ORIGINAL ARTICLE
Transpulmonary pressure and lung elastance can be estimated by a PEEP-step manoeuvre S. Lundin, C. Grivans and O. Stenqvist Department of Anesthesiology and Intensive Care, Sahlgrenska University Hospital, Gothenburg, Sweden
Correspondence S. Lundin, Department of Anesthesiology and Intensive Care, Sahlgrenska University Hospital, 413 45 Gothenburg, Sweden E-mail: [email protected] Conflicts of interest O. S. and S. L. have shares in the Lung Barometry Company, which owns a patent on measurement of lung elastance and transpulmonary pressure. C. G. has no conflict of interest. Funding This study was supported by grants from the Swedish Heart and Lung Foundation, Sahlgrenska Academy at the University of Gothenburg and the Medical Society of Gothenburg, Sweden. Submitted 13 October 2014; accepted 15 October 2014; submission 27 June 2014. Citation Lundin S, Grivans C, Stenqvist O. Transpulmonary pressure and lung elastance can be estimated by a PEEP-step manoeuvre. Acta Anaesthesiologica Scandinavica 2014 doi: 10.1111/aas.12442
Background: 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. Methods: A total of 12 patients with acute respiratory failure were subjected to PEEP trials of 0-4-8-12-16 cmH2O. Changes in endexpiratory 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. Results: Following a PEEP increase from 0 to 16 cmH2O endexpiratory 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, r2 = 0.80, y = 0.96x, mean bias −0.4 ± 3.0 cmH2O with limits of agreement from 5.4 to −6.2 cmH2O (2 standard deviations). Conclusion: 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.
Editorial comment: what this article tells us This study shows that the change in end-expiratory lung volume following a PEEP increase is determined by the size of the PEEP step and lung compliance. The likely explanation is that the rib cage springs out force, which at end-expiration seems to tense the diaphragm, and prevents the abdominal pressure from affecting the lung, even when PEEP is increased. As a consequence, lung compliance and transpulmonary pressure, which is the key factor of ventilator-induced lung injury, can be determined by a simple PEEP-step procedure.
Acta Anaesthesiologica Scandinavica (2014) © 2014 The Acta Anaesthesiologica Scandinavica Foundation. Published by John Wiley & Sons Ltd
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The key factor for protective ventilation is the pressure affecting the lung: the transpulmonary pressure. A prerequisite for transpulmonary pressure determination is oesophageal pressure measurements, but in spite of scientific consensus and promotion since many years, the use in intensive care units (ICUs) is still rare.1 A simple method to calculate lung elastance (El) and transpulmonary pressure may change this disappointing progress as suggested by a previous animal study.2 In 1982, Katz and colleagues3 described the time-course of a positive end-expiratory pressure (PEEP) inflation of the respiratory system as a process involving multiple breaths, before a new pressure/volume (P/V) equilibrium at a higher PEEP level was established. It was later shown that fast and slow compartments were involved in a PEEP-induced inflation of the respiratory system.4 Later an incremental PEEP trial was introduced as an alternative method to the super syringe technique for slow inflation of the respiratory system to determine static compliance.5,6 The right-upwards shift of consecutive airway P/V curves when increasing PEEP was interpreted as recruitment, but Gattinoni and coworkers showed that a PEEP increase resulted in an inflation of the lung from non-dependent to dependent regions7 and that recruitment was not a major event during PEEP inflation of the respi-
ratory system.8–10 It has also been shown in a study of PEEP steps using electric impedance tomography that not only a PEEP increase, but also a tidal inflation causes inflation of the lung from non-dependent to dependent regions.11 As collapsed alveoli are mainly a dependent phenomenon, PEEP increase can be regarded as another way of inflating the lung as compared with tidal inflation.8,9 During PEEP-step inflation in an isolated lung to a certain lung volume, static end-expiratory airway pressure at that lung volume will be equal to the static end-inspiratory plateau pressure of a tidal inspiration to the same lung volume. In the isolated lung, the airway pressure is equal to the transpulmonary pressure, and as a consequence, transpulmonary pressure at that lung volume is the same and independent of mode of inflation, PEEP or tidal inflation. Thus, irrespective of method of inflation – a PEEP-step or a tidal inflation – end-inspiratory and end-expiratory transpulmonary P/V points are positioned on a common lung P/V curve. We hypothesize that also in the lung in situ, during a PEEP-step inflation, the transpulmonary end-inspiratory and endexpiratory P/V points are positioned on a common lung P/V curve (Fig. 1). The aim of the study was to elucidate the physiological course of events and their time dependency, i.e. changes in airway and oesophageal
Fig. 1. Shows two principal ways to inflate the lungs with equally large increases in lung volume. Left panel: Airway (red) and hypothesized lung (blue) pressure/volume curves. Right panel: The airway pressure needed to inflate the lung and displace the chest wall is equal to tidal variation in airway pressure (ΔPaw). The change in PEEP needed to inflate the lung to the same volume as the tidal volume from the lower PEEP level is considerably lower, indicating that the difference between the end-inspiratory airway pressure of a tidal volume from the lower PEEP level and the end-expiratory pressure at the high PEEP level may be equal to the tidal variation in oesophageal pressure of the tidal volume (ΔPes) from the low PEEP level (green). ΔEELV, change in end-expiratory lung volume; ΔPEEP, change in end-expiratory airway pressure; ΔPawEE, change in end-expiratory airway pressure; ΔPaw, tidal variation in airway pressure; ΔPes, tidal variation in oesophageal pressure; ΔPtpVT=ΔEELV, tidal variation in transpulmonary pressure of a tidal volume equal to the change in end-expiratory lung volume. Acta Anaesthesiologica Scandinavica (2014)
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Table 1 Patient characteristics at baseline. Patient
Sex
Age, year
BMI
P/F ratio, kPa
PEEP, cmH2O
Intrinsic PEEP, cmH2O
Infiltrate on X-ray
Diagnosis
1 2 3 4 5 6 7 8 9 10 11 12
F M F M F M F M M F M F
78 65 70 47 70 86 29 64 57 64 60 45
27 28 38 24 21 26 18 29 31 27 23 35
33 29 23 31 29 37 46 20 41 39 23 35
10 12 10 8 6 12 10 14 5 10 10 10
3 4 10 1 0 0 0 1 3 0 4 4
2/4 2/4 2/4 1/4 2/4 2/4 2/4 2/4 0/4 1/4 2/4 2/4
Pneumonia Pancreatitis Aspiration pneumonia Aspiration pneumonia AAA, pleural exudate Abdominal sepsis Aspiration pneumonia AAA, ischemic colitis Hepatic failure Polytrauma Traumatic brain injury Urosepsis Scoliosis
BMI, body mass index; P/F ratio, PaO2/FiO2; FRC, functional residual capacity; AAA, acute abdominal aneurysm; TBI, traumatic brain injury; PEEP, positive end-expiratory pressure.
pressure and in lung volume following a PEEP increase in patients with acute respiratory failure. Methods Patients The study was performed in a mixed ICU of a university hospital and approved by the Local Ethics Committee of Gothenburg, Sweden, Box 100, S-405 30 Gothenburg, protocol number: 112-08 approval date Aug 24, 2008. Informed consent was obtained from next of kin. Patients with chronic obstructive pulmonary disease were excluded. Twelve mechanically ventilated patients with acute respiratory failure were included (Table 1). Before the start of protocol, sedation was deepened and muscle relaxant (rocuronium 40–50 mg) given. Pressure and volume measurements Tracheal pressure was measured via a pressure line introduced through the endotracheal tube, connected to a standard pressure receptor for intravascular measurements (PVB Medizintechnik, Kirchseeon, Germany). Oesophageal pressure was measured with a balloon catheter (Nutrivent, SIDAM S.R.L., Mirandola, Italy) positioned in the lower part of the oesophagus.12 Correct positioning was verified by a modified ‘Baydur maneuver’,13 where the rib cage was com-
pressed during airway occlusion.14–16 Ventilatory flow and volume were measured at the Y-piece with a D-lite side-stream spirometer connected to an AS/3 multi-module monitor (GE Healthcare, Helsinki, Finland). End-expiratory lung volume increase was determined during the first 10 breaths following a PEEP step as the cumulative difference in inspiratory-expiratory tidal volume (Vt) using the spirometer of the Servo-i ventilator (Maquet Critical Care, Solna, Sweden).17 Electric impedance tomography (Dräger Medical, Lübeck, Germany) with an electrode belt placed around the chest wall at the 5th intercostal space was used for online visualisation of volume changes (Fig. 1).17–19
Study protocol Patients in supine position were ventilated in a volume-control mode at a rate of 20 breaths/min, with Vts of 6–7 ml/kg ideal body weight. Correct positioning of the oesophageal catheter was verified at start and end of the protocol and between every PEEP manoeuvre. To obtain a reference level of absolute oesophageal pressure at functional residual capacity (FRC), PEEP trials were started at ZEEP. Three PEEP-step manoeuvres; 0-4-8-12-16-0 cmH2O twice; and then 0-48-12-16-12-8-4-0 cmH2O, with 2 min at each PEEP level were performed. This study reports results from the incremental PEEP manoeuvres.
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conventionally determined at the higher PEEP level.
Calculations Inspiratory driving pressure of the total respiratory system (ΔPaw) was PawEI – PawEE, where PawEI and PawEE were end-inspiratory and endexpiratory airway plateau pressures, respectively. Tidal transpulmonary pressure variation (ΔPtp) was calculated as the ΔPaw − ΔPes, where ΔPes was the tidal oesophageal pressure variation. Total respiratory system elastance (Etot) was calculated as ΔPaw/Vt, where ΔPaw was the tidal airway pressure variation and Vt the tidal volume. Tidal chest wall elastance (EcwVT) was calculated as ΔPes/Vt. Conventional lung elastance (Elconv) was calculated as Etot – EcwVT. Expiratory chest wall elastance of a PEEP inflation (EcwEXP) between ZEEP and 16 cmH2O of PEEP was calculated as the difference in endexpiratory oesophageal pressure between 16 and 0 cmH2O of PEEP, divided by the change in endexpiratory lung volume (ΔEELV) between these PEEP levels. The expected increase in end-expiratory oesophageal pressure following a PEEP step, if the chest wall is regarded as an elastic entity, was calculated from the spirometrically determined cumulative increase in lung volume (ΔEELV) from 0 to 16 cmH2O of PEEP multiplied by mean chest wall elastance and compared with the observed increase in end-expiratory oesophageal pressure in each patient.
