The Experts below are selected from a list of 252 Experts worldwide ranked by ideXlab platform
John J. Marini - One of the best experts on this subject based on the ideXlab platform.
-
reliability of Transpulmonary Pressure time curve profile to identify tidal recruitment hyperinflation in experimental unilateral pleural effusion
Journal of Clinical Monitoring and Computing, 2017Co-Authors: P. Formenti, Alexander B. Adams, David J. Dries, Michele Umbrello, Jerónimo Graf, John J. MariniAbstract:The stress index (SI) is a parameter that characterizes the shape of the airway Pressure-time profile (P/t). It indicates the slope progression of the curve, reflecting both lung and chest wall properties. The presence of pleural effusion alters the mechanical properties of the respiratory system decreasing Transpulmonary Pressure (Ptp). We investigated whether the SI computed using Ptp tracing would provide reliable insight into tidal recruitment/overdistention during the tidal cycle in the presence of unilateral effusion. Unilateral pleural effusion was simulated in anesthetized, mechanically ventilated pigs. Respiratory system mechanics and thoracic computed tomography (CT) were studied to assess P/t curve shape and changes in global lung aeration. SI derived from airway Pressure (Paw) was compared with that calculated by Ptp under the same conditions. These results were themselves compared with quantitative CT analysis as a gold standard for tidal recruitment/hyperinflation. Despite marked changes in tidal recruitment, mean values of SI computed either from Paw or Ptp were remarkably insensitive to variations of PEEP or condition. After the instillation of effusion, SI indicates a preponderant over-distension effect, not detected by CT. After the increment in PEEP level, the extent of CT-determined tidal recruitment suggest a huge recruitment effect of PEEP as reflected by lung compliance. Both SI in this case were unaffected. We showed that the ability of SI to predict tidal recruitment and overdistension was significantly reduced in a model of altered chest wall-lung relationship, even if the parameter was computed from the Ptp curve profile.
-
Reliability of Transpulmonary Pressure–time curve profile to identify tidal recruitment/hyperinflation in experimental unilateral pleural effusion
Journal of clinical monitoring and computing, 2016Co-Authors: P. Formenti, Alexander B. Adams, David J. Dries, Michele Umbrello, Jerónimo Graf, John J. MariniAbstract:The stress index (SI) is a parameter that characterizes the shape of the airway Pressure-time profile (P/t). It indicates the slope progression of the curve, reflecting both lung and chest wall properties. The presence of pleural effusion alters the mechanical properties of the respiratory system decreasing Transpulmonary Pressure (Ptp). We investigated whether the SI computed using Ptp tracing would provide reliable insight into tidal recruitment/overdistention during the tidal cycle in the presence of unilateral effusion. Unilateral pleural effusion was simulated in anesthetized, mechanically ventilated pigs. Respiratory system mechanics and thoracic computed tomography (CT) were studied to assess P/t curve shape and changes in global lung aeration. SI derived from airway Pressure (Paw) was compared with that calculated by Ptp under the same conditions. These results were themselves compared with quantitative CT analysis as a gold standard for tidal recruitment/hyperinflation. Despite marked changes in tidal recruitment, mean values of SI computed either from Paw or Ptp were remarkably insensitive to variations of PEEP or condition. After the instillation of effusion, SI indicates a preponderant over-distension effect, not detected by CT. After the increment in PEEP level, the extent of CT-determined tidal recruitment suggest a huge recruitment effect of PEEP as reflected by lung compliance. Both SI in this case were unaffected. We showed that the ability of SI to predict tidal recruitment and overdistension was significantly reduced in a model of altered chest wall-lung relationship, even if the parameter was computed from the Ptp curve profile.
-
Unilateral mechanical asymmetry: positional effects on lung volumes and Transpulmonary Pressure
Intensive care medicine experimental, 2014Co-Authors: Gustavo A. Cortes-puentes, Kenneth Gard, Alexander B. Adams, David J. Dries, Joseph C. Keenan, John J. MariniAbstract:Background Ventilated patients with asymmetry of lung or chest wall mechanics may be vulnerable to differing lung stresses or strains dependent on body position. Our purpose was to examine Transpulmonary Pressure (PTP) and end-expiratory lung volume (functional residual capacity (FRC)) during body positioning changes in an animal model under the influence of positive end-expiratory Pressure (PEEP) or experimental pleural effusion (PLEF).
