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Transpulmonary pressure monitoring in critically ill patients: pros and cons

Abstract

The use of transpulmonary pressure monitoring based on measurement of esophageal pressure has contributed importantly to the personalization of mechanical ventilation based on respiratory pathophysiology in critically ill patients. However, esophageal pressure monitoring is still underused in the clinical practice. This technique allows partitioning of the respiratory mechanics between the lungs and the chest wall, provides information on lung recruitment and risk of barotrauma, and helps titrating mechanical ventilation settings in patients with respiratory failure. In assisted ventilation modes and during non-invasive respiratory support, esophageal pressure monitoring provides important information on the inspiratory effort and work of breathing. Nonetheless, several controversies persist on technical aspects, interpretation and clinical decision-making based on values derived from this monitoring technique. The aim of this review is to summarize the physiological bases of esophageal pressure monitoring, discussing the pros and cons of its clinical applications and different interpretations in critically ill patients undergoing invasive and non-invasive respiratory support.

Introduction

Transpulmonary pressure (PL) corresponds to the distending force (stress) applied to the lungs which results in their mechanical deformation (strain) [1]. Stress and strain are linked by a linear relationship in healthy subjects and in patients with acute respiratory distress syndrome (ARDS), namely \(stress=k \bullet strain\), where k is specific elastance [2]. The correct physiological definition of transpulmonary pressure is \({P}_{L}={P}_{ALV}-{P}_{pl}\), where PALV is the alveolar pressure and Ppl is the pleural pressure. While PALV equals the airway pressure (PAW) under static conditions at end-inspiration or end-expiration, Ppl requires indirect estimation. Due to the anatomical position of the esophagus in the pleural space, esophageal pressure (Pes) represents a surrogate of the Ppl [1, 3]: therefore, in the clinical practice, transpulmonary pressure can be estimated as \({P}_{L}={P}_{AW}-{P}_{es}\). The use of such approximation has contributed importantly to the knowledge of the respiratory pathophysiology in critically ill patients and individualization of mechanical ventilation [4]. The use of esophageal balloons to measure Pes requires expertise and the correct interpretation of Pes-derived transpulmonary pressure warrants deep understanding of the assumptions underlying the use of Pes as an estimate of Ppl. Possibly as a consequence of this complexity, esophageal pressure monitoring is still underused in the clinical practice [1] and less than 1% of patients with ARDS received this monitoring tool in a recent large international observational study [5].

The aim of this review is to summarize the physiological bases of esophageal pressure monitoring, discussing the pros and cons of its clinical applications and different interpretations in critically ill patients undergoing non-invasive and invasive respiratory support.

Determinants of esophageal pressure

In the upright position, esophageal pressure changes reflect accurately the overall changes occurring in pleural pressure applied to the lungs’ surface at a specific site [6]. However, in the supine position, several factors may influence the value of pressure measured inside the esophagus using an air-filled balloon. Among them, the most important determinants of Pes are the following: chest wall elastance, the height of the chest wall, the distension of the abdomen pushing the diaphragm upwards and the weight of mediastinal organs lying above the esophageal balloon [7]. Moreover, the elastance of the esophageal wall, the reaction of smooth musculature to the presence of the balloon and the elastance of the esophageal balloon itself affect the measurement, while the transmission of cardiac contractions introduces artifacts which may further complicate the interpretation of Ppl.

Despite these known limitations, correct placement of the device allows an acceptable estimation of Ppl changes also in the supine position, with a good correlation with the pressure measured directly in the middle pleural space shown in experimental studies [8, 9]. Changes in body postures have been applied in a study in healthy subjects to estimate the influence of mediastinal and lung weight on Pes, which resulted in a mean of 3 cmH2O [10]. If not accounted for, this additional pressure results in slight overestimation of the Ppl, thus underestimation of the PL, in the dependent lung regions and in slight underestimation of the Ppl, thus overestimation of the PL, in the most non-dependent lung regions. Moreover, esophageal balloons are often placed in patients requiring enteral feeding, however, the presence of a nasogastric tube does not alter significantly the measurement of Pes [11], and the industry has made available catheters combining the function of a nasogastric tube and an esophageal pressure probe [12].

Esophageal balloon positioning

The pressure inside the esophagus varies along its axis. Pressure is irregular in different portions of the esophagus as assessed using multi-probe high resolution manometry [13]. Nonetheless, all studies in respiratory physiology focused on measurements performed in the distal third of the esophagus: correct placement of the probe is therefore crucial. However, a study comparing middle (20–35 cm from the mouth) versus distal (40–45 cm from the mouth) esophageal probe positioning showed minimal influence on estimates of PL [14], suggesting that a certain margin of flexibility can be accepted. The presence of cardiac pulse artifacts further confirms the positioning in the lower esophageal third. Certain manufacturers of esophageal balloons inserted a radio-opaque marker to allow radiological confirmation of the correct positioning [12]. In addition to correct positioning, adequate inflation volume of the probe is key to correct interpretation of esophageal pressure.

