Esophageal Pressure Monitoring During Mechanical Ventilation: Principles and Practice – A Comprehensive Review

2. Static and Dynamic Trans-pulmonary Pressure

During periods of no (or zero) airflow—achieved clinically with an inspiratory or expiratory hold maneuver—airway pressure (Paw) equilibrates with alveolar pressure (Palv). Under these static conditions, the pressure difference between the alveoli and the pleural space directly represents the static trans-pulmonary pressure (PL), defined as:

Plstatic=Palv−Ppl

This measurement reflects the true distending pressure of the lung parenchyma when resistive pressure components are absent, thereby providing a reliable index of alveolar stress at a given lung volume [12].

In contrast, during active airflow, Paw is influenced not only by the elastic recoil of the respiratory system but also by resistive pressure arising from gas flow through the conducting airways. In this context, the trans-pulmonary pressure is termed dynamic PL, and can be approximated as:

Pldynamic=Paw−Ppl

Here, Paw exceeds Palv by the amount of pressure needed to overcome airway resistance. Thus, dynamic PL incorporates both the elastic and resistive loads, making it dependent on flow conditions and inspiratory effort [12].

Clinically, differentiation between static and dynamic PL is essential:

• Static PL provides insight into alveolar distending pressure and the risk of over distension under set ventilatory conditions.
• Dynamic PL reflects the combined mechanical forces during tidal breathing and is useful for understanding the interaction of airflow, resistance, and patient effort with ventilator-delivered pressure.

Static PL, measured during no-flow conditions, isolates the elastic distending pressure of the lung, whereas dynamic PL, measured during airflow, integrates both resistive and elastic components. Together, they provide complementary perspectives on lung mechanics and ventilator-induced stress [12].

3. Stress, Strain, and Ventilator-Associated Lung Injury (VALI)

The concepts of stress and strain provide a mechanistic framework for understanding ventilator-induced lung injury.

• Stress refers to the distending force per unit area applied to lung tissue. Clinically, this is represented by the trans-pulmonary pressure (PL), which reflects the difference between alveolar and pleural pressures. It is the direct mechanical load experienced by the alveolar walls and interstitium during ventilation [13].
• Strain denotes the resultant deformation of the lung parenchyma, expressed as the ratio of the change in lung volume (ΔV) to the reference resting volume, usually the functional residual capacity (FRC). Thus, strain quantifies how much the lung is inflated relative to its baseline size, independent of absolute volume [13].

When stress and strain remain within physiological ranges, ventilation supports gas exchange without injury. However, excessive stress (over-distending pressure) or excessive strain (volumes far above FRC) can disrupt the structural integrity of alveolar–capillary units. This mechanical overload may lead to epithelial and endothelial cell injury, increased permeability pulmonary edema, biotrauma, with the release of inflammatory mediators and ultimately ventilator-associated lung injury (VALI). This underscore the rationale for monitoring pleural pressure [13].

Esophageal Pressure Monitoring

1. Esophageal pressure as a surrogate of Pleural Pressure

Early esophageal manometry began as a research tool to approximate pleural pressure, and is increasingly being used for lung-protective strategies in Acute respiratory distress syndrome (ARDS). Current adoption remains highest in academic and research ICUs. Barriers include training, setup/calibration time, and perceived complexity [14].

Direct measurement of pleural pressure (Ppl) in vivo is not routinely feasible at the bedside. Instead, esophageal pressure (Pes), obtained via a balloon catheter positioned in the mid-thoracic esophagus, has been established as a practical surrogate. The rationale for this approach is based on the anatomical location of the esophagus within the thoracic cavity, where it is exposed to the surrounding pleural space and thus experiences pressure changes that closely parallel pleural pressure [15].

Experimental and clinical studies have demonstrated a strong correlation between Pes and regional pleural pressure, particularly in the mid-thoracic region where gravitational and chest wall effects are relatively balanced. This makes Pes a valuable tool for estimating trans-pulmonary pressure (PL = Paw – Pes) and for guiding individualized ventilator management. However, limitations exist. The thoracic cavity is not a uniform pressure chamber; pleural pressures vary between dependent lung regions (where pressures tend to be more positive due to the weight of lung tissue and abdominal contents) and non-dependent regions (where pressures are relatively negative) [15]. This regional heterogeneity is especially pronounced in pathological states such as acute respiratory distress syndrome (ARDS), where alterations in compliance and regional collapse amplify the differences. Consequently, Pes represents an average or regional estimate of Ppl rather than an absolute measurement across the entire lung [16].

Despite these limitations, monitoring esophageal pressure provides a clinically relevant approximation of pleural pressure dynamics. When interpreted carefully, it offers unique insight into patient-specific respiratory mechanics, informs the calculation of trans-pulmonary pressures, and supports lung-protective ventilation strategies aimed at minimizing ventilator-associated lung injury (VALI).

2. Factors Influencing the Accuracy of Esophageal Pressure Monitoring

Although esophageal pressure (Pes) serves as a practical surrogate for pleural pressure (Ppl), its accuracy is subject to several technical and physiological considerations:

Balloon Positioning

Correct placement of the esophageal balloon catheter is critical. The most reliable measurements are obtained when the balloon lies in the mid-thoracic esophagus, posterior to the left atrium (retro-cardiac position). Malpositioning, such as placement too high in the cervical esophagus or too low in the gastric fundus, can introduce artifacts that distort the pressure signal [17].

Body Position and Mediastinal Weight

The esophagus is subject to external influences, particularly the weight of mediastinal structures and the heart, which can transmit additional pressure to the balloon. These effects vary with body position; for example, in the supine position, the retro cardiac location may exaggerate Pes readings, whereas lateral or prone positioning may alter pressure transmission differently [16].

Regional Heterogeneity of Pleural Pressure

Pleural pressure is not uniform across the lung. Dependent regions typically experience more positive pressures due to the weight of the lung and abdominal contents, while non-dependent regions are exposed to more negative pressures. In pathological conditions such as acute respiratory distress syndrome (ARDS), regional compliance differences and alveolar collapse further amplify this heterogeneity. Consequently, Pes provides an approximation of average pleural pressure, rather than a direct measure of pressures in all lung regions [15].

3. Contraindications to Esophageal Balloon Placement

The insertion of an esophageal balloon catheter carries similar contraindications to nasogastric tube placement [18]. Situations where the procedure should be avoided include:

• Esophageal varices, due to the risk of rupture and life-threatening hemorrhage.
• Coagulopathy, which increases the risk of bleeding from mucosal trauma.
• Severe facial or basilar skull fractures, where transnasal passage of the catheter may be hazardous [18].

In such cases, alternative approaches to estimate pleural pressure or guide ventilatory management should be considered.

4. Equipment and Catheters for Esophageal Pressure Monitoring

Accurate measurement of esophageal pressure (Pes) requires specialized catheters and monitoring equipment designed to optimize signal fidelity while minimizing patient risk. Several catheter systems are available, each with distinct advantages and limitations [19]:

Balloon Catheters

Traditional air-filled balloon catheters (e.g., Cooper, Nutrivent systems) remain the most commonly used devices. When properly inflated with a small, standardized volume of air, the balloon provides a compliant interface between the esophageal wall and the pressure transduction system. This minimizes the risk of mucosal apposition or occlusion, ensuring that the measured pressure reflects intrathoracic changes rather than localized wall contact [20,21].

Dual-Balloon Catheters

More advanced configurations incorporate two balloons, one positioned in the esophagus and the other in the stomach. This design enables simultaneous measurement of esophageal pressure (Pes) and gastric pressure (Pga), allowing calculation of trans-diaphragmatic pressure (Pdi = Pga – Pes). Such measurements are particularly valuable in evaluating diaphragmatic function and guiding ventilatory strategies in certain critically ill patients.

Microsensor Catheters

Catheters equipped with solid-state microsensors at their distal end provide faster response times and are less prone to signal dampening compared with balloon-based systems. However, they may be more susceptible to artifacts from direct wall contact or secretions, and their cost and fragility can limit widespread use in clinical practice.

Tubing and Transducer Systems

Regardless of catheter type, accurate signal acquisition depends on a rigid, non-compliant pressure transmission system. High-pressure tubing is typically used to connect the catheter to a pressure transducer, which interfaces with either a standard patient monitor or the auxiliary monitoring ports of a mechanical ventilator. Proper calibration and zeroing are essential to ensure valid pressure readings [19].

