End-expiratory Esophageal Pressure Research Articles

Advanced respiratory mechanics assessment in mechanically ventilated obese and non-obese patients with or without acute respiratory distress syndrome

BackgroundRespiratory mechanics is a key element to monitor mechanically ventilated patients and guide ventilator settings. Besides the usual basic assessments, some more complex explorations may allow to better characterize patients’ respiratory mechanics and individualize ventilation strategies. These advanced respiratory mechanics assessments including esophageal pressure measurements and complete airway closure detection may be particularly relevant in critically ill obese patients. This study aimed to comprehensively assess respiratory mechanics in obese and non-obese ICU patients with or without ARDS and evaluate the contribution of advanced respiratory mechanics assessments compared to basic assessments in these patients.MethodsAll intubated patients admitted in two ICUs for any cause were prospectively included. Gas exchange and respiratory mechanics including esophageal pressure and end-expiratory lung volume (EELV) measurements and low-flow insufflation to detect complete airway closure were assessed in standardized conditions (tidal volume of 6 mL kg−1 predicted body weight (PBW), positive end-expiratory pressure (PEEP) of 5 cmH2O) within 24 h after intubation.ResultsAmong the 149 analyzed patients, 52 (34.9%) were obese and 90 (60.4%) had ARDS (65.4% and 57.8% of obese and non-obese patients, respectively, p = 0.385). A complete airway closure was found in 23.5% of the patients. It was more frequent in obese than in non-obese patients (40.4% vs 14.4%, p < 0.001) and in ARDS than in non-ARDS patients (30% vs. 13.6%, p = 0.029). Respiratory system and lung compliances and EELV/PBW were similarly decreased in obese patients without ARDS and obese or non-obese patients with ARDS. Chest wall compliance was not impacted by obesity or ARDS, but end-expiratory esophageal pressure was higher in obese than in non-obese patients. Chest wall contribution to respiratory system compliance differed widely between patients but was not predictable by their general characteristics.ConclusionsMost respiratory mechanics features are similar in obese non-ARDS and non-obese ARDS patients, but end-expiratory esophageal pressure is higher in obese patients. A complete airway closure can be found in around 25% of critically ill patients ventilated with a PEEP of 5 cmH2O. Advanced explorations may allow to better characterize individual respiratory mechanics and adjust ventilation strategies in some patients.Trial registration NCT03420417 ClinicalTrials.gov (February 5, 2018).

A280 DOES THE PLACEMENT OF A MANOMETRY PROBE WITH ENDOSCOPY AND CONSCIOUS SEDATION EFFECT MEASUREMENTS ON ENSUING HIGH RESOLUTION MANOMETRY? A RETROSPECTIVE COHORT STUDY IN PATIENTS POST-PERORAL ENDOSCOPIC MYOTOMY

Abstract Background High resolution manometry (HRM) is the gold standard for diagnosis of esophageal motility disorders. This is traditionally conducted without sedation, using intranasal intubation with a manometry probe. Inserting the HRM probe immediately after endoscopic examination allows for endoscopic visualization and sedation for probe placement. This method is used commonly used for our patients who are post-peroral endoscopic myotomy (POEM). However, it is unclear whether short acting sedative drugs administered during endoscopy can affect contractility measurements during HRM. Purpose The purpose of this study was to determine if conscious sedation with short-acting anaesthetic agents (Midazolam and Fentanyl) influenced HRM readings in patients undergoing evaluation post-perioral endoscopic myotomy (POEM). Method We conducted a retrospective cohort study, comparing patients post-POEM who had endoscopy under conscious sedation with placement of the manometry probe versus those without preceeding endoscopy/sedation. Post-POEM patients who had undergone HRM over a 3-year period (2019-2022) were identified from motility lab records. Electronic charts were reviewed for data abstraction, and HRM parameters (resting lower esophageal pressure and integrated relaxation pressure) were determined for both groups and compared using t-tests, and error listed as standard error of the mean. Result(s) From 2019-2022, 15 patients underwent manometry using a non-endoscopic approach with no sedation and 25 underwent manometry following endoscopy with conscious sedation and placement of the probe during the procedure. In the latter group, HRM occurred within 2 hours of probe placement. The mean doses of fentanyl and midazolam were 115mcg (+/-29.7) and 3.3mg (+/-1.3) respectively. The mean end-expiratory lower esophageal sphincter pressure was 9.8 mmHg (+/- 2.9) in the non-endoscopic group and 26.24mmHg (+/- 5) in the endoscopy group (p &amp;lt;0.02). The median integrated relaxation pressure was 11.2 mmHg (+/-1.2) in the non-endoscopic group and 14.52mmHg (+/- 0.9) in those in the endoscopy group (p &amp;lt;0.04). Conclusion(s) In conclusion, this small, retrospective cohort study shows that manometry probe placement after endoscopy with conscious sedation may affect esophgeal HRM measurement parameters in the post-POEM patient population. Physicians should consider delaying HRM measurements for &amp;gt;4 hours to maximize clearance of the sedative medications. Please acknowledge all funding agencies by checking the applicable boxes below None Disclosure of Interest None Declared

Pleural Pressure Targeted Positive Airway Pressure Improves Cardiopulmonary Function in Spontaneously Breathing Patients With Obesity

