Effects of volume history and vagotomy on pulmonary and chest wall mechanics in cats

1991 ◽  
Vol 71 (2) ◽  
pp. 498-508 ◽  
Author(s):  
F. R. Shardonofsky ◽  
M. Skaburskis ◽  
J. Sato ◽  
W. A. Zin ◽  
J. Milic-Emili

Using the technique of rapid airway occlusion during constant-flow inflation, we studied the effects of inflation volume, different baseline tidal volumes (10, 20, and 30 ml/kg), and vagotomy on the resistive and elastic properties of the lungs and chest wall in six anesthetized tracheotomized paralyzed mechanically ventilated cats. Before vagotomy, airway resistance decreased significantly with increasing inflation volume at all baseline tidal volumes. At any given inflation volume, airway resistance decreased with increasing baseline tidal volume. After vagotomy, airway resistance decreased markedly and was no longer affected by baseline tidal volume. Prevagotomy, pulmonary tissue resistance increased progressively with increasing lung volume and was not affected by baseline tidal volume. Pulmonary tissue resistance decreased postvagotomy. Chest wall tissue resistance increased during lung inflation but was not affected by either baseline tidal volume or vagotomy. The static volume-pressure relationships of the lungs and chest wall were not affected by either baseline tidal volume or vagotomy. The data were interpreted in terms of a linear viscoelastic model of the respiratory system (J. Appl. Physiol. 67: 2276–2285, 1989).

1964 ◽  
Vol 19 (4) ◽  
pp. 653-658 ◽  
Author(s):  
B. G. Ferris ◽  
J. Mead ◽  
L. H. Opie

Measurements of flow resistance of various components of the respiratory system were measured in adult male subjects in the sitting position. Nasal resistance is the largest single component being nearly one-half the total and two-thirds of the airway resistance during nose breathing. It is highly nonlinear, and shows much variability. During mouth breathing upper airway resistance (mouth, pharynx, glottis, larynx and upper trachea) is also markedly nonlinear, and accounts for one-third the total airway resistance. Lower airway resistance is approximately linear up to flows of 2 liters/sec. Pulmonary tissue resistance is low as reported in this study. Chest wall resistance is nearly linear up to flow rates of 2 liters/sec and accounts for slightly less than half the total respiratory resistance during mouth breathing and 10–19% during nasal breathing. larynx; airways; chest wall; nose Submitted on December 16, 1963


1991 ◽  
Vol 70 (6) ◽  
pp. 2602-2610 ◽  
Author(s):  
E. D'Angelo ◽  
F. M. Robatto ◽  
E. Calderini ◽  
M. Tavola ◽  
D. Bono ◽  
...  

Pulmonary and chest wall mechanics were studied in 18 anesthetized paralyzed supine humans by use of the technique of rapid airway occlusion during constant-flow inflation. Analysis of the changes in transpulmonary pressure after flow interruption allowed partitioning of the overall resistance of the lung (RL) into two compartments, one (Rint,L) reflecting airway resistance and the other (delta RL) representing the viscoelastic properties of the pulmonary tissues. Similar analysis of the changes in esophageal pressure indicates that chest wall resistance (RW) was due entirely to the viscoelastic properties of the chest wall tissues (delta RW = RW). In line with previous measurements of airway resistance, Rint,L increased with increasing flow and decreased with increasing volume. The opposite was true for both delta RL and delta RW. This behavior was interpreted in terms of a viscoelastic model that allowed computation of the viscoelastic constants of the lung and chest wall. This model also accounts for frequency, volume, and flow dependence of elastance of the lung and chest wall. Static and dynamic elastances, as well as delta R, were higher for the lung than for the chest wall.