Transpulmonary pressure based on oesophageal pressure measurements Transpulmonary pressure was calculated at ZEEP, end-expiration and end-inspiration of PEEP 4 (EE4, EI4), end-expiration and end-inspiration of PEEP 8 (EE8, EI8), end-expiration and endinspiration of PEEP 12 (EE12, EI12) and endexpiration and end-inspiration of PEEP 16 (EE16, EI16) to form a lung P/V curve. End-expiratory transpulmonary pressure was calculated as ΔEELV × Elconv1, where ΔEELV is the change in end-expiratory lung volume between two PEEP levels and Elconv determined from the tidal airway and oesophageal pressure variations (ΔPaw, ΔPes) at the lower of the PEEP level, as (ΔPaw-ΔPes)/Vt. End-inspiratory transpulmonary pressure at the higher PEEP level is the ΔEELV × El1 + Vt × El2, where El2 is the El
Transpulmonary pressure based on El determined as ΔPEEP/ΔEELV, the PEEP-step method (ElPSM) End-expiratory transpulmonary pressure increase between two adjacent PEEP levels is equal to ΔPEEP. End-inspiratory transpulmonary pressure of a Vt from the low PEEP level was calculated as ΔPEEP + ElPSM × Vt, where ElPSM = ΔPEEP/ ΔEELV at the same lung volume above FRC as the end-inspiratory Vt from the lower PEEP level. At the final (highest) PEEP level, ElPSM was determined as the ΔPawEIP/ΔEELV, where ΔPawEIP is the difference in end-inspiratory airway plateau pressure between the second highest and the highest PEEP level, assuming that chest wall elastance is constant when changing PEEP.2,20 As the calculation was performed PEEP step by PEEP step, transpulmonary pressure at all endexpiratory and end-inspiratory P/V points (ZEEP, EE4, EI4, EE8, EI8, EE12, EI12 and EE16 and EI16) was determined and non-linearity of lung mechanics identified. Statistical analysis Data are presented as mean ± standard deviation (SD). Power analysis was performed using a web-based statistical tool (http://www .quantitativeskills.com). To detect a 50% difference, with an SD for the difference of 50% (paired design), between predicted versus observed increase in end-expiratory oesophageal pressure between ZEEP and 16 cmH2O PEEP increase, 10 patients were needed at a power of 80%, a significance level of 0.05. To allow for missing values, 12 patients were included. Comparison between predicted and measured changes in oesophageal pressure and increase in EELV between 1st and 10th expiration were analysed by Wilcoxon matched-pairs signed rank test. Data from PEEP trials were analysed using mean values from three manoeuvres. Data consisted of replicated data in pairs, where the underlying true value changes from pair to pair. By performing two-way analysis of variance, the correlation coefficient within subjects was calculated.21,22 Analyses were performed using StatView for Windows, version 5.0.1 (SAS Institute Inc., Cary, NC, USA) Acta Anaesthesiologica Scandinavica (2014)
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and Prism 6 for Windows, version 6.02 (GraphPad Software Inc., La Jolla, CA, USA). Results Incremental PEEP trial 0, 4, 8, 12 and 16 cmH2O A representative recording during the PEEP trial is shown in Fig. 2. The successive increase in lung volume during the incremental PEEP steps was not accompanied by an increase in end-expiratory oesophageal pressure, PesEE. After zeroing PesEE at ZEEP, PesEE was 0.3 ± 1.4 cmH2O at PEEP 4, 1.0 ± 3.1 cmH2O at PEEP 8, 1.3 ± 3.7 cmH2O at PEEP 12 and 0.5 ± 4.0 cmH2O at PEEP 16 cmH2O. If the chest wall was an elastic entity, the PesEE would have been 7.5 ± 4.3 cmH2O at 16 cmH2O of PEEP as compared with the observed value of 0.5 ± 4.0 cmH2O, P < 0.0005 (Figs 2 and 3). Static (expiratory) chest wall elastance between ZEEP and PEEP 16, obtained by dividing the change in end-expiratory oesophageal pressure with the ΔEELV, was 0.6 ± 2.2 cmH2O/l corresponding to an expiratory chest wall compliance of around 1800 ml/cmH2O. The increase in PesEE after the first expiration after a step increase in PEEP of 4 cmH2O was 2.4 ± 4.2 cmH2O, but 2 min later, just before the next increase in PEEP, the PesEE had decreased significantly to 0.7 ± 3.0 cmH2O, P < 0.0001, whereas end-expiratory lung volume increased significantly from 140 ± 69 ml to 230 ± 132 ml, P < 0.0001 (Figs 2 and 3). There was a very good correlation between the change in ΔEELV following the PEEP steps from PEEP 4 to 16 cmH2O, measured by spirometry and the corresponding volume calculated from the change in PEEP and Elconv as ΔPEEP/Elconv, r2 = 0.83, y = 0.93x, within subject correlation 0.95. There was a good correlation between conventional and PEEP step derived El, r2 = 0.76, y = 1.08x. Cumulative increase in end-expiratory transpulmonary pressure when increasing PEEP was closely related to changes in PEEP, and when PEEP was increased to 3.7 ± 0.2, 7.7 ± 0.3, 11.6 ± 0.5 and 15.4 ± 0.7 cmH2O, the increase in end-expiratory transpulmonary pressure was 2.3 ± 1.1, 5.9 ± 1.7, 10.5 ± 2.4 and 15.3 ± 2.0 cmH2O, respectively (Figs 2 and 3).
Fig. 2. Representative PEEP step recording from 0 to 16 cmH2O. Airway (red) and oesophageal (green), transpulmonary (dark blue) pressure and volume by EIT (light blue). The sudden large increase in oesophageal pressure is a peristaltic artifact. Note that the absolute end-expiratory oesophageal pressure does not increase when lung volume increases following PEEP increases. As a consequence, the end-expiratory transpulmonary pressure increases as much as PEEP is increased (indicated by the light blue arrow in the Paw and Ptp panels which are of equal size). EIT, electric impedance tomography; VOLEIT, volume by EIT; Pes, oesophageal pressure; Paw, airway pressure; Ptp, transpulmonary pressure.
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A
B
Fig. 3. (A) Figure based on mean values from the 12 patients. The end-inspiratory airway pressure/volume (P/V) points are connected to form a PEEP inflation P/V curve (thin red line). The end-expiratory airway P/V points (red/blue circles) are connected to form an expiratory P/V curve. Data based on the mean values from the conventional oesophageal pressure measurements form a mean transpulmonary P/V curve (black triangles, open: end-expiratory, filled: end-inspiratory). The conventional transpulmonary P/V curve is closely related to the end-expiratory airway P/V curve. Tidal chest wall P/V curves (green) are depicted starting from measured end-expiratory oesophageal pressure level. The end-inspiratory oesophageal P/V points are connected to a PEEP inflation P/V curve, which together with the fact that the end-expiratory chest wall P/V points are positioned almost vertically, indicate that the PEEP inflation expiratory chest wall elastance is negligible. (B) Manual reconstruction of breath by breath (only inspirations for clarity) of airway (red), oesophageal (green)and transpulmonary (blue) P/V curves of mean data from all patients. Thick arrows indicate P/V curves at P/V equilibrium at each PEEP level. Red/blue circles are the common airway and transpulmonary end-expiratory P/V points. Red, green and blue open circles indicate first end-expiration (and start of first inspiration) P/V points of airway, chest wall and lung after changing PEEP. Note that while the end-expiratory airway P/V points lie constant on the new PEEP level, the corresponding oesophageal P/V points decline towards the baseline level at ZEEP, indicated by black arrows. The consequence of the subsiding end-expiratory oesophageal pressure at each PEEP level results in the end-expiratory transpulmonary pressure of a PEEP step changing as much as the magnitude PEEP change as PawEE-PesEE = PtpEE (PawEE, end-expiratory airway pressure; PesEE, end-expiratory oesophagel pressure; PtpEE, end-expiratory transpulmonary pressure).
There was a good correlation between transpulmonary pressure at ZEEP, EE4, EI4, EE8, EI8, EE12, EI12, EE16 and EI16 (i.e. multiple values for each patient) by conventional oesophageal pressure measurements and transpulmonary pressure based on El determined as ΔPEEP/ ΔEELV (ElPSM), r2 = 0.80, y = 0.96x, with a mean bias of −0.4 ± 3.0 cmH2O with limits of agreement from 5.4 to −6.2 cmH2O (2 SD) (see Fig. 4). Several values for each patients are included, which maybe a limitation in the regression and Bland and Altman analysis.21,22 EcwVT was 10.0 ± 4.8 cmH2O/l at baseline (ZEEP), 9.6 ± 4.7 cmH2O/l at 4 cmH2O PEEP, 8.5 ± 4.1 cmH2O/l at 8 cmH2O PEEP, 7.9 ± 4.1 cmH2O/l at 12 cmH2O PEEP and 8.1 ± 4.3 cmH2O/l at 16 cmH2O PEEP (ns). Patients were also ranked according to cumulative lung volume response to a PEEP increase from 0 to 16 cmH2O, as lung compliance is correlated to aerated lung volume (23). The quartile with the
lowest response had an Etot of 41.0 ± 9.4 cmH2O/l, an El of 36.4 ± 10.8 cmH2O/l and a chest wall elastance of 4.6 ± 3.0 cmH2O/l. Corresponding values for the quartile with the high responders to PEEP were 20.3 ± 3.5, 12.6 ± 2.1 and 7.5 ± 2.8 cmH2O/l, respectively. The low responders had an El/Etot of 0.88 ± 0.08 similar to pulmonary acute respiratory distress syndrome (ARDS) and high responders had an El/Etot of 0.63 ± 0.08, similar to ARDS21 (Fig. 5). Individual transpulmonary pressure-volume curves based on conventional calculation and the corresponding P/V plot based on cumulated ΔEELV versus PEEP showed similar pattern over a wide range of lung compliances, 90–28 ml/ cmH2O (Fig. 6). Discussion We have shown in patients with acute respiratory failure in supine position that during PEEP inflaActa Anaesthesiologica Scandinavica (2014)
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Fig. 4. Correlation and Bland–Altman plots of transpulmonary pressure based on lung elastance determined by conventional oesophageal pressure measurements and based on ΔPEEP/ΔEELV. It is noteworthy that the variability in measurements most likely is mainly related to the oesophageal pressure measurement, which may have a 30% variability,12 whereas ΔEELV measurements seems to have a lower variability.2,17 ΔEELV, change in end-expiratory lung volume; ΔPEEP, change in end-expiratory airway pressure.