Increased pleural pressure affects the mechanics of breathing of people with class III obesity (BMI > 40kg/m2). What are the acute effects of CPAP titrated to match pleural pressure on cardiopulmonary function in spontaneously breathing patients with class III obesity? We enrolled six participants with BMI within normal range (control participants, group I) and 12 patients with class III obesity (group II) divided into subgroups: IIa, BMI of 40 to 50kg/m2; and IIb, BMI of≥ 50kg/m2. The study was performed in two phases: in phase 1, participants were supine and breathing spontaneously at atmospheric pressure, and in phase 2, participants were supine and breathing with CPAP titrated to match their end-expiratory esophageal pressure in the absence of CPAP. Respiratory mechanics, esophageal pressure, and hemodynamic data were collected, and right heart function was evaluated by transthoracic echocardiography. The levels of CPAP titrated to match pleural pressure in group I, subgroup IIa, and subgroup IIb were 6 ± 2cmH2O, 12 ± 3cmH2O, and 18 ± 4cmH2O, respectively. In both subgroups IIa and IIb, CPAP titrated to match pleural pressure decreased minute ventilation (IIa, P= .03; IIb, P= .03), improved peripheral oxygen saturation (IIa, P= .04; IIb, P= .02), improved homogeneity of tidal volume distribution between ventral and dorsal lung regions (IIa, P= .22; IIb, P= .03), and decreased work of breathing (IIa, P< .001; IIb, P= .003) with a reduction in both the work spent to initiate inspiratory flow as well as tidal ventilation. In five hypertensive participants with obesity, BP decreased to normal range, without impairment of right heart function. In ambulatory patients with class III obesity, CPAP titrated to match pleural pressure decreased work of breathing and improved respiratory mechanics while maintaining hemodynamic stability, without impairing right heart function. ClinicalTrials.gov; No.: NCT02523352; URL: www.clinicaltrials.gov.

Prevalence of Complete Airway Closure According to Body Mass Index in Acute Respiratory Distress Syndrome.

Complete airway closure during expiration may underestimate alveolar pressure. It has been reported in cases of acute respiratory distress syndrome (ARDS), as well as in morbidly obese patients with healthy lungs. The authors hypothesized that complete airway closure was highly prevalent in obese ARDS and influenced the calculation of respiratory mechanics. In a post hoc pooled analysis of two cohorts, ARDS patients were classified according to body mass index (BMI) terciles. Low-flow inflation pressure-volume curve and partitioned respiratory mechanics using esophageal manometry were recorded. The authors' primary aim was to compare the prevalence of complete airway closure according to BMI terciles. Secondary aims were to compare (1) respiratory system mechanics considering or not considering complete airway closure in their calculation, and (2) and partitioned respiratory mechanics according to BMI. Among the 51 patients analyzed, BMI was less than 30 kg/m2 in 18, from 30 to less than 40 in 16, and greater than or equal to 40 in 17. Prevalence of complete airway closure was 41% overall (95% CI, 28 to 55; 21 of 51 patients), and was lower in the lowest (22% [3 to 41]; 4 of 18 patients) than in the highest BMI tercile (65% [42 to 87]; 11 of 17 patients). Driving pressure and elastances of the respiratory system and of the lung were higher when complete airway closure was not taken into account in their calculation. End-expiratory esophageal pressure (ρ = 0.69 [95% CI, 0.48 to 0.82]; P < 0.001), but not chest wall elastance, was associated with BMI, whereas elastance of the lung was negatively correlated with BMI (ρ = -0.27 [95% CI, -0.56 to -0.10]; P = 0.014). Prevalence of complete airway closure was high in ARDS and should be taken into account when calculating respiratory mechanics, especially in the most morbidly obese patients.

The assessment of esophageal pressure using different devices: a validation study.

Although esophageal pressure measurement could help clinicians to improve the ventilatory management of acute respiratory distress syndrome (ARDS) patients, it has been mainly used in clinical research. Aim of this study was to compare the measurements of end-expiratory esophageal pressure, end-expiratory transpulmonary pressure and lung stress by three systems: a dedicated manual device, taken as gold standard, a new automatic system (Optivent) and a bedside equipment, consisting of a mechanical ventilator and a hemodynamic monitor. In sedated and paralyzed mechanically ventilated ARDS patients the esophageal pressure was measured at three PEEP levels in random fashion (baseline level, 50% higher and 50% lower). Forty patients were enrolled (BMI 25 [23-28] kg/m2, PaO<inf>2</inf>/FiO<inf>2</inf> 187 [137-223] and PEEP 9±3 cmH<inf>2</inf>O). The mean esophageal pressure measured during an expiratory pause by the dedicated system, the bedside system and Optivent were 10.0±4.2, 10±4 and 9.9±4.0 cmH<inf>2</inf>O, respectively. The respective bias and limits of agreement between the dedicated system and Optivent and between the dedicated system and the bedside system were as follows: end-expiratory esophageal pressure, 0.2 cmH<inf>2</inf>O, (-0.4 to 0.9) and -0.1 cmH<inf>2</inf>O (-1.9 to 1.7); end-expiratory transpulmonary pressure, -0.6 cmH<inf>2</inf>O (-1.7 to 0.4) and -0.4 cmH<inf>2</inf>O, (-2.2 to 1.5); lung stress -0.9 cmH<inf>2</inf>O (-3.0 to 1.1) and -1.5 cmH<inf>2</inf>O (-4.4 to 1.4). Both Optivent and the bedside system showed clinically acceptability if compared to the gold standard device. The possibility to apply one of these systems could allow a wider use of esophageal pressure in clinical practice.

Comparison of pleural and esophageal pressure in supine and prone positions in a porcine model of acute respiratory distress syndrome.

