Lung mechanics following aspiration of 0.1 N hydrochloric acid

1983 ◽  
Vol 55 (4) ◽  
pp. 1051-1056 ◽  
Author(s):  
R. Winn ◽  
J. Stothert ◽  
B. Nadir ◽  
J. Hildebrandt

Pressure-volume curves were obtained from excised left lungs of goats at 4, 24, and 48 h after tracheal instillation of 2.5 ml/kg of 0.1 N HCl. Air total lung capacity (TLC) at transpulmonary pressure (PL) = 35 cmH2O was 38.8 ml/kg body weight before acid, and was reduced sharply to 21.1 at 4 h, then increased to 25.6 at 24 h and 32.1 at 48 h. Excess extravascular lung water (EVLW) could account for only part of the volume reductions. Specific compliance ratio of transpulmonary pressure to total lung capacity (CL/TLC) between PL of 5 and 0 cmH2O was reduced from 0.074/cmH2O to 0.050, 0.048, and 0.053/cmH2O, respectively. Saline TLC (PL = 10 cmH2O) changed from 44.8 to 32.4, 34.3, and 45.4 ml/kg, respectively, but CL/TLC did not, suggesting airway obstruction. After injury, trapped volume at PL = 0 increased from 24.9 to 29.2, 43.3, and 37.3% TLC with air, and from 20.3 to 38.5, 33.1, and 28.5%, respectively, with saline. Air volume at a PL = 10 cmH2O on deflation fell from 82.0 to 72.1% TLC at 4 h, but was near control at 24 and 48 h. The reduction in ventilated volume was not reflected in proportionately increased shunt; therefore, some compensatory vasoconstriction must have occurred. We suggest that in affected regions increased surface forces, increased EVLW, and airway obstruction caused reductions of lung volume.

1982 ◽  
Vol 53 (3) ◽  
pp. 567-575 ◽  
Author(s):  
H. Inoue ◽  
C. Inoue ◽  
J. Hildebrandt

Effects of temperature on lung pressure-volume (PV) curves and on the reversibility of changes were studied in the range of 4–52 degrees C. Air curves were obtained first at 21 degrees C, then after 60 min equilibration at one of seven test temperatures (4, 21, 32, 37, 42, 47, and 52 degrees C) and finally again at 21 degrees C. In a given lung, peak inflation volume was made identical at all temperatures. Warming from 4 to 42 degrees C steadily diminished both inflation and deflation pressures, but thereafter the trend reversed except on the upper part of the inflation curve. On returning to 21 degrees C, all PV curves were indistinguishable except from 52 degrees C. Liquid PV curves were obtained in a similar way at four temperatures (4, 21, 37, and 52 degrees C). Warming from 4 to 52 degrees C diminished tissue elastic recoil at total lung capacity (TLC) from 17 to 5 cmH2O but raised recoil slightly at lower lung volumes. Liquid PV curves were also reversible except after 52 degrees C. At 37 degrees C the estimated tissue component of the total recoil of air-filled lungs exceeded 95% at 40–60% TLC, and at 21 degrees was 85–90%. This fraction fell to 50% or less at 4 and 52 degrees C, where surface forces failed to reach low levels and alveolar instability resulted.


1980 ◽  
Vol 49 (6) ◽  
pp. 946-952 ◽  
Author(s):  
C. A. Bradley ◽  
N. R. Anthonisen

The effects of a variety of restrictive procedures on lung mechanics were studied in eight healthy subjects. Rib cage restriction decreased total lung capacity (TLC) by 43% and significantly increased elastic recoil and maximum expiratory flow (MEF). Subsequent immersion of four subjects with rib cage restriction resulted in no further change in either parameter; shifts of blood volume did not reverse recoil changes during rib cage restriction. Abdominal restriction decreased TLC by 40% and increased MEF and elastic recoil, but recoil was increased significantly less than was the case with rib cage restriction. Further, at a given recoil pressure, MEF was less during rib cage restriction than during either abdominal restriction or no restriction. Measurements of the unevenness of inspired gas distribution by the single-breath nitrogen technique showed increased unevenness during rib cage restriction, which was significantly greater than that during abdominal restriction. We conclude that lung volume restriction induces changes in lung function, but the nature of these changes depends on how the restriction is applied and therefore cannot be ascribed to low lung volume breathing per se.


1964 ◽  
Vol 207 (1) ◽  
pp. 235-238 ◽  
Author(s):  
Nicholas R. Anthonisen

Relative pulmonary shunt flow (Qs/Qt), was measured in denitrogenated open-chested cats during apnea over the full range of lung volumes. The particular lung volume and transpulmonary pressure were also measured. When completely collapsed lungs were inflated, Qs/Qt decreased sharply to 3% at total lung capacity (TLC). During deflation from TLC Qs/Qt was insensitive to changes in lung volume. Qs/Qt remained low during reinflation after deflation from TLC. These changes in shunt flow can be interpreted as due to either recruitment or collapse of gas exchange units during lung volume change. It appears that completely collapsed lungs inflate very unevenly but that deflation from TLC proceeds remarkably evenly. Reinflation after deflation from TLC also seems to proceed evenly, and the manifest pressure-volume hysteresis is most likely due to hysteresis of the surface-active properties of the alveolar lining material.


