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American Journal of Respiratory and Critical Care Medicine Vol 173. pp. 1291a-1292, (2006)
© 2006 American Thoracic Society


Correspondence

Pleural Cavity Exploitation in beta-Agonist–treated ARDS Patients

From the Authors:

We thank Drs. Effros, Frost, Zarogiannis and colleagues for their interest in our randomized controlled trial of the effects of intravenous salbutamol upon extravascular lung water (EVLW) in patients with ARDS (1). The ideal tool for the assessment of pulmonary edema in ARDS patients remains elusive. The gold standard of gravimetric lung water, which is used in experimental animal models of acute lung injury, is not practical for human application. Quantification of the amount of edema fluid on the chest radiograph is limited by substantial inter-observer variation. Other chest imaging modalities, such as MRI, CT, or PET scanning, are limited by logistical constraints. The PaO2:FIO2 ratio is influenced by several variables, and in the ARDSnet low tidal volume study, the PaO2:FIO2 ratio was worse in the low tidal volume group during the early stages of the trial, despite ultimate improvement in survival (2).

In our study, we used the PiCCO single indicator thermodilution system (Pulsion Medical, Munich, Germany), which allows the noninvasive quantification of EVLW. Experimental studies using the PiCCO system have demonstrated a close correlation (r = 0.97) between EVLW and gravimetric lung water (3). Moreover, EVLW measured using this technique has been shown to predict outcome in patients with sepsis (4) and ARDS (5). In a randomized controlled trial, the use of EVLW measurements to guide the management of patients with ARDS resulted in a reduction in the duration of mechanical ventilation and a trend toward reduced mortality (6).

There are some limitations to this technique, as highlighted by Effros and Frost and Wise. Impairment of lung perfusion, which is present in ARDS, can lead to an underestimation of both intrathoracic blood volume and EVLW (7). In contrast, salbutamol as a pulmonary vasodilator could have increased lung perfusion and masked any reduction in the amount of pulmonary edema. In BALTI, the absence of any significant difference in intrathoracic blood volume (1) reduces the likelihood that the findings were solely due to changes in pulmonary perfusion. Frost highlights work which showed that EVLW can be underestimated in patients receiving dialysis. In BALTI, there was no significant difference between groups in the number of patients receiving dialysis at baseline (4 placebo, 6 salbutamol) or day 7 (3 placebo, 2 salbutamol).

Zarogiannis and colleagues report their interesting observations on the effect of beta2-agonists on pleural fluid clearance. We did not systematically measure the presence of pleural fluid in our study. Fluid in the pleural cavity is not detected by the PiCCO thermodilution system, so the effect reported in our study is independent of any effect on pleural fluid volume.

Despite these potential limitations, the BALTI study demonstrated a clear reduction in EVLW in the salbutamol-treated group. Consistent with the resolution of pulmonary edema, plateau airway pressures fell significantly in the salbutamol-treated group, and there was a trend toward reduced lung injury score. Based upon these promising results the West Midlands Critical Care Network, in collaboration with the UK Intensive Care Society, intends to set up BALTI-2, a randomized placebo-controlled trial powered to assess the effects of intravenous salbutamol upon mortality in ARDS.

Gavin D. Perkins, Danny F. McAuley, David R. Thickett and Fang Gao

West Midlands Critical Care Research Centre, Birmingham Heartlands Hospital, Birmingham, United Kingdom

FOOTNOTES

Conflict of Interest Statement: None of the authors has a financial relationship with a commercial entity that has an interest in the subject of this manuscript.

REFERENCES

  1. Perkins GD, McAuley DF, Thickett DR, Gao F. The beta-agonist lung injury trial (BALTI): a randomized placebo-controlled clinical trial. Am J Respir Crit Care Med 2006;173:281–287.[Abstract/Free Full Text]
  2. The Acute Respiratory Distress Syndrome Network. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. New Engl J Med 2000;342:301–308.[Abstract/Free Full Text]
  3. Katzenelson R, Perel A, Berkenstadt H, Preisman S, Kogan S, Sternik L, Segal E. Accuracy of transpulmonary thermodilution versus gravimetric measurement of extravascular lung water. Crit Care Med 2004;32:1550–1554.[CrossRef][Medline]
  4. Martin GS, Eaton S, Mealer M, Moss M. Extravascular lung water in patients with severe sepsis: a prospective cohort study. Crit Care 2005;9:R74–R82.[CrossRef][Medline]
  5. Perkins GD, Giles SP, McAuley DF, Thickett DR, Gao F. Resolution of pulmonary oedema predicts outcome in ARDS. Br J Anaesth 2004;92:621–622P.
  6. Mitchell JP, Schuller D, Calandrino FS, Schuster DP. Improved outcome based on fluid management in critically ill patients requiring pulmonary artery catheterization. Am Rev Respir Dis 1992;145:990–998.[Medline]
  7. Schreiber T, Huter L, Schwarzkopf K, Schubert H, Preussler N, Bloos F, Gaser E, Karzai W. Lung perfusion affects preload assessment and lung water calculation with the transpulmonary double indicator method. Intensive Care Med 2001;27:1814–1818.[CrossRef][Medline]




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Copyright © 2006 American Thoracic Society