5. Technique: Insertion and Positioning

Esophageal balloon catheters can be introduced via the nasal or oral route, following a technique similar to nasogastric tube placement. The catheter is typically advanced to a depth of 50–60 cm, positioning the balloon first within the stomach. Correct gastric placement can be confirmed by performing an epigastric pressure test, in which gentle external compression of the epigastrium produces a synchronous rise in recorded pressure.

Once gastric placement is verified, the catheter is gradually withdrawn to a depth of approximately 35–45 cm, allowing the balloon to reside in the mid-thoracic esophagus. At this position, the tracing should display characteristic cardiac oscillations and respiratory pressure fluctuations, confirming its exposure to intrathoracic pressure dynamics [17].

Figure 3. Schematic illustration of optimal position of esophageal catheter. Suboptimal position can lead to artifacts or loss of signal. Too high in the esophagus as shown in this figure as “suboptimal position” can lead to falsely low pressures. Absence of cardiac oscillations may indicate a suboptimal position.

Figure 3. Schematic illustration of optimal position of esophageal catheter. Suboptimal position can lead to artifacts or loss of signal. Too high in the esophagus as shown in this figure as “suboptimal position” can lead to falsely low pressures. Absence of cardiac oscillations may indicate a suboptimal position.

Confirmation of Correct Positioning

Several methods are used to validate accurate balloon placement and ensure reliable Pes recordings:

Cardiac Oscillations

The presence of small rhythmic fluctuations on the esophageal pressure tracing, synchronous with the cardiac cycle, indicates appropriate retro cardiac positioning [17]. See Figure 3 for schematic illustration of optimal position of esophageal catheter.

Comparison with Airway Pressure Waveforms

Respiratory swings in Pes should closely mirror those in airway pressure (Paw), though with different absolute values, reflecting parallel changes in pleural and airway pressures during the respiratory cycle [19]. See Figure 4 for pressure swings with optimal placement. See Figure 5 for pressure swings with gastric pattern when the catheter is inappropriately positioned in the stomach.

Figure 4. Schematic illustration of Paw and Pes on pressure time scalar (Pressure on Y axis, time on x axis). Note that the Pes swings closely mirror the Paw swings. This indicates an optimal placement. Cardiac oscillations may be seen on the Pes curve, which is not illustrated here.(Please note the scale on the Y-axis has not been adjusted. This is for illustration purposes only).

Figure 4. Schematic illustration of Paw and Pes on pressure time scalar (Pressure on Y axis, time on x axis). Note that the Pes swings closely mirror the Paw swings. This indicates an optimal placement. Cardiac oscillations may be seen on the Pes curve, which is not illustrated here.(Please note the scale on the Y-axis has not been adjusted. This is for illustration purposes only).

Figure 5. Schematic illustration of Paw and Pes on pressure time scalar (Pressure on Y axis, time on x axis). Note that the Pes has high baseline and abdominal spikes can be seen which are induced by positive pressure ventilation. This is considered a gastric pattern and the catheter should be withdrawn 5 – 10 cm in graded steps. (Please note the scale on the Y-axis has not been adjusted. This is for illustration purposes only). .

Figure 5. Schematic illustration of Paw and Pes on pressure time scalar (Pressure on Y axis, time on x axis). Note that the Pes has high baseline and abdominal spikes can be seen which are induced by positive pressure ventilation. This is considered a gastric pattern and the catheter should be withdrawn 5 – 10 cm in graded steps. (Please note the scale on the Y-axis has not been adjusted. This is for illustration purposes only). .

Occlusion Test

The most rigorous validation method involves an airway occlusion maneuver. The airway is occluded during an inspiratory effort and ratio of the change in airway pressure (ΔPaw) to the change in esophageal pressure (ΔPes) is measured and should approximate 0.8 to 1.2. A ratio within this range confirms that Pes is accurately reflecting intrathoracic pressure changes. This maneuver can also be performed with gentle external thoracic compression to assess the consistency of pressure transmission [19].

Balloon Inflation and Calibration

Zeroing the System: Before inflation, the pressure monitoring system should be zeroed to atmospheric pressure, ensuring that subsequent readings reflect only physiological pressures

Accurate measurement of esophageal pressure (Pes) depends not only on correct catheter positioning but also on appropriate balloon inflation. Both under inflation and overinflation can distort the pressure signal, either by failing to maintain consistent balloon–wall contact or by transmitting balloon wall tension rather than intrathoracic pressure [22] .

Inflation and Deflation Protocol

The balloon is first fully inflated to eliminate any folds or wall apposition. It is then gradually deflated to a volume recommended by the manufacturer, termed the optimal balloon volume (Vbest). At this volume, the balloon is compliant enough to transmit surrounding pressure changes without introducing significant elastic recoil of its own.

• Cooper catheter: Typically inflated with 2 mL of air and then deflated to approximately 1.2 mL [20].
• Nutrivent catheter: Inflated with 4 mL of air and deflated to approximately 1.5 mL [21].

Definition of Vbest

Vbest is defined as the balloon volume at which the swing in esophageal pressure (ΔPes) is maximal and artifacts from balloon recoil or esophageal wall contact are minimal. At this point, the recorded Pes most accurately represents surrounding pleural pressure.

Selecting the correct balloon inflation volume is critical for obtaining valid Pes measurements. Overinflation risks overestimating pleural pressure due to balloon wall stiffness, whereas under inflation can lead to signal dampening and loss of fidelity. Thus, careful titration to Vbest is a fundamental step in ensuring reliable esophageal pressure monitoring [22]. See figure 6 for the compliance curve of the balloon to determine Vbest and how under inflation and overinflation affects the pressure reading.

Figure 6. Schematic illustration of compliance curve of esophageal balloon. Overinflation or under inflation can affect the pressure signal. The optimal volume of the balloon that transmit the signal with maximum amplitude is called “Vbest”.

Troubleshooting

Even when the catheter is correctly positioned and the balloon optimally inflated, artifacts and technical difficulties can compromise the reliability of esophageal pressure (Pes) measurements. Recognizing and addressing these issues is essential for obtaining physiologically valid data [19].See Figure-7 for a schematic illustration of normal Pes waveform on a simulated ventilator screen.

Prominent Cardiac Oscillations

Excessive cardiac-related pressure fluctuations may dominate the Pes tracing, obscuring respiratory pressure changes. This typically indicates balloon placement immediately posterior to the heart. Troubleshooting strategies include slight withdrawal or advancement of the catheter to relocate the balloon within the mid-thoracic esophagus, or repositioning the patient (e.g., modest changes such as head-of-bed elevation) to reduce mediastinal compression effects [17,23]. See Figure-8 for schematic illustration of prominent cardiac oscillation on Pes monitoring with absent respiratory swings.

Figure 7. Schematic illustration of normal Pes waveform on a simulated ventilator screen. Please note the airway swings seen on the esophageal pressure waveform (last line in the scalar figure) during controlled ventilation. Negative deflections if present indicate spontaneous breathing that may be seen in assisted or support ventilation, which are not seen in this ventilator screen. Image obtained from ventrainer module.

Figure 7. Schematic illustration of normal Pes waveform on a simulated ventilator screen. Please note the airway swings seen on the esophageal pressure waveform (last line in the scalar figure) during controlled ventilation. Negative deflections if present indicate spontaneous breathing that may be seen in assisted or support ventilation, which are not seen in this ventilator screen. Image obtained from ventrainer module.

Figure 8. Schematic illustration of prominent cardiac oscillation on Pes monitoring with absent respiratory swings. This requires reposition the patient such as elevation in the head of the bed or slight adjustment to the length of catheter.(Please note the scale on the Y-axis has not been adjusted. This is for illustration purposes only).

Figure 8. Schematic illustration of prominent cardiac oscillation on Pes monitoring with absent respiratory swings. This requires reposition the patient such as elevation in the head of the bed or slight adjustment to the length of catheter.(Please note the scale on the Y-axis has not been adjusted. This is for illustration purposes only).

Esophageal Spasm

Swallowing and spontaneous esophageal smooth muscle contraction may intermittently generate sharp, high amplitude non-respiratory pressure artifacts on the tracing. These are usually transient, but in some cases can persist even under deep sedation or neuromuscular blockade. A lack of correlation between Pes and Paw changes suggests an artifact. When present, clinicians must interpret Pes data cautiously and, if possible, repeat measurements at a later time when spasm subsides [17].

