Fundamental concepts and the latest evidence for esophageal pressure monitoring

PEEP titration using transpulmonary pressure

Talmor et al. conducted a randomized controlled trial (EPVENT) in adult patients with acute respiratory failure, which targeted setting PEEP based on maintaining a positive PL at end-expiration (direct method) versus using an empirical approach using the ARDS Network low PEEP/high FIO2 table [15]. The P/F ratio at 72 h was 88 mmHg higher in the esophageal pressure group than in the control group. Importantly, there was a trend for lower 28-day mortality in the esophageal pressure group. These results prompted a multicenter RCT, EPVENT-2 [16].

EPVENT-2 found no difference between the intervention and control groups with respect to the primary composite outcome of mortality and time off the ventilator or secondary endpoints such as mortality at 28 days and ventilator-free days. An important difference between EPVENT-2 included use of the ARDS Network high PEEP/low FiO2 table in the control group, instead of the low PEEP/high FiO2 table used in EPVENT-1. Post hoc analysis demonstrated heterogeneity in treatment effect based on severity of illness [17], as PEEP guided by the esophageal pressure was associated with lower mortality in patients with APACHE-II below the median value and may have had the opposite effect in patients with higher APACHE-II. Regardless of the treatment group or severity of multiorgan failure, mortality was lowest when PEEP titration brought PL end-expiration to approximately 0 cm H2O. This highlights that while on a population level end-expiratory PL aligns with the high PEEP/low FiO2 table, there is variation on an individual patient basis and esophageal pressure can help individualize PEEP management for a given patient, which may not be apparent with the PEEP/FIiO2 table.

A recent multicenter prospective observational study [18] again highlights potential advantages to PL measurements in subsets of patients. Specifically, they found that PL end-expiration > 0 was associated with lower 60-day mortality in obese patients with a BMI greater than 30. This also reinforces the value of esophageal pressure measurements for PEEP titration, specifically for patients with impaired chest wall compliance.

Extubation readiness

Assessment of patient effort is crucial in determining extubation readiness, and can be estimated using esophageal manometry [19]. Extubation failure (or weaning failure) is caused by an imbalance between respiratory load (respiratory work) and respiratory capacity (respiratory muscle strength), making it important to assess the total balance between respiratory load and capacity in the evaluation of ventilator liberation. Pi/Pimax is a measure of the balance between these two and is calculated as the ratio of change in the airway or esophageal pressure during inspiration over the maximum change in the inspiratory airway or esophageal pressure during occlusion. It has been reported that a high Pi/Pimax measured immediately after extubation is associated with reintubation in children [20]. A limitation of Pi/Pimax is that it does not capture the duration of time spent in inspiration, and does not isolate the diaphragm from other respiratory muscles. Tension-time index (TTI) is calculated as (Pdi/Pdimax)/(TI/Ttot) (Pdi: mean transdiaphragmatic pressure during inspiration (Pes-Pgastric), Pdimax: transdiaphragmatic pressure during maximum inspiration, TI: inspiration time, Ttot: time for one respiratory cycle). Previous studies have highlighted TTI of < 0.15 predicts respiratory muscle fatigue in adults and children [21,22,23].

Upper airway obstruction (UAO)

Esophageal manometry has also been used as a tool to detect upper airway obstruction after extubation in children when combined with respiratory inductance plethysmography. The diagnosis of UAO is made with inspiratory flow limitation, characterized by disproportionately high inspiratory effort (negative esophageal pressure) relative to the change in flow (Fig. 6) [24]. The authors identified that EM with respiratory inductance plethysmography could provide objective warning signs indicating UAO earlier than the bedside clinician's subjective assessment, and is particularly useful in children, where UAO is a frequent cause of failed extubation.

