Transpulmonary driving pressure, without esophageal pressure measurements, instead of airway driving pressure.
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ABSTRACT:
SUBMITTER: Stenqvist O
PROVIDER: S-EPMC7498560 | biostudies-literature | 2020 Nov
REPOSITORIES: biostudies-literature
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Transpulmonary driving pressure, without esophageal pressure measurements, instead of airway driving pressure.
Intensive care medicine 20200918 11
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| S-EPMC10399046 | biostudies-literature
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| S-EPMC9710035 | biostudies-literature
Project description:BackgroundMechanical ventilation is applied to unload the respiratory muscles, but knowledge about transpulmonary driving pressure (ΔPL) is important to minimize lung injury. We propose a method to estimate ΔPL during neurally synchronized assisted ventilation, with a simple intervention of lowering the assist for one breath ("lower assist maneuver", LAM).MethodsIn 24 rabbits breathing spontaneously with imposed loads, titrations of increasing assist were performed, with two neurally synchronized modes: neurally adjusted ventilatory assist (NAVA) and neurally triggered pressure support (NPS). Two single LAM breaths (not sequentially, but independently) were performed at each level of assist by acutely setting the assist to zero cm H2O (NPS) or NAVA level 0 cm H2O/uV (NAVA) for one breath. NPS and NAVA titrations were followed by titrations in controlled-modes (volume control, VC and pressure control, PC), under neuro-muscular blockade. Breaths from the NAVA/NPS titrations were matched (for flow and volume) to VC or PC. Throughout all runs, we measured diaphragm electrical activity (Edi) and esophageal pressure (PES). We measured ΔPL during the spontaneous modes (PL_PES) and controlled mechanical ventilation (CMV) modes (PL_CMV) with the esophageal balloon. From the LAMs, we derived an estimation of ΔPL ("PL_LAM") using a correction factor (ratio of volume during the LAM and volume during assist) and compared it to measured ΔPL during passive (VC or PC) and spontaneous breathing (NAVA or NPS). A requirement for the LAM was similar Edi to the assisted breath.ResultsAll animals successfully underwent titrations and LAMs for NPS/NAVA. One thousand seven-hundred ninety-two (1792) breaths were matched to passive ventilation titrations (matched Vt, r = 0.99). PL_LAM demonstrated strong correlation with PL_CMV (r = 0.83), and PL_PES (r = 0.77). Bland-Altman analysis revealed little difference between the predicted PL_LAM and measured PL_CMV (Bias = 0.49 cm H2O and 1.96SD = 3.09 cm H2O). For PL_PES, the bias was 2.2 cm H2O and 1.96SD was 3.4 cm H2O. Analysis of Edi and PES at peak Edi showed progressively increasing uncoupling with increasing assist.ConclusionDuring synchronized mechanical ventilation, a LAM breath allows for estimations of transpulmonary driving pressure, without measuring PES, and follows a mathematical transfer function to describe respiratory muscle unloading during synchronized assist.
| S-EPMC10463600 | biostudies-literature
Project description:Mechanical forces are increasingly recognized as important determinants of cell and tissue phenotype and also appear to play a critical role in organ development. During the fetal stages of lung morphogenesis, the pressure of the fluid within the lumen of the airways is higher than that within the chest cavity, resulting in a positive transpulmonary pressure. Several congenital defects decrease or reverse transpulmonary pressure across the developing airways and are associated with a reduced number of branches and a correspondingly underdeveloped lung that is insufficient for gas exchange after birth. The small size of the early pseudoglandular stage lung and its relative inaccessibility in utero have precluded experimental investigation of the effects of transpulmonary pressure on early branching morphogenesis. Here, we present a simple culture model to explore the effects of negative transpulmonary pressure on development of the embryonic airways. We found that negative transpulmonary pressure decreases branching, and that it does so in part by altering the expression of fibroblast growth factor 10 (Fgf10). The morphogenesis of lungs maintained under negative transpulmonary pressure can be rescued by supplementing the culture medium with exogenous FGF10. These data suggest that Fgf10 expression is regulated by mechanical stress in the developing airways. Understanding the mechanical signaling pathways that connect transpulmonary pressure to FGF10 can lead to the establishment of novel non-surgical approaches for ameliorating congenital lung defects.
| S-EPMC8673560 | biostudies-literature
Project description:High-frequency oscillation (HFO) is used for the treatment of refractory hypoxic respiratory failure.To demonstrate that the mean transpulmonary pressure (PL) cannot be inferred from mean airway pressure (mPaw).In seven patients already undergoing HFO for refractory acute respiratory distress syndrome, esophageal pressure (Pes) was measured using an esophageal balloon catheter. Pleural pressure (Ppl) and PL were calculated from Pes.In the seven patients (mean [± SD] age 59 ± 9 years) treated with HFO at 5 ± 1 Hz and amplitude 75 ± 10 cmH2O, the mPaw was 27 ± 6 cmH2O, Ppl was 9 ± 6 cmH2O and PL was 18 ± 11 cmH2O. Successful catheter placement and measurement of Pes occurred in 100% of subjects. There was no correlation between PL and mPaw. The majority of subjects required hemodynamic support during the use of HFO; the frequency and degree of support during the study period was no different than that before the study.The present report is the first to describe measuring Pes and calculating Ppl during HFO for acute respiratory distress syndrome. While both current guidelines and recent trials have titrated treatment based on mPaw and oxygenation, there is wide variability in PL during HFO and PL cannot be predicted from mPaw.