Loss of Signal

A sudden absence or dampening of pressure fluctuations suggests a circuit air leak, balloon leak, rupture, or migration out of the thoracic esophagus. Mediastinal weight or contact pressures may dampen or distort the signal, particularly in supine or obese patients. Signal drift can occur over time due to temperature, pressure equilibration, or catheter migration. In such cases, the integrity of the catheter should be checked, balloon inflation volume reverified, and the catheter repositioned if migration into the stomach or oropharynx is suspected. Replacement of the catheter may be required if equipment failure is confirmed [22]. See Figure 9 for the appearance of “loss of signal” on the Pes waveform, which could be seen with balloon rupture.

Prone positioning

Esophageal balloon mechanics may change with body orientation. After proning, the optimal balloon inflation volume (Vbest) should be re-established, and an occlusion test repeated to confirm accuracy [24].

Paralysis or sedation

Controlled conditions (no spontaneous effort) provide the most reliable measurements of end-expiratory (Plexp) and end-inspiratory (Plinsp) transpulmonary pressures. Any change in sedation or paralysis level warrants repeat calibration and verification [24,25].

In these cases, sometimes re-calibration and re-verification should be performed. Check the depth of insertion. Absence of cardiac oscillations and flat signals imply oropharyngeal placement indicating a too shallow placement, while a gastric pressure pattern (sharp rises with abdominal compression, high baseline) indicates migration below the diaphragm. Always re-zero the system and repeat an occlusion test (ΔPaw/ΔPes ratio 0.8–1.2) after changes in patient position, sedation, paralysis, or proning. Inflate to the manufacturer’s recommended maximum volume, then gradually deflate to the best-volume (Vbest)—the point at which Pes swings are maximal and free of artifact. Presence of cardiac oscillations in the Pes trace, and maintenance of the expected Pes–Paw relationships during occlusion holds, provide strong assurance of accuracy [26]. See Table 2 for various artifacts that may be seen during Pes monitoring and corrective strategies.

Summary of Technique:

Insertion and Positioning

1. Insert catheter nasally or orally to ~50–60 cm, confirming gastric placement via epigastric pressure test.

2. Withdraw to ~35–45 cm until cardiac oscillations and respiratory swings are visible.

3. Confirm position with:

• Cardiac oscillations
• Comparison of airway and esophageal pressure waveforms
• Occlusion test: ΔPaw/ΔPes ratio 0.8–1.2 (thoracic compression or inspiratory effort during occlusion).

Balloon Inflation

• Zero system to atmosphere.
• Fully inflate balloon, then gradually deflate to manufacturer-recommended volume (Vbest).
• Examples:
• Cooper: inflate 2 ml → deflate to 1.2 ml
• Nutrivent: inflate 4 ml → deflate to 1.5 ml
• Vbest defined as balloon volume yielding maximal ΔPes with minimal artifact.

Troubleshooting

• Large cardiac oscillations → reposition or slightly ramp patient.
• Esophageal spasm → transient artifact, sometimes refractory to paralysis.
• Loss of signal → balloon leak or migration.
• Prone position or Paralysis: may need recalibration.

See algorithm 1 for Summary of stepwise procedure of inserting esophageal catheter and verification.

Clinical Applications of Esophageal Pressure monitoring

Esophageal manometry has been proposed to have myriad of clinical applications during mechanical ventilation, the most important being lung and diaphragm protective ventilation. See Figure 10 for a various clinical applications of esophageal manometry.

1. Patient–Ventilator Dyssynchrony

Dyssynchrony is common in ARDS, particularly when lung mechanics are heterogeneous and patient drive is high. Airway pressure and flow alone often underestimate the problem. Esophageal manometry reveals inspiratory efforts, expiratory muscle activity, and the timing of neural vs. mechanical breaths and often improves detection and classification of dyssynchronies [27].

Double Triggering

Double triggering is a form of patient–ventilator asynchrony in which two consecutive ventilator-delivered breaths occur in response to a single, sustained patient inspiratory effort. Mechanistically, the initial negative Pes deflection represents the patient’s inspiratory effort, which successfully triggers a mechanical breath. However, when the patient’s inspiratory drive persists beyond the ventilator’s inspiratory cycle, a second trigger may occur, resulting in delivery of a subsequent tidal volume without an intervening exhalation. The consequence is breath stacking, in which two tidal volumes are superimposed. This phenomenon is readily identifiable on esophageal pressure (Pes) tracings as a large, prolonged negative swing, reflecting strong diaphragmatic contraction that outlasts the ventilator’s preset inspiratory time.

This pattern is clinically significant because it exposes the lung to excessive stress and strain. Volutrauma from delivery of stacked volumes that exceed the intended tidal volume, barotrauma due to elevated transpulmonary pressures, and potentially biotrauma, as overstretching promotes inflammatory mediator release.

Identification of double triggering via Pes monitoring underscores the value of esophageal pressure as a tool for detecting occult asynchronies. Recognition should prompt adjustment of ventilator settings—such as prolonging inspiratory time, modifying flow patterns, or optimizing sedation and analgesia—to better match ventilator support with patient effort, thereby reducing the risk of ventilator-induced lung injury (VILI) [27].

Reverse Triggering

Reverse triggering is a distinctive form of patient–ventilator asynchrony in which a passive, ventilator-initiated breath elicits a subsequent reflex diaphragmatic contraction. Unlike conventional triggering, in which patient effort initiates a mechanical breath, reverse triggering arises when lung inflation from the ventilator stimulates afferent mechanoreceptors, leading to delayed activation of the patient’s inspiratory muscles via neural reflex pathways. On esophageal pressure (Pes) monitoring, reverse triggering is characterized by an initial rise in airway pressure (Paw) from the passive ventilator breath, with no preceding negative deflection in Pes and a delayed negative swing in Pes that follows the ventilator insufflation, indicating diaphragmatic contraction after lung stretch rather than before it. This sequence reflects the ventilator entraining the patient’s neural respiratory activity, a phenomenon sometimes referred to as “ventilator-induced breathing” [28].

The clinical significance of reverse triggering lies in its potential to contribute to patient–ventilator dyssynchrony and ventilator-induced lung injury (VILI). Depending on the timing and intensity of the diaphragmatic effort, reverse triggering can augment tidal volume and increase transpulmonary pressure, raising the risk of volutrauma. Reverse triggering can generate eccentric diaphragmatic loading, as contraction occurs while the diaphragm is being stretched by the ventilator, potentially leading to muscle injury [28].

Recognition of reverse triggering requires careful waveform analysis, often facilitated by Pes monitoring, since conventional airway pressure and flow tracings may not reveal the underlying diaphragmatic activity. Identifying this pattern highlights the importance of integrating patient neural effort into ventilatory management and considering interventions such as adjusting ventilator mode, synchrony optimization, or, in selected cases, modifying sedation strategies [28].

Ineffective Effort

Ineffective effort is among the most common forms of patient–ventilator asynchrony, characterized by an inspiratory effort generated by the patient that fails to trigger a ventilator-assisted breath. On esophageal pressure (Pes) tracings, this appears as a negative deflection in Pes—reflecting diaphragmatic contraction and pleural pressure reduction—without a corresponding rise in airway pressure (Paw) or delivered tidal volume [29].

The pathophysiology of ineffective effort typically involves a mismatch between the timing of patient neural inspiration and ventilator trigger sensitivity. Contributing factors include:

• High levels of positive end-expiratory pressure (PEEP) or intrinsic PEEP (“auto-PEEP”), which impose an inspiratory threshold load that the patient cannot consistently overcome.
• Over-assistance or deep sedation, leading to reduced patient drive and delayed or insufficient inspiratory effort relative to the ventilator’s trigger window.
• Short inspiratory times or high cycling thresholds, resulting in early termination of mechanical inspiration and difficulty for the patient to reinitiate a breath.
• Muscle weakness or diaphragmatic dysfunction, where inspiratory force is inadequate to trigger the ventilator [29,30].

From a clinical standpoint, ineffective efforts are important because they may increase patient work of breathing, as inspiratory efforts fail to produce effective ventilation and contribute to dyssynchrony-related discomfort, manifesting as agitation or tachypnea. Since patient effort does not translate into alveolar ventilation, these are considered wasted efforts decreasing the ventilatory efficiency. Ineffective efforts may lead to diaphragmatic injury from repeated unassisted contractions against a closed system [30] .

Recognition with Pes monitoring is particularly valuable, as airway pressure and flow waveforms alone may obscure these “hidden” efforts. Once identified, management strategies include optimizing trigger sensitivity, adjusting PEEP to counteract intrinsic PEEP, titrating sedation, or modifying ventilator mode to improve synchrony.