Fig. 6figure 6

Copyright © 2022 American Thoracic Society. All rights reserved. Cite: Khemani RG, Hotz J, Morzov R, et al. 2016 Evaluating Risk Factors for Pediatric Post-extubation Upper Airway Obstruction Using a Physiology-based Tool. Am J Respir Crit Care Med. 193:198–209. The American Journal of Respiratory and Critical Care Medicine is an official journal of the American Thoracic Society. Example of subglottic upper airway obstruction data of an infant after extubation. The data indicate inspiratory flow limitation (left), that is, no increase in flow despite a continual decrease in esophageal pressure. A significant improvement was observed 20 minutes after racemic epinephrine administration (right). Esophageal pressure was measured in centimeters of water. RIP respiratory inductance plethysmography

Example of a flow-limitation pattern in a patient with subglottic upper airway obstruction after extubation. Applying permission to reprint from [24] with permission of the American Thoracic Society. Example of subglottic upper airway obstruction data of an infant after extubation. The data indicate inspiratory flow limitation (left), that is, no increase in flow despite a continual decrease in esophageal pressure. A significant improvement was observed 20 min after racemic epinephrine administration (right). Esophageal pressure was measured in centimeters of water. RIP = respiratory inductance plethysmography.

Ventilator-induced diaphragm dysfunction (VIDD) and P-SILI

The preservation of spontaneous breathing has many advantages during critical illness. Contraction of the diaphragm by spontaneous breathing distributes ventilation to areas of better perfusion in the dorsal lungs compared with ventilation under neuromuscular blockade [25]. Spontaneous breathing during ventilation may improve gas exchange, maintain peripheral muscles, and prevent diaphragm atrophy [26, 27]. Subphysiological levels of patient effort, often from over assistance from the ventilator, are a major risk factor for ventilator-induced diaphragm dysfunction (VIDD). VIDD has been associated with prolonged mechanical ventilation, reintubation, functional impairment, and mortality [28,29,30,31]. Over-assistance is reported to occur frequently in both adult and pediatric ventilated patients [32, 33]. In contrast, excessive spontaneous respiratory effort leads to increased pulmonary stress and strain, increased pulmonary perfusion, and patient–ventilator asynchrony, resulting in lung injury known as effort-dependent lung injury or patient self-inflicted lung injury (P-SILI) [3, 27]. P-SILI has been shown to be associated with multiple organ dysfunction, progression of lung injury, and death [3, 27, 34].

It has recently become a therapeutic target to maintain patient effort at physiological levels to balance the risks of P-SILI against the risks of VIDD. A recent consensus conference of experts on adult and pediatric ventilation emphasized the importance of balancing protective ventilation of the lung and diaphragm in ARDS [29]. The principle is that lung-protective ventilation is the first priority because of the solid evidence that ventilator-induced lung injury is harmful; however, whenever possible, treatment goals should consider the risk of P-SILI and VIDD and try to maintain patient effort at physiologic levels. Currently, these principles are being tested in clinical trials [35]. Therefore, it is important for bedside physicians to be able to assess the degree of respiratory effort required to make informed ventilator management decisions. Esophageal manometry represents the accepted standard for estimating patient effort or work of breathing.

Work of breathing (WOB)

WOB can be calculated by plotting a curve of one respiratory cycle with esophageal pressure on the x-axis and lung capacity on the y-axis, and the area enclosed by a straight line whose slope is the chest wall compliance. (Fig. 7) [36]. This represents the most precise measure of the work being performed by the respiratory muscles, but has a disadvantage of requiring an accurate measure of volume, limiting application to invasively ventilated patients, for the most part.

Fig. 7figure 7

Method of calculating WOB. Permitted to reprint from [36] with permission form Springer Nature. x-axis: esophageal pressure, y-axis: lung volume. Since the patient's Work of breathing (WOB) includes the work of expanding the thorax in addition to the work of expanding the lungs, WOB is the area bounded by the straight line whose slope is the chest wall compliance and the esophageal pressure (x-axis) and lung capacity (y-axis) plot curves in the inspiratory phase [21]

Pressure time product (PTP)

PTP is a measure of EOB, calculated as the time-based integral of Pmus, that is, the difference between the estimated recoil pressure of the chest wall calculated from the tidal volume and Ccw and Pes during inspiration (Fig. 8). PTP is commonly reported over a 1-min interval. It may be more strongly correlated with respiratory muscle oxygen consumption than with WOB [21, 37, 38]. In adults, the optimal PTP in ventilated patients remains an issue of debate, but suggested targets have been proposed at 50–150 cm H2O·s/min [39].

