Pulmonary and chest wall mechanics in anesthetized paralyzed humans

1991 ◽  
Vol 70 (6) ◽  
pp. 2602-2610 ◽  
Author(s):  
E. D'Angelo ◽  
F. M. Robatto ◽  
E. Calderini ◽  
M. Tavola ◽  
D. Bono ◽  
...  
Keyword(s):  
Chest Wall ◽  
Viscoelastic Properties ◽  
Airway Resistance ◽  
Viscoelastic Model ◽  
Transpulmonary Pressure ◽  
Esophageal Pressure ◽  
Airway Occlusion ◽  
Chest Wall Mechanics ◽  
Overall Resistance ◽  
Viscoelastic Constants

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.

Effect of PEEP on respiratory mechanics in anesthetized paralyzed humans

1992 ◽  
Vol 73 (5) ◽  
pp. 1736-1742 ◽  
Author(s):  
E. D′Angelo ◽  
E. Calderini ◽  
M. Tavola ◽  
D. Bono ◽  
J. Milic-Emili
Keyword(s):  
Chest Wall ◽  
Lung Volume ◽  
Respiratory Mechanics ◽  
Viscoelastic Model ◽  
Esophageal Pressure ◽  
Airway Occlusion ◽  
Flow Interruption ◽  
Peep Ventilation ◽  
Overall Resistance ◽  
Viscoelastic Constants

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.

Viscoelastic behavior of lung and chest wall in dogs determined by flow interruption

1989 ◽  
Vol 67 (6) ◽  
pp. 2219-2229 ◽  
Author(s):  
T. Similowski ◽  
P. Levy ◽  
C. Corbeil ◽  
M. Albala ◽  
R. Pariente ◽  
...  
Keyword(s):  
Frequency Dependence ◽  
Chest Wall ◽  
Viscoelastic Behavior ◽  
Constant Flow ◽  
Pulmonary Tissue ◽  
Airway Occlusion ◽  
Chest Wall Mechanics ◽  
Flow Interruption ◽  
Overall Resistance ◽  
Pressure Changes

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.

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
Keyword(s):  
Tidal Volume ◽  
Chest Wall ◽  
Airway Resistance ◽  
Viscoelastic Model ◽  
Pulmonary Tissue ◽  
Lung Inflation ◽  
Airway Occlusion ◽  
Tissue Resistance ◽  
Linear Viscoelastic ◽  
Inflation Volume

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).

Forces involved in lobar atelectasis in intact dogs

1980 ◽  
Vol 48 (1) ◽  
pp. 29-33 ◽  
Author(s):  
G. T. Ford ◽  
C. A. Bradley ◽  
N. R. Anthonisen
Keyword(s):  
Chest Wall ◽  
Lower Lobe ◽  
Transpulmonary Pressure ◽  
Esophageal Pressure ◽  
Lateral Position ◽  
Relative Volume ◽  
Left Lower Lobe ◽  
Lung Lobe ◽  
Left Lateral Position ◽  
The Difference

When an excised lung lobe undergoes atelectasis, its shape differs from that observed when lobar atelectasis occurs in an intact animal: the chest wall deforms the collapsing lobe. In eight anesthetized dogs in the left lateral position we measured lung volume and transpulmonary pressure during the development of atelectasis. We then induced atelectasis of the left lower lobe with the rest of the lung maintained at FRC and measured lobar volume and "translobar" (lobar minus esophageal) pressure. Lung and lobar volumes were measured by prebreathing the animal with 88% O2-12% N2, occluding the airway and observing the increase in lung or lobar N2 concentration. When the left lower lobe alone collapsed, translobar pressures were more negative than transpulmonary pressure at the same relative volume when the whole lung collapsed. This pressure difference, which represents the deforming force applied to the lobe minus the pressure costs of deformation, averaged 3 cmH2O at 50% FRC. Infusion of 25 ml of normal saline into the pleural space sharply reduced the difference pulmonary pressure during lung collapse: this difference was abolished at 80% FRC and halved at 50% FRC. The large effect of the small volume of fluid suggested that deforming forces were largely generated in relatively local areas, such as regions of the chest wall with sharp angulation.

Effect of the chest wall and blood volume on pulmonary distensibility

1992 ◽  
Vol 72 (1) ◽  
pp. 186-193 ◽  
Author(s):  
H. J. Colebatch ◽  
C. K. Ng ◽  
N. Berend ◽  
F. J. Maccioni
Keyword(s):  
Chest Wall ◽  
Blood Volume ◽  
Surface Pressure ◽  
Supine Position ◽  
Transpulmonary Pressure ◽  
Esophageal Pressure ◽  
Relative Increase ◽  
Alveolar Volume ◽  
Pulmonary Blood Volume ◽  
Gas Volume