Patients with moderate to severe acute respiratory distress syndrome (ARDS) benefit from prone positioning. Although the accuracy of esophageal pressure (Pes) to estimate regional pleural pressure (Ppl) has previously been assessed in the supine position, such data are not available in the prone position in ARDS. In six anesthetized, paralyzed, and mechanically ventilated female pigs, we measured Pes and Ppl into dorsal and ventral parts of the right pleural cavity. Airway pressure (Paw) and flow were measured at the airway opening. Severe ARDS [arterial partial pressure of oxygen ()/fraction of inspired oxygen () < 100 mmHg at positive end-expiratory pressure (PEEP) of 5 cmH2O] was induced by surfactant depletion. In supine and prone positions assigned in a random order, PEEP was set to 20, 15, 10, and 5 cmH2O and static end-expiratory chest wall pressures were measured from Pes (PEEPtot,es) and dorsal (PEEPtot,PplD) and ventral (PEEPtot,PplV) Ppl. The magnitude of the difference between PEEPtot,es and PEEPtot,PplD was similar in each position [−3.6 cmH2O in supine vs. −3.8 cmH2O in prone at PEEP 20 cmH2O (PEEP 20)]. The difference between PEEPtot,es and PEEPtot,PplV became narrower in the prone position (−8.3 cmH2O supine vs. −3.0 cmH2O prone at PEEP 20). PEEPtot,PplV was overestimated by Pes in the prone position at higher pressures. The median (1st–3rd quartiles) dorsal-to-ventral Ppl gradient was 4.4 (2.4–6.8) cmH2O in the supine position and −1.5 (−3.5 to +1.1) cmH2O in the prone position (P < 0.0001) and marginally influenced by PEEP (P = 0.058). Prone position narrowed end-expiratory dorsal-to-ventral Ppl vertical gradient, likely because of a more even distribution of mechanical forces over the chest wall.NEW & NOTEWORTHY In a porcine model of acute respiratory distress syndrome, we found that static end-expiratory esophageal pressure did not change significantly in prone position compared with supine position at any positive end-expiratory pressure (PEEP) tested between 5 and 20 cmH2O. Prone position was associated with an increased ventral pleural pressure and reduced end-expiratory dorsal-to-ventral pleural pressure (Ppl) vertical gradient, likely due to a more even distribution of mechanical forces over the chest wall.

Mechanical Ventilation Guided by Uncalibrated Esophageal Pressure May Be Potentially Harmful.

Esophageal balloon calibration was proposed in acute respiratory failure patients to improve esophageal pressure assessment. In a clinical setting characterized by a high variability of abdominal load and intrathoracic pressure (i.e., pelvic robotic surgery), the authors hypothesized that esophageal balloon calibration could improve esophageal pressure measurements. Accordingly, the authors assessed the impact of esophageal balloon calibration compared to conventional uncalibrated approach during pelvic robotic surgery. In 30 adult patients, scheduled for elective pelvic robotic surgery, calibrated end-expiratory and end-inspiratory esophageal pressure, and the associated respiratory variations were obtained at baseline, after pneumoperitoneum-Trendelenburg application, and with positive end-expiratory pressure (PEEP) administration and compared to uncalibrated values measured at 4-ml filling volume, as per manufacturer recommendation. Data are expressed as median and [25th, 75th percentile]. Ninety calibrations were successfully performed. Chest wall elastance worsened with pneumoperitoneum-Trendelenburg and PEEP (19.0 [15.5, 24.6] and 16.7 [11.4, 21.7] cm H2O/l) compared to baseline (8.8 [6.3, 9.8] cm H2O/l; P < 0.0001 for both comparisons). End-expiratory and end-inspiratory calibrated esophageal pressure progressively increased from baseline (3.7 [2.2, 6.0] and 7.7 [5.9, 10.2] cm H2O) to pneumoperitoneum-Trendelenburg (6.2 [3.8, 10.2] and 16.1 [13.1, 20.6] cm H2O; P = 0.014 and P < 0.001) and PEEP (8.8 [7.7, 15.6] and 18.9 [16.3, 22.0] cm H2O; P < 0.0001 vs. baseline for both comparison; P < 0.001 and P = 0.002 vs. pneumoperitoneum-Trendelenburg) and, at each study step, they were persistently lower than uncalibrated esophageal pressure (P < 0.0001 for all comparisons). Overall, difference among uncalibrated and calibrated esophageal pressure was 5.1 [3.8, 8.4] cm H2O at end-expiration and 3.8 [3.0, 6.3] cm H2O at end-inspiration. Uncalibrated esophageal pressure swing was always lower than calibrated one (P < 0.0001 for all comparisons) with a difference of -1.0 [-1.8, -0.4] cm H2O. In a clinical setting with variable chest wall mechanics, uncalibrated measurements substantially overestimated absolute values and underestimated respiratory variations of esophageal pressure. Calibration could substantially improve mechanical ventilation guided by esophageal pressure.

Body Position Alters Mechanical Power and Respiratory Mechanics During Thoracic Surgery.