Fig. 8figure 8

Method of calculating PTP. Applying permission to reprint from [21] with permission from Daedalus Enterprises; permission conveyed through Copyright Clearance Center, Inc. The upper curve is the time-flow curve, the middle curve is the time-airway pressure curve, and the lower curve is the time-esophageal pressure curve in the ventilated patient with spontaneous breathing. Pressure time product (PTP) can be calculated as the area bounded by the curve of the esophageal pressure in the negative direction during one inspiration (i.e., the pressure that inflates the lungs, color) and the straight line with thoracic compliance taken as the slope (i.e., the pressure that inflates the thorax), multiplied by respiratory rate

Pressure rate product (PRP)

PRP is a measure of breathing effort and is the product of the respiratory rate and the change in esophageal pressure during the respiratory cycle. PRP typically does not subtract the component related to chest wall elastance and has been used most extensively in children. It has the advantage of not requiring a measurement of volume or flow (unlike WOB and PTP), which makes it optimal for studying patients who may not be intubated. Using data measured both before and after extubation in children, a PRP in the range of 200–400 cmH2O/min is considered physiologic and has a low risk of reintubation [19, 40]. In children, this PRP range roughly corresponds to the proposed PTP range of 50–150 cm H2O·s/min for adult targets [19].

Delta esophageal pressure (delta Pes)

Delta Pes is the difference between the lowest Pes value during inspiration and the Pes value just before the beginning of the inspiration. Of all the estimates of patient effort using esophageal manometry, it is the easiest to measure. Delta Pes targets have been suggested to be between − 2 cmH2O and  − 12 cmH2O [29]. Of note, delta Pes is a surrogate for Pmus, but does not correct for the elastic recoil of the chest wall.

Although there are still few reports on the clinical outcomes of maintaining respiratory effort in a target range, Phase I studies highlight the feasibility and possible improvement in clinical outcomes, such as time to the first SBT and more VFDs [41]. A randomized controlled trial in pediatric patients is currently ongoing [35], and one in adults is under development.

Patient–ventilator asynchrony (PVA)

PVA is a major problem in ventilated patients and is related to a mismatch between the patient and the ventilator related to spontaneous breathing efforts. The frequency of PVA is estimated to be as high as 80% [42]. However, the impact of PVA on clinical outcomes in ventilated patients appears to be inconsistent across studies; Thille et al. reported that a higher incidence of PVA is associated with a longer duration of ventilation but not with increased mortality [43]. On the contrary, Blanch et al. found that patients with a higher incidence of PVA had a significantly higher mortality rate in the ICU than those with a lower incidence, but the duration of ventilation did not differ significantly between the two groups [44]. A systematic review and meta-analysis by Kyo reported that PVA might be associated with clinical outcomes; and that more attention should be paid to PVA [45].

Understanding PVA and its severity requires assessment of the patient’s effort. Esophageal manometry can serve as the gold standard method to characterize the timing, phase, magnitude, and duration of patient effort, all of which can contribute to different forms of PVA. For example, reverse triggering is a PVA subtype that is more clearly identified by esophageal manometry. Reverse triggering has been reported in animals and humans since the 1970s [46]. However, it was not until 2013 that this was reported as a ventilator asynchrony [47]. This occurs when the patient’s effort begins after lung inflation from a controlled breath. Recognizing the timing of spontaneous respiratory effort is very important for its diagnosis, and esophageal pressure can provide a direct measure of this timing (Fig. 9). The incidence of reverse triggering during mechanical ventilator management with acute respiratory failure may be as high as 40–50% in both adults and children [48, 49]. Reverse triggering may lead to double cycling (breath stacks) and contribute to lung injury; however, its clinical impact has not yet been fully elucidated.

Fig. 9figure 9

Reverse triggering waveforms. Waveforms of non-breath stacking (left) and breath stacking (right). Black arrows indicate airway pressure and flow at the initiation of spontaneous efforts. The breath on the left has reverse triggering, without a breath stack

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