-
Value and limitations of Transpulmonary Pressure calculations during intra-abdominal hypertension.
Critical care medicine, 2013Co-Authors: Gustavo A. Cortes-puentes, Kenneth Gard, Alexander B. Adams, Katherine Faltesek, Christopher P. Anderson, David J. Dries, John J. MariniAbstract:Objective: To clarify the effect of progressively increasing intra-abdominal Pressure on esophageal Pressure, Transpulmonary Pressure, and functional residual capacity. Design: Controlled application of increased intra-abdominal Pressure at two positive end-expiratory Pressure levels (1 and 10 cm H2O) in an anesthetized porcine model of controlled ventilation. Setting: Large animal laboratory of a university-affiliated hospital. Subjects: Eleven deeply anesthetized swine (weight 46.2 ± 6.2 kg). Interventions: Air-regulated intra-abdominal hypertension (0–25 mm Hg). Measurements: Esophageal Pressure, tidal compliance, bladder Pressure, and end-expiratory lung aeration by gas dilution. Main Results: Functional residual capacity was significantly reduced by increasing intra-abdominal Pressure at both positive end-expiratory Pressure levels (p ≤ 0.0001) without corresponding changes of end-expiratory esophageal Pressure. Above intra-abdominal Pressure 5 mm Hg, plateau airway Pressure increased linearly by ~ 50% of the applied intra-abdominal Pressure value, associated with commensurate changes of esophageal Pressure. With tidal volume held constant, negligible changes occurred in Transpulmonary Pressure due to intra-abdominal Pressure. Driving Pressures calculated from airway Pressures alone (plateau airway Pressure – positive end-expiratory Pressure) did not equate to those computed from Transpulmonary Pressure (tidal changes in Transpulmonary Pressure). Increasing positive end-expiratory Pressure shifted the predominantly negative end-expiratory Transpulmonary Pressure at positive end-expiratory Pressure 1 cm H2O (mean –3.5 ± 0.4 cm H2O) into the positive range at positive end-expiratory Pressure 10 cm H2O (mean 0.58 ± 1.2 cm H2O). Conclusions: Despite its insensitivity to changes in functional residual capacity, measuring Transpulmonary Pressure may be helpful in explaining how different levels of positive end-expiratory Pressure influence recruitment and collapse during tidal ventilation in the presence of increased intra-abdominal Pressure and in calculating true Transpulmonary driving Pressure (tidal changes of Transpulmonary Pressure). Traditional interpretations of respiratory mechanics based on unmodified airway Pressure were misleading regarding lung behavior in this setting.
Luciano Gattinoni - One of the best experts on this subject based on the ideXlab platform.
-
Targeting Transpulmonary Pressure to prevent ventilator-induced lung injury
Expert review of respiratory medicine, 2019Co-Authors: Luciano Gattinoni, Lorenzo Giosa, Matteo Bonifazi, Iacopo Pasticci, Mattia Busana, Matteo Maria Macrì, Federica Romitti, Francesco Vassalli, Michael QuintelAbstract:Introduction: Transpulmonary Pressure (PL) is the Pressure distending the lung. This Pressure equals the stress which develops into the parenchyma at each insufflation and it depends, for a given airway Pressure, on the relationship between the lung and the chest wall elastance: a given stress is associated to a given strain, therefor PL is strictly related to ventilator-induced lung injury (VILI). Insufficient knowledge and increased workload account for its limited use in the clinical setting: indeed, the current recommendations for protective ventilation still rely only on the Pressures applied to the respiratory system in total (Plateau Pressure), without a direct measurement of the real lung stress. Areas covered: We reviewed the significance, the assessment, the application and the limits of Transpulmonary Pressure in the clinical setting. Expert opinion: Transpulmonary Pressure represents a physiologically sound safety limit for mechanical ventilation that should be measured and targeted at least in the most severe ARDS patients. Targeting Transpulmonary Pressure means 'personalizing' the ventilatory settings.