1989 ◽  
Vol 67 (4) ◽  
pp. 1623-1629 ◽  
Author(s):  
B. Suki ◽  
R. Peslin ◽  
C. Duvivier ◽  
R. Farre

Lung impedance was measured from 0.01 to 0.1 Hz in six healthy adults by superimposing small-amplitude forced oscillations on spontaneous breathing. Measurements were made with an almost constant-volume input (160–180 ml) or with an almost constant-flow input (20–30 ml.s-1). No significant difference was found between the two conditions. Lung resistance (RL) sharply decreased from 0.97 kPa.l-1.s at 0.01 Hz to 0.27 kPa.l-1.s at 0.03 Hz and then mildly to 0.23 kPa.l-1.s at 0.1 Hz. Lung effective compliance (CL) decreased slightly and regularly from 0.01 Hz (2.38 l.kPa-1) to 0.1 Hz (1.93 l.kPa-1). The data were analyzed using a linear viscoelastic model adapted from Hildebrandt (J. Appl. Physiol. 28:365–372, 1970) and complemented by a Newtonian resistance (R): RL = R + B/(9.2f); CL = 1/(A + 0.25B + B.log2 pi f), where f is the frequency and B/A is an index of lung tissue viscoelasticity. A good fit was generally obtained, with an average difference of 10% between the observed and predicted values. The ratio B/A was not affected by the breathing and was 10.6 and 13.6% in the constant-volume and constant-flow conditions, respectively, which agrees with Hildebrandt's observations in isolated cat lungs. R was systematically larger than the plethysmographic airway resistance, suggesting that lung tissue resistance might also include a Newtonian component.


1984 ◽  
Vol 113 (1) ◽  
pp. 187-202 ◽  
Author(s):  
WILLIAM K. MILSOM ◽  
TIMOTHY Z. VITALIS

Measurements of pulmonary mechanics made on anaesthetized specimens of the Tokay gecko Gekkogecko (Linné), indicate that both static and dynamic pulmonary mechanics are dominated by the mechanics of the body cavity and chest wall. The lungs are relatively large and compliant and offer little resistance to air flow at any of the ventilation frequencies (f) used in this study. The body wall is relatively stiff and becomes less compliant with increasing ventilation frequency and with increasing tidal volume (VT) at the higher frequencies. The vast majority of the work performed in breathing is used to overcome elastic forces in the chest wall resisting lung inflation. This work increases exponentially with increases in volume. As a consequence, in terms of total ventilation, the most economic breathing pattern is a high frequency, low tidal volume pattern in which changes in minute ventilation (VE) are most economically produced solely by changes in f. Because reductions in tidal volume drastically reduce alveolar ventilation volume while dead space remains constant, the same arguments do not apply to alveolar minute ventilation (VA). In terms of alveolar minute ventilation, there is an optimum combination of f and VT for each level of VA, with changes in VA being most economically produced by almost equal changes in both f and VT


1994 ◽  
Vol 76 (5) ◽  
pp. 2037-2046 ◽  
Author(s):  
F. R. Shardonofsky ◽  
J. Sato ◽  
D. H. Eidelman

The frequency (f) dependence of pulmonary and chest wall mechanics was assessed in nine kittens and four cats. Kittens and cats were anesthetized, paralyzed, and mechanically ventilated at various f between 0.13 and 1.6 Hz and 0.09 and 0.79 Hz, respectively. Resistance and dynamic compliance pertaining to the respiratory system (Rrs and Cdyn,rs), lungs (RL and Cdyn,L), and chest wall (RW and Cdyn,W) were estimated by fitting a single-compartment model to data obtained from regular ventilation. Static lung and chest wall compliances (Cst,L and Cst,W) were computed from quasi-static pressure-volume data. Lung tissue resistance (Rti) was estimated with alveolar capsules in open-chest animals. The f dependence of the two-compartment viscoelastic model of the respiratory system was assessed by computing the effective resistance [Rmod,rs(omega)] and compliance [Cmod,rs(omega)] from data obtained at the lowest experimental f. Both Cdyn,L and Cdyn,W decreased with increasing f in all animals. Cdyn,L/Cst,L and Cdyn,W/Cst,W were lower in kittens than in cats. RL and RW decreased markedly with f in all animals. Rti/RL showed a marked f dependence, its values being similar in both young and adult cats at their respective resting f. CstW/Cst,L ratio was higher in kittens than in cats. A better agreement was found between Cmod,rs(omega) and Cdyn,rs than between Rmod,rs(omega) and Rrs.