Fig. 5. High and low lung volume responders to PEEP. Airway P/V curve at different PEEP levels, red line; end-expiratory airway P/V curve, including an end-inspiratory P/V point calculated as described in methods under ‘Transpulmonary pressure based on El = ΔPEEP/ΔEELV’, blue line. Note that end-expiratory and end-inspiratory airway P/V points are aligned along a common P/V curve in the low responders, where lung elastance is 88% of total respiratory system elastance, while lung elastance in the high volume responders is 63% of total respiratory system elastance and the end-inspiratory airway P/V points are right shifted from the end-expiratory airway P/V curve. ΔEELV, change in end-expiratory lung volume; ΔPEEP, change in end-expiratory airway pressure; P/V, pressure/volume.
tion of the respiratory system, end-expiratory oesophageal pressure remains largely unchanged, and PEEP inflation-related chest wall elastance, calculated as the change in end-expiratory oesophageal pressure divided by the lung volume increase between ZEEP and a PEEP of 16 cmH2O was negligible. EcwVT remained unchanged when increasing PEEP. The tidal lung P/V curves of all the breaths involved in the incremental PEEP steps are lying on a single, common, global lung P/V curve. The increase in lung volume is closely correlated to the PEEP change divided by conventional, oesophageal pressure-derived El.
Thus, if the change in lung volume is determined, El can be determined as the change in PEEP divided by the change in lung volume, ΔPEEP/ ΔEELV. If we study an isolated ventilated lung (without a chest wall), where airway pressure is equal to the transpulmonary pressure, and perform an incremental PEEP trial, end-inspiratory airway pressure at a certain lung volume will be equal to the end-expiratory airway pressure at the same lung volume. This means that without the chest wall, transpulmonary pressure at a certain lung volume is independent of mode of inflation and
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Fig. 6. Individual transpulmonary pressure/volume curves based on conventional calculation and the corresponding pressure/volume plot based on lung elastance calculated as ΔPEEP/ΔEELV. The transpulmonary pressure/volume curves based on oesophageal pressure measurements and on ΔPEEP/ΔEELV correlated very well. The patients are displayed in order of lung volume response to PEEP. Note that lung compliance (Cl) calculated as the ratio of the change in end-expiratory lung volume between PEEP level 0 and 16 cmH2O, plus a tidal volume and the end-inspiratory transpulmonary pressure at PEEP 16 cmH2O, was closely related to the volume response to PEEP, which is in accordance with Cl being correlated to aerated lung volume.23 ΔEELV, change in end-expiratory lung volume; ΔPEEP, change in end-expiratory airway pressure.
end-expiratory and end-inspiratory airway P/V points are aligned on a common transpulmonary P/V curve. If we study patients in vivo with pulmonary ARDS, with little influence of the chest wall, the airway P/V points are positioned on a common P/V curve. In contrast, we observed that in patients with extrapulmonary ARDS, the endinspiratory airway P/V points from the low PEEP level were right shifted from the end-expiratory airway P/V point of the higher PEEP level, as a result of chest wall influence.20 In the present study, we ranked the patients according to the end-expiratory lung volume response to change in PEEP from 0 to 16 cmH2O. Airway P/V points
of the quartile of patients with the least response, where El was 88 % of Etot, showed a pattern similar to the isolated lung and to pulmonary ARDS, whereas P/V points of the most responsive quartile, where El was 63% of Etot, showed a pattern similar to extrapulmonary ARDS, with the end-inspiratory airway P/V points right shifted from the end-expiratory airway P/V curve (Fig. 5). Thus, the right shift seems to be a consequence of chest wall influence and the change in end-expiratory transpulmonary pressure between two PEEP levels is equal to the change in endexpiratory airway pressure, ΔPEEP. This is confirmed in the present study, where tidal variation in transpulmonary pressure of a Vt equal to the Acta Anaesthesiologica Scandinavica (2014)
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ΔEELV from the low PEEP level was closely correlated to change in PEEP and increase in endexpiratory lung volume was closely related to ΔPEEP divided by Elconv. In accordance with this, the difference between the end-inspiratory airway pressure of a Vt equal to the ΔEELV (Vt=ΔEELV) from the low PEEP level and the endexpiratory airway pressure at the high PEEP level, is equal to the tidal variation in oesophageal (pleural) pressure of a Vt=ΔEELV from the low PEEP level (Fig. 1). The implication of the pressure changes following a PEEP increase, i.e. that the end-expiratory transpulmonary pressure changes as much as ΔPEEP, is that there is no or minimal change in end-expiratory oesophageal pressure when increasing PEEP. This was supported by the finding that when increasing PEEP from 0 to 16 cmH2O, resulting in an average end-expiratory lung volume increase of 900 ml, average endexpiratory oesophageal pressure increased only 0.5 cmH2O (Fig. 3B). It has been shown that there is no relation between changes in end-expiratory oesophageal pressure and chest wall elastance,24–28 but there is no generally accepted explanation for the dissociative behaviour of oesophageal pressure in response to tidal and PEEP inflation of the respiratory system.27–34 If there was a relation between chest wall elastance and changes in PesEE following a change in PEEP, the PesEE at 16 cmH2O in PEEP would have been significantly higher, 7.5 ± 4.3 cmH2O compared with the measured value of 0.5 ± 2.0 cmH2O. The lack of, or minimal change in end-expiratory oesophageal pressure is not consistent with the concept of the chest wall as an elastic entity outside another elastic entity, the lung, both trying to recoil to a lower volume.35 If this was the case, the lung would collapse at FRC, when there is no pressure gradient between the outside of the thorax and the alveoli. In reality, the rib cage prevents collapse, as it strives to spring out to a higher volume, counterbalancing the recoil of the lung. The chest wall has previously been described as an elastic entity. As an alternative, we now propose that the rib cage and the diaphragm passively interacts with the abdomen, which can be regarded as a fluid-filled container, a weight, that is displaced in caudal direction, rather than inflated during inspirations.35–37 The position of
the diaphragm at end-expiration is determined by the balance between the rib cage spring-out force, the abdominal pressure and the recoil of the lung, resulting in a negative pleural pressure.38 If abdominal pressure is increased, as in extrapulmonary ARDS, the diaphragm is pushed in cranial direction and the ventral rib cage wall is pulled in dorsal direction, reducing the vertical diameter of the thoracic cavity.39,40 This will reduce lung volume, whereas end-expiratory oesophageal pressure remains largely unchanged. Even when PEEP is applied to expand the lungs, the rib cage spring-out force, which is active up to 70–80% of total lung capacity,35,37 will counteract the last part of the expiration.41 This will cause the diaphragm to be tensed at end-expiration, preventing the abdominal pressure to be transmitted to the thoracic cavity. As a result, end-expiratory oesophageal pressure will remain unchanged2,33,42,43 even when lung volume is increased by PEEP in accordance with a previous study.2 A PEEP-induced inflation of the respiratory system involves multiple breaths (Fig. 3B), and establishment of a new P/V equilibrium; requires a driving pressure to inflate the lung and displace the chest wall complex, which is exerted during inspirations; and is equal to ΔEELV × Etot. The driving pressure to displace the chest wall is equal to ΔEELV × EcwVT, and the pressure needed for inflating the lung is ΔEELV × (Etot − EcwVT), which is equal to El times the ΔEELV. If tidal inflation is equal to the ΔEELV by a PEEP increase, the tidal transpulmonary pressure, of such a Vt will be equal to the change in PEEP. The breath-by-breath build-up of volume after an increase in PEEP is an expiratory phenomenon, where less breathing gas is expired than inspired. The first expiration increase in lung volume after increasing PEEP is equal to ΔPEEP/ Etot due to closing of the expiratory valve at the set PEEP level before the expiration is complete, detaining a volume equal to ΔPEEP/Etot.3 The following44 breath-by-breath volume build-up is also an expiratory phenomenon, which is a result of the retardation of the last part of each expiration and the tensing of the diaphragm by the rib cage spring-out force,17 whereby expiratory gas is detained in the lung. The PEEP-inflated volume is distributed 50–70% to the rib cage, which means that less than half of the lung volume increase is distributed to the diaphragm.41,45 The abdominal
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cavity has a volume of ≈ 10 l and the upper surface area is ≈ 1000 cm2.41 As less than half of an increase in lung volume is distributed to the diaphragm,41 an increase of 1000 ml will lead to, at the most, a 500 ml of intrusion of the diaphragm into the abdomen, increasing the vertical height of abdominal container by ≈ 0.5 cm, influencing abdominal pressure minimally.34,46 Also, the slow, multi-breath caudal displacement of the diaphragm seems to result in a yielding and adapting of the abdominal wall in other areas (than the diaphragm) to accommodate the part of increase in lung volume that is directed versus the diaphragm. This process is time consuming and more prominent at high volumes,47 and it has been shown that the volume increase may continue for up to an hour.6 Conclusions and clinical implications The interaction among the rib cage, diaphragm and abdominal container indicates that the chest wall works as a hydraulic entity, which impedes inflation as a weight, which is displaced during inspiration. This is supported by the finding that chest wall elastance does not increase with increasing PEEP levels. When an extremely slow inflation of the respiratory system, such as PEEP inflation is used, ample time is provided for the chest wall complex, especially the abdomen, to adapt and yield to the intrusion of the diaphragm. The rib cage spring-out force keeps the diaphragm tensed at end-expiration, preventing the abdominal pressure to be transmitted to the thoracic cavity, which results in unchanged endexpiratory oesophageal pressure when increasing PEEP. As the lung is unaffected by the chest wall complex at end-expiratory P/V equilibrium, the increase in end-expiratory lung volume following a PEEP step is equal to the magnitude of the PEEP step divided by Elconv. If the change in lung volume can be determined by the ventilator pneumotachograph,16 El and consequently transpulmonary pressure may be estimated without using oesophageal pressure measurements just by performing a PEEP change. In contrast to oesophageal pressure measurements, this technique is simple and rapid, demanding only a software addition to the ventilator. We have tested this new concept using mean values from 9 patients with pulmonary and 12
patients with extrapulmonary ARDS, the two extremes of the syndrome,20 and found a very good correlation between transpulmonary pressure calculated using oesophageal pressure measurements compared with the new PEEP-step concept (r2 = 0.98, y = 1.1x + 1.7), supporting our findings.48 Further studies are needed to define suitable PEEP changes, repeatability and precision of measurements for this new method, which may improve rational protective ventilator settings of PEEP and Vt.