-
The assessment of Transpulmonary Pressure in mechanically ventilated ARDS patients
Intensive Care Medicine, 2014Co-Authors: Davide Chiumello, Giovanni Babini, Matteo Brioni, Francesco Crimella, Massimo Cressoni, Stefan Lundin, Ola Stenqvist, Andrea Colombo, Luciano GattinoniAbstract:Purpose The optimal method for estimating Transpulmonary Pressure (i.e. the fraction of the airway Pressure transmitted to the lung) has not yet been established. Methods In this study on 44 patients with acute respiratory distress syndrome (ARDS), we computed the end-inspiratory Transpulmonary Pressure as the change in airway and esophageal Pressure from end-inspiration to atmospheric Pressure (i.e. release derived) and as the product of the end-inspiratory airway Pressure and the ratio of lung to respiratory system elastance (i.e. elastance derived). The end-expiratory Transpulmonary Pressure was estimated as the product of positive end-expiratory Pressure (PEEP) minus the direct measurement of esophageal Pressure and by the release method. Results The mean elastance- and release-derived Transpulmonary Pressure were 14.4 ± 3.7 and 14.4 ± 3.8 cmH_2O at 5 cmH_2O of PEEP and 21.8 ± 5.1 and 21.8 ± 4.9 cmH_2O at 15 cmH_2O of PEEP, respectively ( P = 0.32, P = 0.98, respectively), indicating that these parameters were significantly related ( r ^2 = 0.98, P < 0.001 at 5 cmH_2O of PEEP; r ^2 = 0.93, P < 0.001 at 15 cmH_2O of PEEP). The percentage error was 5.6 and 12.0 %, respectively. The mean directly measured and release-derived Transpulmonary Pressure were −8.0 ± 3.8 and 3.9 ± 0.9 cmH_2O at 5 cmH_2O of PEEP and −1.2 ± 3.2 and 10.6 ± 2.2 cmH_2O at 15 cmH_2O of PEEP, respectively, indicating that these parameters were not related ( r ^2 = 0.07, P = 0.08 at 5 cmH_2O of PEEP; r ^2 = 0.10, P = 0.53 at 15 cmH_2O of PEEP). Conclusions Based on our observations, elastance-derived Transpulmonary Pressure can be considered to be an adequate surrogate of the release-derived Transpulmonary Pressure, while the release-derived and directly measured end-expiratory Transpulmonary Pressure are not related.
-
The assessment of Transpulmonary Pressure in mechanically ventilated ARDS patients
Intensive care medicine, 2014Co-Authors: Davide Chiumello, Giovanni Babini, Matteo Brioni, Francesco Crimella, Massimo Cressoni, Stefan Lundin, Ola Stenqvist, Andrea Colombo, Luciano GattinoniAbstract:Purpose The optimal method for estimating Transpulmonary Pressure (i.e. the fraction of the airway Pressure transmitted to the lung) has not yet been established.
-
ECMO criteria for influenza A (H1N1)-associated ARDS: role of Transpulmonary Pressure
Intensive care medicine, 2012Co-Authors: Salvatore Grasso, Pierpaolo Terragni, Alberto Birocco, Rosario Urbino, Lorenzo Del Sorbo, Claudia Filippini, Luciana Mascia, Antonio Pesenti, Alberto Zangrillo, Luciano GattinoniAbstract:To assess whether partitioning the elastance of the respiratory system (E RS) between lung (E L) and chest wall (E CW) elastance in order to target values of end-inspiratory Transpulmonary Pressure (PPLATL) close to its upper physiological limit (25 cmH2O) may optimize oxygenation allowing conventional treatment in patients with influenza A (H1N1)-associated ARDS referred for extracorporeal membrane oxygenation (ECMO). Prospective data collection of patients with influenza A (H1N1)-associated ARDS referred for ECMO (October 2009–January 2010). Esophageal Pressure was used to (a) partition respiratory mechanics between lung and chest wall, (b) titrate positive end-expiratory Pressure (PEEP) to target the upper physiological limit of PPLATL (25 cmH2O). Fourteen patients were referred for ECMO. In seven patients PPLATL was 27.2 ± 1.2 cmH2O; all these patients underwent ECMO. In the other seven patients, PPLATL was 16.6 ± 2.9 cmH2O. Raising PEEP (from 17.9 ± 1.2 to 22.3 ± 1.4 cmH2O, P = 0.0001) to approach the upper physiological limit of Transpulmonary Pressure (PPLATL = 25.3 ± 1.7 cm H2O) improved oxygenation index (from 37.4 ± 3.7 to 16.5 ± 1.4, P = 0.0001) allowing patients to be treated with conventional ventilation. Abnormalities of chest wall mechanics may be present in some patients with influenza A (H1N1)-associated ARDS. These abnormalities may not be inferred from measurements of end-inspiratory plateau Pressure of the respiratory system (PPLATRS). In these patients, titrating PEEP to PPLATRS may overestimate the incidence of hypoxemia refractory to conventional ventilation leading to inappropriate use of ECMO.
