Pulmonary Blood Volume in Chronic Bronchitis

1977 ◽  
Vol 53 (6) ◽  
pp. 587-593
Author(s):  
B. Raffestin ◽  
H. Valette ◽  
J. L. Hebert ◽  
P. Duhaze ◽  
A. Lockhart

1. Pulmonary blood volume was measured in 39 patients with severe chronic bronchitis, of whom 29 had recently recovered from an acute exacerbation. Pa,o2 was below 10·3 kPa in all but five patients, Pa,co2 was above 5·6 kPa in 26 cases, and pulmonary artery mean pressure was above 20 mmHg in 29 cases. Pulmonary blood volume was measured with the double-injection—single-sampling technique using Indocyanine Green and pulmonary wedge injection. 2. Pulmonary blood volume in the 39 patients was significantly lower (343 ± 95 ml) than in a group of 16 normal subjects (469 ± 117 ml) studied previously by the same method. There was no correlation between pulmonary blood volume and driving pressure across the pulmonary circulation, or between pulmonary blood volume and Pa,o2. 3. Breathing 26–29% oxygen in 19 patients caused no significant changes in either pulmonary blood volume or pulmonary vascular resistance. Therefore the reduced pulmonary blood volume could not be attributed to hypoxic pulmonary vasoconstriction. 4. The finding of a diminished pulmonary blood volume in chronic bronchitis is best explained by a loss of pulmonary vessels. Pulmonary blood volume was not correlated with total lung capacity nor with the residual volume/total lung capacity ratio, nor was it significantly higher in the 16 patients with normal total lung capacity (352 ± 73 ml) than in the 23 patients with a total lung capacity greater than 110% of normal (331 ± 110 ml). There was therefore no correlation between the amount of emphysema and the reduction in pulmonary blood volume.

1961 ◽  
Vol 1 (04) ◽  
pp. 353-379
Author(s):  
Jacques Lammerant ◽  
Norman Veall ◽  
Michel De Visscher

Summary1. The technique for the measurement of cardiac output by external recording of the intracardiac flow of 131I labelled human serum albumin has been extended to provide a measure of the mean circulation time from right to left heart and hence a new approach to the estimation of the pulmonary blood volume.2. Values for the basal cardiac output in normal subjects and its variations with age are in good agreement with the previously published data of other workers.3. The pulmonary blood volume in normal man in the basal state was found to be 28.2 ± 0.6% of the total blood volume.4. There was no correlation between cardiac output and pulmonary blood volume in a series of normal subjects in the basal state.5. The increase in cardiac output during digestion was associated with a decrease in pulmonary blood volume equal to 6.3 ± 1.2% of the total blood volume, that is, about 280 ml.6. The increase in cardiac output during exercise was associated with a decrease in pulmonary blood volume equal to 4.5 ± 1.0% of the total blood volume, that is, about 200 ml.7. The increase in cardiac output attributed to alarm is not associated with a decrease in pulmonary blood volume, the latter may in fact be increased.8. The total blood volume is advocated as a standard of reference for studies of this type in normal subjects in preference to body weight or surface area.9. The significance of these results and the validity of the method are discussed.


1988 ◽  
Vol 64 (6) ◽  
pp. 2482-2489 ◽  
Author(s):  
P. Leblanc ◽  
E. Summers ◽  
M. D. Inman ◽  
N. L. Jones ◽  
E. J. Campbell ◽  
...  

The capacity of inspiratory muscles to generate esophageal pressure at several lung volumes from functional residual capacity (FRC) to total lung capacity (TLC) and several flow rates from zero to maximal flow was measured in five normal subjects. Static capacity was 126 +/- 14.6 cmH2O at FRC, remained unchanged between 30 and 55% TLC, and decreased to 40 +/- 6.8 cmH2O at TLC. Dynamic capacity declined by a further 5.0 +/- 0.35% from the static pressure at any given lung volume for every liter per second increase in inspiratory flow. The subjects underwent progressive incremental exercise to maximum power and achieved 1,800 +/- 45 kpm/min and maximum O2 uptake of 3,518 +/- 222 ml/min. During exercise peak esophageal pressure increased from 9.4 +/- 1.81 to 38.2 +/- 5.70 cmH2O and end-inspiratory esophageal pressure increased from 7.8 +/- 0.52 to 22.5 +/- 2.03 cmH2O from rest to maximum exercise. Because the estimated capacity available to meet these demands is critically dependent on end-inspiratory lung volume, the changes in lung volume during exercise were measured in three of the subjects using He dilution. End-expiratory volume was 52.3 +/- 2.42% TLC at rest and 38.5 +/- 0.79% TLC at maximum exercise.


