Lung Function in Chronic Uraemia before and after Removal of Excess of Fluid by Haemodialysis

1974 ◽  
Vol 47 (2) ◽  
pp. 143-151 ◽  
Author(s):  
D. C. Stănescu ◽  
C. Veriter ◽  
J. F. De Plaen ◽  
A. Frans ◽  
C. Van Ypersele De Strihou ◽  
...  

1. Measurements of lung volumes, airway resistance, maximal expiratory flow rates and closing volume were made in twelve patients with chronic renal insufficiency and fluid overload, before and after haemodialysis. 2. Before dialysis, these measurements were within normal limits, except for peak expiratory flow rate, which was significantly lower, and closing volume, which was significantly higher than predicted values. 3. After dialysis body weight decreased significantly and the removal of excess of fluid was accompanied by a significant decrease of closing volume. 4. Measurements of closing volume and the other pulmonary tests were made in six healthy subjects, the same timing being observed as in the patients. Mean as well as individual values of closing volume did not alter, thus excluding the possibility that the changes observed in the patients were due to a circadian rhythm. 5. It is suggested that the higher than predicted closing volume was due to the accumulation of fluid in the dependent areas of the lung, promoting a premature airway closure. Removal of excess of fluid allowed airways to close at a lower lung volume.

1986 ◽  
Vol 60 (3) ◽  
pp. 1060-1066 ◽  
Author(s):  
R. G. Castile ◽  
O. F. Pedersen ◽  
J. M. Drazen ◽  
R. H. Ingram

The effect of carbachol-induced central bronchoconstriction on density dependence of maximal expiratory flow (MEF) was assessed in five dogs. MEFs were measured on air and an 80% He-20% O2 mixture before and after local application of carbachol to the trachea. Airway pressures were measured using a pitot-static probe, from which central airway areas were estimated. At lower concentrations of carbachol the flow-limiting site remained in the trachea over most of the vital capacity (VC), and tracheal area and compliance decreased in all five dogs. In four dogs, decreases in choke point area predominated and produced decreases in flows. In one dog the increase in airway “stiffness” apparently offset the fall in area to account for an increase in MEF. Density dependence measured as the ratio of MEF on HeO2 to MEF on air at 50% of VC increased in all five dogs. Increases in density dependence appeared to be related to increases in airway stiffness at the choke point rather than decreases in gas-related airway pressure differences. Lower concentrations produced a localized decrease in tracheal area and extended the plateau of the flow-volume curve to lower lung volumes. Higher concentrations caused further reductions in tracheal area and greater longitudinal extension of bronchoconstriction, resulting in upstream movement of the site of flow limitation at higher lung volumes. Density dependence increased if the flow-limiting sites remained in the trachea at mid-VC but fell if the flow-limiting site had moved upstream by that volume.


1976 ◽  
Vol 51 (2) ◽  
pp. 133-139
Author(s):  
J. J. Wellman ◽  
E. R. McFadden ◽  
R. H. Ingram

1. Gas-density-dependence of maximal expiratory flow rates (V̇max), defined as the ratio of V̇max while breathing helium/oxygen (80:20) to V̇max. while breathing air at the same lung volume, was examined in relation to other measurements of airways obstruction in patients with obstructive airways disease before and after administration of bronchodilators. 2. Seventeen patients showed a 45% or greater increase in specific conductance(sGaw) after bronchodilator therapy (group A) and thirteen patients demonstrated a lesser response (group B). 3. Before the administration of bronchodilators, the degree of obstruction in the two groups was not different as measured by lung volumes, sGaw, forced expiratory volume in 1 s, and flow rates high in the vital capacity; yet the maximal mid-expiratory flow rate and the degree of density-dependence were significantly lower in group B. 4. After bronchodilators, both groups of patients showed significant improvements in sGaw flow rates and lung volumes. However, group A patients showed a significant increase in density-dependence whereas group B patients did not. 5. Increased density-dependence after bronchodilators in the group A patients was associated with an increase in the computed resistance of the upstream segment with air and a decrease in resistance with helium/oxygen. These changes could be explained by a more mouthward movement of equal pressure points, and therefore a further increase in the relative contribution of the larger density-dependent airways to limitation of flow. 6. The fact that density-dependence was not altered after bronchodilators in the group B patients suggests that the site of limitation of flow did not change appreciably. The shift in the pressure—flow curve for the upstream airways was such that the computed resistance of these airways fell. Thus it appears that the airways comprising the upstream segment were dilated.