Takeshi Yoshida - One of the best experts on this subject based on the ideXlab platform.
-
Esophageal Manometry and Regional Transpulmonary Pressure in Lung Injury
American journal of respiratory and critical care medicine, 2018Co-Authors: Takeshi Yoshida, Marcelo B. P. Amato, Domenico Luca Grieco, Lu Chen, Cristhiano A. S. Lima, Rollin Roldan, Caio C. A. Morais, Susimeire Gomes, Eduardo L. V. Costa, Paulo Francisco Guerreiro CardosoAbstract:Rationale: Esophageal manometry is the clinically available method to estimate pleural Pressure, thus enabling calculation of Transpulmonary Pressure (Pl). However, many concerns make it uncertain ...
-
Volume-controlled Ventilation Does Not Prevent Injurious Inflation during Spontaneous Effort
American journal of respiratory and critical care medicine, 2017Co-Authors: Takeshi Yoshida, Rollin Roldan, Susimeire Gomes, Vinicius Torsani, Akinori Uchiyama, Susumu Nakahashi, M.a.m. Nakamura, Yukiko Koyama, Roberta R. De Santis, Marcelo B. P. AmatoAbstract:Rationale: Spontaneous breathing during mechanical ventilation increases Transpulmonary Pressure and Vt, and worsens lung injury. Intuitively, controlling Vt and Transpulmonary Pressure might limit injury caused by added spontaneous effort.Objectives: To test the hypothesis that, during spontaneous effort in injured lungs, limitation of Vt and Transpulmonary Pressure by volume-controlled ventilation results in less injurious patterns of inflation.Methods: Dynamic computed tomography was used to determine patterns of regional inflation in rabbits with injured lungs during volume-controlled or Pressure-controlled ventilation. Transpulmonary Pressure was estimated by using esophageal balloon manometry [Pl(es)] with and without spontaneous effort. Local dependent lung stress was estimated as the swing (inspiratory change) in Transpulmonary Pressure measured by intrapleural manometry in dependent lung and was compared with the swing in Pl(es). Electrical impedance tomography was performed to evaluate the infla...
-
spontaneous breathing during lung protective ventilation in an experimental acute lung injury model high Transpulmonary Pressure associated with strong spontaneous breathing effort may worsen lung injury
Critical Care Medicine, 2012Co-Authors: Takeshi Yoshida, Akinori Uchiyama, Nariaki Matsuura, Takashi Mashimo, Yuji FujinoAbstract:Objective:We investigated whether potentially injurious Transpulmonary Pressure could be generated by strong spontaneous breathing and exacerbate lung injury even when plateau Pressure is limited to <30 cm H2O.Design:Prospective, randomized, animal study.Setting:University animal research laboratory
-
Spontaneous breathing during lung-protective ventilation in an experimental acute lung injury model: high Transpulmonary Pressure associated with strong spontaneous breathing effort may worsen lung injury.
Critical care medicine, 2012Co-Authors: Takeshi Yoshida, Akinori Uchiyama, Nariaki Matsuura, Takashi Mashimo, Yuji FujinoAbstract:Objective:We investigated whether potentially injurious Transpulmonary Pressure could be generated by strong spontaneous breathing and exacerbate lung injury even when plateau Pressure is limited to
Daniel Talmor - One of the best experts on this subject based on the ideXlab platform.