Esophageal balloon inflation

Most esophageal probes manufacturers suggest inflating the balloon with a fixed amount of air, in a range from 0.5 to 4 ml, according to the size and elastic properties of the device. However, technical characteristics of the balloon such as diameter, size, material and compliance of the cuff affect the transmission of pressure changes in the chest wall to the balloon according to its inflation volume [15]. Several authors suggest titrating volume inflation individually. In fact, under-filling would result in minimal cardiac artefacts [16] but under-estimation of both baseline Pes and Pes swings during tidal breathing, while over-filling would over-estimate Pes [17]. An optimal inflation should be aimed at maintaining the ratio of changes of the Pes and Paw closest to 1 during an airway occlusion test [18], while other experts suggested inflating it in order to remain in the linear part of the esophageal balloon pressure–volume curve while maximizing the difference between Pes,end-inspiratory and Pes,end-expiratory [15]. Since most balloons are connected to the ventilator auxiliary port or dedicated monitoring system through a three-way stopcock and a tube, air leaks may occur: balloon filling should be checked periodically to ensure quality of measurements. To reduce transmission of cardiac noise and to minimize the risk of leaks, liquid-filling of balloons has been proposed [19], but seldom used in the clinical practice.

Occlusion maneuvers to confirm positioning and inflation

As discussed above, positioning and inflation of the balloon both influence the Pes. Correct positioning and filling can be checked using an occlusion test: when the airway is occluded at end-expiration, changes in Ppl are transmitted to the airway through the lungs. During occlusion, the changes of Pes (ΔPes) equal the changes of the Paw (ΔPaw), thus their ratio should be 1 (ΔPes/ ΔPaw = 1) [18], assuming that Ppl = Pes. A tolerance of 10% or 20% is normally considered acceptable, corresponding to ΔPes/ ΔPaw from 0.9 to 1.1 or from 0.8 to 1.2, respectively. In spontaneously breathing patients, airway pressure changes assessed during the occlusion test correspond to the negative Pes swings due to the isometric inspiratory efforts (Fig. 1). In sedated passive patients, pressure changes must be induced with gentle external chest compressions (Fig. 2), sufficient to generate a safe but measurable ΔPaw, typically values between 5 and 15 cmH2O are aimed for. When ΔPaw and ΔPes are equal, their difference, namely the ΔPL, is zero. In modern ventilators and monitors able to plot the PL tracing in real-time (green plots in Figs. 1 and 2), verifying that PL remains constant during inspiratory efforts or chest compressions at the occlusion test further confirms the correct positioning and inflation of the balloon. Figures 1 and 2 illustrate these concepts and propose an algorithm for assessment of balloon positioning and filling. It must be stressed that aiming for a specific range of acceptability of the ratio between when ΔPes and ΔPaw corresponds mathematically to the introduction of a systematic percent error of 10 to 20%. This has important implications especially in patients in which the calibration was performed with small changes in the ΔPes, namely those that are spontaneously breathing with a limited inspiratory effort or those in controlled ventilation in which chest compressions resulted in small changes of the ΔPes. In these subjects, while during the calibration the absolute differences between ΔPes and ΔPaw are limited, a 10–20% percent error may result in large absolute errors when high inspiratory pressures or elevated inspiratory efforts are generated during tidal breathing.

Fig. 1
figure 1

Occlusion test to confirm correct positioning and inflation of the esophageal balloon in an active patient receiving assisted ventilation. An end-expiratory occlusion is performed, during which negative deflections of the pleural (Pes) and airway (PAW) pressures are observed. During inspiratory efforts, the transpulmonary pressure (PL) remains stable

Fig. 2
figure 2

Occlusion test to confirm correct positioning and inflation of the esophageal balloon in a sedated patient without spontaneous breathing activity receiving controlled ventilation. An end-expiratory occlusion is performed, and gentle external chest compressions are delivered. Positive swings of the pleural (Pes) and airway (PAW) pressures reflect the increase in intrathoracic pressure due to the external compressions. During the occlusion maneuver, the transpulmonary pressure (PL) remains stable

Interpretation of esophageal pressure in controlled ventilation

Once ensured the correct positioning and inflation of the esophageal balloon, further reasoning and computations are necessary to use it as a tool to titrate mechanical ventilation settings.

Absolute values and partitioning of respiratory mechanics

The simplest application of esophageal pressure monitoring in passive mechanically ventilated patients is the partitioning of the respiratory system elastance (Ers) in its two components: lung elastance (EL) and chest wall elastance (Ecw) [1, 3, 20]. Elastance is defined as the ratio between pressure changes and volume changes, is measured in cmH2O/L and is the reciprocal of compliance (C), thus E = 1/C. Elastance has additive properties, therefore Ers = EL + Ecw and since volume changes of the lungs are reflected by equal volume changes of the chest wall due to their anatomical contiguity, such property translates to the driving pressure (ΔP), namely the difference between end-inspiratory and end-expiratory pressure during tidal breathing. Therefore ΔPrs = ΔPL + ΔPcw, where ΔPcw equals the driving esophageal pressure (ΔPes). As illustrated in Fig. 3, at equal plateau pressures measured at the ventilator, a patient with increased Ecw will have lower end-inspiratory transpulmonary pressure and correspondingly a lower lung strain. This is the pathophysiological basis of the concept that higher airway plateau pressures could be tolerated in case of increased Ecw, such as in obese patients [21] or those with intraabdominal hypertension [22].