1992 ◽  
Vol 72 (1) ◽  
pp. 231-235 ◽  
Author(s):  
J. A. Panizza ◽  
K. E. Finucane

Pleural pressure is usually estimated with a balloon catheter (BC) positioned in the middle third of the esophagus. An alternate method, which avoids potential inaccuracies associated with changes in balloon volume, is a catheter-mounted transducer (CMT) system. To assess the accuracy of a CMT system in defining the elastic properties of the lungs, we compared the static pressure-volume (PV) properties of the lungs measured sequentially with CMT and BC systems in six healthy subjects each on two occasions, relating static transpulmonary pressure (Pst,L) to lung volume during interrupted exhalations from total lung capacity (TLC). PV data were fitted with an exponential function (least-squares method), and the exponent (k) was used to define the shape of the PV curve; position was defined by Pst,L at TLC and at 90 and 60% TLC. These data were examined for agreement (paired t test) and repeatability (coefficient of repeatability). No significant differences were demonstrated: k was 0.10 +/- 0.02 and 0.11 +/- 0.03 (SD) and Pst,L at 60% TLC was 8.27 +/- 2.09 and 8.37 +/- 1.63 cmH2O for the CMT and BC systems, respectively. The coefficient of repeatability for each parameter was not significantly different but was consistently less with the BC, suggesting better repeatability. We conclude that a CMT system is an acceptable alternative to a BC system for defining the elastic properties of lungs.


1977 ◽  
Vol 42 (3) ◽  
pp. 413-419 ◽  
Author(s):  
N. A. Saunders ◽  
M. F. Betts ◽  
L. D. Pengelly ◽  
A. S. Rebuck

We measured lung mechanics in seven healthy males during acute isocapnic hypoxia (PAO2 = 40–50 Torr; PACO2 = 38–42 Torr). Hypoxia was accompanied by increases in total lung capacity (mean increase +/- SD; 0.40 +/- 0.24 liters; P less than 0.005) functional residual capacity (0.34 +/- 0.25 liters; P less than 0.01) and residual volume (0.56 +/- 0.44 liters; P less than 0.02) in all subjects. Specific conductance of the lung decreased during hypoxia (P less than 0.02). The static deflation pressure-volume curve of the lung was shifted upward during hypoxia in all subjects. Resting end-expiratory recoil pressure of the lung was slightly, but not significantly lower during hypoxtic expiratory lung compliance was greater during hypoxia (0.39 +/- 0.04 l/cmH2O) than control measurements (0.31 +/- 0.05 l/cmH2O; P less than 0.005). No change was noted in dynamic lung compliance. All changes in lung mechanics were reversed within three minutes of reoxygenation. We conclude that acute isocapnic hypoxia increases total lung capacity in man and suggest that this may be due to the effect of hypoxia on the airways and pulmonary circulation.


2000 ◽  
Vol 89 (5) ◽  
pp. 2030-2040 ◽  
Author(s):  
Béla Suki ◽  
Adriano M. Alencar ◽  
József Tolnai ◽  
Tibor Asztalos ◽  
Ferenc Peták ◽  
...  

In 11 isolated dog lung lobes, we studied the size distribution of recruited alveolar volumes that become available for gas exchange during inflation from the collapsed state. Three catheters were wedged into 2-mm-diameter airways at total lung capacity. Small-amplitude pseudorandom pressure oscillations between 1 and 47 Hz were led into the catheters, and the input impedances of the regions subtended by the catheters were continuously recorded using a wave tube technique during inflation from −5 cmH2O transpulmonary pressure to total lung capacity. The impedance data were fit with a model to obtain regional tissue elastance (Eti) as a function of inflation. First, Eti was high and decreased in discrete jumps as more groups of alveoli were recruited. By assuming that the number of opened alveoli is inversely proportional to Eti, we calculated from the jumps in Eti the distribution of the discrete increments in the number of opened alveoli. This distribution was in good agreement with model simulations in which airways open in cascade or avalanches. Implications for mechanical ventilation may be found in these results.