-
The Esophageal Pressure-Guided Ventilation 2 (EPVent2) trial protocol: a multicentre, randomised clinical trial of mechanical ventilation guided by Transpulmonary Pressure
BMJ open, 2014Co-Authors: Emily Fish, Todd Sarge, Stephen H. Loring, Victor Novack, Valerie Banner-goodspeed, Daniel TalmorAbstract:Introduction: Optimal ventilator management for patients with acute respiratory distress syndrome (ARDS) remains uncertain. Lower tidal volume ventilation appears to be beneficial, but optimal management of positive end-expiratory Pressure (PEEP) remains unclear. The Esophageal PressureGuided Ventilation 2 Trial (EPVent2) aims to examine the impact of mechanical ventilation directed at maintaining a positive Transpulmonary Pressure (PTP) in patients with moderate-to-severe ARDS. Methods and analysis: EPVent2 is a multicentre, prospective, randomised, phase II clinical trial testing the hypothesis that the use of a PTP-guided ventilation strategy will lead to improvement in composite outcomes of mortality and time off the ventilator at 28 days as compared with a high-PEEP control. This study will enrol 200 study participants from 11 hospitals across North America. The trial will utilise a primary composite end point that incorporates death and days off the ventilator at 28 days to test the primary hypothesis that adjusting ventilator Pressure to achieve positive PTP values will result in improved mortality and ventilator-free days.
-
Raising positive end-expiratory Pressures in ARDS to achieve a positive Transpulmonary Pressure does not cause hemodynamic compromise
Intensive care medicine, 2013Co-Authors: Todd Sarge, Stephen H. Loring, Maayan Yitsak-sade, Atul Malhotra, Victor Novack, Daniel TalmorAbstract:Intensive Care Med (2014) 40:126–128 DOI 10.1007/s00134-013-3127-1 Todd Sarge Stephen H. Loring Maayan Yitsak-Sade Atul Malhotra Victor Novack Daniel Talmor Raising positive end-expiratory Pressures in ARDS to achieve a positive Transpulmonary Pressure does not cause hemodynamic compromise Received: 24 September 2013 Accepted: 27 September 2013 Published online: 15 October 2013 O Springer-Verlag Berlin Heidelberg and ESICM 2013 Dear Editor, High positive end-expiratory Pressure (PEEP) is associated with improved survival in patients with moderate to severe acute respiratory distress syn- drome (ARDS) [1], but high PEEP has also been reported to cause right heart failure and hemodynamic com- promise [2]. In our previous trial of ventilator management in ARDS [3], setting PEEP to achieve a positive Transpulmonary Pressure estimated using esophageal manometry usually increased PEEP, often significantly, but also led to better blood oxygena- tion and respiratory compliance than the control PEEP. To determine whether such manipulations of PEEP degrade hemodynamic function, we LETTER performed a retrospective analysis of the 61 patients in the EPVent Trial, who were all ventilated to achieve a target range of arterial oxygenation after hemodynamic resuscitation by protocol [3]. Subjects in the inter- vention group had PEEP set to maintain oxygenation at a positive estimated Transpulmonary Pressure (P L = airway Pressure - esophageal Pressure), whereas those in the con- trol group had PEEP set according to a standard table based on oxygenation as in the ARDSNet low tidal volume trial [4]. Mean arterial Pressure (MAP), heart rate, central venous Pressure (CVP), vasopressor require- ments, fluid balance, and simplified organ failure assessment (SOFA) scores were analyzed for the 3 days following enrollment. The primary between-group comparison was MAP, and secondary comparisons were cardiovascular SOFA score, urine output, creatinine level, and length-of-stay fluid balance. Baseline characteristics and sever- ity of illness were similar between groups. PEEP and plateau Pressures were markedly higher in the inter- vention group (initial PEEP averaged 18.7 vs 11.0 cmH 2 O and plateau Pressure 31.4 vs 25.1 cmH 2 O in intervention and control groups, respectively) [3]. Nonetheless, hemodynamic vari- ables including MAP and cardiovascular SOFA score were similar between groups (Fig. 1). MAP improved slightly over the first 72 h in both groups (between-group P = 0.576), fluid balance was reduced toward zero in both groups (between-group P = 0.245), and urine output improved in both groups (between-group P = 0.701). The cardiovascular component of the SOFA score, fluid balance, creatinine levels, urine output, and MAP were compared between groups and tested by generalized estimating equations with adjustment for covariates. None was significantly affected by group assignment. Although limited by the small sample size, these results indicate that raising PEEP as part of a strategy to optimize Transpulmonary Pressure in adequately resuscitated patients does not result in detectable impairment in hemodynamics, organ function mea- sured by SOFA scores, fluid balance, or vasopressor requirement. With normal lungs, high alveolar Pressures in the absence of adequate volume expansion may compress pulmonary vasculature and increase pulmonary vascular resistance (PVR), reducing cardiac output and impairing right heart function [5]. However, in ARDS, low lung volume and atelec- tasis may also increase PVR. Under these circumstances, raising PEEP could recruit collapsed lung and lower PVR. In this way, raising PEEP to prevent both lung collapse and overdistension may improve the hemodynamic function. We conclude that in patients with ARDS, individualizing PEEP to optimize Transpulmonary Pressures using esophageal manometry does not compromise hemodynamic function. We are currently studying the
-
Targeting Transpulmonary Pressure to prevent ventilator induced lung injury.