Fig. 3
figure 3

Airway pressure (top panels) and esophageal pressure (lower panels) of a patient with normal (left) or increased (right) chest wall elastance. At the same increased airway plateau and driving pressures (27 and 17 cmH2O, respectively), the resulting transpulmonary pressure at end-inspiration and the transpulmonary driving pressure is lower in the patient with increased chest wall elastance. The elastance ratio is reported, showing that in the left patient 76% of the total elastance is constituted by lung elastance, while only 24% in the patient on the right. PAW: airway pressure; Pes: esophageal pressure; PCW: pressure of the chest wall; PL: transpulmonary pressure; Pplat: plateau pressure; PEEP: positive end-expiratory pressure

Elastance-derived interpretation

The elastance-derived method proposes to use the ratio of the lung elastance to the total elastance (elastance ratio, EL/Ers) as a multiplicative correction factor to apply to pressures measured at the ventilator (Fig. 3) [23]. The EL/Ers ratio can be measured as (ΔPrs − ΔPes)/ΔPrs under passive conditions, and typically ranges from 0.5 or lower to 0.9 in critically ill patients with ARDS. It can be seen as the fraction of the airway pressure that is transmitted to the lungs. According to this method, inspiratory transpulmonary pressure is corrected as Pplat,elastance-derived = Pplat EL/Ers and has been shown to reflect accurately the regional transpulmonary pressure in the non-dependent regions [9]. This method has been extensively used by some research groups [24]; however, when used as guidance to set positive end-expiratory pressure (PEEP) it has poor agreement with methods relying on the absolute values of Pes [25].

PEEP-release method

To avoid the possible confounding factor of PEEP on the elastic properties of the chest wall, the PEEP-release method was proposed, based on the comparison of the transpulmonary pressure values during tidal breathing at PEEP with those obtained at zero end-expiratory pressure [2, 26]. Details on this calculation are provided in Fig. 4; as for the elastance-derived method, there is poor agreement between the values obtained with this method and those relying on absolute values of Pes.

Fig. 4
figure 4

Comparison between transpulmonary pressure computed based on absolute values and using the PEEP-release method. From an initial PEEP of 10 cmH2O a peep-release maneuver is performed to measure the value of the end-expiratory esophageal pressure at ZEEP. PAW: airway pressure; Pes: esophageal pressure; PL: transpulmonary pressure; Pplat: plateau pressure; PEEP: positive end-expiratory pressure; ZEEP: zero end-expiratory pressure

PEEP-step method

A research group proposed a method to estimate the transpulmonary pressure without an esophageal balloon, based on the measurement of the end-expiratory lung volume changes following an abrupt change in PEEP [27]. This method has been validated in an in-vitro model [28], but assumes implicitly that the end-expiratory transpulmonary pressure estimated with esophageal manometry is zero regardless of the applied PEEP level, which is contradicted by other clinical studies [29, 30].

Regional variability of pleural pressure and application of correction factors

An important determinant of the Ppl at the regional level is the presence of the hydrostatic pressure due to the weight of lung tissue and mediastinum lying above the level at which Ppl is measured [31, 32]. This results in a ventral to dorsal gradient of the Ppl in the supine position; as a consequence, Pes approximates accurately the Ppl only measured at the level corresponding to the position of the esophagus in the chest wall [9]. As illustrated in Fig. 5A, in healthy lungs the superimposed pressure in the most dorsal regions is around 3 cmH2O [33], therefore assuming that the esophagus lies in an intermediate position in the ventral-dorsal axis, the Ppl in the most ventral or dorsal regions could deviate from the measured Pes by ± 1.5 cmH2O, a negligible value in most clinical settings. In ARDS, the weight of the injured lungs increases this gradient when fully supine to an average value of 10 cmH2O [31] (Fig. 5B), therefore Ppl, dorsal ≈ Pes + 5 cmH2O and Ppl,ventral ≈ Pes − 5 cmH2O [9]. The superimposed pressure in ARDS is therefore in the same order of magnitude of pressure changes applied to titrate mechanical ventilation at the bedside, notably PEEP. This has practical consequences when using Pes to guide clinical decisions. In fact, titrating mechanical ventilation parameters including PEEP using the Pes as estimate of the average PL is equivalent to targeting the middle regions of the lungs. This may lead to airway pressures insufficient to fully recruit dorsal regions, but still resulting in hyperdistension in ventral regions.

Fig. 5
figure 5

Contribution of the superimposed pressure to the esophageal pressure in a healthy patient (A) and in one with ARDS (B). Esophageal pressure under-estimates the transpulmonary pressure in non-dependent regions while over-estimates that in the dorsal ones, especially in injured lungs. PAW: airway pressure; Pes: esophageal pressure; PL: transpulmonary pressure; Pplat: plateau pressure

PEEP titration based on end-expiratory transpulmonary pressure

The absolute end-expiratory transpulmonary pressure, when Pes is assumed equal to Ppl, is PL,end-exp = PEEPtot − Pes,end-exp. Its value in patients with ARDS typically ranges between − 10 to + 10 cmH2O and is influenced by PEEP [34] and positioning [35]. Negative values of PL,end-exp are associated with de-recruitment in dependent lung regions, as confirmed in studies based on electrical impedance tomography (EIT) [36]. A first randomized trial comparing a PEEP titration strategy aimed at maintaining strictly non-negative PL,end-exp showed improvement of oxygenation compared to a conventional low-PEEP/FiO2 table strategy [30]. However, this strategy was not superior to the conventional high-PEEP/FiO2 table in a larger randomized trial [37]. Nonetheless, a sub-study of the latter trial identified that titration of PEEP to PL,end-exp to near-zero values (± 2 cmH2O) was associated with improved mortality, whereas higher values could result in high static strain and higher mortality [38].