References 1. Akoumianaki E, Maggiore SM, Valenza F, Bellani G, Jubran A, Loring SH, Pelosi P, Talmor D, Grasso S, Chiumello D, Guérin C, Patroniti N, Ranieri VM, Gattinoni L, Nava S, Terragni PP, Pesenti A, Tobin M, Mancebo J, Brochard L. The application of esophageal pressure measurement in patients with respiratory failure. Am J Respir Crit Care Med 2014; 189: 520–31. 2. Stenqvist O, Grivans C, Andersson B, Lundin S. Lung elastance and transpulmonary pressure can be determined without using oesophageal pressure measurements. Acta Anaesthesiol Scand 2012; 56: 738–47. 3. Katz JA, Ozanne GM, Zinn SE, Fairley HB. Time course and mechanisms of lung-volume increase with PEEP in acute pulmonary failure. Anesthesiology 1981; 54: 9–16. 4. Fretschner R, Laubscher TP, Brunner JX. New aspects of pulmonary mechanics: ‘slowly’ distensible compartments of the respiratory system, identified by a PEEP step maneuver. Intensive Care Med 1996; 12: 1328–34. 5. Putensen C, Baum M, Koller W, Putz G. [The PEEP wave: an automated technic for bedside determination of the volume/pressure ratio in the lungs of ventilated patients]. Anaesthesist 1989; 38: 214–9. 6. Putensen C, Baum M, Hormann C. Selecting ventilator settings according to variables derived from the quasi-static pressure/volume relationship in patients with acute lung injury. Anesth Analg 1993; 77: 436–47. 7. Gattinoni L, Pelosi P, Crotti S, Valenza F. Effects of positive end-expiratory pressure on regional distribution of tidal volume and recruitment in adult respiratory distress syndrome. Am J Respir Crit Care Med 1995; 151: 1807–14. Acta Anaesthesiologica Scandinavica (2014)
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8. Cressoni MCC, Amini M, Febres D, Gallazzi E, Carlesso E, Cadringher P, Langer T, Chiumello D, Gattinoni L. Recruited lung tissue does not resume normal mechanical properties. Crit Care 2013; 17: P106. 9. Cressoni MGE, Chiurazzi C, Marino A, Briono M, Menga F, Cegada I, Lemos A, Lazzerini M, Carlesso E, Cadringher P, Chiumello D, Gattinoni L. Limits of normality of quantitative thoracic computed tomography analysis. Crit Care 2013; 17: R93. 10. Lowhagen K, Lundin S, Stenqvist O. Regional intratidal gas distribution in acute lung injury and acute respiratory distress syndrome – assessed by electric impedance tomography. Minerva Anestesiol 2010; 76: 1024–35. 11. Stahl CA, Möller K, Steinmann D, Henzler D, Lundin S, Stenqvist O. Determination of ‘recruited volume’ following a PEEP step is not a measure of lung recruitability. Acta Anaesthesiol Scand 2014; Oct 28. [Epub ahead of print]. doi: 10.1111/aas.12432. 12. Chiumello D, Gallazzi E, Marino A, Berto V, Mietto C, Cesana B, Gattinoni L. A validation study of a new nasogastric polyfunctional catheter. Intensive Care Med 2011; 37: 791–5. 13. Baydur A, Behrakis PK, Zin WA, Jaeger M, Milic-Emili J. A simple method for assessing the validity of the esophageal balloon technique. Am Rev Respir Dis 1982; 126: 788–91. 14. Ducros LST, Derenne J-P. Validity of oesophageal pressure measurement for respiratory mechanics studies during ventilation. Eur Respir J 1995; 8 (Suppl 19): 39S. 15. Lanteri CJ, Kano S, Sly PD. Validation of esophageal pressure occlusion test after paralysis. Pediatr Pulmonol 1994; 17: 56–62. 16. Karason S, Karlsen KL, Lundin S, Stenqvist O. A simplified method for separate measurements of lung and chest wall mechanics in ventilator-treated patients. Acta Anaesthesiol Scand 1999; 43: 308–15. 17. Grivans C, Lundin S, Stenqvist O, Lindgren S. Positive end-expiratory pressure-induced changes in end-expiratory lung volume measured by spirometry and electric impedance tomography. Acta Anaesthesiol Scand 2011; 55: 1068–77. 18. Hinz J, Hahn G, Neumann P, Sydow M, Mohrenweiser P, Hellige G, Burchardi H. End-expiratory lung impedance change enables bedside monitoring of end-expiratory lung volume change. Intensive Care Med 2003; 29: 37–43.
19. Frerichs I. Electrical impedance tomography (EIT) in applications related to lung and ventilation: a review of experimental and clinical activities. Physiol Meas 2000; 21: R1–21. 20. Gattinoni L, Pelosi P, Suter PM, Pedoto A, Vercesi P, Lissoni A. Acute respiratory distress syndrome caused by pulmonary and extrapulmonary disease. Different syndromes? Am J Respir Crit Care Med 1998; 158: 3–11. 21. Bland JM, Altman DG. Calculating correlation coefficients with repeated observations: Part 2 – correlation between subjects. BMJ 1995; 310: 633. 22. Bland JM, Altman DG. Calculating correlation coefficients with repeated observations: Part 1 – correlation within subjects. BMJ 1995; 310: 446. 23. Gattinoni L, Pesenti A, Avalli L, Rossi F, Bombino M. Pressure-volume curve of total respiratory system in acute respiratory failure. Computed tomographic scan study. Am Rev Respir Dis 1987; 136: 730–6. 24. Gattinoni L, Mascheroni D, Basilico E, Foti G, Pesenti A, Avalli L. Volume/pressure curve of total respiratory system in paralysed patients: artefacts and correction factors. Intensive Care Med 1987; 13: 19–25. 25. Loring SH, O’Donnell CR, Behazin N, Malhotra A, Sarge T, Ritz R, Novack V, Talmor D. Esophageal pressures in acute lung injury: do they represent artifact or useful information about transpulmonary pressure, chest wall mechanics, and lung stress? J Appl Physiol 2010; 108: 515–22. 26. Pelosi P, Goldner M, McKibben A, Adams A, Eccher G, Caironi P, Losappio S, Gattinoni L, Marini JJ. Recruitment and derecruitment during acute respiratory failure: an experimental study. Am J Respir Crit Care Med 2001; 164: 122–30. 27. Valenza F, Chevallard G, Porro GA, Gattinoni L. Static and dynamic components of esophageal and central venous pressure during intra-abdominal hypertension. Crit Care Med 2007; 35: 1575–81. 28. Plataki M, Hubmayr RD. Should mechanical ventilation be guided by esophageal pressure measurements? Curr Opin Crit Care 2011; 17: 275–80. 29. Gattinoni L, Chiumello D, Carlesso E, Valenza F. Bench-to-bedside review: chest wall elastance in acute lung injury/acute respiratory distress syndrome patients. Crit Care 2004; 8: 350–5. 30. Talmor DS, Loring SH. Esophageal pressures in acute respiratory distress syndrome: how should we interpret and use them? Crit Care Med 2013; 41: e1.
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31. Hubmayr RD. Is there a place for esophageal manometry in the care of patients with injured lungs? J Appl Physiol 2010; 108: 481–2. 32. Guerin C, Richard JC. Comparison of 2 correction methods for absolute values of esophageal pressure in subjects with acute hypoxemic respiratory failure, mechanically ventilated in the ICU. Respir Care 2012; 57: 2045–51. 33. Gulati G, Novero A, Loring SH, Talmor D. Pleural pressure and optimal positive end-expiratory pressure based on esophageal pressure versus chest wall elastance: incompatible results. Crit Care Med 2013; 41: 1951–7. 34. Jakob SM, Knuesel R, Tenhunen JJ, Pradl R, Takala J. Increasing abdominal pressure with and without PEEP: effects on intra-peritoneal, intra-organ and intra-vascular pressures. BMC Gastroenterol 2010; 10: 70. 35. Hedenstierna G. Esophageal pressure: benefit and limitations. Minerva Anestesiol 2012; 78: 959–66. 36. Kubiak BD, Gatto LA, Jimenez EJ, Silva-Parra H, Snyder KP, Vieau CJ, Barba J, Nasseri-Nik N, Falk JL, Nieman GF. Plateau and transpulmonary pressure with elevated intra-abdominal pressure or atelectasis. J Surg Res 2010; 159: e17–24. 37. Agostoni E, Hyatt R. The respiratory system. Mechanics of breathing. Handbook of Physiology, Vol. 3. Bethesda, MD: American Physiological Society, 1986: 113–30. 38. Nunn J. Elastic forces and lung volumes, In: Nunn JF ed. Nunn’s applied respiratory physiology, 4th edn. Oxford: Butterworth-Heinemann, 1995: 36–52. 39. Froese AB, Bryan AC. Effects of anesthesia and paralysis on diaphragmatic mechanics in man. Anesthesiology 1974; 41: 242–55. 40. Butler J. The adaptation of the relaxed lungs and chest wall to changes in volume. Clin Sci (Lond) 1957; 16: 421–33.
41. Hedenstierna G, Strandberg A, Brismar B, Lundquist H, Svensson L, Tokics L. Functional residual capacity, thoracoabdominal dimensions, and central blood volume during general anesthesia with muscle paralysis and mechanical ventilation. Anesthesiology 1985; 62: 247–54. 42. Chelucci GL, Brunet F, Dall’Ava-Santucci J, Dhainaut JF, Paccaly D, Armaganidis A, Milic-Emili J, Lockhart A. A single-compartment model cannot describe passive expiration in intubated, paralysed humans. Eur Respir J 1991; 4: 458–64. 43. de Leon A, Thorn SE, Raoof M, Ottosson J, Wattwil M. Effects of different respiratory maneuvers on esophageal sphincters in obese patients before and during anesthesia. Acta Anaesthesiol Scand 2010; 54: 1204–9. 44. Cortes-Puentes GA, Gard KE, Adams AB, Faltesek KA, Anderson CP, Dries DJ, Marini JJ. Value and limitations of transpulmonary pressure calculations during intra-abdominal hypertension. Crit Care Med 2013; 41: 1870–7. 45. Grimby G, Hedenstierna G, Lofstrom B. Chest wall mechanics during artificial ventilation. J Appl Physiol 1975; 38: 576–80. 46. Wauters J, Claus P, Brosens N, McLaughlin M, Hermans G, Malbrain M, Wilmer A. Relationship between abdominal pressure, pulmonary compliance, and cardiac preload in a porcine model. Crit Care Res Pract 2012; 2012: 763181: 1–6. 47. Sharp JT, Johnson FN, Goldberg NB, Van Lith P. Hysteresis and stress adaptation in the human respiratory system. J Appl Physiol 1967; 23: 487–97. 48. Stenqvist O, Lundin S. Lung elastance and transpulmonary pressure may be determined without using esophageal pressure measurements. Am J Respir Crit Care Med 2014; 190: 120.