Minerva anestesiologica, 2009Co-Authors: Todd Sarge, Daniel TalmorAbstract:Abstract Acute respiratory distress syndrome (ARDS) and ventilator induced lung injury (VILI) continue to challenge clinicians who care for the critically ill. Current research in ARDS has focused on ventilator strategies to improve the outcome for these patients. In this review, we emphasize the limitations of managing ventilators based on airway Pressures alone. Specifically, basic pulmonary mechanics including chest wall compliance and Transpulmonary Pressure are reviewed. This review suggests that perturbations in chest wall compliance and Transpulmonary Pressure may explain the lack of efficacy observed in recent clinical trials of ventilator management. We present a method for estimating pleural and Transpulmonary Pressures from esophageal manometry. Quantifying these variables and individualizing ventilator management based on individual patient physiology may be useful to intensive care clinicians who treat patients with ARDS.
Davide Chiumello - One of the best experts on this subject based on the ideXlab platform.
-
Interpretation of the Transpulmonary Pressure in the critically ill patient.
Annals of translational medicine, 2018Co-Authors: Michele Umbrello, Davide ChiumelloAbstract:Mechanical ventilation is a life-saving procedure, which takes over the function of the respiratory muscles while buying time for healing to take place. However, it can also promote or worsen lung injury, so that careful monitoring of respiratory mechanics is suggested to titrate the level of support and avoid injurious Pressures and volumes to develop. Standard monitoring includes flow, volume and airway Pressure (Paw). However, Paw represents the Pressure acting on the respiratory system as a whole, and does not allow to differentiate the part of Pressure that is spent di distend the chest wall. Moreover, if spontaneous breathing efforts are allowed, the Paw is the sum of that applied by the ventilator and that generated by the patient. As a consequence, monitoring of Paw has significant shortcomings. Assessment of esophageal Pressure (Pes), as a surrogate for pleural Pressure (Ppl), may allow the clinicians to discriminate between the elastic behaviour of the lung and the chest wall, and to calculate the degree of spontaneous respiratory effort. In the present review, the characteristics and limitations of airway and Transpulmonary Pressure monitoring will be presented; we will highlight the different assumptions underlying the various methods for measuring Transpulmonary Pressure (i.e., the elastance-derived and the release-derived method, and the direct measurement), as well as the potential application of Transpulmonary Pressure assessment during both controlled and spontaneous/assisted mechanical ventilation in critically ill patients.
-
Transpulmonary Pressure during high-frequency oscillation ventilation: Is it the culprit?
Annals of intensive care, 2016Co-Authors: Massimo Cressoni, Davide ChiumelloAbstract:High-frequency oscillation ventilation (HFOV) seems the perfect embodiment of the “open lung theory” as it suggests extremely low tidal volumes combined with very high mean airway Pressures. With disappointment clinical trials showed that the application of HFOV was associated with a decreased survival [1]. The culprit has not been identified, and a possible cause is the effect of increased intrathoracic Pressures on the right ventricle and very high intrathoracic Pressures which act as an obstacle to blood flow [1]. When a positive Pressure is applied to the respiratory system, it is spent in part to inflate the lung and in part to inflate the chest wall. The real distending force of the lung is the Transpulmonary Pressure (TP) which is the difference in Pressure between the pleural space and the alveolar units. As pleural Pressure cannot be directly measured, the esophageal Pressure is used as a surrogate.