Use of transpulmonary pressure to assess the risk of VILI

Exposure of lung regions to excessively elevated inspiratory pressures is a major determinant of ventilator-induced lung injury (VILI) [39]. This risk is higher in non-dependent ventral regions that receive most ventilation in ARDS in the supine position during controlled ventilation in passive patients. At end-inspiration, the PL in the ventral lung is correctly estimated by the elastance-derived method or applying a correction of + 5 cmH2O on the absolute measurement of PL [9]; however, also the application of a fixed correction factor is simplistic, as its exact value depends on the severity of ARDS. To assess dynamic strain, the transpulmonary driving pressure (ΔPL) could be used, computed as PL,end-insp minus PL,end-exp.

Interpretation of esophageal pressure in assisted ventilation

The applications of esophageal pressure monitoring in actively breathing patients receiving invasive assisted ventilation require separate considerations. The activation of inspiratory muscles generates a negative deflection of the Ppl, the magnitude of this deflection is referred to as ΔPes (Fig. 6). This negative pressure is maintained for a certain amount of time, that is the neural inspiratory time, and initially is spent to activate the ventilator’s inspiratory trigger and to overcome intrinsic (auto) PEEP and inspiratory resistive forces, then it is released to allow end of inspiration and cycling. The pressure generated by inspiratory muscles is defined as \({P}_{mus}={P}_{CW,recoil}-{P}_{es}\), where Pcw,recoil represents the pressure that would have been generated in the chest wall by the same gas volume in absence of inspiratory effort (Fig. 6, blue line). The maximum inspiratory transpulmonary pressure is the difference between the inspiratory airway pressure and the minimum Pes during the inspiratory effort (Fig. 6, green arrow). In case of increased inspiratory drive, very high PL values could be reached when a highly negative Pes is added to the ventilator’s inspiratory pressure.

Fig. 6
figure 6

Computation of the pressure–time product (PTP) in two patients with equal magnitude of esophageal pressure swings (ΔPes) but short (left) versus prolonged (right) neural inspiratory time. When the inspiratory effort is initiated, the patient has first to overcome the intrinsic PEEP (PTPres, blue area, top panels), then the negative pressure is maintained for the duration of the neural inspiratory time (PTPinsp, yellow regions, top panels). The patient on the right, compared to that on the left, has an higher PTP at the same ΔPes. If the inspiratory effort is terminated before the end of the ventilator inspiratory time, the patient acts as a passive patient in the late phase of inspiration, when the esophageal pressure increases because of the ventilator inspiratory pressure (PTPvent). The slope of the recoil pressure is chest wall elastance; when this is not known, PTP can be approximated integrating the Pes instead of the Pmusc (simplified PTPinsp, lower panels). PAW: airway pressure; Pes: esophageal pressure; PL: transpulmonary pressure; PCW,recoil: pressure of the chest wall under passive conditions; PEEP: positive end-expiratory pressure

Assessment of inspiratory effort and work of breathing

When titrating respiratory support in assisted ventilation modes, clinicians should ideally target the work of breathing (WOB): low WOB may reflect over-assistance or over-sedation, while higher WOB may indicate under-assistance or excessive respiratory effort and risk of patient self-inflicted lung injury [40]. Nonetheless, computation of WOB is complex, as it is defined as the area of the inspiratory portion of the inspiratory muscle pressure (Pmus)—volume loop [3]. From a mathematical standpoint, this corresponds for each breath to:

