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.

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.

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.

The supine position improves but does not normalize the blunted pulmonary capillary blood volume response to exercise in mild COPD

2020 ◽  
Vol 128 (4) ◽  
pp. 925-933
Author(s):  
Bryan A. Ross ◽  
Andrew R. Brotto ◽  
Desi P. Fuhr ◽  
Devin B. Phillips ◽  
Sean van Diepen ◽  
...  
Keyword(s):  
Blood Volume ◽  
Supine Position ◽  
Microvascular Dysfunction ◽  
Chronic Obstructive ◽  
Alveolar Volume ◽  
Obstructive Pulmonary Disease ◽  
Pulmonary Capillary ◽  
Capillary Blood Volume ◽  
Pulmonary Capillary Blood ◽  
Response To Exercise

Patients with mild chronic obstructive pulmonary disease (COPD) demonstrate resting pulmonary vascular dysfunction as well as a blunted pulmonary diffusing capacity (DLCO) and pulmonary capillary blood volume (VC) response to exercise. The transition from the upright to supine position increases central blood volume and perfusion pressure, which may overcome microvascular dysfunction in an otherwise intact alveolar-capillary interface. The present study examined whether the supine position normalized DLCO and VC responses to exercise in mild COPD. Sixteen mild COPD participants and 13 age-, gender-, and height-matched controls completed DLCO maneuvers at rest and during exercise in the upright and supine position. The multiple [Formula: see text]-DLCO method was used to determine DLCO, VC, and membrane diffusion capacity (DM). All three variables were adjusted for alveolar volume (DLCOAdj, VCAdj, and DMAdj). The supine position reduced alveolar volume similarly in both groups, but oxygen consumption and cardiac output were unaffected. DLCOAdj, DMAdj, and VCAdj were all lower in COPD. These same variables all increased with upright and supine exercise in both groups. DLCOAdj was unaffected by the supine position. VCAdj increased in the supine position similarly in both groups. DMAdj was reduced in the supine position in both groups. While the supine position increased exercise VCAdj in COPD, the increase was of similar magnitude to healthy controls; therefore, exercise VC remained blunted in COPD. The persistent reduction in exercise DLCO and VC when supine suggests that pulmonary vascular destruction is a contributing factor to the blunted DLCO and VC response to exercise in mild COPD. NEW & NOTEWORTHY Patients with mild chronic obstructive pulmonary disease demonstrate a combination of reversible pulmonary microvascular dysfunction and irreversible pulmonary microvascular destruction.

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.

Continuous recording of pulmonary blood volume: pulmonary pressure and volume changes

1959 ◽  
Vol 197 (5) ◽  
pp. 959-962 ◽  
Author(s):  
Arthur W. Lindsey ◽  
Arthur C. Guyton
Keyword(s):  
Heart Failure ◽  
Pulmonary Artery ◽  
Chest Wall ◽  
Blood Volume ◽  
Right Heart Failure ◽  
Continuous Recording ◽  
Lung Field ◽  
Left Heart ◽  
Left Heart Failure ◽  
Pulmonary Blood Volume

A method for continuous recording of pulmonary blood volume in the intact animal has been devised, utilizing the detection of I131-tagged blood from a circumscribed portion of lung field. To rule out the interference of blood in the chest wall the counts per minute (cpm) obtained from the chest wall after removing the lung at the end of the experiment were subtracted from the recorded cpm throughout the experiment. The cpm from the chest wall were found to be stable, so that it was concluded that changes in total cpm were caused by changes in pulmonary blood volume. Constriction of the ascending aorta or pulmonary artery by previously placed loops of plastic tubing produced either right or left heart failure. When left heart failure was produced acutely, the pulmonary blood volume increased an average of 79.5%±6.1 S.E. in 23 dogs. Constriction of the pulmonary artery, producing acute right heart failure, decreased the pulmonary blood volume an average of 38%±2.3 S.E. in 23 dogs.