1984 ◽  
Vol 56 (1) ◽  
pp. 52-56 ◽  
Author(s):  
T. S. Hurst ◽  
B. L. Graham ◽  
D. J. Cotton

We studied 10 symptom-free lifetime non-smokers and 17 smokers all with normal pulmonary function studies. All subjects performed single-breath N2 washout tests by either exhaling slowly (“slow maneuver”) from end inspiration (EI) to residual volume (RV) or exhaling maximally (“fast maneuver”) from EI to RV. After either maneuver, subjects then slowly inhaled 100% O2 to total lung capacity (TLC) and without breath holding, exhaled slowly back to RV. In the nonsmokers seated upright phase III slope of single-breath N2 test (delta N2/l) was lower (P less than 0.01) for the fast vs. the slow maneuver, but this difference disappeared when the subjects repeated the maneuvers in the supine position. In contrast, delta N2/l was higher for the fast vs. the slow maneuver (P less than 0.01) in smokers seated upright. For the slow maneuver, delta N2/l was similar between smokers and nonsmokers but for the fast maneuvers delta N2/l was higher in smokers than nonsmokers (P less than 0.01). We suggest that the fast exhalation to RV decreases delta N2/l in normal subjects by decreasing apex-to-base differences in regional ratio of RV to TLC (RV/TLC) but increases delta N2/l in smokers, because regional RV/TLC increases distal to sites of small airways obstruction when the expiratory flow rate is increased.


1986 ◽  
Vol 60 (4) ◽  
pp. 1198-1202 ◽  
Author(s):  
F. D. McCool ◽  
B. M. Pichurko ◽  
A. S. Slutsky ◽  
M. Sarkarati ◽  
A. Rossier ◽  
...  

Previous studies suggest that abdominal binding may affect the interaction of the rib cage and the diaphragm over the tidal range of breathing in quadriplegia. To determine whether abdominal binding influences rib cage motion over the entire range of inspiratory capacity, we used spirometry and the helium-dilution technique to measure functional residual capacity (FRC), inspiratory capacity, and total lung capacity (TLC) in eight quadriplegic and five normal subjects in supine, tilted (37 degrees), and seated positions. Combined data in all three positions indicated that, with abdominal binding, FRC and TLC decreased in normal subjects [delta FRC = -0.33 + 0.151 (SD) P less than 0.01); delta TLC = -0.16 + 0.121, P less than 0.05]. In quadriplegia there was also a reduction in FRC with binding (delta FRC = -0.32 + 0.101, P less than 0.001). However, TLC increased in quadriplegia (delta TLC = 0.07 + 0.061, P less than 0.025). In an additional six quadriplegic and five normal subjects, we used magnetometers to define the influences of abdominal binding on rib cage dimensions and TLC. In quadriplegia, rib cage dimensions were increased at TLC with abdominal binding, whereas there was no change in normals. Our data suggest that this inspiratory effect of abdominal binding on augmenting rib cage volume in quadriplegia is greater than the effect of impeding diaphragm descent, and thus abdominal binding produces a net increase in TLC in quadriplegia.


1961 ◽  
Vol 16 (1) ◽  
pp. 27-29 ◽  
Author(s):  
Francisco Moreno ◽  
Harold A. Lyons

The changes produced by body posture on total lung capacity and its subdivisions have been reported for all positions except the prone position. Twenty normal subjects, twelve males and eight females, had determinations of total lung capacity in the three body positions, sitting, supine and prone. Tidal volume, minute ventilation and O2 consumption were also measured. The changes found on assumption of the supine position from the sitting position were similar to those previously reported. For the prone position, a smaller inspiratory capacity and a larger expiratory reserve volume were found. The mean values were changed, respectively, –8% and +37%. Associated with these changes was a significant increase of the functional residual capacity by 636 ml. Ventilation did not change significantly from that found during sitting, unlike the findings associated with the supine position, in which position the tidal volume was decreased. Respiratory frequency remained the same for all positions. Submitted on April 5, 1960