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Transpulmonary pressure and lung elastance can be estimated by a PEEP-step manoeuvre S. Lundin, C. Grivans and O. Stenqvist Department of Anesthesiology and Intensive Care, Sahlgrenska University Hospital, Gothenburg, Sweden
Correspondence S. Lundin, Department of Anesthesiology and Intensive Care, Sahlgrenska University Hospital, 413 45 Gothenburg, Sweden E-mail: [email protected] Conflicts of interest O. S. and S. L. have shares in the Lung Barometry Company, which owns a patent on measurement of lung elastance and transpulmonary pressure. C. G. has no conflict of interest. Funding This study was supported by grants from the Swedish Heart and Lung Foundation, Sahlgrenska Academy at the University of Gothenburg and the Medical Society of Gothenburg, Sweden. Submitted 13 October 2014; accepted 15 October 2014; submission 27 June 2014. Citation Lundin S, Grivans C, Stenqvist O. Transpulmonary pressure and lung elastance can be estimated by a PEEP-step manoeuvre. Acta Anaesthesiologica Scandinavica 2014 doi: 10.1111/aas.12442
Background: 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. Methods: A total of 12 patients with acute respiratory failure were subjected to PEEP trials of 0-4-8-12-16 cmH2O. Changes in endexpiratory 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. Results: Following a PEEP increase from 0 to 16 cmH2O endexpiratory 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, r2 = 0.80, y = 0.96x, mean bias −0.4 ± 3.0 cmH2O with limits of agreement from 5.4 to −6.2 cmH2O (2 standard deviations). Conclusion: 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.
Editorial comment: what this article tells us This study shows that the change in end-expiratory lung volume following a PEEP increase is determined by the size of the PEEP step and lung compliance. The likely explanation is that the rib cage springs out force, which at end-expiration seems to tense the diaphragm, and prevents the abdominal pressure from affecting the lung, even when PEEP is increased. As a consequence, lung compliance and transpulmonary pressure, which is the key factor of ventilator-induced lung injury, can be determined by a simple PEEP-step procedure.
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The key factor for protective ventilation is the pressure affecting the lung: the transpulmonary pressure. A prerequisite for transpulmonary pressure determination is oesophageal pressure measurements, but in spite of scientific consensus and promotion since many years, the use in intensive care units (ICUs) is still rare.1 A simple method to calculate lung elastance (El) and transpulmonary pressure may change this disappointing progress as suggested by a previous animal study.2 In 1982, Katz and colleagues3 described the time-course of a positive end-expiratory pressure (PEEP) inflation of the respiratory system as a process involving multiple breaths, before a new pressure/volume (P/V) equilibrium at a higher PEEP level was established. It was later shown that fast and slow compartments were involved in a PEEP-induced inflation of the respiratory system.4 Later an incremental PEEP trial was introduced as an alternative method to the super syringe technique for slow inflation of the respiratory system to determine static compliance.5,6 The right-upwards shift of consecutive airway P/V curves when increasing PEEP was interpreted as recruitment, but Gattinoni and coworkers showed that a PEEP increase resulted in an inflation of the lung from non-dependent to dependent regions7 and that recruitment was not a major event during PEEP inflation of the respi-
ratory system.8–10 It has also been shown in a study of PEEP steps using electric impedance tomography that not only a PEEP increase, but also a tidal inflation causes inflation of the lung from non-dependent to dependent regions.11 As collapsed alveoli are mainly a dependent phenomenon, PEEP increase can be regarded as another way of inflating the lung as compared with tidal inflation.8,9 During PEEP-step inflation in an isolated lung to a certain lung volume, static end-expiratory airway pressure at that lung volume will be equal to the static end-inspiratory plateau pressure of a tidal inspiration to the same lung volume. In the isolated lung, the airway pressure is equal to the transpulmonary pressure, and as a consequence, transpulmonary pressure at that lung volume is the same and independent of mode of inflation, PEEP or tidal inflation. Thus, irrespective of method of inflation – a PEEP-step or a tidal inflation – end-inspiratory and end-expiratory transpulmonary P/V points are positioned on a common lung P/V curve. We hypothesize that also in the lung in situ, during a PEEP-step inflation, the transpulmonary end-inspiratory and endexpiratory P/V points are positioned on a common lung P/V curve (Fig. 1). The aim of the study was to elucidate the physiological course of events and their time dependency, i.e. changes in airway and oesophageal
Fig. 1. Shows two principal ways to inflate the lungs with equally large increases in lung volume. Left panel: Airway (red) and hypothesized lung (blue) pressure/volume curves. Right panel: The airway pressure needed to inflate the lung and displace the chest wall is equal to tidal variation in airway pressure (ΔPaw). The change in PEEP needed to inflate the lung to the same volume as the tidal volume from the lower PEEP level is considerably lower, indicating that the difference between the end-inspiratory airway pressure of a tidal volume from the lower PEEP level and the end-expiratory pressure at the high PEEP level may be equal to the tidal variation in oesophageal pressure of the tidal volume (ΔPes) from the low PEEP level (green). ΔEELV, change in end-expiratory lung volume; ΔPEEP, change in end-expiratory airway pressure; ΔPawEE, change in end-expiratory airway pressure; ΔPaw, tidal variation in airway pressure; ΔPes, tidal variation in oesophageal pressure; ΔPtpVT=ΔEELV, tidal variation in transpulmonary pressure of a tidal volume equal to the change in end-expiratory lung volume. Acta Anaesthesiologica Scandinavica (2014)
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Table 1 Patient characteristics at baseline. Patient
Sex
Age, year
BMI
P/F ratio, kPa
PEEP, cmH2O
Intrinsic PEEP, cmH2O
Infiltrate on X-ray
Diagnosis
1 2 3 4 5 6 7 8 9 10 11 12
F M F M F M F M M F M F
78 65 70 47 70 86 29 64 57 64 60 45
27 28 38 24 21 26 18 29 31 27 23 35
33 29 23 31 29 37 46 20 41 39 23 35
10 12 10 8 6 12 10 14 5 10 10 10
3 4 10 1 0 0 0 1 3 0 4 4
2/4 2/4 2/4 1/4 2/4 2/4 2/4 2/4 0/4 1/4 2/4 2/4
Pneumonia Pancreatitis Aspiration pneumonia Aspiration pneumonia AAA, pleural exudate Abdominal sepsis Aspiration pneumonia AAA, ischemic colitis Hepatic failure Polytrauma Traumatic brain injury Urosepsis Scoliosis
BMI, body mass index; P/F ratio, PaO2/FiO2; FRC, functional residual capacity; AAA, acute abdominal aneurysm; TBI, traumatic brain injury; PEEP, positive end-expiratory pressure.
pressure and in lung volume following a PEEP increase in patients with acute respiratory failure. Methods Patients The study was performed in a mixed ICU of a university hospital and approved by the Local Ethics Committee of Gothenburg, Sweden, Box 100, S-405 30 Gothenburg, protocol number: 112-08 approval date Aug 24, 2008. Informed consent was obtained from next of kin. Patients with chronic obstructive pulmonary disease were excluded. Twelve mechanically ventilated patients with acute respiratory failure were included (Table 1). Before the start of protocol, sedation was deepened and muscle relaxant (rocuronium 40–50 mg) given. Pressure and volume measurements Tracheal pressure was measured via a pressure line introduced through the endotracheal tube, connected to a standard pressure receptor for intravascular measurements (PVB Medizintechnik, Kirchseeon, Germany). Oesophageal pressure was measured with a balloon catheter (Nutrivent, SIDAM S.R.L., Mirandola, Italy) positioned in the lower part of the oesophagus.12 Correct positioning was verified by a modified ‘Baydur maneuver’,13 where the rib cage was com-
pressed during airway occlusion.14–16 Ventilatory flow and volume were measured at the Y-piece with a D-lite side-stream spirometer connected to an AS/3 multi-module monitor (GE Healthcare, Helsinki, Finland). End-expiratory lung volume increase was determined during the first 10 breaths following a PEEP step as the cumulative difference in inspiratory-expiratory tidal volume (Vt) using the spirometer of the Servo-i ventilator (Maquet Critical Care, Solna, Sweden).17 Electric impedance tomography (Dräger Medical, Lübeck, Germany) with an electrode belt placed around the chest wall at the 5th intercostal space was used for online visualisation of volume changes (Fig. 1).17–19
Study protocol Patients in supine position were ventilated in a volume-control mode at a rate of 20 breaths/min, with Vts of 6–7 ml/kg ideal body weight. Correct positioning of the oesophageal catheter was verified at start and end of the protocol and between every PEEP manoeuvre. To obtain a reference level of absolute oesophageal pressure at functional residual capacity (FRC), PEEP trials were started at ZEEP. Three PEEP-step manoeuvres; 0-4-8-12-16-0 cmH2O twice; and then 0-48-12-16-12-8-4-0 cmH2O, with 2 min at each PEEP level were performed. This study reports results from the incremental PEEP manoeuvres.
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conventionally determined at the higher PEEP level.
Calculations Inspiratory driving pressure of the total respiratory system (ΔPaw) was PawEI – PawEE, where PawEI and PawEE were end-inspiratory and endexpiratory airway plateau pressures, respectively. Tidal transpulmonary pressure variation (ΔPtp) was calculated as the ΔPaw − ΔPes, where ΔPes was the tidal oesophageal pressure variation. Total respiratory system elastance (Etot) was calculated as ΔPaw/Vt, where ΔPaw was the tidal airway pressure variation and Vt the tidal volume. Tidal chest wall elastance (EcwVT) was calculated as ΔPes/Vt. Conventional lung elastance (Elconv) was calculated as Etot – EcwVT. Expiratory chest wall elastance of a PEEP inflation (EcwEXP) between ZEEP and 16 cmH2O of PEEP was calculated as the difference in endexpiratory oesophageal pressure between 16 and 0 cmH2O of PEEP, divided by the change in endexpiratory lung volume (ΔEELV) between these PEEP levels. The expected increase in end-expiratory oesophageal pressure following a PEEP step, if the chest wall is regarded as an elastic entity, was calculated from the spirometrically determined cumulative increase in lung volume (ΔEELV) from 0 to 16 cmH2O of PEEP multiplied by mean chest wall elastance and compared with the observed increase in end-expiratory oesophageal pressure in each patient.