$${WOB}_{breath}=\int\limits_{{T}_{insp}}{P}_{mus} dV$$

The WOB can be then expressed in Joules per liter of generated volume (\({{WOB}_{volume}=WOB}_{breath}/{V}_{T}\)) or per minute of ventilation (\({{WOB}_{minute}=WOB}_{breath}\bullet RR\)) [41]. A limitation of this definition of WOB is that any inspiratory effort not generating a tidal volume will be zero, leading to a misinterpretation of the role of ineffective inspiratory efforts and other asynchronies. Moreover, integration over a volume is a complex computation, therefore a surrogate based on integration over time is often used: the esophageal pressure–time product (\({PTP}_{es}=\int_{{T}_{insp}}{P}_{mus} dt\), see Fig. 6). The PTPes has been suggested to have a target range of 50 to 150 cmH2O·s [3] and can be calculated also for ineffective efforts. Still, computation of Pcw,recoil to obtain the Pmus requires knowing the ECW (slope of the blue line in Fig. 6), which cannot be easily measured in active patients. Even if ECW is measured in the same patient under passive conditions before initiation of assisted ventilation, it is unknown how ECW varies when sedation is reduced, or neuromuscular blockade withheld to allow spontaneous breathing. Most experimental studies computed the Pcw,recoil based on either the predicted value of ECW or assuming a fixed value of 5 cmH2O/L. The PTPes and WOB are correlated and provide a precise quantification of the strength of inspiratory muscle activity, and PTP is well correlated to the metabolic cost of breathing, namely oxygen consumption [42]. The use of ECW to account for the role of chest wall in inspiratory effort implies that the lung total volume is above the threshold point of the pressure–volume loop where the chest wall is in relaxation conditions [43]: this may not be the case in patients with respiratory failure with reduced total lung volume, thus questioning the routine use of the Pcw,recoil to measure the PTP in patients with ARDS. Thus, a further simplification consists in ignoring the Pcw,recoil when computing the PTPes (simplified PTPes, bottom panels in Fig. 6). Both the conventional and the simplified PTP are computed after off-line post-processing of respiratory tracings in the context of clinical research, with little to no application in the current clinical practice. The only measure that can be obtained in real-time at the bedside is the magnitude of esophageal pressure swings (ΔPes), which is a rough estimate of inspiratory effort. However, this could reflect inaccurately the WOB: the same ΔPes will result in different PTPes if applied for a short versus long neural inspiratory time (Fig. 6, left and right panels).

Esophageal pressure monitoring represents the reference method to measure of inspiratory muscle activity and driving transpulmonary inspiratory pressure. Due to its complexity, several alternative methods based on ventilator measurements not requiring the insertion of an esophageal balloon have been proposed to guide the level of respiratory assistance and weaning from mechanical ventilation. These include the airway occlusion pressure at 100 ms from onset of inspiration (P01) [44], end-inspiratory occlusion [45] and brief end-expiratory occlusion [46] tests.

Assessment of maximum inspiratory transpulmonary pressure

Most research on transpulmonary pressure monitoring in assisted ventilation focused on the quantification of respiratory effort. However, high inspiratory transpulmonary pressures can be achieved also during assisted breathing [40, 47]. Figure 6 illustrates two patients receiving assisted ventilation highlighting the maximum PL achieved during a respiratory cycle; since the end-expiratory PL can be different from 0, this does not necessarily correspond to the sum of ΔPes and ΔPaw (Fig. 6, top panels). Also without esophageal pressure monitoring, an end-inspiratory occlusion performed in a cooperative patient under relaxation conditions could provide an indirect estimate of the maximum inspiratory PL during tidal breathing [45].

Assessment of asynchronies

Unintended interactions between the patient respiratory muscle activity and the ventilator are referred to as patient-ventilator asynchronies and are associated with worse clinical outcomes in critically ill patients [48], even though a causal link between asynchronies and mortality has not been established. Esophageal pressure monitoring allows precise identification of the matching between patient efforts and respiratory acts delivered by the ventilator. While Pes can be considered a reference method for detection of asynchronies, visual inspection of ventilator curves by experienced clinicians identifies correctly most asynchronies [49].

Monitoring of asynchronies using esophageal pressure in active patients

Pros: Allows precise monitoring of all types of patient-ventilator asynchronies.

Cons: In most cases, asynchronies can be detected by visual inspection of flow-time and airway pressure–time curves on the ventilator.

Applications during non-invasive respiratory support

The same considerations discussed in active patients also apply to those receiving non-invasive respiratory support such as conventional or high-flow oxygen therapy, continuous positive airway pressure (CPAP) and bilevel non-invasive ventilation (NIV). In these circumstances, high inspiratory drive may be associated with increased risk of barotrauma [40] and need for endotracheal intubation [50, 51]. Nonetheless, assessing inspiratory effort in these patients is particularly difficult. In patients receiving oxygen therapy few parameters in addition to clinical examination can give rough estimates of the inspiratory effort, including respiratory rate, level of dyspnea, diaphragm ultrasound and nasal pressure swings [52, 53]. In patients receiving positive-pressure respiratory support through a ventilator and non-invasive interfaces such as masks or helmets, occlusion-derived maneuvers on the ventilator typically give unreliable information on the inspiratory effort due to the confounding effect of the interface volume and compliance [54]. Monitoring Pes provides unique information in this setting, but this remains a largely underexplored field as clinicians tend to be reluctant in inserting an esophageal balloon in an awake hypoxemic patient [55].

Conclusions

Transpulmonary pressure monitoring based on measurement of esophageal pressure substantially improved our knowledge of the pathophysiology and management of critically ill patients with respiratory failure. However, the physiology behind its interpretation is complex, and simplistic approaches have so far failed in enlarging the number of clinicians routinely using this technique. The availability of modern esophageal probes, ventilators and dedicated monitors makes this technique applicable in any modern intensive care unit. Despite the availability of alternative methods, the use of esophageal pressure monitoring should be encouraged in the clinical practice as it improves understanding of respiratory failure and personalization of mechanical ventilation in critically ill patients.

Availability of data and materials

Not applicable.

Code availability

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References

  1. Akoumianaki E, Maggiore SM, Valenza F, Bellani G, Jubran A, Loring SH, et al. The application of esophageal pressure measurement in patients with respiratory failure. Am J Respir Crit Care Med. 2014;189:520–31.