1989 ◽  
Vol 67 (6) ◽  
pp. 2219-2229 ◽  
Author(s):  
T. Similowski ◽  
P. Levy ◽  
C. Corbeil ◽  
M. Albala ◽  
R. Pariente ◽  
...  

Pulmonary and chest wall mechanics were studied in six anesthetized paralyzed dogs, by use of the technique of rapid airway occlusion during constant flow inflation. Analysis of the pressure changes after flow interruption allowed us to partition the overall resistance of the lung (Rl) and chest wall (Rw) and total respiratory system (Rrs) into two components, one (Rinit) reflecting in the lung airway resistance (Raw), the other (delta R) reflecting primarily the viscoelastic properties of the pulmonary and chest wall tissues. The effects of varying inspiratory flow and inflation volume were interpreted in terms of frequency dependence of resistance, by using a spring-and-dashpot model previously proposed and substantiated by Bates et al. (Proc. 9th Annu. Conf. IEEE Med. Biol. Soc., 1987, vol. 3, p. 1802-1803). We observed that 1) Raw and Rw,init were nearly equal and small relative to Rl and Rw (both were unaffected by flow); 2) Rrs,init decreased slightly with increasing volume; 3) both delta Rl and delta Rw decreased with increasing flow and increased with increasing lung volume. These changes were manifestations of frequency dependence of delta R, as it is predicted by the model; 4) Rrs, Rl, and Rw followed the same trends as delta R. These results corroborate data previously reported in the literature with the use of different techniques to measure airways and pulmonary tissue resistances and confirm that the use of Rl to assess bronchial reactivity is problematic. The interrupter techniques provides a convenient way to obtain Raw values, as well as analogs of lung and chest wall tissue resistances in intact dogs.


1987 ◽  
Vol 63 (2) ◽  
pp. 603-608 ◽  
Author(s):  
D. W. Hudgel ◽  
M. Mulholland ◽  
C. Hendricks

The purposes of this study were 1) to characterize the immediate inspiratory muscle and ventilation responses to inspiratory resistive loading during sleep in humans and 2) to determine whether upper airway caliber was compromised in the presence of a resistive load. Ventilation variables, chest wall, and upper airway inspiratory muscle electromyograms (EMG), and upper airway resistance were measured for two breaths immediately preceding and immediately following six applications of an inspiratory resistive load of 15 cmH2O.l–1 X s during wakefulness and stage 2 sleep. During wakefulness, chest wall inspiratory peak EMG activity increased 40 +/- 15% (SE), and inspiratory time increased 20 +/- 5%. Therefore, the rate of rise of chest wall EMG increased 14 +/- 10.9% (NS). Upper airway inspiratory muscle activity changed in an inconsistent fashion with application of the load. Tidal volume decreased 16 +/- 6%, and upper airway resistance increased 141 +/- 23% above pre-load levels. During sleep, there was no significant chest wall or upper airway inspiratory muscle or timing responses to loading. Tidal volume decreased 40 +/- 7% and upper airway resistance increased 188 +/- 52%, changes greater than those observed during wakefulness. We conclude that 1) the immediate inspiratory muscle and timing responses observed during inspiratory resistive loading in wakefulness were absent during sleep, 2) there was inadequate activation of upper airway inspiratory muscle activity to compensate for the increased upper airway inspiratory subatmospheric pressure present during loading, and 3) the alteration in upper airway mechanics during resistive loading was greater during sleep than wakefulness.