Flow Starvation

Flow starvation is a patient–ventilator asynchrony that occurs when the inspiratory flow provided by the ventilator is insufficient to meet the patient’s inspiratory demand. This mismatch leads to increased patient effort and can be detected reliably through a combination of airway pressure (Paw) and esophageal pressure (Pes) monitoring. On the Paw waveform, flow starvation manifests as a concave or “scooped” appearance during inspiration, reflecting the patient’s vigorous attempt to draw in additional flow beyond what the ventilator is delivering. Simultaneously, the Pes tracing demonstrates a deep and exaggerated negative deflection, signifying heightened diaphragmatic contraction and increased inspiratory effort [31].

The underlying mechanisms include:

• Fixed inspiratory flow delivery in volume-controlled modes that is inadequate relative to patient demand.
• Excessively low flow settings or slow rise time in pressure-controlled or pressure-support modes, delaying the attainment of sufficient inspiratory pressure.
• Increased respiratory drive, such as in hypoxemia, hypercapnia, metabolic acidosis, or discomfort, amplifying the disparity between demand and supply [31].

The clinical implications of flow starvation are significant. Patients may experience increased work of breathing (WOB) and respiratory muscle load, which can predispose to fatigue, dyspnea and agitation, often prompting higher sedative or analgesic requirements if unrecognized. Eventually this may lead to asynchrony-related lung injury, since forceful inspiratory efforts may increase transpulmonary pressures, contributing to regional over distension and ventilator-induced lung injury (VILI) [30].

Identification through Pes monitoring is particularly valuable because it reveals the magnitude of patient effort that may not be evident on Paw and flow tracings alone. Management strategies include adjusting inspiratory flow rate, shortening rise time, modifying inspiratory pressure support, or switching to ventilatory modes that better match patient demand (e.g., proportional assist or neurally adjusted ventilatory assist) [30].

Cycling Asynchrony

Cycling asynchrony refers to a mismatch between the neural inspiratory time (the duration of the patient’s diaphragmatic effort) and the mechanical inspiratory time imposed by the ventilator. Esophageal pressure (Pes) monitoring provides a sensitive method to detect this phenomenon, as it directly reflects the timing and magnitude of patient inspiratory effort relative to ventilator-delivered support [32].

Premature Cycling

Premature cycling occurs when the ventilator terminates inspiration before the patient has completed their neural inspiratory effort. On Pes tracings, this is evident as a continued negative deflection beyond the point of ventilator cycling, indicating persistent diaphragmatic contraction without ongoing ventilatory assistance. Clinically, this leads to increased work of breathing (WOB) and dyspnea, as the patient continues inspiratory effort unassisted with the ventilator drive the ventilatory cycle feels truncated relative to their neural drive. This also can lead to Ineffective efforts, if the patient attempts to prolong inspiration by initiating another breath that fails to trigger. Common causes include short inspiratory times, high cycling thresholds, or low levels of pressure support [32].

Delayed Cycling

Delayed cycling occurs when the ventilator continues to deliver inspiratory flow after the patient’s neural inspiratory effort has ceased. On Pes tracings, this is recognized by a return of Pes toward baseline (signifying relaxation of the diaphragm) while Paw remains elevated due to ongoing ventilator insufflation. Consequences include dynamic hyperinflation, as late-phase insufflation may oppose the onset of passive exhalation. Increased expiratory muscle activity may be seen, as the patient recruits abdominal muscles to terminate inspiration. This often leads to discomfort, as mechanical breath timing is out of phase with neural effort. Delayed cycling is often caused by long inspiratory times, low cycling thresholds, or excessive pressure support [32].

Cycling asynchrony contributes to inefficient ventilation, increased patient effort, and potential risk of ventilator-induced lung injury (VILI) through excessive stress and strain. By aligning mechanical support with neural timing—as revealed by Pes monitoring—clinicians can optimize ventilatory synchrony. Adjustments may include modifying inspiratory time, altering cycling criteria, or using advanced ventilator modes (e.g., proportional assist ventilation or neurally adjusted ventilatory assist) that better match patient effort [30,32]. See Figure 11 for Identification of patient ventilator dyssynchrony via Pes waveform.

Normal assisted breath: The airway pressure increases almost simultaneously with the negative deflection of esophageal pressure.

Reverse triggering: On esophageal pressure (Pes) monitoring, reverse triggering is characterized by an initial rise in airway pressure (Paw) from the passive ventilator breath, with no preceding negative deflection in Pes and a delayed negative swing in Pes that follows the ventilator insufflation, indicating diaphragmatic contraction after lung stretch rather than before it

Flow starvation: On the Paw waveform, flow starvation typically manifests as a concave or “scooped” appearance during inspiration or blunted rise in airway pressure. Simultaneously, the Pes tracing demonstrates a deep and exaggerated negative deflection, signifying heightened diaphragmatic contraction and increased inspiratory effort reflecting the patient’s vigorous attempt to draw in additional flow beyond what the ventilator is delivering.

Double triggering: Esophageal pressure (Pes) tracings as a large, prolonged negative swing, reflecting strong diaphragmatic contraction that outlasts the ventilator’s preset inspiratory time, hence ventilator triggers the double breath.

Ineffective effort: On esophageal pressure (Pes) tracings, this appears as a negative deflection in Pes; reflecting diaphragmatic contraction, without a corresponding rise in airway pressure (Paw) or delivered tidal volume.

2. Detection of Dynamic Hyperinflation / Intrinsic PEEP

Dynamic hyperinflation, also termed intrinsic PEEP (PEEPi), arises when insufficient time is available for complete exhalation before the initiation of the next breath. This leads to air trapping, progressive increases in end-expiratory lung volume, and the development of a positive alveolar pressure that persists at end-expiration. It is most commonly encountered in patients with severe obstructive lung disease, such as COPD or asthma, where airflow limitation and prolonged expiratory time constants impair full lung emptying [33].

Airway pressure and flow tracings alone often fail to reveal PEEPi, particularly in assisted ventilation, because expiratory muscle activity can obscure evidence of incomplete exhalation. In such cases, standard techniques like end-expiratory occlusion may underestimate the true degree of dynamic hyperinflation [34].

Esophageal manometry provides a more direct means of detecting and quantifying PEEPi. During inspiration, a patient effort is reflected as a negative deflection in Pes, signifying diaphragmatic contraction and pleural pressure reduction. In the presence of PEEPi, no inspiratory flow occurs initially, because the patient’s inspiratory effort must first overcome the elevated alveolar pressure that persists at end-expiration. Flow begins only once the magnitude of the negative Pes swing exceeds the intrinsic threshold imposed by dynamic hyperinflation [34].

This allows clinicians to detect occult PEEPi that may not be evident on airway waveforms alone and quantify the inspiratory threshold load, defined as the amount of negative pressure the patient must generate to initiate airflow in the presence of hyperinflation [35].

Recognition of PEEPi at the bedside has important therapeutic consequences. Dynamic hyperinflation increases the work of breathing, contributes to dyspnea and ventilator asynchrony, and impairs venous return by elevating intrathoracic pressure. Through Pes monitoring, one can tailor ventilator strategies—such as prolonging expiratory time, adjusting external PEEP, or reducing respiratory rate—to minimize intrinsic PEEP and reduce patient burden [33,35,34]. See Figure 12 for detecting intrinsic PEEP using Pes waveform.

3. PEEP Titration

One of the most extensively validated clinical applications of esophageal pressure (Pes) monitoring is the optimization of positive end-expiratory pressure (PEEP) based on estimates of transpulmonary pressure (PL). Pes can decipher the lung parenchymal and pleural components contributing to the airway pressure, thus gives us a better understanding between the pressure required to distend the lung parenchyma versus that required to overcome chest wall elastance. This separation provides a more physiologically sound approach to ventilator management, particularly in patients with heterogeneous respiratory mechanics such as those with acute respiratory distress syndrome (ARDS) or obesity. PEEP titration using esophageal manometry is best guided by measuring transpulmonary pressure and titrating PEEP to a “set” target. As transpulmonary pressure is conceptually the lung distending pressure and the goal is to avoid alveolar collapse at the end of expiration and minimize over distension, certain targets can be defined [36,37].

End-Expiratory Transpulmonary Pressure (Plexp)

Plexp represents the pressure maintaining alveolar patency at the end of expiration. A negative PLexp suggests a tendency toward alveolar collapse, while an excessively positive PLexp risks dynamic tidal hyperinflation. Hence approximately Plexp of 0 to +2 cmH₂O, is just sufficient to keep alveoli open without overdistension [36].

End-Inspiratory Transpulmonary Pressure (Plinsp)

Plinsp reflects the distending pressure applied to lung tissue at peak inspiration. Excessive values predispose to overinflation, volutrauma, and ventilator-induced lung injury (VILI). Hence typically Plinsp is maintained at <15–20 cmH₂O [38].