    Article  PubMed  Google Scholar 

  2. Chiumello D, Carlesso E, Cadringher P, Caironi P, Valenza F, Polli F, et al. Lung stress and strain during mechanical ventilation for acute respiratory distress syndrome. Am J Respir Crit Care Med. 2008;178:346–55.

    Article  PubMed  Google Scholar 

  3. Mauri T, Yoshida T, Bellani G, Goligher EC, Carteaux G, Rittayamai N, et al. Esophageal and transpulmonary pressure in the clinical setting: meaning, usefulness and perspectives. Intensive Care Med. 2016;42:1360–73.

    Article  PubMed  Google Scholar 

  4. Pelosi P, Ball L, Barbas CSV, Bellomo R, Burns KEA, Einav S, et al. Personalized mechanical ventilation in acute respiratory distress syndrome. Crit Care Lond Engl. 2021;25:250.

    Article  Google Scholar 

  5. Bellani G, Laffey JG, Pham T, Fan E, Brochard L, Esteban A, et al. Epidemiology, patterns of care, and mortality for patients with acute respiratory distress syndrome in intensive care units in 50 countries. JAMA. 2016;315:788–800.

    Article  CAS  PubMed  Google Scholar 

  6. Mead J, Gaensler EA. Esophageal and pleural pressures in man, upright and supine. J Appl Physiol. 1959;14:81–3.

    Article  CAS  PubMed  Google Scholar 

  7. Hedenstierna G. Esophageal pressure: benefit and limitations. Minerva Anestesiol. 2012;78:959–66.

    CAS  PubMed  Google Scholar 

  8. Pelosi P, Goldner M, McKibben A, Adams A, Eccher G, Caironi P, et al. Recruitment and derecruitment during acute respiratory failure: an experimental study. Am J Respir Crit Care Med. 2001;164:122–30.

    Article  CAS  PubMed  Google Scholar 

  9. Yoshida T, Amato MBP, Grieco DL, Chen L, Lima CAS, Roldan R, et al. Esophageal manometry and regional transpulmonary pressure in lung injury. Am J Respir Crit Care Med. 2018;197:1018–26.

    Article  PubMed  Google Scholar 

  10. Washko GR, O’Donnell CR, Loring SH. Volume-related and volume-independent effects of posture on esophageal and transpulmonary pressures in healthy subjects. J Appl Physiol. 2006;2006(100):753–8.

    Article  Google Scholar 

  11. Niknam J, Chandra A, Adams AB, Nahum A, Ravenscraft SA, Marini JJ. Effect of a nasogastric tube on esophageal pressure measurement in normal adults. Chest. 1994;106:137–41.

    Article  CAS  PubMed  Google Scholar 

  12. Chiumello D, Gallazzi E, Marino A, Berto V, Mietto C, Cesana B, et al. A validation study of a new nasogastric polyfunctional catheter. Intensive Care Med. 2011;37:791–5.

    Article  CAS  PubMed  Google Scholar 

  13. Persson P, Ahlstrand R, Gudmundsson M, de Leon A, Lundin S. Detailed measurements of oesophageal pressure during mechanical ventilation with an advanced high-resolution manometry catheter. Crit Care Lond Engl. 2019;23:217.

    Article  Google Scholar 

  14. Chiumello D, Consonni D, Coppola S, Froio S, Crimella F, Colombo A. The occlusion tests and end-expiratory esophageal pressure: measurements and comparison in controlled and assisted ventilation. Ann Intensive Care. 2016;6:13.

    Article  PubMed  PubMed Central  Google Scholar 

  15. Mojoli F, Iotti GA, Torriglia F, Pozzi M, Volta CA, Bianzina S, et al. In vivo calibration of esophageal pressure in the mechanically ventilated patient makes measurements reliable. Crit Care Lond Engl. 2016;20:98.

    Article  Google Scholar 

  16. Mojoli F, Chiumello D, Pozzi M, Algieri I, Bianzina S, Luoni S, et al. Esophageal pressure measurements under different conditions of intrathoracic pressure. An in vitro study of second generation balloon catheters. Minerva Anestesiol. 2015;81:855–64.

    CAS  PubMed  Google Scholar 

  17. Mojoli F, Torriglia F, Orlando A, Bianchi I, Arisi E, Pozzi M. Technical aspects of bedside respiratory monitoring of transpulmonary pressure. Ann Transl Med. 2018;6:377.

    Article  PubMed  PubMed Central  Google Scholar 

  18. Baydur A, Behrakis PK, Zin WA, Jaeger M, Milic-Emili J. A simple method for assessing the validity of the esophageal balloon technique. Am Rev Respir Dis. 1982;126:788–91.

    CAS  PubMed  Google Scholar 

  19. Beda A, Güldner A, Carvalho AR, Zin WA, Carvalho NC, Huhle R, et al. Liquid- and air-filled catheters without balloon as an alternative to the air-filled balloon catheter for measurement of esophageal pressure. PLoS ONE. 2014;9:e103057.

    Article  PubMed  PubMed Central  Google Scholar 

  20. Coppola S, Pozzi T, Gurgitano M, Liguori A, Duka E, Bichi F, et al. Radiological pattern in ARDS patients: partitioned respiratory mechanics, gas exchange and lung recruitability. Ann Intensive Care. 2021;11:78.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  21. Pelosi P, Croci M, Ravagnan I, Vicardi P, Gattinoni L. Total respiratory system, lung, and chest wall mechanics in sedated-paralyzed postoperative morbidly obese patients. Chest. 1996;109:144–51.

