help button home button
AJRCCM
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by DE BACKER, D.
Right arrow Articles by VINCENT, J.-L.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by DE BACKER, D.
Right arrow Articles by VINCENT, J.-L.

Am. J. Respir. Crit. Care Med., Volume 156, Number 4, October 1997, 1099-1104

Lactate Production by the Lungs in Acute Lung Injury

DANIEL DE BACKER, JACQUES CRETEUR, HAIBO ZHANG, MICHELLE NORRENBERG, and JEAN-LOUIS VINCENT

Department of Intensive Care, Erasme University Hospital, Free University of Brussels, Belgium

Arteriovenous differences in lactate (AVLAC) across the lungs are usually small and close to zero. However, it has recently been reported that the lungs can produce increased amounts of lactate in some patients with acute respiratory distress syndrome (ARDS). The aim of this study was to evaluate lactate production in various types of acute lung injury requiring mechanical ventilation and hemodynamic monitoring. Since the differences involved are usually small, minor errors in lactate measurement could greatly influence AVLAC. Based on an analysis of these errors (see text for details), we averaged five arterial and venous samples for each measurement. We investigated 122 patients: 43 with acute lung injury (ALI), nine with cardiogenic pulmonary edema (CPE), 37 with bronchopneumonia (BPN), seven with single lung transplantation (LTX), and 26 with other causes of respiratory failure (OTHER). There was no difference in arterial lactate between the various groups. AVLAC was higher in patients with ALI than in the other groups (0.20 ± 0.23 versus 0.07 ± 0.11 mEq/L). In patients with ALI, AVLAC was proportional to the Murray's lung injury score (-0.032 + 0.032x; r = 0.46, p < 0.01). Lung lactate production was calculated as the product of the cardiac index times AVLAC and was significantly higher in patients with ALI than in the other groups (0.69 ± 0.88 versus 0.19 ± 0.30 mEq/min; p < 0.05). In patients with ALI, lung lactate production was inversely related to the PaO2/FIO2 (1.42 - 0.005x; r = 0.35, p < 0.05) but directly related to the venous admixture (-0.36 + 0.003x; r = 0.49, p < 0.01) and the lung injury score (-0.19 + 0.36x; r = 0.45, p < 0.01). Lung lactate production was not significantly related to arterial lactate levels. These data indicate that AVLAC and lung lactate production can be increased in patients with ARDS but remain within the normal range in other types of respiratory failure.




This article has been cited by other articles:


Home page
 Hum Exp ToxicolHome page
E. Borges, M. Pinheiro, A. Eleto-Silva, M. Caliari, and M. Rodrigues-Machado
Glycogen content is affected differently in acute pulmonary and extra-pulmonary lung injury
Human and Experimental Toxicology, September 1, 2009; 28(9): 583 - 590.
[Abstract] [PDF]

Home page
 ChestHome page
M. Zambon and J.-L. Vincent
Mortality Rates for Patients With Acute Lung Injury/ARDS Have Decreased Over Time
Chest, May 1, 2008; 133(5): 1120 - 1127.
[Abstract] [Full Text] [PDF]

Home page
 Annals of Clinical & Laboratory ScienceHome page
A. O. Rashid, H. M. Azam, V. A. DeBari, A. I. Blamoun, M. Q. Moammar, and M. A. Khan
Non-Anion Gap Acidosis in Asthma: Clinical and Laboratory Features and Outcomes for Hospitalized Patients
Ann. Clin. Lab. Sci., January 1, 2008; 38(3): 228 - 234.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Respir. Crit. Care Med.Home page
E. Crimi, H. Zhang, R. N. N. Han, L. D. Sorbo, V.M. Ranieri, and A. S. Slutsky
Ischemia and Reperfusion Increases Susceptibility to Ventilator-induced Lung Injury in Rats
Am. J. Respir. Crit. Care Med., July 15, 2006; 174(2): 178 - 186.
[Abstract] [Full Text] [PDF]

Home page
 J. Appl. Physiol.Home page
S. M. Lobo, D. De Backer, Q. Sun, Z. Tu, G. Dimopoulos, J.-C. Preiser, N. Nagy, B. Vray, V. Vercruy, R. G. G. Terzi, et al.
Gut mucosal damage during endotoxic shock is due to mechanisms other than gut ischemia
J Appl Physiol, November 1, 2003; 95(5): 2047 - 2054.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Respir. Crit. Care Med.Home page
E. L'HER and P. SEBERT
A Global Approach to Energy Metabolism in an Experimental Model of Sepsis
Am. J. Respir. Crit. Care Med., October 15, 2001; 164(8): 1444 - 1447.
[Abstract] [Full Text] [PDF]

Home page
 ChestHome page
C. A. Manthous
Lactic Acidosis in Status Asthmaticus : Three Cases and Review of the Literature
Chest, May 1, 2001; 119(5): 1599 - 1602.
[Abstract] [Full Text] [PDF]

Home page
 ChestHome page
T. S. Walsh, S. McLellan, S. J. Mackenzie, and A. Lee
Hyperlactatemia and Pulmonary Lactate Production in Patients With Fulminant Hepatic Failure
Chest, August 1, 1999; 116(2): 471 - 476.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Proc. Am. Thorac. Soc. Am. J. Respir. Cell Mol. Biol.
Copyright © 1997 American Thoracic Society 		  CCM abstracts