During thoracic surgery, patients are usually positioned in lateral decubitus and only the dependent lung ventilated. The ventilated lung is thus exposed to the weight of the contralateral hemithorax and restriction of the dependent chest wall. We hypothesized that mechanical power would increase during one-lung ventilation in the lateral position. We performed a prospective, observational, single-center study from December 2016 to May 2017. Thirty consecutive patients undergoing general anesthesia with mechanical ventilation (mean age, 68 ± 11 years; body mass index, 25 ± 5 kg·m) for thoracic surgery were enrolled. Total and partitioned mechanical power, lung and chest wall elastance, and esophageal pressure were compared in supine and lateral position with double- and one-lung ventilation and with closed and open chest both before and after surgery. Mixed factorial ANOVA for repeated measurements was performed, with both step and the period before or after surgery as 2 within-subject factors, and left or right body position during surgery as a fixed, between-subject factor. Appropriate interaction terms were included. The mechanical power was higher in lateral one-lung ventilation compared to both supine and lateral position double-lung ventilation (11.1 ± 3.0 vs 8.2 ± 2.7 vs 8.7 ± 2.6; mean difference, 2.9 J·minute [95% CI, 1.4-4.4 J·minute] and 2.4 J·minute [95% CI, 0.9-3.9 J·minute]; P < .001 and P = .002, respectively). Lung elastance was higher during lateral position one-lung ventilation compared to both lateral and supine double-lung ventilation (24.3 ± 8.7 vs 9.5 ± 3.8 vs 10.0 ± 3.8; mean difference, 14.7 cm H2O·L [95% CI, 11.2-18.2 cm H2O·L] and 14.2 cm H2O·L [95% CI, 10.8-17.7 cm H2O·L], respectively) and was higher compared to predicted values (20.1 ± 7.5 cm H2O·L). Chest wall elastance increased in lateral position double-lung ventilation compared to supine (11.1 ± 3.8 vs 6.6 ± 3.4; mean difference, 4.5 cm H2O·L [95% CI, 2.6-6.3 cm H2O·L]) and was lower in lateral position one-lung ventilation with open chest than with a closed chest (3.5 ± 1.9 vs 7.1 ± 2.8; mean difference, 3.6 cm H2O·L [95% CI, 2.4-4.8 cm H2O·L]). The end-expiratory esophageal pressure decreased moving from supine position to lateral position one-lung ventilation while increased with the opening of the chest wall. Mechanical power and lung elastance are increased in the lateral position with one-lung ventilation. Esophageal pressure monitoring may be used to follow these changes.

Airway Closure during Surgical Pneumoperitoneum in Obese Patients.

Airway closure causes lack of communication between proximal airways and alveoli, making tidal inflation start only after a critical airway opening pressure is overcome. The authors conducted a matched cohort study to report the existence of this phenomenon among obese patients undergoing general anesthesia. Within the procedures of a clinical trial during gynecological surgery, obese patients underwent respiratory/lung mechanics and lung volume assessment both before and after pneumoperitoneum, in the supine and Trendelenburg positions, respectively. Among patients included in this study, those exhibiting airway closure were compared to a control group of subjects enrolled in the same trial and matched in 1:1 ratio according to body mass index. Eleven of 50 patients (22%) showed airway closure after intubation, with a median (interquartile range) airway opening pressure of 9 cm H2O (6 to 12). With pneumoperitoneum, airway opening pressure increased up to 21 cm H2O (19 to 28) and end-expiratory lung volume remained unchanged (1,294 ml [1,154 to 1,363] vs. 1,160 ml [1,118 to 1,256], P = 0.155), because end-expiratory alveolar pressure increased consistently with airway opening pressure and counterbalanced pneumoperitoneum-induced increases in end-expiratory esophageal pressure (16 cm H2O [15 to 19] vs. 27 cm H2O [23 to 30], P = 0.005). Conversely, matched control subjects experienced a statistically significant greater reduction in end-expiratory lung volume due to pneumoperitoneum (1,113 ml [1,040 to 1,577] vs. 1,000 ml [821 to 1,061], P = 0.006). With airway closure, static/dynamic mechanics failed to measure actual lung/respiratory mechanics. When patients with airway closure underwent pressure-controlled ventilation, no tidal volume was inflated until inspiratory pressure overcame airway opening pressure. In obese patients, complete airway closure is frequent during anesthesia and is worsened by Trendelenburg pneumoperitoneum, which increases airway opening pressure and alveolar pressure: besides preventing alveolar derecruitment, this yields misinterpretation of respiratory mechanics and generates a pressure threshold to inflate the lung that can reach high values, spreading concerns on the safety of pressure-controlled modes in this setting.

Detailed measurements of oesophageal pressure during mechanical ventilation with an advanced high-resolution manometry catheter

BackgroundOesophageal pressure (PES) is used for calculation of lung and chest wall mechanics and transpulmonary pressure during mechanical ventilation. Measurements performed with a balloon catheter are suggested as a basis for setting the ventilator; however, measurements are affected by several factors. High-resolution manometry (HRM) simultaneously measures pressures at every centimetre in the whole oesophagus and thereby provides extended information about oesophageal pressure. The aim of the present study was to evaluate the factors affecting oesophageal pressure using HRM.MethodsOesophageal pressure was measured using a high-resolution manometry catheter in 20 mechanically ventilated patients (15 in the ICU and 5 in the OR). Different PEEP levels and different sizes of tidal volume were applied while pressures were measured continuously. In 10 patients, oesophageal pressure was also measured using a conventional balloon catheter for comparison. A retrospective analysis of oesophageal pressure measured with HRM in supine and sitting positions in 17 awake spontaneously breathing patients is also included.ResultsHRM showed large variations in end-expiratory PES (PESEE) and tidal changes in PES (ΔPES) along the oesophagus. Mean intra-individual difference between the minimum and maximum end-expiratory oesophageal pressure (PESEE at baseline PEEP) and tidal variations in oesophageal pressure (ΔPES at tidal volume 6 ml/kg) recorded by HRM in the different sections of the oesophagus was 23.7 (7.9) cmH2O and 7.6 (3.9) cmH2O respectively. Oesophageal pressures were affected by tidal volume, level of PEEP, part of the oesophagus included and patient positioning. HRM identified simultaneous increases and decreases in PES within a majority of individual patients. Compared to sitting position, supine position increased PESEE (mean difference 12.3 cmH2O), pressure variation within individual patients and cardiac artefacts. The pressure measured with a balloon catheter did not correspond to the average pressure measured with HRM within the same part of the oesophagus.ConclusionsThe intra-individual variability in PESEE and ΔPES is substantial, and as a result, the balloon on the conventional catheter is affected by many different pressures along its length. Oesophageal pressures are not only affected by lung and chest wall mechanics but are a complex product of many factors, which is not obvious during conventional measurements. For correct calculations of transpulmonary pressure, factors influencing oesophageal pressures need to be known. HRM, which is available at many hospitals, can be used to increase the knowledge concerning these factors.Trial registrationClinicalTrials.gov, NCT02901158