To determine the reason for increased pulmonary distensibility in excised lungs, we performed deflation pressure-volume (PV) studies in 24 dogs. Exponential analysis of PV data gave K, an index of distensibility. Lung volume was measured by dilution of neon. Compared with measurements obtained in the supine position, with the chest closed, and with esophageal pressure (Pes) to obtain transpulmonary pressure, K was not changed significantly with the chest strapped, with pleural pressure to obtain transpulmonary pressure, or with the chest open. From displacement of PV curves obtained in the supine position and with the chest closed or open, we estimated that Pes was 0.18 kPa greater than average lung surface pressure. An increase in K in the prone and head-up positions was attributed to a traction artifact decreasing Pes. Exsanguination increased K and produced a relative increase in gas volume. These results show that overall pulmonary distensibility is unaffected by an intact chest wall. An increase in K and gas volume after exsanguination probably reflects a decreased pulmonary blood volume, with collapse of capillaries increasing the alveolar volume-to-surface ratio.

Frequency dependence of pulmonary and chest wall mechanics in young and adult cats

1994 ◽  
Vol 76 (5) ◽  
pp. 2037-2046 ◽  
Author(s):  
F. R. Shardonofsky ◽  
J. Sato ◽  
D. H. Eidelman
Keyword(s):  
Chest Wall ◽  
Respiratory System ◽  
Viscoelastic Model ◽  
Dynamic Compliance ◽  
Compartment Model ◽  
Volume Data ◽  
Chest Wall Mechanics ◽  
Tissue Resistance ◽  
Single Compartment Model ◽  
Adult Cats

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.

Effects of Prone Positioning on Transpulmonary Pressures and End-expiratory Volumes in Patients without Lung Disease

2018 ◽  
Vol 128 (6) ◽  
pp. 1187-1192 ◽  
Author(s):  
Abirami Kumaresan ◽  
Robert Gerber ◽  
Ariel Mueller ◽  
Stephen H. Loring ◽  
Daniel Talmor
Keyword(s):  
Chest Wall ◽  
Prone Position ◽  
Airway Pressure ◽  
Transpulmonary Pressure ◽  
Esophageal Pressure ◽  
Driving Pressure ◽  
Prone Positioning ◽  
Volume Increase ◽  
Mechanically Ventilated ◽  
Chest Wall Elastance

Abstract Background The effects of prone positioning on esophageal pressures have not been investigated in mechanically ventilated patients. Our objective was to characterize effects of prone positioning on esophageal pressures, transpulmonary pressure, and lung volume, thereby assessing the potential utility of esophageal pressure measurements in setting positive end-expiratory pressure (PEEP) in prone patients. Methods We studied 16 patients undergoing spine surgery during general anesthesia and neuromuscular blockade. We measured airway pressure, esophageal pressures, airflow, and volume, and calculated the expiratory reserve volume and the elastances of the lung and chest wall in supine and prone positions. Results Esophageal pressures at end expiration with 0 cm H2O PEEP decreased from supine to prone by 5.64 cm H2O (95% CI, 3.37 to 7.90; P < 0.0001). Expiratory reserve volume measured at relaxation volume increased from supine to prone by 0.15 l (interquartile range, 0.25, 0.10; P = 0.003). Chest wall elastance increased from supine to prone by 7.32 (95% CI, 4.77 to 9.87) cm H2O/l at PEEP 0 (P < 0.0001) and 6.66 cm H2O/l (95% CI, 3.91 to 9.41) at PEEP 7 (P = 0.0002). Median driving pressure, the change in airway pressure from end expiration to end-inspiratory plateau, increased in the prone position at PEEP 0 (3.70 cm H2O; 95% CI, 1.74 to 5.66; P = 0.001) and PEEP 7 (3.90 cm H2O; 95% CI, 2.72 to 5.09; P < 0.0001). Conclusions End-expiratory esophageal pressure decreases, and end-expiratory transpulmonary pressure and expiratory reserve volume increase, when patients are moved from supine to prone position. Mean respiratory system driving pressure increases in the prone position due to increased chest wall elastance. The increase in end-expiratory transpulmonary pressure and expiratory reserve volume may be one mechanism for the observed clinical benefit with prone positioning.

scholarly journals Goal-Directed Mechanical Ventilation: Are We Aiming at the Right Goals? A Proposal for an Alternative Approach Aiming at Optimal Lung Compliance, Guided by Esophageal Pressure in Acute Respiratory Failure

2012 ◽  
Vol 2012 ◽  
pp. 1-9 ◽  
Author(s):  
Arie Soroksky ◽  
Antonio Esquinas
Keyword(s):  
Mechanical Ventilation ◽  
Respiratory Failure ◽  
Acute Respiratory Failure ◽  
Chest Wall ◽  
Respiratory System ◽  
Transpulmonary Pressure ◽  
Esophageal Pressure ◽  
Plateau Pressure ◽  
Lung Compliance ◽  
Inspiratory Pressure