Transpulmonary Driving Pressure (ΔPL):

Similar to driving pressure, transpulmonary driving pressure is defined as the difference between PLinsp and PLexp, representing the dynamic stress applied during tidal ventilation. Like driving pressure, this may be associated with lung injury risk and outcomes in ARDS. A clinical target of <10–12 cmH₂O is generally considered protective [39]. See Algorithm-2 for Proposed algorithm to titrate PEEP for lung protective ventilation in ARDS using esophageal manometry.

The use of esophageal pressure monitoring for PEEP titration is particularly useful in morbidly obese patients with ARDS. In patients with morbid obesity, airway pressures are often elevated due to reduced chest wall compliance. For instance, plateau pressures may appear dangerously high when measured solely from the airway. Without Pes monitoring, one might reduce PEEP to avoid perceived over distension. However, Pes monitoring may reveal that pleural pressure is also elevated, and thus the transpulmonary pressure is deceptively low or even negative at end-expiration (e.g., PLexp –5 cmH₂O) causing atelectrauma. Despite high Paw, the lungs remain prone to collapse, and higher—not lower—PEEP is required to achieve a safe transpulmonary distending pressure. In this context, Pes-guided titration provides a physiological rationale for maintaining higher PEEP levels to prevent atelectrauma, while still avoiding overdistension by monitoring PLinsp and ΔPL [40].

By tailoring PEEP to achieve “physiological” transpulmonary pressures, Pes monitoring allows clinicians to balance alveolar recruitment against the risk of overinflation, avoid under-recruitment in patients with high chest wall elastance and minimize both atelectrauma and volutrauma, reducing the risk of VILI [38].

This individualized approach underscores the value of Pes monitoring as a tool for precision mechanical ventilation, particularly in complex phenotypes such as obese patients with ARDS, chest wall injury, or abdominal hypertension.

Clinical Evidence for Esophageal Pressure–Guided PEEP Titration

The concept of using esophageal pressure (Pes) monitoring to titrate positive end-expiratory pressure (PEEP) has been evaluated in prospective randomized clinical trials. These studies aimed to determine whether tailoring ventilator settings to achieve physiologically appropriate transpulmonary pressures translates into improved outcomes in patients with acute respiratory distress syndrome (ARDS).

EPVent Trial (2008, Talmor et al.) [39]

The first Esophageal Pressure-Guided Ventilation (EPVent) trial was a single-center, randomized controlled study comparing conventional ARDSNet low-PEEP strategies with Pes-guided PEEP titration.

• Methodology: In the intervention arm, PEEP was adjusted to achieve a transpulmonary pressure at end-expiration (PLexp) of 0 to +2 cmH₂O, thereby preventing alveolar collapse.
• Findings: The Pes-guided group demonstrated:
• Improved oxygenation (higher PaO₂/FiO₂ ratios).
• Better respiratory system compliance.
• A trend toward reduced mortality, though not powered for survival as a primary endpoint.
• Significance: This trial provided proof-of-concept that Pes-guided PEEP titration could physiologically optimize ventilation and potentially improve clinical outcomes.

EPVent-2 Trial (2019, Beitler et al.) [40]

The EPVent-2 trial was a larger, multi center randomized controlled trial designed to validate and extend the findings of EPVent.

• Methodology: Patients with moderate-to-severe ARDS were randomized to Pes-guided PEEP titration (targeting PLexp 0–6 cmH₂O) versus a high-PEEP ARDSNet strategy.
• Findings:
• No significant difference in the primary outcome of 28-day mortality or ventilator-free days between groups.
• Both groups had similar safety profiles, with no excess of barotrauma or hemodynamic compromise.
• Oxygenation and compliance improvements observed in EPVent were not consistently replicated, possibly because the high-PEEP control arm already approximated physiologically appropriate PEEP levels.
• Significance: EPVent-2 suggested that while Pes-guided titration is safe, its benefit may be most pronounced compared with low-PEEP strategies, whereas its advantage over high-PEEP strategies is less clear. Patients in Pes guided PEEP required less rescue therapies and prone position was considered as a rescue therapy rather than a standard of care.

Taken together, these trials highlight that Pes-guided ventilation is feasible and safe in clinical practice. Pes guided PEEP titration may confer a benefit over traditional low-PEEP strategies by improving oxygenation and compliance. However does not clearly outperform high-PEEP strategies, which may already achieve similar physiological effects in many patients. While Pes guided PEEP titration has not been prospectively tested in patients with morbid obesity in these trials specifically, it may be a valuable tool for patients with high chest wall elastance or complex mechanics [39,40]. See Table 3 for comparison of two major trials involving esophageal pressure monitoring during mechanical ventilation in ARDS.

Table 3. Comparison of two major trials involving esophageal pressure monitoring during mechanical ventilation in ARDS.

6. Work of Breathing

The work of breathing (WOB) reflects the energy expenditure required to overcome the elastic and resistive loads of the respiratory system. It represents a critical determinant of both patient comfort and ventilatory adequacy. Precise quantification of WOB enables clinicians to evaluate whether ventilatory support is appropriately matched to patient demand, thereby preventing both fatigue and ventilator-induced complications [5].

An estimated normal WOB is approximately 0.3–0.6 J/L, indicating physiologically sustainable breathing in health. An excessive or unsustainable values exceeding 1.5 J/L denote a level of respiratory muscle load that is unlikely to be sustained, predisposing patients to fatigue, hypercapnia, and potential weaning failure [53].

Esophageal pressure (Pes) monitoring provides a unique means to calculate the pressure–time product of the esophageal pressure (PTPes), which integrates the magnitude and duration of inspiratory effort over time. Pressure time product is thought to strongly correlate with diaphragmatic oxygen consumption and energy expenditure, making it a physiologically robust measure of respiratory muscle workload and work of breathing [54,55].

PTPes (Pressure–Time Product of the Esophagus) [53]

Represents the integrated inspiratory load over time,

• Suggested target range: 60–150 cmH₂O·s/min.
• Low values indicate over-assist and underuse of respiratory muscles.
• High values (>200 cmH₂O·s/min) denote unsustainable loads, predictive of weaning failure and impending fatigue.

By providing an objective index of inspiratory effort, Pes-derived WOB and PTPes can guide the titration of proportional assist ventilation (PAV), neurally adjusted ventilatory assist (NAVA), or optimized levels of pressure support ventilation (PSV). These dynamic, patient-tailored strategies aim to maintain the patient’s effort within the “lung- and diaphragm-protective window”—ensuring sufficient respiratory drive to prevent atrophy, while avoiding injurious levels of strain that risk patient self-inflicted lung injury (P-SILI) [53,55].

7. Weaning from mechanical ventilation

Weaning failure often reflects a load–capacity imbalance, where the mechanical load imposed on the respiratory system exceeds the patient’s neuromuscular capacity. Conventional predictors, such as the rapid shallow breathing index (RSBI), provide only a crude snapshot of breathing pattern and do not directly quantify inspiratory effort or diaphragmatic workload. Esophageal pressure (Pes) monitoring addresses this gap by offering dynamic, physiologic indices that integrate both load and effort, thereby providing a more accurate assessment of readiness to wean. Pes-derived indices allows us to detect load–capacity imbalance during SBTs, even when conventional metrics appear reassuring. It can help us differentiate between respiratory muscle weakness and excessive ventilatory load, informing targeted therapy (e.g., adjusting PEEP, bronchodilation, or rehabilitation strategies) and ultimately guide timing of extubation, improving safety and reducing the risk of failure and potentially consider unloading strategies such as Non-invasive ventilation or heated high flow nasal cannula after extubation. A few Pes-derived indices are briefly mentioned for perusal [4,56,57].

Pes-Derived Indices

• ΔPes (Swing in Esophageal Pressure): Directly measures patient inspiratory effort during spontaneous breathing trials (SBTs). This is calculated as the difference between lowest Pes value just before the beginning and during inspiration. This is considered as a surrogate of muscle power, as this does not incorporate recoil of the chest wall.

Suggested target ΔPes between -2 cm H20 and -12 cmH20.

Excessive ΔPes indicates that the patient is generating abnormally high negative pressures to overcome resistive or elastic loads, suggestive of impending weaning failure. Minimal ΔPes, in contrast, may reflect excessive ventilator assistance during “assisted SBTs,” which can mask underlying respiratory insufficiency [58].

2.

