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.

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 Different contributions from lungs and chest wall to respiratory mechanics in mice, rats, and rabbits

2019 ◽  
Vol 127 (1) ◽  
pp. 198-204 ◽  
Author(s):  
Roberta Südy ◽  
Gergely H. Fodor ◽  
André Dos Santos Rocha ◽  
Álmos Schranc ◽  
József Tolnai ◽  
...  
Keyword(s):  
Chest Wall ◽  
Respiratory System ◽  
Respiratory Mechanics ◽  
Esophageal Pressure ◽  
Tissue Mechanics ◽  
Lung Mechanics ◽  
Laboratory Animals ◽  
Forced Oscillation Technique ◽  
Small Laboratory ◽  
Positive End Expiratory Pressure

Changes in lung mechanics are frequently inferred from intact-chest measures of total respiratory system mechanics without consideration of the chest wall contribution. The participation of lungs and chest wall in respiratory mechanics has not been evaluated systematically in small animals commonly used in respiratory research. Thus, we compared these contributions in intact-chest mice, rats, and rabbits and further characterized the influence of positive end-expiratory pressure (PEEP). Forced oscillation technique was applied to anesthetized mechanically ventilated healthy animals to obtain total respiratory system impedance (Zrs) at 0, 3, and 6 cmH2O PEEP levels. Esophageal pressure was measured by a catheter-tip micromanometer to separate Zrs into pulmonary (ZL) and chest wall (Zcw) components. A model containing a frequency-independent Newtonian resistance (RN), inertance, and a constant-phase tissue damping (G) and elastance (H) was fitted to Zrs, ZL, and Zcw spectra. The contribution of Zcw to RN was negligible in all species and PEEP levels studied. However, the participation of Zcw in G and H was significant in all species and increased significantly with increasing PEEP and animal size (rabbit > rat > mice). Even in mice, the chest wall contribution to G and H was still considerable, reaching 47.0 ± 4.0(SE)% and 32.9 ± 5.9% for G and H, respectively. These findings demonstrate that airway parameters can be assessed from respiratory system mechanical measurements. However, the contribution from the chest wall should be considered when intact-chest measurements are used to estimate lung parenchymal mechanics in small laboratory models (even in mice), particularly at elevated PEEP levels. NEW & NOTEWORTHY In species commonly used in respiratory research (rabbits, rats, mice), esophageal pressure-based estimates revealed negligible contribution from the chest wall to the Newtonian resistance. Conversely, chest wall participation in the viscoelastic tissue mechanical parameters increased with body size (rabbit > rat > mice) and positive end-expiratory pressure, with contribution varying between 30 and 50%, even in mice. These findings demonstrate the potential biasing effects of the chest wall when lung tissue mechanics are inferred from intact-chest measurements in small laboratory animals.

Pleural pressure increases during inspiration in the zone of apposition of diaphragm to rib cage

1988 ◽  
Vol 65 (5) ◽  
pp. 2207-2212 ◽  
Author(s):  
W. F. Urmey ◽  
A. De Troyer ◽  
K. B. Kelly ◽  
S. H. Loring
Keyword(s):  
Esophageal Pressure ◽  
Pleural Pressure ◽  
Abdominal Pressure ◽  
Transdiaphragmatic Pressure ◽  
Rib Cage ◽  
Direct Measurements ◽  
Anesthetized Dogs ◽  
Theoretical Mechanism ◽  
Phrenic Stimulation ◽  
Anatomic Region

The zone of apposition of diaphragm to rib cage provides a theoretical mechanism that may, in part, contribute to rib cage expansion during inspiration. Increases in intra-abdominal pressure (Pab) that are generated by diaphragmatic contraction are indirectly applied to the inner rib cage wall in the zone of apposition. We explored this mechanism, with the expectation that pleural pressure in this zone (Pap) would increase during inspiration and that local transdiaphragmatic pressure in this zone (Pdiap) must be different from conventionally determined transdiaphragmatic pressure (Pdi) during inspiration. Direct measurements of Pap, as well as measurements of pleural pressure (Ppl) cephalad to the zone of apposition, were made during tidal inspiration, during phrenic stimulation, and during inspiratory efforts in anesthetized dogs. Pab and esophageal pressure (Pes) were measured simultaneously. By measuring Ppl's with cannulas placed through ribs, we found that Pap consistently increased during both maneuvers, whereas Ppl and Pes decreased. Whereas changes in Pdi of up to -19 cmH2O were measured, Pdiap never departed from zero by greater than -4.5 cmH2O. We conclude that there can be marked regional differences in Ppl and Pdi between the zone of apposition and regions cephalad to the zone. Our results support the concept of the zone of apposition as an anatomic region where Pab is transmitted to the interior surface of the lower rib cage.

Abdominal distension alters regional pleural pressures and chest wall mechanics in pigs in vivo

1991 ◽  
Vol 70 (6) ◽  
pp. 2611-2618 ◽  
Author(s):  
T. Mutoh ◽  
W. J. Lamm ◽  
L. J. Embree ◽  
J. Hildebrandt ◽  
R. K. Albert
Keyword(s):  
Chest Wall ◽  
Respiratory System ◽  
Functional Residual Capacity ◽  
Total Lung Capacity ◽  
Abdominal Cavity ◽  
Abdominal Distension ◽  
Abdominal Pressure ◽  
Lung Capacity ◽  
Lung Expansion ◽  
Residual Capacity

