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American Journal of Respiratory and Critical Care Medicine Vol 178. pp. 542, (2008)
© 2008 American Thoracic Society


Correspondence

Whole-Body "Negative-Pressure" Ventilation: Is It Really Different?

To the Editor:

The article by Dr. Grasso and colleagues (1) in a rabbit model of acute lung injury claims to show superiority of whole-body "negative-pressure" ventilation (NPV) over conventional positive-pressure ventilation (PPV). They report that NPV resulted in better oxygenation, greater lung volume at FRC, less atelectasis on computed tomography (CT), and less ventilator-induced lung injury on histology. In respiratory mechanics, the term "negative pressure" denotes that the pressure at some location is slightly less positive than ambient atmospheric pressure, not that the pressure is less than zero (i.e., less than absolute vacuum). The idea that whole-body external "negative pressure" can have a different effect on the respiratory system than internal positive pressure has been a point of confusion for at least a century (2).

Conventional respiratory mechanics holds that volume change during passive mechanical ventilation depends on the transrespiratory pressure, Prs (positive pressure at the airway opening minus slightly lower positive pressure at the body surface), and the effects of the pressure difference are the same whether pressure is increased at the airway in PPV or reduced at the body surface in whole-body NPV (2). From this perspective, the dramatic results of Grasso and coworkers are surprising and require critical examination. The authors hypothesize that NPV "applies pressure over the whole lung surface," and that "negative pressure must take effect through the chest wall before impacting on the pleural space." These statements are equally true of ambient pressure.

Before discarding conventional respiratory mechanics, it is important to be sure that there are no differences between NPV and PPV with regard to ventilation parameters known to affect measured outcome variables: atelectasis, oxygenation, and lung injury. Several studies in acute lung injury have shown that these outcome variables improve with higher end-expiratory Prs, usually brought about by higher positive end-expiratory pressure (PEEP) (36). A fair comparison of the different modes requires that Prs and its waveform are matched throughout the duration of NPV and PPV. As the authors correctly point out, pleural and transpulmonary pressure measurements are subject to artifact, but if the respiratory muscles are relaxed, the essential information can be obtained from Prs. Measurements of Prs and its components (airway pressure and body surface pressure) were not reported in this study. Video-CT scans in the online supplement suggest that Prs was substantially greater on NPV than PPV; this would explain the findings without requiring us to relinquish conventional respiratory mechanics.

Stephen H. Loring and Robert B. Banzett

Beth Israel Deaconess Medical Center
and
Harvard Medical School
Boston, Massachusetts

FOOTNOTES

Conflict of Interest Statement: Neither author has a financial relationship with a commercial entity that has an interest in the subject of this manuscript.

REFERENCES

  1. Grasso F, Engelberts D, Helm E, Frndova H, Jarvis S, Talakoub O, McKerlie C, Babyn P, Post M, Kavanagh BP. Negative-pressure ventilation: better oxygenation and less lung injury. Am J Respir Crit Care Med 2008;177:412–418.[Abstract/Free Full Text]
  2. Comroe JH Jr. Inflation—1904 model. Retrospectroscope. Menlo Park, CA: Von Gehr Press; 1977. pp. 110–113.
  3. Chiumello D, Pristine G, Slutsky AS. Mechanical ventilation affects local and systemic cytokines in an animal model of acute respiratory distress syndrome. Am J Respir Crit Care Med 1999;160:109–116.[Abstract/Free Full Text]
  4. Muscedere JG, Mullen JB, Gan K, Slutsky AS. Tidal ventilation at low airway pressures can augment lung injury. Am J Respir Crit Care Med 1994;149:1327–1334.[Abstract]
  5. Webb HH, Tierney DF. Experimental pulmonary edema due to intermittent positive pressure ventilation with high inflation pressures: protection by positive end-expiratory pressure. Am Rev Respir Dis 1974;110:556–565.[Medline]
  6. Wyszogrodski I, Kyei-Aboagye K, Taeusch HW Jr, Avery ME. Surfactant inactivation by hyperventilation: conservation by end-expiratory pressure. J Appl Physiol 1975;38:461–466.[Abstract/Free Full Text]




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Proc. Am. Thorac. Soc. Am. J. Respir. Cell Mol. Biol.
Copyright © 2008 American Thoracic Society