PTPes (Esophageal Pressure–Time Product): This is a time based integral of Pmus (pressure generated by the inspiratory muscles) which captures both the magnitude and duration of inspiratory effort, making it a robust indicator of the energetic cost of breathing. This is calculated as an area bounded by the negative esophageal pressure during inspiration and the chest wall elastance slope multiplied by the respiratory rate. This seems to co-relate with the oxygen consumption of respiratory muscles better than the work of breathing.

Suggested target PTPes: between 50-150 cm H2O.s/min

Elevated PTPes during an SBT indicates unsustainable work of breathing, correlating strongly with weaning failure. Studies have shown that PTP outperforms RSBI because it measures true diaphragmatic load rather than relying on indirect surrogates like respiratory rate and tidal volume [59].

3.

Pi/Pimax: This is the ratio of change in esophageal pressure during inspiration to the maximum change during occlusion.

Suggested target Pi/Pimax: 0.15 to 0.25

A high Pi/Pimax (> 0.46) is associated with re-intubation. A disadvantage to this index is that it does not capture the inspiratory time which contributes to the work of breathing [60].

4.

Tension-time index (TTI): calculated as a ratio of (Pdi/Pdimax) to (TI/Ttot). This is the ratio of fractional diaphragmatic pressure to the inspiratory duty cycle.

Suggested TTI > 0.15

A TTI of < 0.15 correlated with respiratory muscle fatigue [61].

Pdi: mean transdiaphragmatic pressure during inspiration (Pes-Pgastric)

Pdimax: transdiaphragmatic pressure during maximum inspiration

TI: inspiration time

Ttot: time for one respiratory cycle

5.

Pressure rate Product (PRP): As the name suggests, this is the product of respiratory rate and change in esophageal pressure during respiratory cycle. This incorporates the recoil from chest wall and additionally does not require the measurement of flow or volume [62,63].

Suggested target PRP: between 200-400 cm H2O/min.

This range seems to correspond to PTP range of 50–150cm H2O·s/min.

6.

Trend Index: Unlike RSBI (RR/VT), which ignores effort, TI incorporates ΔPes, providing a more direct measure of patient work. This is a composite Pes-derived parameter that integrates ΔPes swings in the first 9-10 minutes, reflecting the trajectory of effort rather than a single time-point measurement. Progressive increases in ΔPes or PTPes during an SBT (even if within acceptable ranges at initiation) may signal fatigue and impending failure, allowing earlier intervention [64,65,66].

Pes trend index = 0.240 + 0.241* X1- 0.111*X2- 0.067*X3 + 0.055*X4

• X1 = max (0, 7.411 –∆Pes 9);
• X2 = max (0, ∆Pes 9- 5.967);
• X3 = max (0, ∆Pes 1-0.094) * max(0, ∆Pes 9-7.411);
• X4 = max (0, ∆Pes 1 + 1.679) * max(0, ∆Pes 9-10.729)
• ∆Pes 9 represents the estimated value of Pes at the ninth-to-tenth minute transition, and ∆Pes 1 represents the slope of the swings in Pes throughout the first minute

Pes trend index of less than or equal to 0.44 after 9 minutes of spontaneous breathing was associated with weaning failure.

8. Hemodynamic Assessment

Esophageal pressure (Pes) monitoring has important implications beyond respiratory mechanics, particularly in the realm of hemodynamic assessment. Because the esophagus lies within the thoracic cavity, Pes reflects changes in intrathoracic pressure, which directly influences the transmural pressures experienced by the heart and great vessels [9].

During spontaneous breathing, negative Pes swings augment venous return and reduce left ventricular afterload, whereas positive intrathoracic pressures during controlled ventilation can impede venous return and elevate right ventricular afterload. These dynamics are critical when interpreting invasive pressure measurements such as central venous pressure (CVP) and pulmonary artery occlusion pressure (PAOP).

A positive Pes (elevated intrathoracic pressure), as may occur during positive-pressure ventilation or in obesity, is transmitted to the intravascular compartment. This transmission causes CVP and PAOP values to appear artificially elevated, even though the true transmural (effective) filling pressures of the heart may be normal or even reduced. Conversely, negative Pes swings during strong inspiratory efforts can artifactually lower measured filling pressures, potentially masking inadequate preload [67].

To correctly interpret hemodynamic data in this context, intravascular pressures should be adjusted by accounting for Pes [68]. The transmural pressure, the true distending pressure of a cardiac chamber or vessel—is obtained by subtracting Pes (or intrathoracic pressure) from the measured intravascular pressure:

Ptransmural=Pmeasured−Pesophageal

This correction is particularly valuable in critically ill patients with acute respiratory distress syndrome (ARDS), obesity, or those receiving high levels of positive end-expiratory pressure (PEEP), where chest wall mechanics significantly distort intravascular pressure readings. Pes monitoring thus provides a means to disentangle cardiac preload and afterload from the confounding influence of intrathoracic pressures, thereby improving the accuracy of hemodynamic assessment and guiding fluid and vasoactive therapy in complex critically ill patients [69,70].

Clinical Example

Consider a patient with moderate-to-severe ARDS, managed on high levels of PEEP (e.g., 16 cmH₂O). Standard invasive monitoring shows a CVP of 18 mmHg and a PAOP of 20 mmHg, both of which would typically suggest elevated preload and possible risk of pulmonary congestion. However, simultaneous esophageal pressure (Pes) monitoring reveals an average Pes of +12 cmH₂O, reflecting markedly elevated pleural pressure due to both chest wall mechanics and applied PEEP. When corrected for Pes, the transmural filling pressures are significantly lower than the measured values suggest:

CVP transmural= CVP measured−Pes=18−12=6 mmHg

PAOP transmural=PAOP measured−Pes=20−12=8 mmHg

These corrected values demonstrate that, despite apparently elevated intravascular pressures, the true preload is low, and the patient may in fact benefit from cautious fluid administration or adjustment of vasoactive support. Without Pes monitoring, reliance on uncorrected CVP/PAOP could lead to erroneous clinical decisions—such as withholding fluids or even initiating unnecessary diuresis—potentially worsening perfusion.

In summary, the incorporation of Pes into hemodynamic assessment allows clinicians to move beyond raw intravascular pressures and instead interpret transmural pressures, yielding a more physiologically accurate representation of preload and afterload in critically ill patients [67,71].

9. Utility in special populations

A. Obesity and Elevated Intra-Abdominal Pressure

In patients with obesity or elevated intra-abdominal pressure (IAP), baseline esophageal pressure (Pes) is typically elevated due to reduced chest wall compliance and upward displacement of the diaphragm. This phenomenon leads to higher measured airway pressures (Paw), which may be misinterpreted as reflecting injurious lung stress if Pes is not accounted for. By partitioning lung and chest wall mechanics, Pes monitoring allows for differentiation between elevated Paw driven by chest wall loading versus true transpulmonary pressure (PL).The elevated airway plateau pressures (Pplat) can be misleading. In such patients, higher Paw is acceptable provided that the end-inspiratory transpulmonary pressure (Plinsp) remains within the safe range (<15–20 cmH₂O). Because elevated Pes often translates into a negative end-expiratory PL (Plexp), higher levels of PEEP are frequently necessary to achieve a Plexp near 0–2 cmH₂O, thereby preventing alveolar collapse. Adequate PEEP counteracts external compressive forces imposed by the chest wall and abdominal pressure, ensuring that alveoli especially in dependent regions remain open without excessive distension of non-dependent lung regions [72,73].

B. Severe COPD (Chronic obstructive pulmonary disease) /Asthma

In severe airflow obstruction, slow expiratory time constants and dynamic airway collapse trap gas at end-expiration, elevating alveolar pressure (Palv) above the airway opening (Paw) when the next inspiration begins. This intrinsic PEEP (PEEPi, “auto-PEEP”) imposes a threshold load and thereby patient must first generate enough negative pleural pressure to bring Palv down to Paw before any inspiratory flow can occur.

With esophageal manometry, the start of an assisted or spontaneous breath classically displays a downward Pes deflection without flow, Paw and flow remain flat until the negative Pes equals the trapped pressure. The magnitude of this pre-flow Pes drop approximates dynamic PEEPi. During an end-expiratory occlusion (“no-flow” hold), the negative Pes required to deflect Paw equals static PEEPi and quantifies the threshold load. External PEEP may be gradually increased while observing pre-flow Pes drop during assisted or support mode. Typically external PEEP is targeted to 70–85% of measured PEEPi to reduce threshold load while avoiding additional hyperinflation. Other ways to treat auto-PEEP include lengthening expiratory time (↓RR, adjusting Inspiratory: expiratory ratio), reduce VT/flow demand, lowering circuit resistance, treating bronchospasm and clearing secretions. Mose sensitive flow trigger or neural triggering may be used [74].

