Online Letters to the Editor

The authors reply:

F

irst of all, we would like to thank Vieillard-Baron et al (1) for their kind words related to our physiological study in Critical Care Medicine (2). We agree with them that the different extent to which the airway pressure is transmitted to the pleura, pericard, and central venous pressure (besides in Table 2 and also shown in Fig. 4B) may potentially result in a collapse of the superior vena cava at the junction between the pleural and pericardial pressure as suggested by VieillardBaron et al (1) using transesophageal echocardiography (3). Second, we will try to explain the absence of change in transmural right atrial pressure. We believe that the venous return is reduced (based on the decrease of the transmural pressure of vena cava), but this decrease is compensated by an increase in right ventricular afterload (as also suggested by Vieillard-Baron et al [1]). In order to find out in which patients the increase in afterload plays a larger role, we divided the patients in two groups based on the observed change in transmural pressure of the right atrium. As a result, we did not find any differences in, for example, airway pressure and mean arterial pressure. After that, we calculated the change in the variation of the right atrial transmural pressure as a result of increasing tidal volume (TV) (a positive change would indicate a more prominent role of the afterload). This change was then related to the pulse pressure variation as a measure of fluid responsiveness (the hypothesis was that in nonresponders, the afterload has a more prominent role). The Pearson correlation (r) of this relationship was 0.72 (p < 0.01) (Fig. 1). This indeed indicates that in fluid-responsive patients, the ventilation-induced decrease in preload is the main determinant for the decrease in the output of the right heart, whereas in nonfluid-responsive patients, the increase in afterload is the main determinant. Finally, we fully agree that our results related to decreased chest wall compliance are in accordance with the equation Ccw= TV_changes/Ppl_changes and that in this situation, the change in pleural pressure is increased for the same delivered TV. This formulation is more appropriate than suggesting that a decrease in chest wall compliance may increase the pressure transmission from the airways to the pleural space. Professor Pickkers served as a board member for Gamla Brogatans Sjukvårdsaffär Aktiebolag, Exponential Biotherapies Inc (EBI), and AM-Pharma; consulted for AM-Pharma and EBI; and lectured for Pfizer, Merck Sharp & Dhome, and Astellas. His institution received grant support from ZonMW, Nierstichting, and Reumafonds. The remaining authors have disclosed that they do not have any potential conflicts of interest. Benno Lansdorp, MSc, PhD, Department of Intensive Care, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands, and University of Twente, MIRA–Institute for Biomedical Technology and Technical Medicine, Enschede, The Netherlands; Joris Lemson, MD, PhD, Johannes G. van der Hoeven, MD, PhD, Peter Pickkers, MD, PhD, Department of Intensive Care, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands

Critical Care Medicine

Figure 1. Change in the transmural pressure variation of the right atrium over the increasing tidal volumes related to the pulse pressure variation (PPV) (as a measure of volume status) (r = 0.72; p < 0.01).

REFERENCES

1. Vieillard-Baron A, Repessé X, Charron C: Heart-Lung Interactions: Have a Look on the Superior Vena Cava and on the Changes in Right Ventricular Afterload. Crit Care Med 2015; 43:e52 2. Lansdorp B, Hofhuizen C, van Lavieren M, et al: Mechanical ventilation-induced intrathoracic pressure distribution and heart-lung interactions. Crit Care Med 2014; 42:1983–1990 3. Vieillard-Baron A, Chergui K, Rabiller A, et al: Superior vena caval collapsibility as a gauge of volume status in ventilated septic patients. Intensive Care Med 2004; 30:1734–1739 DOI: 10.1097/CCM.0000000000000808

Chest Wall Elastance in the Estimation of the Transpulmonary Pressure: How Should We Use It? To the Editor:

I

n a recent issue of Critical Care Medicine, we read with interest the article by Gulati et al (1), describing two methods of estimating transpulmonary pressure. One method measured the esophageal pressure (Pes) and used it directly as a surrogate for pleural pressure (Pes-based method), whereas the other method derived pleural pressure (Ppl) from chest wall elastance (Ecw). At end-inspiration occlusion, both methods calculated the transpulmonary pressure (PL,eio) as the difference between the airway opening pressure (Pao,eio) and pleural pressure (Ppl,eio). In the latter (Ecw-based) method, the equation was written as follows:

PL,eio = Pao,eio × (1 − Ecw / ERS )

(Eq. 1)

where ERS is the respiratory system elastance. As such, the Ecwderived PL,eio, averaging 23.6 cm H2O, was much higher than the PL,eio obtained from the Pes-based method (7.4 cm H2O) in this study. It seems to us that this discordance is mainly due to the mathematical incorrectness of the Ecw-based method. As proposed by Chiumello et al (2), the basic physiological equations remind us that the correct value of PL,eio should be determined as follows:

∆PL = (PL,eio − PL,eeo )

= (Pao,eio − PEEPtot ) × (1 − Ecw / ERS ), www.ccmjournal.org

e53

Online Letters to the Editor

and hence PL,eio = PL,eeo + (Pao,eio − PEEPtot ) × (1 − Ecw / ERS ) (Eq. 2),

Unit, Tianjin Chest Hospital, Teaching Hospital of Tianjin Medical University, Tianjin, China