1981 ◽  
Vol 50 (5) ◽  
pp. 1079-1086 ◽  
Author(s):  
J. E. Fish ◽  
M. G. Ankin ◽  
J. F. Kelly ◽  
V. I. Peterman

We examined the effects of lung inflation on induced airway obstruction in 14 atopic asthmatic and 14 atopic nonasthmatic subjects. Subjects were challenged with aerosols of methacholine (MCh) and pollen antigen (Ag), and the effects of inflation were assessed with partial ad full flow-volume curves and by comparing airway conductance measurements before and after deep inspiration to total lung capacity (TLC). Whereas bronchoconstriction was transiently abolished or reduced with inspiration in nonasthmatics, these effects were absent or diminished in asthmatic subjects. Dissimilarities could not be explained by differences in base-line lung function or degree of obstruction produced. Deep inspiration had a greater effect in reducing airway obstruction produced with MCh than with Ag in nonasthmatics. In addition, atropine pretreatment had no effect on inspiration responses in asthmatics given Ag, suggesting that vagal reflexes were not the cause of an impaired ability to reduce bronchomotor tone by lung inflation. Our findings reveal the existence of an intrinsic means of regulating bronchomotor toe by active changes in lung volume and that such a mechanism is impaired in asthma. We suggest that airway hyperactivity in asthma is perhaps less a reflection of enhanced end-organ responsiveness than a reflection of this impaired capacity.


1975 ◽  
Vol 39 (1) ◽  
pp. 23-29 ◽  
Author(s):  
G. M. Tisi ◽  
V. D. Minh ◽  
P. J. Friedman

We studied four supine dogs that were anesthetized with pentobarbital, intubated, and ventilated with a piston pump. The dimensional response of central (CAW) (greater than 2 mm diam) and peripheral airways (PAW) (smaller than 2 mm diam) to changes in transpulmonary pressure (Ptp) was determined by progressive increments in tidal volume (VT). A specially designed electronics relay circuit permitted this relationship to be obtained for points of no flow during tidal volume breathing: i.e., preinspiration (FRC); end inspiration (FRC + VT). The airways were dusted with powdered tantalum. Six airway divisions were identified: four CAW: trachea, main stem, lobar, segmental; and two PAW: subsegmental, and lobular. AP and lateral roentgenograms were obtained by standard technics and primary magnification (mag factor 2). Airway diameters were plotted as a function of transpulmonary pressure between 3 and 26 cmH2O with the diameter at total lung capacity expressed as 100%. The data show that: 1) there is significant distensibility above 5 cmH2O for all airways from the trachea to the lobular airways; 2) that the pressure-diameter plot is a linear plot for each airway from 3 to 26 cmH2O with R values between 0.846 and 0.957; 3) the peripheral lobular airways are more distensible than the central airways (P smaller than 0.05). We attribute the difference in distensibility of the peripheral lobular airways to their lack of cartilaginous support, and their decreased muscular support when compared to the CAW.


1980 ◽  
Vol 49 (4) ◽  
pp. 558-565 ◽  
Author(s):  
N. Berend ◽  
C. Skoog ◽  
W. M. Thurlbeck

Static deflationary pressure-volume curves were obtained in 28 emphysema-free (18 male and 10 female) and 39 emphysematous excised human lungs inflated to a maximum transpulmonary pressure (Pl) of 30 cmH2O. In emphysema-free lungs, the lung volumes at Pl 30 cmH2O (V30) were significantly related to body length in males and were significantly larger than predicated total lung capacity in vivo. However, corrected for stature (V30/body length), there was no significant age correlation. In both males and females, highly significant correlations between the PL at 50--90% V30 and age were obtained. There were no significant differences in these regressions between males and females. The emphysematous lungs were divided into three groups with increasing emphysema grades. Progressive decreases in the PL at 50--90% V30 and increases in the V30 were seen in the groups with increasing degrees of emphysema. Significant changes occurred in these measurements even in group 2 with mild emphysema, suggesting that the lesions of emphysema are not directly responsible for these changes.


1981 ◽  
Vol 51 (4) ◽  
pp. 823-829 ◽  
Author(s):  
H. Inoue ◽  
C. Inoue ◽  
J. Hildebrandt

This study was designed to determine whether the effects of temperature on lung pressure-volume (PV) curves were influenced by the state of the surface lining at the time of warming or cooling. In successive runs, temperature was varied (21, 37, or 5 degrees C) with lung gas volume fixed at either 55% total lung capacity (TLC) or 0% TLC (degassed), followed by PV curves to TLC. Peak inflation volume in a given lung was made identical at all temperatures. The starting pressure at 55% TLC remained fixed during temperature changes, whereas peak pressure ranged from 24 cmH2O at 37 degrees C to 40 cmH2O at 5 degrees C. However, below 75% TLC all deflation curves differed by less than 1 cmH2O, and the lowest recoil occurred at 5 degrees C. At 0% TLC, a similar dispersion in pressures appeared at TLC. However, on deflation, recoil at 37 degrees C was always less than at 21 degrees C, whereas at 5 degrees C a drastic shift to the right occurred. First-cycle hysteresis and midinflation pressure also increased with cooling. Thus, with cooling, the spreading and adsorption of surfactant during lung expansion are inhibited, and during deflation aggregation is greatly facilitated, accounting for the above results. When an already spread surface is cooled, then expanded, as at 55% TLC, the more rigid lining causes some rise in peak pressure at TLC but little change elsewhere. However, when lungs are degassed and then cooled, the aggregated surfactant spreads extremely poorly, leading to greatly increased recoil throughout the cycle. Changes in pressure at TLC may depend considerably on tissue effects.


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