Occasionally, in COPD/asthma, abdominal/expiratory muscle activity may persist into end-expiration, raising gastric pressure (Pga) and thus Pes even when lungs are still hyperinflated. This can overestimate PEEPi if an elevated end-expiratory Pes is interpreted purely as pleural pressure [34].

Clues to detect this overestimation includes:

• Phasic Pga rises during expiration and a positive end-expiratory Pdi (Pga–Pes).
• Abdominal paradox or visible abdominal muscle recruitment.

Measurement during relaxed breathing and brief expiratory occlusions to eliminate flow-dependent artifacts and track Pga with a dual-balloon catheter, and interpret Pes in conjunction with flow/volume tracings (ensure complete exhalation is not occurring) may mitigate some of these problems [75,76].

It must be remembered that PEEPi varies regionally and Pes reflects a mid-thoracic average when a true threshold loads can be higher in dependent lung. Furthermore, very weak inspiratory muscles may not overcome PEEPi; the pre-flow Pes drop will then underestimate the true auto-PEEP [77,78].

C. ECMO (Extra Corporeal Membrane Oxygenation)

During venovenous ECMO, gas exchange (especially CO₂ removal) is largely off-loaded to the circuit, allowing the ventilator to be set for minimal lung stress and strain. Because airway pressures (Paw) are confounded by chest-wall mechanics—often markedly abnormal in ARDS, obesity, or elevated intra-abdominal pressure—transpulmonary pressure (PL = Paw − Pes) is the most direct bedside surrogate of alveolar distending pressure. Targeting PL rather than Paw operationalizes lung rest by capping true tissue stress [79] . Definitive randomized data specifically linking Pes-guided PL targets to ECMO outcomes are limited; current support is physiologic and pragmatic rather than trial-proven.

Proposed “lung rest” ventilation strategy at bedside:

• End-inspiratory stress (PLinsp). Use paralysis or deep sedation (at least during measurement) to eliminate patient effort, then titrate VT/pressure support to keep PLinsp low (commonly ≤10–12 cmH₂O, and even 5–10 cmH₂O in the early “ultraprotective” phase).
• End-expiratory stability (Plexp). Adjust PEEP to maintain Plexp ≈ 0 to +2 cmH₂O, preventing cyclic collapse without overdistending non-dependent lung.
• Driving pressure. Minimize ΔPL (PLinsp − Plexp)—ideally <10–12 cmH₂O. With sweep gas handling CO₂, accept very low VT (3–4 mL/kg PBW or less) and lower respiratory rates as needed to achieve these PL targets.
• Obesity/high IAP. Expect higher measured Paw at any given PL because Pes is elevated. With Pes guidance, accept higher Pplat/Paw (and often higher PEEP) so long as PL targets are respected—a strategy that sustains recruitment in dependent lung without exceeding safe distending pressures.

Other clinical applications include

“Pre-ECMO candidacy assessment”: When high Paw appears “unsafe” in obese ARDS, Pes may reveal acceptable PL, supporting continuation of non-ECMO strategies or more confident use of higher PEEP while monitoring PL [79].

“Weaning ECMO”: As sweep is reduced, monitor PL while gradually increasing ventilator contribution, while monitoring the transpulmonary driving pressure [79,80].

10. Integration with other monitoring for comprehensive assessment

Electrical Activity of the Diaphragm (EAdi): Neuro-mechanical coupling

The electrical activity of the diaphragm (EAdi) represents the integrated neural output from the respiratory centers in the brainstem to the diaphragm via the phrenic nerves. It is captured using specialized esophageal catheters equipped with multiple electrodes. Unlike Pes, which measures the mechanical consequence of inspiratory effort, EAdi quantifies the neural command itself. Thus, EAdi provides a direct link between central respiratory drive and ventilatory effort, bridging physiology with patient–ventilator interaction. Eadi (neuro-ventilatory drive) reflects the intensity of central drive to breathe, integrating chemical (PaCO₂, PaO₂, pH) and mechanical (load, stretch receptor input) stimuli. EAdi provides precise temporal information, marking inspiratory onset and termination. Elevated EAdi signals heightened respiratory drive, often in response to hypoxemia, hypercapnia, or increased mechanical load (e.g., in ARDS or COPD). Low EAdi may reflect over sedation, excessive ventilator assist, or impaired central drive. Whereas Pes reflects pressure transmission and mechanical consequences, EAdi reflects the central respiratory command. Together, they offer a more holistic assessment of patient effort, synchrony, and ventilatory support adequacy [48].

By comparing EAdi with Pes or tidal volume, one can assess the efficiency of translating neural drive into mechanical output (neuro-mechanical coupling), a measure that becomes particularly relevant in conditions like neuromuscular weakness or diaphragm dysfunction [81].

Integrating EAdi with Pes monitoring improves detection of patient–ventilator asynchronies such as delayed triggering, premature cycling, or reverse triggering and can be used to titrate ventilator output proportionally to neural effort, aligning mechanical assistance with patient demand especially in proportional assist ventilation (PAV) or neurally adjusted ventilatory assist (NAVA) modes. This can help avoid both over-assist (leading to diaphragm unloading and atrophy) and under-assist (leading to excessive effort and potential patient self-inflicted lung injury, P-SILI). Furthermore can be used to assess readiness to wean [82].

Diaphragm Ultrasound

Diaphragm ultrasound provides a noninvasive, real-time assessment of diaphragmatic structure and function. Two main parameters typically evaluated include diaphragmatic thickening and displacement [83].

1. Diaphragmatic thickening (TF, thickening fraction):

Measured at the zone of apposition, typically between the 8th and 10th intercostal space. Thickening during inspiration reflects active fiber recruitment.

TF = (Thickness at end-inspiration − Thickness at end-expiration) / Thickness at end-expiration × 100%.

Moderate thickening fractions (typically 20–40%) during spontaneous breathing trials correlate with successful extubation, while minimal or absent thickening suggests diaphragmatic weakness or fatigue.

2. Excursion (displacement)

Measured in M-mode, reflecting diaphragmatic caudal displacement during inspiration.

These ultrasound-derived indices are indirect surrogates of diaphragmatic effort and contractility, though they measure movement and morphology, not pressure generation. Serial measurements can track changes in diaphragmatic activity, particularly during prolonged mechanical ventilation. Reduced excursion or thickening may indicate ventilator-induced diaphragmatic dysfunction (VIDD), phrenic nerve injury, or myopathic changes. Unlike Pes, diaphragm ultrasound requires no invasive equipment and can be repeated frequently. However there are some limitations. The relationship between thickening fraction/excursion and true inspiratory effort (quantified via Pes or pressure–time product [PTPes]) is modest. Thickening reflects regional recruitment but does not directly quantify pressure generation. Excursion may be influenced by passive lung mechanics, ventilator support, or patient positioning. Ultrasound is dependent on operator expertise, probe placement, patient body habitus, and intercostal window. Ultrasound measures a limited region of the diaphragm (zone of apposition), which may not represent global diaphragmatic activity [84,85].

Diaphragm ultrasound is best viewed as a qualitative and trend tool for diaphragm activity, with value in predicting weaning success and identifying dysfunction. However, for accurate quantification of inspiratory effort and work of breathing, Pes-derived indices (ΔPes, PTPes) remain superior. Integrating Diaphragm ultrasound with Pes monitoring may be used for more comprehensive assessment for diaphragmatic function [83,84,85].

Electrical Impedance Tomography (EIT)

Electrical Impedance Tomography (EIT) is a noninvasive, radiation-free imaging modality that provides real-time, bedside monitoring of regional ventilation distribution. A belt containing multiple surface electrodes is placed circumferentially around the patient’s thorax. Low-amplitude alternating electrical currents are applied between electrode pairs, and the resulting voltage changes are measured. Because air has much higher impedance than surrounding tissues, variations in thoracic impedance correspond to regional changes in lung aeration throughout the respiratory cycle. Unlike global airway pressure measurements (Paw, Pes, PL), which provide averaged data, EIT captures spatial heterogeneity of lung inflation. It identifies regions of collapse, under-ventilation, or overdistension, guiding more individualized ventilator settings. By observing recruitment vs. overdistension in real time, EIT is believed to allow titration of PEEP to balance alveolar opening with avoidance of hyperinflation [86,87].