REFERENCES where ∆PL is the difference of the transpulmonary pressure at end-inspiration (PL,eio) and end-expiration occlusions (PL,eeo) and PEEPtot is the total positive end-expiratory pressure. Unfortunately, Gulati et al (1) used a simplified equation (Eq. 1) including only the Ecw/ERS ratio and Pao,eio, which neglects the values of PEEPtot and PL,eeo. Thus, the overestimation of PL,eio should not come as a surprise when considering the low mean Ecw/ERS ratio (0.25) and a marked discrepancy between PEEPtot and PL,eeo (i.e., a high mean PEEPtot of 17.4 cm H2O and a negative mean PL,eeo value of –2.9 cm H2O) in this population. In a similar acute respiratory distress syndrome (ARDS) population (3) with a mean Ecw/ERS of 0.22, it has been shown that PL,eeo averaged –2.8 cm H2O and ranged widely from –15 to 5 cm H2O. Such substantially negative values of PL,eeo in such populations will make the overestimation of PL,eio by the Ecw-based method even unavoidable, given that PL,eeo should always be taken into account when calculating PL,eio (Eq. 2). Our reasoning agrees perfectly well with findings from a previous study in a similar population (i.e., mean Ecw/ERS of 0.22). In this study, Loring et al (3) demonstrated that the value of PL,eeo, which was completely ignored by Gulati et al (1), was the most important determinant of PL,eio, such that 62% of the variance in PL,eio was explained by PL,eeo. In addition, the combination of lung elastance and tidal volume, which is equal to (Pao,eio – PEEPtot) × (1 – Ecw/ERS), correlated weakly with PL,eio (R2 = 0.23) (3), further supporting our conclusion that PL,eio calculated as Pao,eio × (1 – Ecw/ERS) is not an adequate surrogate for the real transpulmonary pressure at end-inspiration occlusion, at least in the study population of Gulati et al (1). Actually, the Ecw-based method used in this study, which is a simplified version of the standard method (2), is correct and can provide reliable estimation of PL,eio only if both Ppl and airway pressure are equal to zero at functional residual capacity (4). Unfortunately, this minimum prerequisite is highly unlikely to be fulfilled in patients with ARDS (5). Thus, we believe that such Ecw-based method used by Gulati et al (1) for estimating PL,eio does not account for the key determinant of PL,eio (i.e., PL,eeo and PEEPtot) and the resulting erroneous estimation is unavoidable, especially in their study population with a low Ecw/ERS ratio. We are not saying that such Ecw-based method is useless in all clinical circumstances and are convinced that further work is needed to identify illustrative subgroups of patients with ARDS, in whom the use of Ecw-based method proposed by Gulati et al (1) can still be justified. The authors have disclosed that they do not have any potential conflicts of interest. Yang Liu, MD, Medical Intensive Care Unit, Pingjin Hospital, Logistics College of the Chinese People’s Armed Police Forces, Tianjin, China; Yu Mu, MD, PhD, Coronary Care e54

www.ccmjournal.org

1. Gulati G, Novero A, Loring SH, et al: Pleural Pressure and Optimal Positive End-Expiratory Pressure Based on Esophageal Pressure Versus Chest Wall Elastance: Incompatible Results. Crit Care Med 2013; 41:1951–1957 2. Chiumello D, Carlesso E, Cadringher P, et al: Lung stress and strain during mechanical ventilation for acute respiratory distress syndrome. Am J Respir Crit Care Med 2008; 178:346–355 3. Loring SH, O’Donnell CR, Behazin N, et al: 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 (1985) 2010; 108:515–522 4. Staffieri F, Stripoli T, De Monte V, et al: Physiological effects of an open lung ventilatory strategy titrated on elastance-derived end-inspiratory transpulmonary pressure: Study in a pig model. Crit Care Med 2012; 40:2124–2131 5. Pelosi P, Goldner M, McKibben A, et al: Recruitment and derecruitment during acute respiratory failure: An experimental study. Am J Respir Crit Care Med 2001; 164:122–130 DOI: 10.1097/CCM.0000000000000741

The authors reply:

W

e thank Drs. Liu and Mu (1) for their thoughtful analysis of the mathematics and physiology underlying the elastance-based method for determining transpulmonary pressure. They describe the flawed mathematics and logical inconsistency of the simplified formula that we presented (Eq. 1 in [1]), relating transpulmonary pressure (PL) to airway pressure (Paw) and the ratio of lung elastance to total respiratory elastance (EL/Ers or EL/Etot). They go on to derive the correct expression (Eq. 2 in [1]) relating transpulmonary pressure to elastances of chest wall and respiratory system, including measured values of airway and esophageal pressure (thereby including the constant of integration). Drs. Liu and Mu (1) support the validity of this equation by citing our previous article (2), concluding, “… the value of [transpulmonary pressure during end-expiratory occlusion], which was completely ignored [in Eq. 1 presented] by Gulati et al (3), was the most important determinant of the value of [transpulmonary pressure at endinspiratory plateau]…” We agree with this analysis by Drs. Liu and Mu (1). However, we would emphasize that the elastance-based method now in use is, in fact, the simplified and mathematically incomplete Equation 1 presented in our report! This method, originally described in articles by Gattinoni et al (4, 5) and used by others (6, 7), is summarized by the equations “Ppl = Paw × Ecw/Etot” (6) and “PL = Paw × EL/Ers” (5), in which pleural (Ppl) and transpulmonary pressures are calculated from elastances and airway pressure. Although the correct Equation 2 is based on an equation presented by Chiumello et al (8), that article only reports changes in transpulmonary pressure and presents no equation that directly relates transpulmonary pressure to elastances. Recent articles using the elastance-based method show that February 2015 • Volume 43 • Number 2

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Chest wall elastance in the estimation of the transpulmonary pressure: how should we use it?

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