Comments
To the Editor:
We read with interest the review on esophageal pressure (Pes) measurements (1). The importance of transpulmonary pressure (Ptp), when selecting a protective and optimal ventilatory strategy, was profoundly emphasized. However, the authors admit that the introduction of Pes measurements in the intensive care unit has been disappointingly slow, in spite of the continuous promotion by the most influential and respected researchers in the field. This is not surprising, as Pes measurements are technically complicated and there is a lack of consensus on the interpretation of the absolute Pes variations with changes in positive end-expiratory pressure (PEEP), making it difficult for clinicians to use Pes to optimize mechanical ventilation (2).
A simpler method for determining lung elastance (El) and Ptp seems to be needed: If a PEEP trial is performed in isolated lungs, where airway pressure (Paw) equals Ptp, end-expiratory Paw (PawEE, PEEP) at a certain lung volume is the same as end-inspiratory airway plateau pressure (PawEI) at the same lung volume; that is, Ptp at a certain lung volume is independent of mode of inflation, tidal or PEEP-induced. However, when a PEEP trial is performed in vivo, PawEI of a low PEEP level is right shifted in comparison with the PawEE of the high PEEP level. If the tidal volume from the low PEEP is equal to the change in PEEP-induced end-expiratory lung volume (∆EELV), the difference between PawEILoPEEP (∆Ptp + ∆Pes) and PawEEHiPEEP constitutes the ∆Pes of the tidal volume at low PEEP, and consequently the ∆Ptp is equal to the change in PEEP (∆PEEP) and lung elastance can be determined as ∆PEEP/∆EELV, where ∆EELV is determined by the pneumotachograph of the ventilator.
This method for determining lung elastance was tested on data of 24 patients with lung elastance between 26 and 9 cm H2O/L (lung-healthy patients, and patients with moderate and severe acute respiratory distress syndrome [ARDS]), resulting in a correlation of r2 = 0.96 (3), and also on 21 patients with pulmonary and extrapulmonary ARDS, corresponding to nonresponders and responders to PEEP, the two extremes of the syndrome (4), where mean end-expiratory and end-inspiratory transpulmonary pressures of four PEEP levels of both pulmonary and extrapulmonary ARDS were positioned on a common correlation line, y = 1.1x with a correlation of r2 = 0.99.
The implication of El = ∆PEEP/∆EELV is that the ∆EELV after a PEEP change can be predicted as ∆PEEP divided by conventionally obtained lung elastance and that the increase in absolute Ptp after a PEEP step is equal to the change in PEEP. In a porcine study we verified these assumptions—the change in absolute Ptp after a PEEP increase was closely related to the change in PEEP and the spirometrically measured ∆EELV was closely related to ∆PEEP divided by conventional El, y = 0.98x + 6.2 (5). In 12 patients with ARDS we found that conventional El and El determined as ∆PEEP/∆EELV correlated, r2 = 0.95 and y = 1.15x, and the increase in absolute Ptp after a PEEP step was closely related to the size of the PEEP steps (6). So far PEEP changes up to 16 cm H2O have been used.
The most likely explanations of these findings are as follows:
| 1. | The chest wall complex behaves like a weight that is displaced in the caudal direction during tidal or PEEP inflation rather than expanding like an elastic entity. | ||||
| 2. | The abdominal wall yields to the intrusion of the diaphragm during the slow, multibreath inflation induced by a PEEP increase, leaving the absolute Pes mostly unchanged. | ||||
| 3. | The rib cage spring-out force tenses the diaphragm and prevents the transmittal of abdominal pressure to the thoracic cavity and pleural space at end-expiration, also at increased PEEP. | ||||
In conclusion, data representative of a total of 57 patients in three studies (3, 4, 6) indicate that lung elastance can be determined as ∆PEEP/∆EELV and consequently Ptp can be calculated without using Pes measurements. This method is so simple that Ptp could be determined on a routine basis in all ventilated patients, providing a rationale for optimizing PEEP and tidal volume.
| 1. | Akoumianaki E, Maggiore SM, Valenza F, Bellani G, Jubran A, Loring SH, Pelosi P, Talmor D, Grasso S, Chiumello D, et al. The application of esophageal pressure measurement in patients with respiratory failure. Am J Respir Crit Care Med 2014;189:520–531. |
| 2. | 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;41:1951–1957. |
| 3. | Pelosi P, Cereda M, Foti G, Giacomini M, Pesenti A. Alterations of lung and chest wall mechanics in patients with acute lung injury: effects of positive end-expiratory pressure. Am J Respir Crit Care Med 1995;152:531–537. |
| 4. | 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. |
| 5. | 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;56:738–747. |
| 6. | Grivans C, Lundin S, Stenqvist O. Lung elastance can be determined without oesophageal pressure measurements. Crit Care 2013;17(Suppl 2):P130. |
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