    Article  CAS  PubMed  Google Scholar 

  22. Regli A, Pelosi P, Malbrain MLNG. Ventilation in patients with intra-abdominal hypertension: what every critical care physician needs to know. Ann Intensive Care. 2019;9:52.

    Article  PubMed  PubMed Central  Google Scholar 

  23. Gattinoni L, Chiumello D, Carlesso E, Valenza F. Bench-to-bedside review: chest wall elastance in acute lung injury/acute respiratory distress syndrome patients. Crit Care. 2004;8:350.

    Article  PubMed  PubMed Central  Google Scholar 

  24. Gattinoni L, Marini JJ, Collino F, Maiolo G, Rapetti F, Tonetti T, et al. The future of mechanical ventilation: lessons from the present and the past. Crit Care. 2017;21:183.

    Article  PubMed  PubMed Central  Google Scholar 

  25. Gulati G, Novero A, Loring SH, Talmor D. Pleural pressure and optimal positive end-expiratory pressure based on esophageal pressure versus chest wall elastance: incompatible results*. Crit Care Med. 2013;41:1951–7.

    Article  PubMed  Google Scholar 

  26. Mietto C, Malbrain MLNG, Chiumello D. Transpulmonary pressure monitoring during mechanical ventilation: a bench-to-bedside review. Anaesthesiol Intensive Ther. 2015;47(Spec No):s27-37.

    Article  PubMed  Google Scholar 

  27. Stenqvist O, Lundin S. Lung elastance and transpulmonary pressure may be determined without using esophageal pressure measurements. Am J Respir Crit Care Med. 2014;190:120–120.

    Article  PubMed  Google Scholar 

  28. Persson P, Lundin S, Stenqvist O. Transpulmonary and pleural pressure in a respiratory system model with an elastic recoiling lung and an expanding chest wall. Intensive Care Med Exp. 2016;4:26.

    Article  PubMed  PubMed Central  Google Scholar 

  29. Chiumello D, Cressoni M, Colombo A, Babini G, Brioni M, Crimella F, et al. The assessment of transpulmonary pressure in mechanically ventilated ARDS patients. Intensive Care Med. 2014;40:1670–8.

    Article  PubMed  Google Scholar 

  30. Talmor D, Sarge T, Malhotra A, O’Donnell CR, Ritz R, Lisbon A, et al. Mechanical ventilation guided by esophageal pressure in acute lung injury. N Engl J Med. 2008;359:2095–104.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  31. Pelosi P, D’Andrea L, Vitale G, Pesenti A, Gattinoni L. Vertical gradient of regional lung inflation in adult respiratory distress syndrome. Am J Respir Crit Care Med. 1994;149:8–13.

    Article  CAS  PubMed  Google Scholar 

  32. Cressoni M, Chiumello D, Carlesso E, Chiurazzi C, Amini M, Brioni M, et al. Compressive forces and computed tomography-derived positive end-expiratory pressure in acute respiratory distress syndrome. Anesthesiology. 2014;121:572–81.

    Article  PubMed  Google Scholar 

  33. Cressoni M, Gallazzi E, Chiurazzi C, Marino A, Brioni M, Menga F, et al. Limits of normality of quantitative thoracic CT analysis. Crit Care Lond Engl. 2013;17:R93.

    Article  Google Scholar 

  34. Talmor D, Sarge T, O’Donnell CR, Ritz R, Malhotra A, Lisbon A, et al. Esophageal and transpulmonary pressures in acute respiratory failure. Crit Care Med. 2006;34:1389–94.

    Article  PubMed  PubMed Central  Google Scholar 

  35. Boesing C, Graf PT, Schmitt F, Thiel M, Pelosi P, Rocco PRM, et al. Effects of different positive end-expiratory pressure titration strategies during prone positioning in patients with acute respiratory distress syndrome: a prospective interventional study. Crit Care Lond Engl. 2022;26:82.

    Article  Google Scholar 

  36. Bikker IG, Blankman P, Specht P, Bakker J, Gommers D. Global and regional parameters to visualize the “best” PEEP during a PEEP trial in a porcine model with and without acute lung injury. Minerva Anestesiol. 2013;79:983–92.

    CAS  PubMed  Google Scholar 

  37. Beitler JR, Sarge T, Banner-Goodspeed VM, Gong MN, Cook D, Novack V, et al. Effect of titrating positive end-expiratory pressure (PEEP) with an esophageal pressure-guided strategy vs an empirical High PEEP-Fio2 strategy on death and days free from mechanical ventilation among patients with acute respiratory distress syndrome: a randomized clinical trial. JAMA. 2019;321:846–57.

    Article  PubMed  PubMed Central  Google Scholar 

  38. Sarge T, Baedorf-Kassis E, Banner-Goodspeed V, Novack V, Loring SH, Gong MN, et al. Effect of esophageal pressure-guided positive end-expiratory pressure on survival from acute respiratory distress syndrome: a risk-based and mechanistic reanalysis of the EPVent-2 trial. Am J Respir Crit Care Med. 2021;204:1153–63.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  39. Silva PL, Ball L, Rocco PRM, Pelosi P. Physiological and pathophysiological consequences of mechanical ventilation. Semin Respir Crit Care Med. 2022;43:321–34.