Pes-derived transpulmonary pressure reflects global lung stress, but cannot differentiate regional ventilation patterns. EIT complements this by identifying regional strain and overdistension, ensuring that maintaining “safe” global pressures (e.g., Plinsp <15–20 cmH₂O) does not mask harmful regional mechanics. This can be important as EIT can reveal non-dependent lung overdistension even when Pes-guided PL values remain within target ranges. Furthermore, EIT can show delayed emptying, regional air trapping, or asymmetric ventilation, and may be useful in COPD and asthma. However EIT provides only a cross-sectional slice of the lung (typically at the 4th–6th intercostal space), which may not fully represent global lung mechanics. Image resolution is modest compared to CT, though temporal resolution is superior (real-time monitoring) and is not yet universally standardized [88,89,90,91].

Occlusion pressure indices (P0.1 and Pocc)

P0.1 (Occlusion Pressure at 100 ms) is defined as the negative airway pressure generated during the first 100 milliseconds of an inspiratory effort against an occluded airway. It reflects the neural respiratory drive, independent of patient effort duration or respiratory system mechanics, because it is measured before significant lung or chest wall displacement occurs [92].

High P0.1 (>3.5–4 cmH₂O): Suggests excessive respiratory drive, which may predispose to patient self-inflicted lung injury (P-SILI) [93].

Low P0.1 (<1 cmH₂O): May indicate over-assist, deep sedation, or central suppression [93].

Pocc (Maximum Occlusion Pressure) is measured during a brief airway occlusion, Pocc represents the maximal inspiratory pressure a patient can generate. It provides an estimate of patient inspiratory effort and load–capacity balance, capturing the combined effect of neural drive, muscle strength, and chest wall mechanics [94].

High Pocc: Reflects strong inspiratory effort, suggesting under-assistance or increased mechanical load [94].

Low Pocc: Suggests diaphragmatic weakness, over-assist, or impaired neural drive [95].

Both P0.1 and Pocc can be measured easily using standard ventilators without specialized equipment and are useful as rapid adjuncts to measure respiratory drive. Abnormal values of P0.1 and Pocc may signal excessive effort or insufficient drive, both of which increase the risk of weaning failure. However these indices do not distinguish neural drive from mechanical load (e.g., high P0.1 may reflect either strong drive or high resistance) and could be sensitive to sedation, ventilator settings, and patient–ventilator synchrony. Additionally they lack the precision of Pes or EAdi for quantifying effort and transpulmonary stress, hence together, they provide more pragmatic assessment of respiratory drive [96,97,98].

See Table 4 for summary of various physiological (proposed) targets for esophageal derived indices during mechanical ventilation for lung and diaphragm protective strategy.

Limitations and Cautions for Esophageal Pressure Monitoring

While esophageal pressure (Pes) monitoring provides unique physiologic insights into transpulmonary mechanics, its application carries several important limitations and caveats that must be acknowledged for accurate interpretation and safe use in clinical practice.

1. Regional Representation of Pleural Pressure:

Pes primarily reflects pleural pressure in the dependent, mid-thoracic regions of the lung. However, pleural pressure is heterogeneous across the thorax, especially in acute respiratory distress syndrome (ARDS), where gravitational and structural forces create marked regional differences. Thus, while Pes offers a useful approximation of pleural pressure, it may underestimate the stress in non-dependent lung regions, where overdistension can occur even when transpulmonary pressure appears within “safe” limits [25,99].

2. Technical Sources of Artifact

Accurate Pes measurement is highly dependent on technique. Common sources of error include, esophageal spasm, which can transiently increase local pressure and distort readings, cardiac oscillations, transmitted to the esophagus, which may obscure respiratory pressure swings, catheter malposition (e.g., gastric placement or shallow esophageal location), which can lead to inaccurate reflection of thoracic pressures [100].

3. Balloon Inflation and Calibration

The accuracy of Pes monitoring is sensitive to balloon volume and calibration technique. Under inflation risks poor transmission of pleural pressure, whereas overinflation can cause esophageal wall apposition and artifactually elevated readings. Manufacturers recommend initial balloon inflation followed by stepwise deflation to a “best volume” (Vbest), the point at which respiratory swings are most faithfully transmitted with minimal artifact. In addition, periodic occlusion tests (ΔPaw/ΔPes ≈ 1 during inspiratory effort against a closed airway) are essential to verify measurement reliability [100].

4. Outcome Evidence and Clinical Individualization

Although Pes-guided strategies consistently improve oxygenation and compliance compared with low-PEEP protocols, evidence for mortality benefit remains mixed. The EPVent-1 trial suggested potential survival advantage, but the larger EPVent-2 trial did not confirm this benefit compared with high-PEEP strategies. Consequently, Pes monitoring should be viewed as a physiologic adjunct, particularly valuable in specific phenotypes (e.g., obesity, altered chest-wall mechanics, equivocal weaning), rather than a universal mandate [101].

See Table 5 for summary on the strengths and limitations of esophageal pressure monitoring during mechanical ventilation. See Figure 13 for the summary of various clinical applications and proposed targets during mechanical ventilation using esophageal pressure monitoring.

Future directions

Targeted trials:

Future research on esophageal pressure (Pes) monitoring should focus on targeted, stratified clinical trials that address patient heterogeneity in chest-wall mechanics, positioning, and spontaneous effort. Prior studies such as EPVent and EPVent-2 suggest physiologic benefits of Pes-guided ventilation but highlight the need for phenotype-specific strategies. Carefully designed multi-center trials should randomize patients to Pes-guided versus standardized approaches while stratifying by obesity or elevated chest-wall elastance (BMI ≥35–40), proning status, and degree of spontaneous effort. Endpoints should include ventilator-free days, mortality, and physiologic measures of lung stress and effort, complemented by mechanistic sub-studies (e.g., EIT for regional strain, biomarkers of biotrauma, diaphragm ultrasound). Such trials would clarify whether individualized, physiology-driven ventilatory management improves outcomes in select populations—particularly obese patients, those requiring prone positioning, and patients with high inspiratory effort—ultimately defining the most clinically impactful and safe role for Pes monitoring in critical care.

Closed-loop ventilation:

Closed-loop ventilation represents a promising future direction by integrating real-time esophageal pressure (Pes) monitoring into automated controllers that titrate PEEP, inspiratory support, and assist levels. Using end-expiratory and end-inspiratory transpulmonary pressures (Plexp, Plinsp) alongside effort-based indices (ΔPes, PTPes), these systems can dynamically balance lung protection, avoiding overdistension and collapse. It can incorporate diaphragm protection preventing both excessive effort and disuse atrophy. Early prototypes of physiologically adaptive modes, such as proportional assist ventilation (PAV) and neurally adjusted ventilatory assist (NAVA), demonstrate feasibility, but true closed-loop systems integrating Pes remain largely experimental. Future development should focus on algorithms that continuously adapt to changes in chest-wall mechanics, spontaneous effort, and patient–ventilator synchrony, with validation in multi-center trials. Such technology has the potential to transform Pes from a specialized monitoring tool into a bedside-integrated, automated controller, delivering individualized lung- and diaphragm-protective ventilation. It may have a role in weaning process.

Catheter advancements

Advances in catheter technology are central to expanding the clinical utility of esophageal pressure (Pes) monitoring. Next-generation designs featuring wide-range, thin-wall balloons can improve signal fidelity across diverse patient populations, including those with altered chest-wall mechanics. Enhanced signal-processing algorithms, particularly improved filtering of cardiac oscillations, would reduce artifacts and allow more reliable interpretation during dynamic conditions. Integration of Pes-derived metrics such as real-time transpulmonary pressures (PL), ΔPes, and PTPes—directly into ventilator displays would streamline workflow, minimize operator dependence, and promote wider adoption. Future innovation should prioritize user-friendly, robust, and artifact-resistant systems that deliver clinically actionable data at the bedside, thereby transforming Pes monitoring from a research tool into a routine standard for precision-guided mechanical ventilation.

11. Conclusions

Esophageal pressure monitoring offers a valuable window into patient–ventilator interaction, lung–chest wall mechanics, and inspiratory effort. It provides a physiologically sound method for tailoring PEEP, tidal volume, and support levels, particularly in complex cases such as ARDS with obesity, COPD, or severe dyssynchrony. While limitations exist including heterogeneity of pleural pressures and technical artifacts, when applied thoughtfully, Pes monitoring facilitates more precise, lung- and diaphragm-protective ventilation. Pes guided ventilation may be helpful in weaning, outperforming conventional indices by quantifying true muscle effort. Further large-scale trials are needed to clarify its impact on clinical outcomes, but its role as a bedside physiological tool is firmly established.