| S-EPMC4128514 | biostudies-literature
Project description:BackgroundThere is a strong rationale for proposing transpulmonary pressure-guided protective ventilation in acute respiratory distress syndrome. The reference esophageal balloon catheter method requires complex in vivo calibration, expertise and specific material order. A simple, inexpensive, accurate and reproducible method of measuring esophageal pressure would greatly facilitate the measure of transpulmonary pressure to individualize protective ventilation in the intensive care unit.ResultsWe propose an air-filled esophageal catheter method without balloon, using a disposable catheter that allows reproducible esophageal pressure measurements. We use a 49-cm-long 10 Fr thin suction catheter, positioned in the lower-third of the esophagus and connected to an air-filled disposable blood pressure transducer bound to the monitor and pressurized by an air-filled infusion bag. Only simple calibration by zeroing the transducer to atmospheric pressure and unit conversion from mmHg to cmH2O are required. We compared our method with the reference balloon catheter both ex vivo, using pressure chambers, and in vivo, in 15 consecutive mechanically ventilated patients. Esophageal-to-airway pressure change ratios during the dynamic occlusion test were close to one (1.03 ± 0.19 and 1.00 ± 0.16 in the controlled and assisted modes, respectively), validating the proper esophageal positioning. The Bland-Altman analysis revealed no bias of our method compared with the reference and good precision for inspiratory, expiratory and delta esophageal pressure measurements in both the controlled (largest bias -0.5 cmH2O [95% confidence interval: -0.9; -0.1] cmH2O; largest limits of agreement -3.5 to 2.5 cmH2O) and assisted modes (largest bias -0.3 [-2.6; 2.0] cmH2O). We observed a good repeatability (intra-observer, intraclass correlation coefficient, ICC: 0.89 [0.79; 0.96]) and reproducibility (inter-observer ICC: 0.89 [0.76; 0.96]) of esophageal measurements. The direct comparison with pleural pressure in two patients and spectral analysis by Fourier transform confirmed the reliability of the air-filled catheter-derived esophageal pressure as an accurate surrogate of pleural pressure. A calculator for transpulmonary pressures is available online.ConclusionsWe propose a simple, minimally invasive, inexpensive and reproducible method for esophageal pressure monitoring with an air-filled esophageal catheter without balloon. It holds the promise of widespread bedside use of transpulmonary pressure-guided protective ventilation in ICU patients.
| S-EPMC8445653 | biostudies-literature
Project description:BackgroundAPRV has been used for ARDS in the past. Little is known about the risk of ventilator- induced lung- injury (VILI) in APRV vs. BIPAP in the management of in COVID19-associated ARDS (CARDS). This study aimed to compare transpulmonary pressures (TPP) in APRV vs. BIPAP in CARDS in regard to lung protective ventilator settings.MethodsThis retrospective, monocentric cohort study (ethical approval: 21-1553) assessed all adult ICU- patients with CARDS who were ventilated with BIPAP vs. APRV and monitored with TPP from 03/2020 to 10/2021. Ventilator-settings / -pressures, TPP, hemodynamic and arterial blood gas parameters were compared in both modes.Results20 non- spontaneously breathing patients could be included in the study: Median TPPendexpiratory was lower / negative in APRV (-1.20mbar; IQR - 4.88 / +4.53) vs. positive in BIPAP (+ 3.4mbar; IQR + 1.95 / +8.57; p < .01). Median TPPendinspiratory did not differ. In APRV, mean tidal- volume per body- weight (7.05 ± 1.28 vs. 5.03 ± 0.77 ml; p < .01) and mean airway- pressure (27.08 ± 1.67 vs. 22.68 ± 2.62mbar; p < .01) were higher. There was no difference in PEEP, peak-, plateau- or driving- pressure, compliance, oxygenation and CO2- removal between both modes.ConclusionDespite higher tidal- volumes / airway-pressures in APRV vs. BIPAP, TPPendinspiratory was not increased. However, in APRV median TPPendexpiratory was negative indicating an elevated risk of occult atelectasis in APRV- mode in CARDS. Therefore, TPP- monitoring could be a useful tool for monitoring a safe application of APRV- mode in CARDS.