    Article  PubMed  Google Scholar 

  40. Battaglini D, Robba C, Ball L, Silva PL, Cruz FF, Pelosi P, et al. Noninvasive respiratory support and patient self-inflicted lung injury in COVID-19: a narrative review. Br J Anaesth. 2021;127:353–64.

    Article  CAS  PubMed  Google Scholar 

  41. Carteaux G, Mancebo J, Mercat A, Dellamonica J, Richard J-CM, Aguirre-Bermeo H, et al. Bedside adjustment of proportional assist ventilation to target a predefined range of respiratory effort. Crit Care Med. 2013;41:2125–32.

    Article  PubMed  Google Scholar 

  42. Field S, Sanci S, Grassino A. Respiratory muscle oxygen consumption estimated by the diaphragm pressure-time index. J Appl Physiol. 1984;57:44–51.

    Article  CAS  PubMed  Google Scholar 

  43. Cereda M. How does one evaluate and monitor respiratory function in the intensive care unit? Evid-Based Pract Crit Care. Elsevier; 2010 [cited 2022 Nov 27]. p. 3–10. https://linkinghub.elsevier.com/retrieve/pii/B9781416054764000018

  44. Beloncle F, Piquilloud L, Olivier P-Y, Vuillermoz A, Yvin E, Mercat A, et al. Accuracy of P0.1 measurements performed by ICU ventilators: a bench study. Ann Intensive Care. 2019;9:104.

    Article  PubMed  PubMed Central  Google Scholar 

  45. Foti G, Cereda M, Banfi G, Pelosi P, Fumagalli R, Pesenti A. End-inspiratory airway occlusion: a method to assess the pressure developed by inspiratory muscles in patients with acute lung injury undergoing pressure support. Am J Respir Crit Care Med. 1997;156:1210–6.

    Article  CAS  PubMed  Google Scholar 

  46. Bertoni M, Telias I, Urner M, Long M, Del Sorbo L, Fan E, et al. A novel non-invasive method to detect excessively high respiratory effort and dynamic transpulmonary driving pressure during mechanical ventilation. Crit Care Lond Engl. 2019;23:346.

    Article  Google Scholar 

  47. Bellani G, Grasselli G, Teggia-Droghi M, Mauri T, Coppadoro A, Brochard L, et al. Do spontaneous and mechanical breathing have similar effects on average transpulmonary and alveolar pressure? A clinical crossover study. Crit Care Lond Engl. 2016;20:142.

    Article  Google Scholar 

  48. Blanch L, Villagra A, Sales B, Montanya J, Lucangelo U, Luján M, et al. Asynchronies during mechanical ventilation are associated with mortality. Intensive Care Med. 2015;41:633–41.

    Article  PubMed  Google Scholar 

  49. Garofalo E, Bruni A, Pelaia C, Liparota L, Lombardo N, Longhini F, et al. Recognizing, quantifying and managing patient-ventilator asynchrony in invasive and noninvasive ventilation. Expert Rev Respir Med. 2018;12:557–67.

    Article  CAS  PubMed  Google Scholar 

  50. Tonelli R, Fantini R, Tabbì L, Castaniere I, Pisani L, Pellegrino MR, et al. Early inspiratory effort assessment by esophageal manometry predicts noninvasive ventilation outcome in de novo respiratory failure. A pilot study. Am J Respir Crit Care Med. 2020;202:558–67.

    Article  PubMed  PubMed Central  Google Scholar 

  51. Ball L, Robba C, Herrmann J, Gerard SE, Xin Y, Pigati M, et al. Early versus late intubation in COVID-19 patients failing helmet CPAP: a quantitative computed tomography study. Respir Physiol Neurobiol. 2022;301:103889.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  52. Pelosi P, Tonelli R, Torregiani C, Baratella E, Confalonieri M, Battaglini D, et al. Different methods to improve the monitoring of noninvasive respiratory support of patients with severe pneumonia/ARDS due to COVID-19: an update. J Clin Med. 2022;11:1704.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  53. Tonelli R, Cortegiani A, Marchioni A, Fantini R, Tabbì L, Castaniere I, et al. Nasal pressure swings as the measure of inspiratory effort in spontaneously breathing patients with de novo acute respiratory failure. Crit Care Lond Engl. 2022;26:70.

    Article  Google Scholar 

  54. Grieco DL, Maggiore SM, Roca O, Spinelli E, Patel BK, Thille AW, et al. Non-invasive ventilatory support and high-flow nasal oxygen as first-line treatment of acute hypoxemic respiratory failure and ARDS. Intensive Care Med. 2021;47:851–66.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  55. Tobin MJ, Jubran A, Laghi F. P-SILI as justification for intubation in COVID-19: readers as arbiters. Ann Intensive Care. 2020;10:156.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

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Ball, L., Talmor, D. & Pelosi, P. Transpulmonary pressure monitoring in critically ill patients: pros and cons. Crit Care 28, 177 (2024). https://doi.org/10.1186/s13054-024-04950-y

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