The occlusion tests and end-expiratory esophageal pressure: measurements and comparison in controlled and assisted ventilation.

Background Esophageal pressure is used as a reliable surrogate of the pleural pressure. It is conventionally measured by an esophageal balloon placed in the lower part of the esophagus. To validate the correct position of the balloon, a positive pressure occlusion test by compressing the thorax during an end-expiratory pause or a Baydur test obtained by occluding the airway during an inspiratory effort is used. An acceptable catheter position is defined when the ratio between the changes in esophageal and airway pressure (∆Pes/∆Paw) is close to unity. Sedation and paralysis could affect the accuracy of esophageal pressure measurements. The aim of this study was to evaluate, in mechanically ventilated patients, the effects of paralysis, two different esophageal balloon positions and two PEEP levels on the ∆Pes/∆Paw ratio measured by the positive pressure occlusion and the Baydur tests and on the end-expiratory esophageal pressure and respiratory mechanics (lung and chest wall).MethodsTwenty-one intubated and mechanically ventilated patients (mean age 64.8 ± 14.0 years, body mass index 24.2 ± 4.3 kg/m2, PaO2/FiO2 319.4 ± 117.3 mmHg) were enrolled. In step 1, patients were sedated and paralyzed during volume-controlled ventilation, and in step 2, they were only sedated during pressure support ventilation. In each step, two esophageal balloon positions (middle and low, between 25–30 cm and 40–45 cm from the mouth) and two levels of PEEP (0 and 10 cmH2O) were applied. The ∆Pes/∆Paw ratio and end-expiratory esophageal pressure were evaluated.ResultsThe ∆Pes/∆Paw ratio was slightly higher (+0.11) with positive occlusion test compared with Baydur’s test. The level of PEEP and the esophageal balloon position did not affect this ratio. The ∆Pes and ∆Paw were significantly related to a correlation coefficient of r = 0.984 during the Baydur test and r = 0.909 in the positive occlusion test. End-expiratory esophageal pressure was significantly higher in sedated and paralyzed patients compared with sedated patients (+2.47 cmH2O) and when esophageal balloon was positioned in the low position (+2.26 cmH2O). The esophageal balloon position slightly influenced the lung elastance, while the PEEP reduced the chest wall elastance without affecting the lung and total respiratory system elastance.ConclusionsParalysis and balloon position did not clinically affect the measurement of the ∆Pes/∆Paw ratio, while they significantly increased the end-expiratory esophageal pressure.

Association Between High-Flow Nasal Cannula and End-Expiratory Esophageal Pressures in Premature Infants.

High-flow nasal cannula (HFNC) is commonly being used to provide noninvasive respiratory support in newborn infants. Continuous distending pressure generated by these devices in preterm infants has not been elucidated. The aim of this work was to determine the association between HFNC flow in L/min and end-expiratory esophageal pressure in cm H2O in premature infants. In a prospective observational study, end-expiratory esophageal pressure measurements were conducted in clinically stable premature infants who required HFNC. The end-expiratory esophageal pressure generated by the HFNC was measured by a regular feeding tube overlying the lower esophagus and connected to a pressure transducer. Each infant had different end-expiratory esophageal pressure measurements at different high flows ranging from 2 to 8 L/min. Nineteen premature infants were studied. Their birthweight (mean ± SD) was 904 ± 574 g, and gestational age was 26.6 ± 3.1 weeks. Overall, 93 end-expiratory esophageal pressure measurements were conducted. At the time of the end-expiratory esophageal pressure measurements, infants were 1,458 ± 828 g and 7.2 ± 4.8 weeks old. At HFNC flows ranging from 2 to 8 L/min, the corresponding esophageal pressures ranged from 2 to 15 cm H2O. There was a statistically significant association between esophageal pressures and flows. In a linear regression model with the end-expiratory esophageal pressure as the dependent variable and HFNC flow as the independent variable, there was a significant correlation between the 2 variables: end-expiratory esophageal pressure (cm H2O) = 1.18 × HFNC (L/min) (r(2) = 0.95, P < .001). HFNC-associated end-expiratory esophageal pressure is measurable in premature infants. There is a significant association between flows and generated esophageal pressures. There is also variability in the amount of end-expiratory esophageal pressure generated. These observations should be kept in mind when using high HFNC flows in preterm infants.