Transpulmonary pressure based on oesophageal pressure measurements Transpulmonary pressure was calculated at ZEEP, end-expiration and end-inspiration of PEEP 4 (EE4, EI4), end-expiration and end-inspiration of PEEP 8 (EE8, EI8), end-expiration and endinspiration of PEEP 12 (EE12, EI12) and endexpiration and end-inspiration of PEEP 16 (EE16, EI16) to form a lung P/V curve. End-expiratory transpulmonary pressure was calculated as ΔEELV × Elconv1, where ΔEELV is the change in end-expiratory lung volume between two PEEP levels and Elconv determined from the tidal airway and oesophageal pressure variations (ΔPaw, ΔPes) at the lower of the PEEP level, as (ΔPaw-ΔPes)/Vt. End-inspiratory transpulmonary pressure at the higher PEEP level is the ΔEELV × El1 + Vt × El2, where El2 is the El
Transpulmonary pressure based on El determined as ΔPEEP/ΔEELV, the PEEP-step method (ElPSM) End-expiratory transpulmonary pressure increase between two adjacent PEEP levels is equal to ΔPEEP. End-inspiratory transpulmonary pressure of a Vt from the low PEEP level was calculated as ΔPEEP + ElPSM × Vt, where ElPSM = ΔPEEP/ ΔEELV at the same lung volume above FRC as the end-inspiratory Vt from the lower PEEP level. At the final (highest) PEEP level, ElPSM was determined as the ΔPawEIP/ΔEELV, where ΔPawEIP is the difference in end-inspiratory airway plateau pressure between the second highest and the highest PEEP level, assuming that chest wall elastance is constant when changing PEEP.2,20 As the calculation was performed PEEP step by PEEP step, transpulmonary pressure at all endexpiratory and end-inspiratory P/V points (ZEEP, EE4, EI4, EE8, EI8, EE12, EI12 and EE16 and EI16) was determined and non-linearity of lung mechanics identified. Statistical analysis Data are presented as mean ± standard deviation (SD). Power analysis was performed using a web-based statistical tool (http://www .quantitativeskills.com). To detect a 50% difference, with an SD for the difference of 50% (paired design), between predicted versus observed increase in end-expiratory oesophageal pressure between ZEEP and 16 cmH2O PEEP increase, 10 patients were needed at a power of 80%, a significance level of 0.05. To allow for missing values, 12 patients were included. Comparison between predicted and measured changes in oesophageal pressure and increase in EELV between 1st and 10th expiration were analysed by Wilcoxon matched-pairs signed rank test. Data from PEEP trials were analysed using mean values from three manoeuvres. Data consisted of replicated data in pairs, where the underlying true value changes from pair to pair. By performing two-way analysis of variance, the correlation coefficient within subjects was calculated.21,22 Analyses were performed using StatView for Windows, version 5.0.1 (SAS Institute Inc., Cary, NC, USA) Acta Anaesthesiologica Scandinavica (2014)
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and Prism 6 for Windows, version 6.02 (GraphPad Software Inc., La Jolla, CA, USA). Results Incremental PEEP trial 0, 4, 8, 12 and 16 cmH2O A representative recording during the PEEP trial is shown in Fig. 2. The successive increase in lung volume during the incremental PEEP steps was not accompanied by an increase in end-expiratory oesophageal pressure, PesEE. After zeroing PesEE at ZEEP, PesEE was 0.3 ± 1.4 cmH2O at PEEP 4, 1.0 ± 3.1 cmH2O at PEEP 8, 1.3 ± 3.7 cmH2O at PEEP 12 and 0.5 ± 4.0 cmH2O at PEEP 16 cmH2O. If the chest wall was an elastic entity, the PesEE would have been 7.5 ± 4.3 cmH2O at 16 cmH2O of PEEP as compared with the observed value of 0.5 ± 4.0 cmH2O, P < 0.0005 (Figs 2 and 3). Static (expiratory) chest wall elastance between ZEEP and PEEP 16, obtained by dividing the change in end-expiratory oesophageal pressure with the ΔEELV, was 0.6 ± 2.2 cmH2O/l corresponding to an expiratory chest wall compliance of around 1800 ml/cmH2O. The increase in PesEE after the first expiration after a step increase in PEEP of 4 cmH2O was 2.4 ± 4.2 cmH2O, but 2 min later, just before the next increase in PEEP, the PesEE had decreased significantly to 0.7 ± 3.0 cmH2O, P < 0.0001, whereas end-expiratory lung volume increased significantly from 140 ± 69 ml to 230 ± 132 ml, P < 0.0001 (Figs 2 and 3). There was a very good correlation between the change in ΔEELV following the PEEP steps from PEEP 4 to 16 cmH2O, measured by spirometry and the corresponding volume calculated from the change in PEEP and Elconv as ΔPEEP/Elconv, r2 = 0.83, y = 0.93x, within subject correlation 0.95. There was a good correlation between conventional and PEEP step derived El, r2 = 0.76, y = 1.08x. Cumulative increase in end-expiratory transpulmonary pressure when increasing PEEP was closely related to changes in PEEP, and when PEEP was increased to 3.7 ± 0.2, 7.7 ± 0.3, 11.6 ± 0.5 and 15.4 ± 0.7 cmH2O, the increase in end-expiratory transpulmonary pressure was 2.3 ± 1.1, 5.9 ± 1.7, 10.5 ± 2.4 and 15.3 ± 2.0 cmH2O, respectively (Figs 2 and 3).
Fig. 2. Representative PEEP step recording from 0 to 16 cmH2O. Airway (red) and oesophageal (green), transpulmonary (dark blue) pressure and volume by EIT (light blue). The sudden large increase in oesophageal pressure is a peristaltic artifact. Note that the absolute end-expiratory oesophageal pressure does not increase when lung volume increases following PEEP increases. As a consequence, the end-expiratory transpulmonary pressure increases as much as PEEP is increased (indicated by the light blue arrow in the Paw and Ptp panels which are of equal size). EIT, electric impedance tomography; VOLEIT, volume by EIT; Pes, oesophageal pressure; Paw, airway pressure; Ptp, transpulmonary pressure.
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A
B
Fig. 3. (A) Figure based on mean values from the 12 patients. The end-inspiratory airway pressure/volume (P/V) points are connected to form a PEEP inflation P/V curve (thin red line). The end-expiratory airway P/V points (red/blue circles) are connected to form an expiratory P/V curve. Data based on the mean values from the conventional oesophageal pressure measurements form a mean transpulmonary P/V curve (black triangles, open: end-expiratory, filled: end-inspiratory). The conventional transpulmonary P/V curve is closely related to the end-expiratory airway P/V curve. Tidal chest wall P/V curves (green) are depicted starting from measured end-expiratory oesophageal pressure level. The end-inspiratory oesophageal P/V points are connected to a PEEP inflation P/V curve, which together with the fact that the end-expiratory chest wall P/V points are positioned almost vertically, indicate that the PEEP inflation expiratory chest wall elastance is negligible. (B) Manual reconstruction of breath by breath (only inspirations for clarity) of airway (red), oesophageal (green)and transpulmonary (blue) P/V curves of mean data from all patients. Thick arrows indicate P/V curves at P/V equilibrium at each PEEP level. Red/blue circles are the common airway and transpulmonary end-expiratory P/V points. Red, green and blue open circles indicate first end-expiration (and start of first inspiration) P/V points of airway, chest wall and lung after changing PEEP. Note that while the end-expiratory airway P/V points lie constant on the new PEEP level, the corresponding oesophageal P/V points decline towards the baseline level at ZEEP, indicated by black arrows. The consequence of the subsiding end-expiratory oesophageal pressure at each PEEP level results in the end-expiratory transpulmonary pressure of a PEEP step changing as much as the magnitude PEEP change as PawEE-PesEE = PtpEE (PawEE, end-expiratory airway pressure; PesEE, end-expiratory oesophagel pressure; PtpEE, end-expiratory transpulmonary pressure).
There was a good correlation between transpulmonary pressure at ZEEP, EE4, EI4, EE8, EI8, EE12, EI12, EE16 and EI16 (i.e. multiple values for each patient) by conventional oesophageal pressure measurements and transpulmonary pressure based on El determined as ΔPEEP/ ΔEELV (ElPSM), r2 = 0.80, y = 0.96x, with a mean bias of −0.4 ± 3.0 cmH2O with limits of agreement from 5.4 to −6.2 cmH2O (2 SD) (see Fig. 4). Several values for each patients are included, which maybe a limitation in the regression and Bland and Altman analysis.21,22 EcwVT was 10.0 ± 4.8 cmH2O/l at baseline (ZEEP), 9.6 ± 4.7 cmH2O/l at 4 cmH2O PEEP, 8.5 ± 4.1 cmH2O/l at 8 cmH2O PEEP, 7.9 ± 4.1 cmH2O/l at 12 cmH2O PEEP and 8.1 ± 4.3 cmH2O/l at 16 cmH2O PEEP (ns). Patients were also ranked according to cumulative lung volume response to a PEEP increase from 0 to 16 cmH2O, as lung compliance is correlated to aerated lung volume (23). The quartile with the
lowest response had an Etot of 41.0 ± 9.4 cmH2O/l, an El of 36.4 ± 10.8 cmH2O/l and a chest wall elastance of 4.6 ± 3.0 cmH2O/l. Corresponding values for the quartile with the high responders to PEEP were 20.3 ± 3.5, 12.6 ± 2.1 and 7.5 ± 2.8 cmH2O/l, respectively. The low responders had an El/Etot of 0.88 ± 0.08 similar to pulmonary acute respiratory distress syndrome (ARDS) and high responders had an El/Etot of 0.63 ± 0.08, similar to ARDS21 (Fig. 5). Individual transpulmonary pressure-volume curves based on conventional calculation and the corresponding P/V plot based on cumulated ΔEELV versus PEEP showed similar pattern over a wide range of lung compliances, 90–28 ml/ cmH2O (Fig. 6). Discussion We have shown in patients with acute respiratory failure in supine position that during PEEP inflaActa Anaesthesiologica Scandinavica (2014)
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Fig. 4. Correlation and Bland–Altman plots of transpulmonary pressure based on lung elastance determined by conventional oesophageal pressure measurements and based on ΔPEEP/ΔEELV. It is noteworthy that the variability in measurements most likely is mainly related to the oesophageal pressure measurement, which may have a 30% variability,12 whereas ΔEELV measurements seems to have a lower variability.2,17 ΔEELV, change in end-expiratory lung volume; ΔPEEP, change in end-expiratory airway pressure.