Abdominal distension (AD) occurs in pregnancy and is also commonly seen in patients with ascites from various causes. Because the abdomen forms part of the "chest wall," the purpose of this study was to clarify the effects of AD on ventilatory mechanics. Airway pressure, four (vertical) regional pleural pressures, and abdominal pressure were measured in five anesthetized, paralyzed, and ventilated upright pigs. The effects of AD on the lung and chest wall were studied by inflating a liquid-filled balloon placed in the abdominal cavity. Respiratory system, chest wall, and lung pressure-volume (PV) relationships were measured on deflation from total lung capacity to residual volume, as well as in the tidal breathing range, before and 15 min after abdominal pressure was raised. Increasing abdominal pressure from 3 to 15 cmH2O decreased total lung capacity and functional residual capacity by approximately 40% and shifted the respiratory system and chest wall PV curves downward and to the right. Much smaller downward shifts in lung deflation curves were seen, with no change in the transdiaphragmatic PV relationship. All regional pleural pressures increased (became less negative) and, in the dependent region, approached 0 cmH2O at functional residual capacity. Tidal compliances of the respiratory system, chest wall, and lung were decreased 43, 42, and 48%, respectively. AD markedly alters respiratory system mechanics primarily by "stiffening" the diaphragm/abdomen part of the chest wall and secondarily by restricting lung expansion, thus shifting the lung PV curve as seen after chest strapping. The less negative pleural pressures in the dependent lung regions suggest that nonuniformities of ventilation could also be accentuated and gas exchange impaired by AD.

Respiratory mechanics in the anesthetized rat

1978 ◽  
Vol 45 (2) ◽  
pp. 255-260 ◽  
Author(s):  
Y. L. Lai ◽  
J. Hildebrandt
Keyword(s):  
Chest Wall ◽  
Respiratory System ◽  
Esophageal Pressure ◽  
Gas Content ◽  
Lung Capacity ◽  
Consistent Change ◽  
Residual Capacity ◽  
Wall Compliance ◽  
The Difference ◽  
Body Plethysmograph

Functional residual capacity (FRC) and pressure-volume (PV) curves of the lung, chest wall, and total respiratory system were studied in 15 anesthetized rats, weighing 307 +/- 10 (SE) g. Pleural pressure was estimated from the esophageal pressure measured with a water-filled catheter. The FRC determined by body plethysmograph was slightly and significantly larger than FRC determined from saline displacement of excised lungs. The difference may be accounted for by O2 uptake by lung tissue, escape of CO2 through the pleura, and abdominal gas. Paralysis in the prone position did not affect FRC, and abdominal gas content contributed only slightly to the FRC measured by body plethysmograph. Values of various pulmonary parameters (mean +/- SE) were as follows: residual volume, 1.26 +/- 0.13 ml; FRC, 2.51 +/- 0.20 ml; total lung capacity, 12.23 +/- 0.55 ml; compliance of the lung, 0.90 +/- 0.06 ml/cmH2O; chest wall compliance, 1.50 +/- 0.11 ml/cmH2O; and respiratory system compliance, 0.57 +/- 0.03 ml/cmH2O. The lung PV curve did not show a consistent change after the chest was opened.

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.

scholarly journals Determinants of the esophageal-pleural pressure relationship in humans

2020 ◽  
Vol 128 (1) ◽  
pp. 78-86 ◽  
Author(s):  
Iacopo Pasticci ◽  
Paolo Cadringher ◽  
Lorenzo Giosa ◽  
Michele Umbrello ◽  
Paolo Formenti ◽  
...  
Keyword(s):  
Tidal Volume ◽  
Chest Wall ◽  
Supine Position ◽  
Body Position ◽  
Esophageal Pressure ◽  
Lateral Position ◽  
Pleural Pressure ◽  
Absolute Value ◽  
Gravitational Forces ◽  
Chest Wall Elastance

Esophageal pressure has been suggested as adequate surrogate of the pleural pressure. We investigate after lung surgery the determinants of the esophageal and intrathoracic pressures and their differences. The esophageal pressure (through esophageal balloon) and the intrathoracic/pleural pressure (through the chest tube on the surgery side) were measured after surgery in 28 patients immediately after lobectomy or wedge resection. Measurements were made in the nondependent lateral position (without or with ventilation of the operated lung) and in the supine position. In the lateral position with the nondependent lung, collapsed or ventilated, the differences between esophageal and pleural pressure amounted to 4.4 ± 1.6 and 5.1 ± 1.7 cmH2O. In the supine position, the difference amounted to 7.3 ± 2.8 cmH2O. In the supine position, the estimated compressive forces on the mediastinum were 10.5 ± 3.1 cmH2O and on the iso-gravitational pleural plane 3.2 ± 1.8 cmH2O. A simple model describing the roles of chest, lung, and pneumothorax volume matching on the pleural pressure genesis was developed; modeled pleural pressure = 1.0057 × measured pleural pressure + 0.6592 ( r2 = 0.8). Whatever the position and the ventilator settings, the esophageal pressure changed in a 1:1 ratio with the changes in pleural pressure. Consequently, chest wall elastance (Ecw) measured by intrathoracic (Ecw = ΔPpl/tidal volume) or esophageal pressure (Ecw = ΔPes/tidal volume) was identical in all the positions we tested. We conclude that esophageal and pleural pressures may be largely different depending on body position (gravitational forces) and lung-chest wall volume matching. Their changes, however, are identical. NEW & NOTEWORTHY Esophageal and pleural pressure changes occur at a 1:1 ratio, fully justifying the use of esophageal pressure to compute the chest wall elastance and the changes in pleural pressure and in lung stress. The absolute value of esophageal and pleural pressures may be largely different, depending on the body position (gravitational forces) and the lung-chest wall volume matching. Therefore, the absolute value of esophageal pressure should not be used as a surrogate of pleural pressure.

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