Effect of transpulmonary pressure-directed mechanical ventilation on respiration in severe acute pancreatitis patient with intraabdominal hypertension

To assess the effect of mehanical ventilation (MV) guided by transpulmonary pressure (Ptp) on respiratory mechanics and gas exchange in severe acute pancreatitis patient with intraabdominal hypertension. Twelve severe acute pancreatitis patient with intraabdominal hypertension and acute respiratory distress syndrome(ARDS) underwent mechanical ventilation were involved from Jan to Dec 2013. PEEP levels were set to achieve a Ptp of 0 to 10 cm of water at end expiration. We also limited tidal volume to keep Ptp at less than 25 cm of water at end inspiration. Respiratory mechanics and gas-exchange were measured. Plat pressure (Pplat) increased and the compliance of chest wall (Ccw) decreased when intraabdominal pressure (IAP) increased. Pplat correlated with IAP positively (r2=0.741 9, P<0.05) and Ccw correlated with IAP negtively (r2=0.722 2, P<0.05), respectively.There were not corrletions between IAP and end-expiratory Ptp (Ptp-e) and end-inspiratory Ptp (Ptp-i) (P>0.05). Compared with baseline, after guiding MV with Ptp, the Level of PEEP (14.6±4.2) cmH2O vs (8.3±2.0) cmH2O, and Ptp-e (1.5±0.5) cmH2O vs (-2.3±1.4) cmH2O increased (P<0.05) and Ptp-i did not increase significantly (P>0.05). Ptp-e correlated with PEEP (r2=0.549, P<0.05) and end-expiratory esophageal pressure (Pes-e) (r2=0.260, P<0.05). Ptp-i correlated with Pplat (r2=0.523, P<0.05) and end-inspiratory esophageal pressure (Pes-i) (r2=0.231, P<0.05), but did not correlate with Tidal volume(VT) (r2=0.052 4, P>0.05). Compared with baseline, lung compliance (CL) (48.1±10.3) cmH2O vs (25.7±6.4) cmH2O and oxygenation index (PaO2/FiO2) (235±48) mmHg vs (160±35) mmHg improved obviously (P<0.05), dead space fraction (VD/VT) (0.48±0.07) vs (0.59±0.06) decreased (P<0.05), but Ccw and respiratory compliance(Cr) didn't improve (P>0.05). Transpulmonary pressure-directed mechanical ventilation in ARDS secondary to severe acute pancreatitis patient with intraabdominal hypertension could not only recruit the collapsed alveoli, improve lung compliance, increase oxygenation index and decrease dead space ventilation but also monitor lung stress to avoid alveoli overinflation, which might be lung protective.

Transpulmonary pressure and lung elastance can be estimated by a PEEP-step manoeuvre.

Transpulmonary pressure is a key factor for protective ventilation. This requires measurements of oesophageal pressure that is rarely used clinically. A simple method may be found, if it could be shown that tidal and positive end-expiratory pressure (PEEP) inflation of the lungs with the same volume increases transpulmonary pressure equally. The aim of the present study was to compare tidal and PEEP inflation of the respiratory system. A total of 12 patients with acute respiratory failure were subjected to PEEP trials of 0-4-8-12-16 cmH2O. Changes in end-expiratory lung volume (ΔEELV) following a PEEP step were determined from cumulative differences in inspiratory-expiratory tidal volumes. Oesophageal pressure was measured with a balloon catheter. Following a PEEP increase from 0 to 16 cmH2O end-expiratory oesophageal pressure did not increase (0.5 ± 4.0 cmH2O). Average increase in EELV following a PEEP step of 4 cmH2O was 230 ± 132 ml. The increase in EELV was related to the change in PEEP divided by lung elastance (El) derived from oesophageal pressure as ΔPEEP/El. There was a good correlation between transpulmonary pressure by oesophageal pressure and transpulmonary pressure based on El determined as ΔPEEP/ΔEELV, r(2) = 0.80, y = 0.96x, mean bias -0.4 ± 3.0 cmH2 O with limits of agreement from 5.4 to -6.2 cmH2O (2 standard deviations). PEEP inflation of the respiratory system is extremely slow, and allows the chest wall complex, especially the abdomen, to yield and adapt to intrusion of the diaphragm. As a consequence a change in transpulmonary pressure is equal to the change in PEEP and transpulmonary pressure can be determined without oesophageal pressure measurements.

Positive end-expiratory pressure adjustment in parenchimal respiratory failure: static pressure-volume loop or transpulmonary pressure?