Fig. 5. High and low lung volume responders to PEEP. Airway P/V curve at different PEEP levels, red line; end-expiratory airway P/V curve, including an end-inspiratory P/V point calculated as described in methods under ‘Transpulmonary pressure based on El = ΔPEEP/ΔEELV’, blue line. Note that end-expiratory and end-inspiratory airway P/V points are aligned along a common P/V curve in the low responders, where lung elastance is 88% of total respiratory system elastance, while lung elastance in the high volume responders is 63% of total respiratory system elastance and the end-inspiratory airway P/V points are right shifted from the end-expiratory airway P/V curve. ΔEELV, change in end-expiratory lung volume; ΔPEEP, change in end-expiratory airway pressure; P/V, pressure/volume.
tion of the respiratory system, end-expiratory oesophageal pressure remains largely unchanged, and PEEP inflation-related chest wall elastance, calculated as the change in end-expiratory oesophageal pressure divided by the lung volume increase between ZEEP and a PEEP of 16 cmH2O was negligible. EcwVT remained unchanged when increasing PEEP. The tidal lung P/V curves of all the breaths involved in the incremental PEEP steps are lying on a single, common, global lung P/V curve. The increase in lung volume is closely correlated to the PEEP change divided by conventional, oesophageal pressure-derived El.
Thus, if the change in lung volume is determined, El can be determined as the change in PEEP divided by the change in lung volume, ΔPEEP/ ΔEELV. If we study an isolated ventilated lung (without a chest wall), where airway pressure is equal to the transpulmonary pressure, and perform an incremental PEEP trial, end-inspiratory airway pressure at a certain lung volume will be equal to the end-expiratory airway pressure at the same lung volume. This means that without the chest wall, transpulmonary pressure at a certain lung volume is independent of mode of inflation and
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Fig. 6. Individual transpulmonary pressure/volume curves based on conventional calculation and the corresponding pressure/volume plot based on lung elastance calculated as ΔPEEP/ΔEELV. The transpulmonary pressure/volume curves based on oesophageal pressure measurements and on ΔPEEP/ΔEELV correlated very well. The patients are displayed in order of lung volume response to PEEP. Note that lung compliance (Cl) calculated as the ratio of the change in end-expiratory lung volume between PEEP level 0 and 16 cmH2O, plus a tidal volume and the end-inspiratory transpulmonary pressure at PEEP 16 cmH2O, was closely related to the volume response to PEEP, which is in accordance with Cl being correlated to aerated lung volume.23 ΔEELV, change in end-expiratory lung volume; ΔPEEP, change in end-expiratory airway pressure.
end-expiratory and end-inspiratory airway P/V points are aligned on a common transpulmonary P/V curve. If we study patients in vivo with pulmonary ARDS, with little influence of the chest wall, the airway P/V points are positioned on a common P/V curve. In contrast, we observed that in patients with extrapulmonary ARDS, the endinspiratory airway P/V points from the low PEEP level were right shifted from the end-expiratory airway P/V point of the higher PEEP level, as a result of chest wall influence.20 In the present study, we ranked the patients according to the end-expiratory lung volume response to change in PEEP from 0 to 16 cmH2O. Airway P/V points
of the quartile of patients with the least response, where El was 88 % of Etot, showed a pattern similar to the isolated lung and to pulmonary ARDS, whereas P/V points of the most responsive quartile, where El was 63% of Etot, showed a pattern similar to extrapulmonary ARDS, with the end-inspiratory airway P/V points right shifted from the end-expiratory airway P/V curve (Fig. 5). Thus, the right shift seems to be a consequence of chest wall influence and the change in end-expiratory transpulmonary pressure between two PEEP levels is equal to the change in endexpiratory airway pressure, ΔPEEP. This is confirmed in the present study, where tidal variation in transpulmonary pressure of a Vt equal to the Acta Anaesthesiologica Scandinavica (2014)
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ΔEELV from the low PEEP level was closely correlated to change in PEEP and increase in endexpiratory lung volume was closely related to ΔPEEP divided by Elconv. In accordance with this, the difference between the end-inspiratory airway pressure of a Vt equal to the ΔEELV (Vt=ΔEELV) from the low PEEP level and the endexpiratory airway pressure at the high PEEP level, is equal to the tidal variation in oesophageal (pleural) pressure of a Vt=ΔEELV from the low PEEP level (Fig. 1). The implication of the pressure changes following a PEEP increase, i.e. that the end-expiratory transpulmonary pressure changes as much as ΔPEEP, is that there is no or minimal change in end-expiratory oesophageal pressure when increasing PEEP. This was supported by the finding that when increasing PEEP from 0 to 16 cmH2O, resulting in an average end-expiratory lung volume increase of 900 ml, average endexpiratory oesophageal pressure increased only 0.5 cmH2O (Fig. 3B). It has been shown that there is no relation between changes in end-expiratory oesophageal pressure and chest wall elastance,24–28 but there is no generally accepted explanation for the dissociative behaviour of oesophageal pressure in response to tidal and PEEP inflation of the respiratory system.27–34 If there was a relation between chest wall elastance and changes in PesEE following a change in PEEP, the PesEE at 16 cmH2O in PEEP would have been significantly higher, 7.5 ± 4.3 cmH2O compared with the measured value of 0.5 ± 2.0 cmH2O. The lack of, or minimal change in end-expiratory oesophageal pressure is not consistent with the concept of the chest wall as an elastic entity outside another elastic entity, the lung, both trying to recoil to a lower volume.35 If this was the case, the lung would collapse at FRC, when there is no pressure gradient between the outside of the thorax and the alveoli. In reality, the rib cage prevents collapse, as it strives to spring out to a higher volume, counterbalancing the recoil of the lung. The chest wall has previously been described as an elastic entity. As an alternative, we now propose that the rib cage and the diaphragm passively interacts with the abdomen, which can be regarded as a fluid-filled container, a weight, that is displaced in caudal direction, rather than inflated during inspirations.35–37 The position of
the diaphragm at end-expiration is determined by the balance between the rib cage spring-out force, the abdominal pressure and the recoil of the lung, resulting in a negative pleural pressure.38 If abdominal pressure is increased, as in extrapulmonary ARDS, the diaphragm is pushed in cranial direction and the ventral rib cage wall is pulled in dorsal direction, reducing the vertical diameter of the thoracic cavity.39,40 This will reduce lung volume, whereas end-expiratory oesophageal pressure remains largely unchanged. Even when PEEP is applied to expand the lungs, the rib cage spring-out force, which is active up to 70–80% of total lung capacity,35,37 will counteract the last part of the expiration.41 This will cause the diaphragm to be tensed at end-expiration, preventing the abdominal pressure to be transmitted to the thoracic cavity. As a result, end-expiratory oesophageal pressure will remain unchanged2,33,42,43 even when lung volume is increased by PEEP in accordance with a previous study.2 A PEEP-induced inflation of the respiratory system involves multiple breaths (Fig. 3B), and establishment of a new P/V equilibrium; requires a driving pressure to inflate the lung and displace the chest wall complex, which is exerted during inspirations; and is equal to ΔEELV × Etot. The driving pressure to displace the chest wall is equal to ΔEELV × EcwVT, and the pressure needed for inflating the lung is ΔEELV × (Etot − EcwVT), which is equal to El times the ΔEELV. If tidal inflation is equal to the ΔEELV by a PEEP increase, the tidal transpulmonary pressure, of such a Vt will be equal to the change in PEEP. The breath-by-breath build-up of volume after an increase in PEEP is an expiratory phenomenon, where less breathing gas is expired than inspired. The first expiration increase in lung volume after increasing PEEP is equal to ΔPEEP/ Etot due to closing of the expiratory valve at the set PEEP level before the expiration is complete, detaining a volume equal to ΔPEEP/Etot.3 The following44 breath-by-breath volume build-up is also an expiratory phenomenon, which is a result of the retardation of the last part of each expiration and the tensing of the diaphragm by the rib cage spring-out force,17 whereby expiratory gas is detained in the lung. The PEEP-inflated volume is distributed 50–70% to the rib cage, which means that less than half of the lung volume increase is distributed to the diaphragm.41,45 The abdominal
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cavity has a volume of ≈ 10 l and the upper surface area is ≈ 1000 cm2.41 As less than half of an increase in lung volume is distributed to the diaphragm,41 an increase of 1000 ml will lead to, at the most, a 500 ml of intrusion of the diaphragm into the abdomen, increasing the vertical height of abdominal container by ≈ 0.5 cm, influencing abdominal pressure minimally.34,46 Also, the slow, multi-breath caudal displacement of the diaphragm seems to result in a yielding and adapting of the abdominal wall in other areas (than the diaphragm) to accommodate the part of increase in lung volume that is directed versus the diaphragm. This process is time consuming and more prominent at high volumes,47 and it has been shown that the volume increase may continue for up to an hour.6 Conclusions and clinical implications The interaction among the rib cage, diaphragm and abdominal container indicates that the chest wall works as a hydraulic entity, which impedes inflation as a weight, which is displaced during inspiration. This is supported by the finding that chest wall elastance does not increase with increasing PEEP levels. When an extremely slow inflation of the respiratory system, such as PEEP inflation is used, ample time is provided for the chest wall complex, especially the abdomen, to adapt and yield to the intrusion of the diaphragm. The rib cage spring-out force keeps the diaphragm tensed at end-expiration, preventing the abdominal pressure to be transmitted to the thoracic cavity, which results in unchanged endexpiratory oesophageal pressure when increasing PEEP. As the lung is unaffected by the chest wall complex at end-expiratory P/V equilibrium, the increase in end-expiratory lung volume following a PEEP step is equal to the magnitude of the PEEP step divided by Elconv. If the change in lung volume can be determined by the ventilator pneumotachograph,16 El and consequently transpulmonary pressure may be estimated without using oesophageal pressure measurements just by performing a PEEP change. In contrast to oesophageal pressure measurements, this technique is simple and rapid, demanding only a software addition to the ventilator. We have tested this new concept using mean values from 9 patients with pulmonary and 12
patients with extrapulmonary ARDS, the two extremes of the syndrome,20 and found a very good correlation between transpulmonary pressure calculated using oesophageal pressure measurements compared with the new PEEP-step concept (r2 = 0.98, y = 1.1x + 1.7), supporting our findings.48 Further studies are needed to define suitable PEEP changes, repeatability and precision of measurements for this new method, which may improve rational protective ventilator settings of PEEP and Vt.