Pulmonary diffusing capacity and capillary blood volume in aging dogs

1975 ◽  
Vol 38 (4) ◽  
pp. 647-650 ◽  
Author(s):  
N. E. Robinson ◽  
J. R. Gillespie
Keyword(s):  
Blood Volume ◽  
Morphological Changes ◽  
Transpulmonary Pressure ◽  
Capillary Blood ◽  
Diffusing Capacity ◽  
Alveolar Volume ◽  
Single Breath ◽  
Age Related ◽  
Capillary Blood Volume ◽  
Pulmonary Capillary Blood

Single-breath carbon monoxide diffusing capacity (DLco), pulmonary capillary blood volume (Vc), and membrane diffusing capacity (Dm) were measured in 24 beagle dogs aged 289–3,882 days. DLco and Vc were a function of age and alveolar volume (Va). Vc decreased with age resulting in changes in DLco. Changes in Vc may have been due to pulmonary morphological changes or to an exaggerated decrease in pulmonary blood flow in old dogs in response to 20–30 cmH-2O transpulmonary pressure. There was no age-related change in Dm.

Human Chest Wall Function while Awake and during Halothane Anesthesia 

1995 ◽  
Vol 82 (1) ◽  
pp. 6-19 ◽  
Author(s):  
David O. Warner ◽  
Mark A. Warner ◽  
Erik L. Ritman
Keyword(s):  
Chest Wall ◽  
Blood Volume ◽  
Functional Residual Capacity ◽  
Muscle Activity ◽  
Respiratory Muscle ◽  
Halothane Anesthesia ◽  
Intercostal Muscles ◽  
Residual Capacity ◽  
Gas Volume ◽  
Respiratory Muscle Activity

Background Data concerning chest wall configuration and the activities of the major respiratory muscles that determine this configuration during anesthesia in humans are limited. The aim of this study was to determine the effects of halothane anesthesia on respiratory muscle activity and chest wall shape and motion during spontaneous breathing. Methods Six human subjects were studied while awake and during 1 MAC halothane anesthesia. Respiratory muscle activity was measured using fine-wire electromyography electrodes. Chest wall configuration was determined using images of the thorax obtained by three-dimensional fast computed tomography. Tidal changes in gas volume were measured by integrating respiratory gas flow, and the functional residual capacity was measured by a nitrogen dilution technique. Results While awake, ribcage expansion was responsible for 25 +/- 4% (mean +/- SE) of the total change in thoracic volume (delta Vth) during inspiration. Phasic inspiratory activity was regularly present in the diaphragm and parasternal intercostal muscles. Halothane anesthesia (1 MAC) abolished activity in the parasternal intercostal muscles and increased phasic expiratory activity in the abdominal muscles and lateral ribcage muscles. However, halothane did not significantly change the ribcage contribution to delta Vth (18 +/- 4%). Intrathoracic blood volume, measured by comparing changes in total thoracic volume and gas volume, increased significantly during inspiration both while awake and while anesthetized (by approximately 20% of delta Vth, P < 0.05). Halothane anesthesia significantly reduced the functional residual capacity (by 258 +/- 78 ml), primarily via an inward motion of the end-expiratory position of the ribcage. Although the diaphragm consistently changed shape, with a cephalad displacement of posterior regions and a caudad displacement of anterior regions, the diaphragm did not consistently contribute to the reduction in the functional residual capacity. Halothane anesthesia consistently increased the curvature of the thoracic spine measured in the saggital plane. Conclusions The authors conclude that (1) ribcage expansion is relatively well preserved during halothane anesthesia despite the loss of parasternal intercostal muscle activity; (2) an inward displacement of the ribcage accounts for most of the decrease in functional residual capacity caused by halothane anesthesia, accompanied by changes in diaphragm shape that may be related to motion of its insertions on the thoracoabdominal wall; and (3) changes in intrathoracic blood volume constitute a significant fraction of delta Vth during tidal breathing.

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.

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.

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.

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