The aim of the study was compare the prognostic value, efficacy and safety ofpositive end-expiratory pressure (PEEP) adjustment in conformity with lower inflection point of static "pressure-volume" loop (LIP) or end-expiratory esophageal pressure (EEEP) in parenchymal respiratory failure. We included in the study 56 patients (39 males) at age 47 +/- 17.8 years with parenchymal respiratory failure (PaO2/FiO2 < 250 mmHg, bilateral infiltrates on chest X-ray or lung CT scan, no signs of left ventricular failure), who were mecAanically ventilated for less than 48 hours. All patients were sedated and paralyzed. We measured intra- Sabdominal pressure, PaO2/FiO2, PaCO2, alveolar dead space (Vdalv), plotted static "pressure-volume" loop by low flow technique in range of 0 to 40 mbar, recording LIP Then we placed nasogastric tube with balloon for esophageal pressure measurement and measured esophageal pressure at PEEP range from 8 to 20 mbar (with 2 mbar steps) and recorded plateau pressure (Pplat), transpulmonary plateau pressure (Ptp plat), transpulmonary pressure at PEEP level (Ptp PEEP), static compliance of respiratory system (Cstat), lung compliance (Clung), chest wall compliance (Ccw) at every step. Also by volumetric capnography technique we measured end-tidal carbon dioxide concentration (EtCO2), minute volume of exhaled carbon dioxide (VCO2) volume of exhaled carbon dioxide by single breath (VtCO2) and calculate VC2/EtCO2 as a surrogate marker of pulmnonary perfusion. After that we set PEEP at EEEP level (at zero end-expirato- my ranspulmonary pressure) and recorded changes of PaO2/FiO2 and Vdalv. LIP value was 5 (6-10) mbar and it was less than empirically set PEEP in most of patients before enrollment and had no prognostic value for PEEP setting. EEEP level was 14 (12-18.25) mbar and it was higher than LIP in 96.4% patients. Distribution of EEEP values was close to normal unlike LIP Chest wall compliance was less than normal (100 ml/mbar) in 46% of patients. EEEP has correlation with body mass index (rho 0.554, p=0.002). We did not find any correlation between intra-abdominal pres- sure (IAP) and EEEP (p=0.376) or IAP and LIP (p=0.464). PEEP levels higher than 14 mbar led to significant decrease in Cstat and Clung (p<0.001). We observed significant decrease in VCO at PEEP levels more than 16 mbar, i.e., more than EEEP median. PEEP levels more than 16 mbar decreased VCO2/EtCO2, (decreased pulmonary perfusion) from 7.47 (6.54-8.7) at PEEP 14 mbar to 7.32 (6.35-8.76) at PEEP 20 mbar (p=0.004). PEEP setting at EEEP level increased PaO/FiO2 from 205 (154-235) to 280 (208-358) mmHg (p<0.001), did hot change Vdalv (p=0.093) and decreased Cstat and Clung in the most of patients (64.3%). L1P was lower than empirically set PEEP in most patients and did not help to optimize gas exchange. PEEP setting at EEEP level in patients with parenchimal respiratory failure increases PaO/FiO, (reflects opening of collapsed alveoli), decreases volume of expired carbon dioxide and decreases lung compliance (reflects overdistenion of opened alveoli). VCO2/EtCO2 ratio decreases (decreased pulmonary perfusion) at PEEP levels more than 16 mbar, which was more than EEEP.

Pleural Pressure and Optimal Positive End-Expiratory Pressure Based on Esophageal Pressure Versus Chest Wall Elastance

1) To compare two published methods for estimating pleural pressure, one based on directly measured esophageal pressure and the other based on chest wall elastance. 2) To evaluate the agreement between two published positive end-expiratory pressure optimization strategies based on these methods, one targeting an end-expiratory esophageal pressure-based transpulmonary pressure of 0 cm H2O and the other targeting an end-inspiratory elastance-based transpulmonary pressure of 26 cm H2O.Retrospective study using clinical data.Medical and surgical ICUs.Sixty-four patients mechanically ventilated for acute respiratory failure with esophageal balloons placed for clinical management.Esophageal pressure and chest wall elastance-based methods for estimating pleural pressure and setting positive end-expiratory pressure were retrospectively applied to each of the 64 patients. In patients who were ventilated at two positive end-expiratory pressure levels, chest wall and respiratory system elastances were calculated at each positive end-expiratory pressure level.The pleural pressure estimates using both methods were discordant and differed by as much as 10 cm H2O for a given patient. The two positive end-expiratory pressure optimization strategies recommended positive end-expiratory pressure changes in opposite directions in 33% of patients. The ideal positive end-expiratory pressure levels recommended by the two methods for each patient were discordant and uncorrelated (R = 0.05). Chest wall and respiratory system elastances grew with increases in positive end-expiratory pressure in patients with positive end-expiratory esophageal pressure-based transpulmonary pressures (p < 0.05).Esophageal pressure and chest wall elastance-based methods for estimating pleural pressure do not yield similar results. The strategies of targeting an end-expiratory esophageal pressure-based transpulmonary pressure of 0 cm H2O and targeting an end-inspiratory elastance-based transpulmonary pressure of 26 cm H2O cannot be considered interchangeable. Finally, chest wall and respiratory system elastances may vary unpredictably with changes in positive end-expiratory pressure.

Value and Limitations of Transpulmonary Pressure Calculations During Intra-Abdominal Hypertension

To clarify the effect of progressively increasing intra-abdominal pressure on esophageal pressure, transpulmonary pressure, and functional residual capacity. Controlled application of increased intra-abdominal pressure at two positive end-expiratory pressure levels (1 and 10 cm H2O) in an anesthetized porcine model of controlled ventilation. Large animal laboratory of a university-affiliated hospital. Eleven deeply anesthetized swine (weight 46.2 ± 6.2 kg). Air-regulated intra-abdominal hypertension (0-25 mm Hg). Esophageal pressure, tidal compliance, bladder pressure, and end-expiratory lung aeration by gas dilution. Functional residual capacity was significantly reduced by increasing intra-abdominal pressure at both positive end-expiratory pressure levels (p ≤ 0.0001) without corresponding changes of end-expiratory esophageal pressure. Above intra-abdominal pressure 5 mm Hg, plateau airway pressure increased linearly by ~ 50% of the applied intra-abdominal pressure value, associated with commensurate changes of esophageal pressure. With tidal volume held constant, negligible changes occurred in transpulmonary pressure due to intra-abdominal pressure. Driving pressures calculated from airway pressures alone (plateau airway pressure--positive end-expiratory pressure) did not equate to those computed from transpulmonary pressure (tidal changes in transpulmonary pressure). Increasing positive end-expiratory pressure shifted the predominantly negative end-expiratory transpulmonary pressure at positive end-expiratory pressure 1 cm H2O (mean -3.5 ± 0.4 cm H2O) into the positive range at positive end-expiratory pressure 10 cm H2O (mean 0.58 ± 1.2 cm H2O). Despite its insensitivity to changes in functional residual capacity, measuring transpulmonary pressure may be helpful in explaining how different levels of positive end-expiratory pressure influence recruitment and collapse during tidal ventilation in the presence of increased intra-abdominal pressure and in calculating true transpulmonary driving pressure (tidal changes of transpulmonary pressure). Traditional interpretations of respiratory mechanics based on unmodified airway pressure were misleading regarding lung behavior in this setting.