References 1. Akoumianaki E, Maggiore SM, Valenza F, Bellani G, Jubran A, Loring SH, Pelosi P, Talmor D, Grasso S, Chiumello D, Guérin C, Patroniti N, Ranieri VM, Gattinoni L, Nava S, Terragni PP, Pesenti A, Tobin M, Mancebo J, Brochard L. The application of esophageal pressure measurement in patients with respiratory failure. Am J Respir Crit Care Med 2014; 189: 520–31. 2. Stenqvist O, Grivans C, Andersson B, Lundin S. Lung elastance and transpulmonary pressure can be determined without using oesophageal pressure measurements. Acta Anaesthesiol Scand 2012; 56: 738–47. 3. Katz JA, Ozanne GM, Zinn SE, Fairley HB. Time course and mechanisms of lung-volume increase with PEEP in acute pulmonary failure. Anesthesiology 1981; 54: 9–16. 4. Fretschner R, Laubscher TP, Brunner JX. New aspects of pulmonary mechanics: ‘slowly’ distensible compartments of the respiratory system, identified by a PEEP step maneuver. Intensive Care Med 1996; 12: 1328–34. 5. Putensen C, Baum M, Koller W, Putz G. [The PEEP wave: an automated technic for bedside determination of the volume/pressure ratio in the lungs of ventilated patients]. Anaesthesist 1989; 38: 214–9. 6. Putensen C, Baum M, Hormann C. Selecting ventilator settings according to variables derived from the quasi-static pressure/volume relationship in patients with acute lung injury. Anesth Analg 1993; 77: 436–47. 7. Gattinoni L, Pelosi P, Crotti S, Valenza F. Effects of positive end-expiratory pressure on regional distribution of tidal volume and recruitment in adult respiratory distress syndrome. Am J Respir Crit Care Med 1995; 151: 1807–14. Acta Anaesthesiologica Scandinavica (2014)
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8. Cressoni MCC, Amini M, Febres D, Gallazzi E, Carlesso E, Cadringher P, Langer T, Chiumello D, Gattinoni L. Recruited lung tissue does not resume normal mechanical properties. Crit Care 2013; 17: P106. 9. Cressoni MGE, Chiurazzi C, Marino A, Briono M, Menga F, Cegada I, Lemos A, Lazzerini M, Carlesso E, Cadringher P, Chiumello D, Gattinoni L. Limits of normality of quantitative thoracic computed tomography analysis. Crit Care 2013; 17: R93. 10. Lowhagen K, Lundin S, Stenqvist O. Regional intratidal gas distribution in acute lung injury and acute respiratory distress syndrome – assessed by electric impedance tomography. Minerva Anestesiol 2010; 76: 1024–35. 11. Stahl CA, Möller K, Steinmann D, Henzler D, Lundin S, Stenqvist O. Determination of ‘recruited volume’ following a PEEP step is not a measure of lung recruitability. Acta Anaesthesiol Scand 2014; Oct 28. [Epub ahead of print]. doi: 10.1111/aas.12432. 12. Chiumello D, Gallazzi E, Marino A, Berto V, Mietto C, Cesana B, Gattinoni L. A validation study of a new nasogastric polyfunctional catheter. Intensive Care Med 2011; 37: 791–5. 13. Baydur A, Behrakis PK, Zin WA, Jaeger M, Milic-Emili J. A simple method for assessing the validity of the esophageal balloon technique. Am Rev Respir Dis 1982; 126: 788–91. 14. Ducros LST, Derenne J-P. Validity of oesophageal pressure measurement for respiratory mechanics studies during ventilation. Eur Respir J 1995; 8 (Suppl 19): 39S. 15. Lanteri CJ, Kano S, Sly PD. Validation of esophageal pressure occlusion test after paralysis. Pediatr Pulmonol 1994; 17: 56–62. 16. Karason S, Karlsen KL, Lundin S, Stenqvist O. A simplified method for separate measurements of lung and chest wall mechanics in ventilator-treated patients. Acta Anaesthesiol Scand 1999; 43: 308–15. 17. Grivans C, Lundin S, Stenqvist O, Lindgren S. Positive end-expiratory pressure-induced changes in end-expiratory lung volume measured by spirometry and electric impedance tomography. Acta Anaesthesiol Scand 2011; 55: 1068–77. 18. Hinz J, Hahn G, Neumann P, Sydow M, Mohrenweiser P, Hellige G, Burchardi H. End-expiratory lung impedance change enables bedside monitoring of end-expiratory lung volume change. Intensive Care Med 2003; 29: 37–43.
19. Frerichs I. Electrical impedance tomography (EIT) in applications related to lung and ventilation: a review of experimental and clinical activities. Physiol Meas 2000; 21: R1–21. 20. Gattinoni L, Pelosi P, Suter PM, Pedoto A, Vercesi P, Lissoni A. Acute respiratory distress syndrome caused by pulmonary and extrapulmonary disease. Different syndromes? Am J Respir Crit Care Med 1998; 158: 3–11. 21. Bland JM, Altman DG. Calculating correlation coefficients with repeated observations: Part 2 – correlation between subjects. BMJ 1995; 310: 633. 22. Bland JM, Altman DG. Calculating correlation coefficients with repeated observations: Part 1 – correlation within subjects. BMJ 1995; 310: 446. 23. Gattinoni L, Pesenti A, Avalli L, Rossi F, Bombino M. Pressure-volume curve of total respiratory system in acute respiratory failure. Computed tomographic scan study. Am Rev Respir Dis 1987; 136: 730–6. 24. Gattinoni L, Mascheroni D, Basilico E, Foti G, Pesenti A, Avalli L. Volume/pressure curve of total respiratory system in paralysed patients: artefacts and correction factors. Intensive Care Med 1987; 13: 19–25. 25. Loring SH, O’Donnell CR, Behazin N, Malhotra A, Sarge T, Ritz R, Novack V, Talmor D. Esophageal pressures in acute lung injury: do they represent artifact or useful information about transpulmonary pressure, chest wall mechanics, and lung stress? J Appl Physiol 2010; 108: 515–22. 26. Pelosi P, Goldner M, McKibben A, Adams A, Eccher G, Caironi P, Losappio S, Gattinoni L, Marini JJ. Recruitment and derecruitment during acute respiratory failure: an experimental study. Am J Respir Crit Care Med 2001; 164: 122–30. 27. Valenza F, Chevallard G, Porro GA, Gattinoni L. Static and dynamic components of esophageal and central venous pressure during intra-abdominal hypertension. Crit Care Med 2007; 35: 1575–81. 28. Plataki M, Hubmayr RD. Should mechanical ventilation be guided by esophageal pressure measurements? Curr Opin Crit Care 2011; 17: 275–80. 29. Gattinoni L, Chiumello D, Carlesso E, Valenza F. Bench-to-bedside review: chest wall elastance in acute lung injury/acute respiratory distress syndrome patients. Crit Care 2004; 8: 350–5. 30. Talmor DS, Loring SH. Esophageal pressures in acute respiratory distress syndrome: how should we interpret and use them? Crit Care Med 2013; 41: e1.
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31. Hubmayr RD. Is there a place for esophageal manometry in the care of patients with injured lungs? J Appl Physiol 2010; 108: 481–2. 32. Guerin C, Richard JC. Comparison of 2 correction methods for absolute values of esophageal pressure in subjects with acute hypoxemic respiratory failure, mechanically ventilated in the ICU. Respir Care 2012; 57: 2045–51. 33. Gulati G, Novero A, Loring SH, Talmor D. Pleural pressure and optimal positive end-expiratory pressure based on esophageal pressure versus chest wall elastance: incompatible results. Crit Care Med 2013; 41: 1951–7. 34. Jakob SM, Knuesel R, Tenhunen JJ, Pradl R, Takala J. Increasing abdominal pressure with and without PEEP: effects on intra-peritoneal, intra-organ and intra-vascular pressures. BMC Gastroenterol 2010; 10: 70. 35. Hedenstierna G. Esophageal pressure: benefit and limitations. Minerva Anestesiol 2012; 78: 959–66. 36. Kubiak BD, Gatto LA, Jimenez EJ, Silva-Parra H, Snyder KP, Vieau CJ, Barba J, Nasseri-Nik N, Falk JL, Nieman GF. Plateau and transpulmonary pressure with elevated intra-abdominal pressure or atelectasis. J Surg Res 2010; 159: e17–24. 37. Agostoni E, Hyatt R. The respiratory system. Mechanics of breathing. Handbook of Physiology, Vol. 3. Bethesda, MD: American Physiological Society, 1986: 113–30. 38. Nunn J. Elastic forces and lung volumes, In: Nunn JF ed. Nunn’s applied respiratory physiology, 4th edn. Oxford: Butterworth-Heinemann, 1995: 36–52. 39. Froese AB, Bryan AC. Effects of anesthesia and paralysis on diaphragmatic mechanics in man. Anesthesiology 1974; 41: 242–55. 40. Butler J. The adaptation of the relaxed lungs and chest wall to changes in volume. Clin Sci (Lond) 1957; 16: 421–33.
41. Hedenstierna G, Strandberg A, Brismar B, Lundquist H, Svensson L, Tokics L. Functional residual capacity, thoracoabdominal dimensions, and central blood volume during general anesthesia with muscle paralysis and mechanical ventilation. Anesthesiology 1985; 62: 247–54. 42. Chelucci GL, Brunet F, Dall’Ava-Santucci J, Dhainaut JF, Paccaly D, Armaganidis A, Milic-Emili J, Lockhart A. A single-compartment model cannot describe passive expiration in intubated, paralysed humans. Eur Respir J 1991; 4: 458–64. 43. de Leon A, Thorn SE, Raoof M, Ottosson J, Wattwil M. Effects of different respiratory maneuvers on esophageal sphincters in obese patients before and during anesthesia. Acta Anaesthesiol Scand 2010; 54: 1204–9. 44. Cortes-Puentes GA, Gard KE, Adams AB, Faltesek KA, Anderson CP, Dries DJ, Marini JJ. Value and limitations of transpulmonary pressure calculations during intra-abdominal hypertension. Crit Care Med 2013; 41: 1870–7. 45. Grimby G, Hedenstierna G, Lofstrom B. Chest wall mechanics during artificial ventilation. J Appl Physiol 1975; 38: 576–80. 46. Wauters J, Claus P, Brosens N, McLaughlin M, Hermans G, Malbrain M, Wilmer A. Relationship between abdominal pressure, pulmonary compliance, and cardiac preload in a porcine model. Crit Care Res Pract 2012; 2012: 763181: 1–6. 47. Sharp JT, Johnson FN, Goldberg NB, Van Lith P. Hysteresis and stress adaptation in the human respiratory system. J Appl Physiol 1967; 23: 487–97. 48. Stenqvist O, Lundin S. Lung elastance and transpulmonary pressure may be determined without using esophageal pressure measurements. Am J Respir Crit Care Med 2014; 190: 120.
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