Patients with acute respiratory failure and decreased respiratory system compliance due to ARDS frequently present a formidable challenge. These patients are often subjected to high inspiratory pressure, and in severe cases in order to improve oxygenation and preserve life, we may need to resort to unconventional measures. The currently accepted ARDSNet guidelines are characterized by a generalized approach in which an algorithm for PEEP application and limited plateau pressure are applied to all mechanically ventilated patients. These guidelines do not make any distinction between patients, who may have different chest wall mechanics with diverse pathologies and different mechanical properties of their respiratory system. The ability of assessing pleural pressure by measuring esophageal pressure allows us to partition the respiratory system into its main components of lungs and chest wall. Thus, identifying the dominant factor affecting respiratory system may better direct and optimize mechanical ventilation. Instead of limiting inspiratory pressure by plateau pressure, PEEP and inspiratory pressure adjustment would be individualized specifically for each patient's lung compliance as indicated by transpulmonary pressure. The main goal of this approach is to specifically target transpulmonary pressure instead of plateau pressure, and therefore achieve the best lung compliance with the least transpulmonary pressure possible.

scholarly journals Respiratory mechanical effects of surgical pneumoperitoneum in humans

2014 ◽  
Vol 117 (9) ◽  
pp. 1074-1079 ◽  
Author(s):  
Stephen H. Loring ◽  
Negin Behazin ◽  
Aileen Novero ◽  
Victor Novack ◽  
Stephanie B. Jones ◽  
...  
Keyword(s):  
Chest Wall ◽  
Respiratory System ◽  
Transpulmonary Pressure ◽  
Esophageal Pressure ◽  
Pleural Pressure ◽  
Abdominal Pressure ◽  
Positive End Expiratory Pressure ◽  
Before And After ◽  
Show Evidence ◽  
Obese Subjects

Pneumoperitoneum for laparoscopic surgery is known to stiffen the chest wall and respiratory system, but its effects on resting pleural pressure in humans are unknown. We hypothesized that pneumoperitoneum would raise abdominal pressure, push the diaphragm into the thorax, raise pleural pressure, and squeeze the lung, which would become stiffer at low volumes as in severe obesity. Nineteen predominantly obese laparoscopic patients without pulmonary disease were studied supine (level), under neuromuscular blockade, before and after insufflation of CO2 to a gas pressure of 20 cmH2O. Esophageal pressure (Pes) and airway pressure (Pao) were measured to estimate pleural pressure and transpulmonary pressure (Pl = Pao − Pes). Changes in relaxation volume (Vrel, at Pao = 0) were estimated from changes in expiratory reserve volume, the volume extracted between Vrel, and the volume at Pao = −25 cmH2O. Inflation pressure-volume (Pao-Vl) curves from Vrel were assessed for evidence of lung compression due to high Pl. Respiratory mechanics were measured during ventilation with a positive end-expiratory pressure of 0 and 7 cmH2O. Pneumoperitoneum stiffened the chest wall and the respiratory system (increased elastance), but did not stiffen the lung, and positive end-expiratory pressure reduced Ecw during pneumoperitoneum. Contrary to our expectations, pneumoperitoneum at Vrel did not significantly change Pes [8.7 (3.4) to 7.6 (3.2) cmH2O; means (SD)] or expiratory reserve volume [183 (142) to 155 (114) ml]. The inflation Pao-Vl curve above Vrel did not show evidence of increased lung compression with pneumoperitoneum. These results in predominantly obese subjects can be explained by the inspiratory effects of abdominal pressure on the rib cage.

Lung and chest wall mechanics in mechanically ventilated COPD patients

1993 ◽  
Vol 74 (4) ◽  
pp. 1570-1580 ◽  
Author(s):  
C. Guerin ◽  
M. L. Coussa ◽  
N. T. Eissa ◽  
C. Corbeil ◽  
M. Chasse ◽  
...  
Keyword(s):  
Chest Wall ◽  
Time Constant ◽  
Viscoelastic Behavior ◽  
Normal Subjects ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Mechanically Ventilated ◽  
Airway Occlusion ◽  
Chest Wall Mechanics ◽  
Copd Patients

By use of the technique of rapid airway occlusion, the effects of inspiratory flow, volume, and time on lung and chest wall mechanics were investigated in 10 chronic obstructive pulmonary disease (COPD) patients mechanically ventilated for acute respiratory failure. We measured the interrupter resistance (Rint), which in humans reflects airway resistance; the additional resistances due to time constant inequality and viscoelastic pressure dissipations within the lungs (delta RL) and the chest wall; and the static and dynamic elastances of lung and chest wall. We observed that 1) static elastances of lung and chest wall in COPD patients were similar to those of normal subjects; 2) Rint of the lung was markedly increased and flow dependent in COPD patients, whereas Rint of the chest wall was negligible as in normal subjects; and 3) in COPD patients, delta RL was markedly increased at all inflation flows and volumes, reflecting increased time constant inequalities within the lungs and/or altered viscoelastic behavior. The results imply increased dynamic work due to Rint and delta RL and marked time dependency of pulmonary resistance and elastance in COPD patients.

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