| S-EPMC11786409 | biostudies-literature
Project description:BackgroundStress index at post-recruitment maneuvers could be a method of positive end-expiratory pressure (PEEP) titration in acute respiratory distress syndrome (ARDS) patients. However, airway pressure (Paw) stress index may not reflect lung mechanics in the patients with high chest wall elastance. This study was to evaluate the Pawstress index on lung mechanics and the correlation between Pawstress index and transpulmonary pressure (PL) stress index in acute respiratory failure (ARF) patients.MethodsTwenty-four ARF patients with mechanical ventilation (MV) were consecutively recruited from July 2011 to April 2013 in Zhongda Hospital, Nanjing, China and Ospedale S. Giovanni Battista-Molinette Hospital, Turin, Italy. All patients underwent MV with volume control (tidal volume 6 ml/kg) for 20 min. PEEP was set according to the ARDSnet study protocol. The patients were divided into two groups according to the chest wall elastance/respiratory system elastance ratio. The high elastance group (H group, n = 14) had a ratio ≥30%, and the low elastance group (L group, n = 10) had a ratio <30%. Respiratory elastance, gas-exchange, Pawstress index, and PLstress index were measured. Student's t-test, regression analysis, and Bland-Altman analysis were used for statistical analysis.ResultsPneumonia was the major cause of respiratory failure (71.0%). Compared with the L group, PEEP was lower in the H group (5.7 ± 1.7 cmH2O vs. 9.0 ± 2.3 cmH2O, P < 0.01). Compared with the H group, lung elastance was higher (20.0 ± 7.8 cmH2O/L vs. 11.6 ± 3.6 cmH2O/L, P < 0.01), and stress was higher in the L group (7.0 ± 1.9 vs. 4.9 ± 1.9, P = 0.02). A linear relationship was observed between the Pawstress index and the PLstress index in H group (R2 = 0.56, P < 0.01) and L group (R2 = 0.85, P < 0.01).ConclusionIn the ARF patients with MV, Pawstress index can substitute for PLto guide ventilator settings.Trial registrationClinicalTrials.gov NCT02196870 (https://clinicaltrials.gov/ct2/show/NCT02196870).
| S-EPMC4960953 | biostudies-literature
Project description:BackgroundLung-protective ventilation strategy suggests the use of low tidal volume, depending on ideal body weight, and adequate levels of PEEP. However, reducing tidal volume according to ideal body weight does not always prevent overstress and overstrain. On the contrary, titrating mechanical ventilation on airway driving pressure, computed as airway pressure changes from PEEP to end-inspiratory plateau pressure, equivalent to the ratio between the tidal volume and compliance of respiratory system, should better reflect lung injury. However, possible changes in chest wall elastance could affect the reliability of airway driving pressure. The aim of this study was to evaluate if airway driving pressure could accurately predict lung stress (the pressure generated into the lung due to PEEP and tidal volume).MethodsOne hundred and fifty ARDS patients were enrolled. At 5 and 15 cmH2O of PEEP, lung stress, driving pressure, lung and chest wall elastance were measured.ResultsThe applied tidal volume (mL/kg of ideal body weight) was not related to lung gas volume (r (2) = 0.0005 p = 0.772). Patients were divided according to an airway driving pressure lower and equal/higher than 15 cmH2O (the lower and higher airway driving pressure groups). At both PEEP levels, the higher airway driving pressure group had a significantly higher lung stress, respiratory system and lung elastance compared to the lower airway driving pressure group. Airway driving pressure was significantly related to lung stress (r (2) = 0.581 p < 0.0001 and r (2) = 0.353 p < 0.0001 at 5 and 15 cmH2O of PEEP). For a lung stress of 24 and 26 cmH2O, the optimal cutoff value for the airway driving pressure were 15.0 cmH2O (ROC AUC 0.85, 95 % CI = 0.782-0.922); and 16.7 (ROC AUC 0.84, 95 % CI = 0.742-0.936).ConclusionsAirway driving pressure can detect lung overstress with an acceptable accuracy. However, further studies are needed to establish if these limits could be used for ventilator settings.
| S-EPMC4993008 | biostudies-literature
Project description:Transpulmonary pressure (PL) is computed as the difference between airway pressure and pleural pressure and separates the pressure delivered to the lung from the one acting on chest wall and abdomen. Pleural pressure is measured as esophageal pressure (PES) through dedicated catheters provided with esophageal balloons. We discuss the role of PL in assessing the effects of mechanical ventilation in patients with acute respiratory distress syndrome (ARDS). In the supine position, directly measured PL represents the pressure acting on the alveoli and airways. Because there is a pressure gradient in the pleural space from the non-dependent to the dependent zones, the pressure in the esophagus probably represents the pressure at a mid-level between sternal and vertebral regions. For this reason, it has been proposed to set the end-expiratory pressure in order to get a positive value of PL. This improves oxygenation and compliance. PL can also be estimated from airway pressure plateau and the ratio of lung to respiratory elastance (elastance-derived method). Some data suggest that this latter calculation may better estimate PL in the nondependent lung zones, at risk for hyperinflation. Elastance-derived PL at end-inspiration (PLend-insp) may be a good surrogate of end-inspiratory lung stress for the "baby lung", at least in non-obese patients. Limiting end-inspiratory PL to 20-25 cmH2O appears physiologically sound to mitigate ventilator-induced lung injury (VILI). Last, lung driving pressure (∆PL) reflects the tidal distending pressure. Changes in PL may also be assessed during assisted breathing to take into account the additive effects of spontaneous breathing and mechanical breaths on lung distension. In summary, despite limitations, assessment of PL allows a deeper understanding of the risk of VILI and may potentially help tailor ventilator settings.
| S-EPMC5537111 | biostudies-other