2000 ◽  
Vol 88 (4) ◽  
pp. 1413-1420 ◽  
Author(s):  
David Peter Johns ◽  
John Wilson ◽  
Richard Harding ◽  
E. Haydn Walters

Anatomic dead space (Vd) is known to increase with end-inspiratory lung volume (EILV), and the gradient of the relationship has been proposed as an index of airway distensibility (ΔVd). The aims of this study were to apply a rapid method for measuring ΔVd and to determine whether it was affected by lung volume history. Vd of 16 healthy and 16 mildly asthmatic subjects was measured at a number of known EILVs by using a tidal breathing, CO2-washout method. The effect of lung volume history was assessed by using three tidal breathing regimens: 1) three discrete EILVs (low/medium/high; LMH); 2) progressively decreasing EILVs from total lung capacity (TLC; TLC-RV); and 3) progressively increasing EILVs from residual volume (RV; RV-TLC). ΔVd was lower in the asthmatic group for the LMH (25.3 ± 2.24 vs. 21.2 ± 1.66 ml/l, means ± SE) and TLC-RV (24.3 ± 1.69 vs. 18.7 ± 1.16 ml/l) regimens. There was a trend for a lower ΔVd in the asthmatic group for the RV-TLC regimen (23.3 ± 2.19 vs. 18.8 ± 1.68 ml/l). There was no difference in ΔVd between groups. In conclusion, mild asthmatic subjects have stiffer airways than normal subjects, and this is not obviously affected by lung volume history.


1983 ◽  
Vol 54 (6) ◽  
pp. 1618-1623 ◽  
Author(s):  
C. H. Fanta ◽  
D. E. Leith ◽  
R. Brown

Normal subjects can increase their vital capacity by appropriate training. We tested whether that change can be achieved by greater maximal shortening of the inspiratory muscles without concomitant increases in peak static inspiratory pressures. Sixteen healthy volunteers participated in the study: eight were randomly assigned to make 20 inhalations to total lung capacity, held for 10 s with the glottis open, each day for 6 wk; the remainder served as nontraining controls. Before and after the 6-wk study period, we made multiple determinations of lung volumes and of curves relating lung volume to maximal static inspiratory (and expiratory) pressure. Control subjects had no significant changes from base line in any variable. In the training group, the mean vital capacity increased 200 +/- 74 ml (P less than 0.05) or 3.9 +/- 1.3% (P less than 0.02), without a significant change in residual volume. After training, the mean maximal inspiratory pressure at the airway opening (PI) at a lung volume equal to the base-line total lung capacity was 27 +/- 8 cmH2O in this group (vs. zero before training; P less than 0.02). Values of PI in the mid-vital capacity range did not change. We conclude that in response to appropriate training stimuli inspiratory muscles can contract to shorter minimal lengths, a capacity potentially important in progressive pulmonary hyperinflation.


1981 ◽  
Vol 50 (5) ◽  
pp. 950-955 ◽  
Author(s):  
J. D. Hirasuna ◽  
A. B. Gorin

We have observed a progressive decrease in pulmonary blood volume during sustained recumbency measured using two independent methods. Pulmonary capillary blood volume (Vc) was estimated by the method of Roughton and Forster (J. Appl. Physiol. 11: 290, 1957). We measured regional pulmonary blood volume (PBVR) using 99mTc-labeled erythrocytes (Gorin et al., J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 45: 225, 1978). In 21 studies in 19 normal subjects, we measured pulmonary CO diffusing capacity by the single-breath technique and calculated Vc with the subjects seated and at fixed times after lying down. After 5 min in the recumbent position, there was a mean 49% increase in Vc over the value in the seated position. With sustained recumbency Vc decreased 18.3%/h over 90 min. In 12 studies in 8 normal subjects, PBVR declined 16.7%/h with prolonged recumbency in studies lasting 60-90 min. The initial increase in Vc after subjects assumed a supine position has been well described. The subsequent fall in pulmonary blood volume to levels equal to or below that measured with the subject seated has not previously been reported.


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