-
Transpulmonary Pressure monitoring during mechanical ventilation: a bench-to-bedside review
Anaesthesiology Intensive Therapy, 2015Co-Authors: Cristina Mietto, Manu L N G Malbrain, Davide ChiumelloAbstract:Different ventilation strategies have been suggested in the past in patients with acute respiratory distress syndrome (ARDS). Airway Pressure monitoring alone is inadequate to assure optimal ventilatory support in ARDS patients. The assessment of Transpulmonary Pressure (PTP) can help clinicians to tailor mechanical ventilation to the individual patient needs. Transpulmonary Pressure monitoring, defined as airway Pressure (Paw) minus intrathoracic Pressure (ITP), provides essential information about chest wall mechanics and its effects on the respiratory system and lung mechanics. The positioning of an esophageal catheter is required to measure the esophageal Pressure (Peso), which is clinically used as a surrogate for ITP or pleural Pressure (Ppl), and calculates the Transpulmonary Pressure. The benefits of such a ventilation approach are avoiding excessive lung stress and individualizing the positive end-expiratory Pressure (PEEP) setting. The aim is to prevent over-distention of alveoli and the cyclic recruitment/derecruitment or shear stress of lung parenchyma, mechanisms associated with ventilator-induced lung injury (VILI). Knowledge of the real lung distending Pressure, i.e. the Transpulmonary Pressure, has shown to be useful in both controlled and assisted mechanical ventilation. In the latter ventilator modes, Peso measurement allows one to assess a patient's respiratory effort, patient-ventilator asynchrony, intrinsic PEEP and the calculation of work of breathing. Conditions that have an impact on Peso, such as abdominal hypertension, will also be discussed briefly.
-
The assessment of Transpulmonary Pressure in mechanically ventilated ARDS patients
Intensive Care Medicine, 2014Co-Authors: Davide Chiumello, Giovanni Babini, Matteo Brioni, Francesco Crimella, Massimo Cressoni, Stefan Lundin, Ola Stenqvist, Andrea Colombo, Luciano GattinoniAbstract:Purpose The optimal method for estimating Transpulmonary Pressure (i.e. the fraction of the airway Pressure transmitted to the lung) has not yet been established. Methods In this study on 44 patients with acute respiratory distress syndrome (ARDS), we computed the end-inspiratory Transpulmonary Pressure as the change in airway and esophageal Pressure from end-inspiration to atmospheric Pressure (i.e. release derived) and as the product of the end-inspiratory airway Pressure and the ratio of lung to respiratory system elastance (i.e. elastance derived). The end-expiratory Transpulmonary Pressure was estimated as the product of positive end-expiratory Pressure (PEEP) minus the direct measurement of esophageal Pressure and by the release method. Results The mean elastance- and release-derived Transpulmonary Pressure were 14.4 ± 3.7 and 14.4 ± 3.8 cmH_2O at 5 cmH_2O of PEEP and 21.8 ± 5.1 and 21.8 ± 4.9 cmH_2O at 15 cmH_2O of PEEP, respectively ( P = 0.32, P = 0.98, respectively), indicating that these parameters were significantly related ( r ^2 = 0.98, P < 0.001 at 5 cmH_2O of PEEP; r ^2 = 0.93, P < 0.001 at 15 cmH_2O of PEEP). The percentage error was 5.6 and 12.0 %, respectively. The mean directly measured and release-derived Transpulmonary Pressure were −8.0 ± 3.8 and 3.9 ± 0.9 cmH_2O at 5 cmH_2O of PEEP and −1.2 ± 3.2 and 10.6 ± 2.2 cmH_2O at 15 cmH_2O of PEEP, respectively, indicating that these parameters were not related ( r ^2 = 0.07, P = 0.08 at 5 cmH_2O of PEEP; r ^2 = 0.10, P = 0.53 at 15 cmH_2O of PEEP). Conclusions Based on our observations, elastance-derived Transpulmonary Pressure can be considered to be an adequate surrogate of the release-derived Transpulmonary Pressure, while the release-derived and directly measured end-expiratory Transpulmonary Pressure are not related.
-
The assessment of Transpulmonary Pressure in mechanically ventilated ARDS patients
Intensive care medicine, 2014Co-Authors: Davide Chiumello, Giovanni Babini, Matteo Brioni, Francesco Crimella, Massimo Cressoni, Stefan Lundin, Ola Stenqvist, Andrea Colombo, Luciano GattinoniAbstract:Purpose The optimal method for estimating Transpulmonary Pressure (i.e. the fraction of the airway Pressure transmitted to the lung) has not yet been established.
