model and the mathematical analysis are described. Factors (such as functional inhomogeneities, central blood volume, haemoglobin concentration, oxygen partial pressure, etc.) affecting this complex parameter of gas exchange are discussed. As the rebreathing technique for DCO seems to be influenced least by functional inhomogeneities in the diseased lung, it is advantageously qualified for measurements in intensive care patients. By adding an insoluble inert gas (for instance argon), functional residual capacity (FRC) can be determined at the same time. The method is well reproducible (+/- 3.8% for DCO and +/- 2.1% for FRC in duplicate determinations). During mechanical ventilation, the borderline towards pathological values determined by this method proved to be about 10 ml . min-1 . mmHg-1. First experimental and clinical results are presented which demonstrate DCO to be a qualified parameter for evaluating the pulmonary gas exchange function, indicating a progression of respiratory failure.
Pulmonary diffusing capacity (DL) for carbon monoxide (CO) and nitric oxide (NO) were simultaneously measured in man using the single breath method, by adding 4O ppm of NO to the inspired gas and analysing the expirate for NO by a chemiluminescent method. The mean ratio of DLNO to DLCO in thirteen subjects was 4.3 (SD 0.3), mean DLNO = 49 mmol.min-1.kPa-1 (SD 10) and mean DLCO = 11 mmol.min-1.kPa-1 (SD 2). An increase in alveolar oxygen concentration from a mean of 18 to 68% in five subjects was associated with a 54% fall in DLCO but no change in DLNO. A reduction of lung volume from total lung capacity (TLC) (mean of 7 l) to a mean volume of 3.9 l in five subjects caused a fall in both DLNO (by 34%) and DLCO (by 8%). With 175 watts cycle exercise in three subjects the DLCO rose by 45% and DLNO by 25%. Since NO reacts much faster with haemoglobin than CO, DLNO should be influenced much less by reaction with haemoglobin, and perhaps represents a better index for the diffusing capacity of the alveolar-capillary membrane (Dm) than DLCO.
Pulmonary diffusing capacity (DLCO) has been measured at 3500 m in highlander and lowlander subjects. DLCO is more elevated in highlanders than in lowlanders. In these subjects, a transient increase of DLCO is observed during the first hours of hypoxia which is related to transient changes in pulmonary circulation.
The pulmonary diffusing capacity (DLCO--steady state method according to Bates and coworkers) was measured at the time of heart catheterization in 12 patients with mitral stenosis without mitral incompetence. DLCO correlates with the tidal volume at rest and during exercise and with pulmonary vascular resistance during exercise only. DLCO and left atrial pressure exhibit a positive correlation up to 22.5 mm Hg only. In patients with mitral stenosis DLCO depends on the alveolar surface area and DLCO is influenced by regional changes in the pulmonary vascular resistance.
Single-breath carbon monoxide diffusing capacity (DLco), pulmonary capillary blood volume (Vc), and membrane diffusing capacity (Dm) were measured in 24 beagle dogs aged 289-3,882 days. DLco and Vc were a function of age and alveolar volume (Va). Vc decreased with age resulting in changes in DLco. Changes in Vc may have been due to pulmonary morphological changes or to an exaggerated decrease in pulmonary blood flow in old dogs in response to 20-30 cmH-2O transpulmonary pressure. There was no age-related change in Dm.