1982 ◽  
Vol 52 (4) ◽  
pp. 874-878 ◽  
Author(s):  
J. W. Weiss ◽  
E. R. McFadden ◽  
R. H. Ingram

Using normal human subjects we have measured maximal expiratory flow rates with air (Vmaxair) and after a washin of 80% He-20% O2 (VmaxHeO2) and static elastic recoil pressures of the lung [Pst(L)] both before and after administration of a beta-agonist, terbutaline. The effects of inhaled drug were compared with those of the subcutaneously administered agent, each given in doses to produce maximal bronchodilatation as assessed by increases in Vmaxair in the mid-vital capacity. Although there was a significant yet modest decrease in Pst(L) only after injection of the agent, density dependence (DD), assessed as the ratio of VmaxHeO2 to Vmaxair, increased significantly and comparably after either route of administration. A modest decrease in Pst(L), therefore, did not affect the changes in DD.


CHEST Journal ◽  
1992 ◽  
Vol 102 (5) ◽  
pp. 1636-1637
Author(s):  
Sema Umut ◽  
Bilun Gemicioğlu ◽  
Nurhayat Yildirim

1982 ◽  
Vol 53 (2) ◽  
pp. 392-396 ◽  
Author(s):  
J. W. Weiss ◽  
E. R. McFadden ◽  
R. H. Ingram

Using forced vital capacity maneuvers, we measured maximal expiratory flow rates (Vmax) and static elastic recoil pressures of the lung [Pst(L)] using quasi-static maneuvers in normal nonsmoking human subjects who were breathing air and after a washing of 80% helium-20% oxygen before and after both inhaled and intravenously administered atropine sulfate. By both routes there were equivalent increases in Vmaxair but different effects on density dependence (DD) of Vmax (DD = ratio of VmaxHeO2 to Vmaxair) and on Pst(L). At 30% of vital capacity, DD decreased from an average of 1.47 to 1.32 (P less than 0.01, paired t test) after inhaled drug and did not change after parenteral administration [1.44 vs. 1.48 (P greater than 0.2)]. After inhalation Pst(L) did not change, but after parenteral administration Pst(L) significantly decreased. We interpret these findings to indicate a predominantly large-airway effect with the inhalation route and a more uniform dilatation after the parenteral dose. These results contrast with beta-adrenergic dilatation following which small-airway effects predominate regardless of route of administration.


1978 ◽  
Vol 45 (2) ◽  
pp. 238-243 ◽  
Author(s):  
E. C. Deal ◽  
E. R. McFadden ◽  
R. H. Ingram ◽  
J. J. Jaeger

The role of vagal efferent activity in the cold air potentiation of exercise-induced asthma was assessed by exercising nine subjects who breathed air at ambient and subfreezing temperatures before and after cholinergic blockade. Lung volumes and maximal expiratory flow volume curves with air and with 80% helium-20% oxygen were obtained before and 5--10 min after each challenge. Isovolume comparisons of maximal expiratory flow rates with the two gases were used to assess relative contributions of large and small airways to flow limitation. Exercise under ambient conditions resulted in the expected airway obstruction and cold air exaggerated the response. Atropine pretreatment had no effect on the cold air potentiation. After atropine with ambient air exercise, there was an increase in the relative contribution of large airways to flow limitation, whereas exercise with cold air resulted in an increase in the contribution of small airways. We concluded that the potentiating effects of cold air are local and suggest that the immediate stimulus is related to cooling of intrathoracic airways.