End-expiratory esophageal pressure versus lower inflection point in acute lung injury

No recommendations available concerning protocols of static PV loop and esophageal pressure measurements use set positive end-expiratory pressure (PEEP). The aim of the study was evaluation of the significance of the lower inflection point (LIP) and esophageal pressure monitoring for PEEP adjustment in ALI and ARDS.

Lung elastance and transpulmonary pressure can be determined without using oesophageal pressure measurements

The aim of the present study was to demonstrate that lung elastance and transpulmonary pressure can be determined without using oesophageal pressure measurements. Studies were performed on 13 anesthetized and sacrificed ex vivo pigs. Tracheal and oesophageal pressures were measured and changes in end-expiratory lung volume (ΔEELV) determined by spirometry as the cumulative inspiratory-expiratory tidal volume difference. Studies were performed with different end-expiratory pressure steps [change in end-expiratory airway pressure (ΔPEEP)], body positions and with abdominal load. A PEEP increase results in a multi-breath build-up of end-expiratory lung volume. End-expiratory oesophageal pressure did not increase further after the first expiration, constituting half of the change in ΔEELV following a PEEP increase, even though end-expiratory volume continued to increase. This resulted in a successive left shift of the chest wall pressure-volume curve. Even at a PEEP of 12 cmH(2) O did the end-expiratory oesophageal (pleural) pressure remain negative. A PEEP increase resulted in a less than expected increase in end-expiratory oesophageal pressure, indicating that the chest wall and abdomen gradually can accommodate changes in lung volume. The rib cage end-expiratory spring-out force stretches the diaphragm and prevents the lung from being compressed by abdominal pressure. The increase in transpulmonary pressure following a PEEP increase was closely related to the increase in PEEP, indicating that lung compliance can be calculated from the ratio of the change in end-expiratory lung volume and the change in PEEP, ΔEELV/ΔPEEP.

Comparison of Conventional and Segmental Analysis on High Resolution Manometry (HRM)

Purpose: HRM demonstration of three contraction segments in the esophageal body has added to our understanding of esophageal motor physiology. Despite this advance, pre-HRM parameters continue to be applied to HRM analysis. We investigated differences between conventional and segmental analysis of HRM Clouse plots in symptomatic subjects and normal controls. Methods: HRM contour plots were compared between a reflux group (n=110, 49±1.4 yr, 55F/55M) with abnormal pH study, erosive esophagitis on endoscopy or Barrett's esophagus on histopathology; a non-reflux group (n=74, 48±2.3 yr, 48F/26M) with esophageal symptoms but normal pH study and endoscopy; and controls (n=12, 30±0.9 yr, 7F/5M). Achalasia and its variants, aperistalsis and post surgical states were excluded. Peristaltic performance, peak contraction amplitude (PCA) in either smooth muscle segment, averaged contraction amplitude (ACA, 3 & 8 cm proximal to LES), segment anatomy, and end-expiratory lower esophageal sphincter pressure (LESP) were extracted. At 30 mmHg, sequences were designated fragmented if one smooth muscle segment was absent or if the two segments were separated by a pressure trough and failed if both smooth muscle segments were absent. Results: A total of 1827 swallows were analyzed in symptomatic subjects, and 120 in controls. As expected, reflux subjects had lower ACA (82.9 ±3.3 vs. 116.6 ±5.7 mmHg, p<0.0001) and LESP (7.8±0.7 vs. 16.2±1.6 mmHg, p<0.0001) compared to non-reflux group; similar findings were seen using PCA (119.7±1.5 vs. 161.3±2.6 mmHg, p<0.0001). PCA in controls (160± 3.7 mmHg) was comparable to non-reflux but significantly higher than reflux subjects. There were 44.4% (reflux) and 38.3% (non-reflux) gains in measured amplitude using PCA rather than ACA. Further, 41.1% fewer failed sequences (87 vs. 123) were seen in the reflux group with segment analysis (p=0.01); in the non-reflux group, the change from 20 to 15 failed was not significant; no change was noted in the controls. Fragmented contractions were significantly more prevalent in the reflux group (18.1%) compared to non-reflux (4.1%) or controls (7.5%, p<0.0001). Discordance between conventional and segmental analysis was 27.2% in the reflux group, but only 5.4% in the non-reflux group (p<0.001). Composite failed and fragmented sequences amounting to >30% of the evaluated wet swallows significantly segregated the reflux group from the non-reflux group (34.5% vs. 4.1%, OR 12.5, 95% CI 3.5-34.6, p<0.0001). Conclusion: New HRM analysis paradigms may provide novel insight into esophageal peristaltic function, especially in subjects with hypomotile patterns. Further studies are required to determine if these new parameters improve prediction of patient outcome.