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
Copyright of Critical Care Medicine is the property of Lippincott Williams & Wilkins and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
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
Copyright of Critical Care Medicine is the property of Lippincott Williams & Wilkins and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