1973 ◽  
Vol 45 (3) ◽  
pp. 407-410 ◽  
Author(s):  
J. V. Collins ◽  
G. M. Cochrane ◽  
Jane Davis ◽  
S. R. Benatar ◽  
T. J. H. Clark

1. Rapid intravenous (i.v.) infusions of saline were administered to five healthy male volunteers. Measurements were made of static and dynamic lung volumes, ‘closing volume’ and pulmonary compliance before and after infusion; all measurements were made in the seated upright position. 2. Following a 1 litre infusion small decreases occurred in static and dynamic lung volumes in all studies and were associated in each case with an increase in ‘closing volume’. ‘Closing volume’ returned to normal within 1 h of the infusion. 3. After 2 litre infusions more marked decreases in all lung volumes occurred and were associated with variable changes in ‘closing volume’. The pattern of change varied between individual subjects and this is thought to reflect differences in localization within the lungs of the effects of the saline load in different subjects. 4. After 2 litre infusions static compliance was decreased in all subjects during the first 10–15 min. Changes in dynamic compliance showed marked individual variation.


1988 ◽  
Vol 64 (4) ◽  
pp. 1650-1658 ◽  
Author(s):  
J. Solway

Using our transistor model of the lung during forced expiration (J. Appl. Physiol. 62: 2013-2025, 1987), we recently predicted that 1) axially arranged choke points can exist simultaneously during forced expiration with sufficient effort, and 2) overall maximal expiratory flow may be relatively insensitive to nonuniform airways obstruction because of flow interdependence between parallel upstream branches. We tested these hypotheses in excised central airways obtained from five canine lungs. Steady expiratory flow was induced by supplying constant upstream pressure (Pupstream = 0-16 cmH2O) to the bronchi of both lungs while lowering pressure at the tracheal airway opening (16 to -140 cmH2O). Intra-airway pressure profiles obtained during steady maximal expiratory flow disclosed a single choke point in the midtrachea when Pupstream was high (2-16 cmH2O). However, when Pupstream was low (0 cmH2O), two choke sites were evident: the tracheal site persisted, but another upstream choke point (main carina or both main bronchi) was added. Flow interdependence was studied by comparing maximal expiratory flow through each lung before and after introduction of a unilateral external resistance upstream of the bronchi of one lung. When this unilateral resistance was added, ipsilateral flow always fell, but changes in flow through the contralateral lung depended on the site of the most upstream choke. When a single choke existed in the trachea, addition of the external resistance increased contralateral flow by 38 +/- 28% (SD, P less than 0.003). In contrast, when the most upstream choke existed at the main carina or in the bronchi, addition of the external resistance had no effect on contralateral maximal expiratory flow.(ABSTRACT TRUNCATED AT 250 WORDS)


1981 ◽  
Vol 50 (3) ◽  
pp. 575-579 ◽  
Author(s):  
K. P. Strohl ◽  
C. F. O'Cain ◽  
R. H. Ingram ◽  
M. A. Yanta ◽  
W. D. Kaplan ◽  
...  

To determine the relationship between changes in density dependence of maximal expiratory flow and changes in the predominant site of bronchoconstriction, we altered the pattern of inhalation of a methacholine aerosol to achieve deposition either centrally (by short choppy breaths) or peripherally (by slow deep breaths). Partial expiratory flow volume curves on air and on 80% helium-20% oxygen (HeO2) were recorded in six healthy subjects before and after each pattern of methacholine inhalation. We varied concentrations of methacholine and number of inhalations to achieve equivalent degrees of bronchoconstriction as assessed by decreases in maximal flow (Vmax) on air, which fell 27% from control values. Vmax on HeO2 also fell after both inhalation patterns. Density dependence (Vmax on HeO2 divided by Vmax on air) decreased following slow deep breaths of bronchoconstrictor aerosol, and increased following short choppy breaths. In three subjects, inhalation of radiolabeled methacholine aerosol confirmed that the slow deep pattern was associated with a diffuse, more peripheral deposition, whereas the short choppy pattern led to central deposition. We conclude that changes in density dependence reflect the predominant site of obstruction after acute methacholine aerosol challenge in healthy subjects.


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