1992 ◽  
Vol 73 (5) ◽  
pp. 1736-1742 ◽  
Author(s):  
E. D′Angelo ◽  
E. Calderini ◽  
M. Tavola ◽  
D. Bono ◽  
J. Milic-Emili

With the use of the technique of rapid airway occlusion during constant flow inflation, respiratory mechanics were studied in eight anesthetized paralyzed supine normal humans during zero (ZEEP) and positive end-expiratory pressure (PEEP) ventilation. PEEP increased the end-expiratory lung volume by 0.49 liter. The changes in transpulmonary and esophageal pressure after flow interruption were analyzed in terms of a seven-parameter “viscoelastic” model. This allowed assessment of static lung and chest wall elastance (Est,L and Est,W), partitioning of overall resistance into airway interrupter (Rint,L) and tissue resistances (delta RL and delta RW), and computation of lung and chest wall “viscoelastic constants.” With increasing flow, Rint,L increased, whereas delta RL and delta RW decreased, as predicted by the model. Est,L, Est,W, and Rint,L decreased significantly with PEEP because of increased lung volume, whereas delta R and viscoelastic constants of lung and chest wall were independent of PEEP. The results indicate that PEEP caused a significant decrease in Rint,L, Est,L, and Est,W, whereas the dynamic tissue behavior, as reflected by delta RL and delta RW, did not change.


1989 ◽  
Vol 67 (6) ◽  
pp. 2296-2302 ◽  
Author(s):  
E. van Lunteren ◽  
M. A. Haxhiu ◽  
N. S. Cherniack

Complex relationships exist among electromyograms (EMGs) of the upper airway muscles, respective changes in muscle length, and upper airway volume. To test the effects of preventing lung inflation on these relationships, recordings were made of EMGs and length changes of the geniohyoid (GH) and sternohyoid (SH) muscles as well as of tidal changes in upper airway volume in eight anesthetized cats. During resting breathing, tracheal airway occlusion tended to increase the inspiratory lengthening of GH and SH. In response to progressive hypercapnia, the GH eventually shortened during inspiration in all animals; the extent of muscle shortening was minimally augmented by airway occlusion despite substantial increases in EMGs. SH lengthened during inspiration in six of eight animals under hypercapnic conditions, and in these cats lengthening was greater during airway occlusion even though EMGs increased. Despite the above effects on SH and GH length, upper airway tidal volume was increased significantly by tracheal occlusion under hypercapnic conditions. These data suggest that the thoracic and upper airway muscle reflex effects of preventing lung inflation during inspiration act antagonistically on hyoid muscle length, but, because of the mechanical arrangement of the hyoid muscles relative to the airway and thorax, they act agonistically to augment tidal changes in upper airway volume. The augmentation of upper airway tidal volume may occur in part as a result of the effects of thoracic movements being passively transmitted through the hyoid muscles.


1992 ◽  
Vol 73 (5) ◽  
pp. 1908-1913 ◽  
Author(s):  
F. M. Robatto ◽  
S. Simard ◽  
H. Orana ◽  
P. T. Macklem ◽  
M. S. Ludwig

We have recently shown in dogs that much of the increase in lung resistance (RL) after induced constriction can be attributed to increases in tissue resistance, the pressure drop in phase with flow across the lung tissues (Rti). Rti is dependent on lung volume (VL) even after induced constriction. As maximal responses in RL to constrictor agonists can also be affected by changes in VL, we questioned whether changes in the plateau response with VL could be attributed in part to changes in the resistive properties of lung tissues. We studied the effect of changes in VL on RL, Rti, airway resistance (Raw), and lung elastance (EL) during maximal methacholine (MCh)-induced constriction in 8 anesthetized, paralyzed, open-chest mongrel dogs. We measured tracheal flow and pressure (Ptr) and alveolar pressure (PA), the latter using alveolar capsules, during tidal ventilation [positive end-expiratory pressure (PEEP) = 5.0 cmH2O, tidal volume = 15 ml/kg, frequency = 0.3 Hz]. Measurements were recorded at baseline and after the aerosolization of increasing concentrations of MCh until a clear plateau response had been achieved. VL was then altered by changing PEEP to 2.5, 7.5, and 10 cmH2O. RL changed only when PEEP was altered from 5 to 10 cmH2O (P < 0.01). EL changed when PEEP was changed from 5 to 7.5 and 5 to 10 cmH2O (P < 0.05). Rti and Raw varied significantly with all three maneuvers (P < 0.05). Our data demonstrate that the effects of VL on the plateau response reflect a complex combination of changes in tissue resistance, airway caliber, and lung recoil.


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