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Emanuel P. Rivers, MD, MPH, FCCP; Ronald Elkin, MD; Chad Cannon, MD
Author and Funding Information

From the Department of Emergency Medicine and Surgery (Dr Rivers), Henry Ford Hospital, Wayne State University; the Department of Medicine (Dr Elkin), Pulmonary and Critical Care Medicine, California Pacific Medical Center; and the Department of Emergency Medicine (Dr Cannon), University of Kansas Hospital.

Correspondence to: Emanuel P. Rivers, MD, MPH, FCCP, Department of Emergency Medicine, Wayne State University, 270-Clara Ford Pavilion, Henry Ford Hospital, 2799 W Grand Blvd, Detroit, MI 48202; e-mail: erivers1@hfhs.org


Financial/nonfinancial disclosures: The authors have reported to CHEST the following conflicts of interest: In the past 3 years, Dr Rivers has received funding from the National Institutes of Health, Aggennix AG, and Alere Corporation. He has been a one-time consultant for Aggennix AG; Eisai Co, Ltd; Idaho Technologies Inc; AstraZeneca; Massimo; and Sangard. He is a consultant to the Institute of Medicine, National Academies. The Early Goal-Directed Therapy (EGDT) study was performed without external industry support or funding of any kind. Any intellectual properties associated with Dr Rivers’ research are exclusively owned by Henry Ford Hospital. Dr Rivers holds no past or present intellectual properties and has never received royalties or stock interest related to technologies in EGDT research and practice. Dr Elkin has received funding from the Gordon and Betty Moore Foundation, has been a one-time consultant for Eisai Co, Ltd, and participated on the speaker’s bureau for Edwards Lifesciences LLC on three occasions. Dr Cannon has been a one-time consultant for Aggennix AG and Eisai Co, Ltd.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (http://www.chestpubs.org/site/misc/reprints.xhtml).


© 2012 American College of Chest Physicians


Chest. 2012;141(5):1363-1364. doi:10.1378/chest.12-0740
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Published online

To the Editor:

We appreciate the interest of Dr Manthous in our Counterpoint Editorial1 in CHEST that lactate clearance is an insufficient replacement for central venous oxygen saturation (Scvo2) as a goal in the treatment of severe sepsis and septic shock. Mathematic coupling results from using cardiac output to calculate both oxygen delivery (Do2) and oxygen consumption (V˙ o2). This “artifact” can be overcome by directly measuring V˙ o2 by expired gas analysis.2 In both animal3 and human4 models of early septic shock, decreased Scvo2, intracardiac filling pressures, and cardiac output (hypodynamic state) give way to a hyperdynamic state after adequate resuscitation.4 Thus, a biphasic response in V˙ o2 (independent of measurement method) is part of the pathogenesis of this disease and is not an artifact.5 The critical Do2 and V˙ o2 (where anaerobic metabolism occurs) can vary because of comorbidities, such as chronic cardiopulmonary disorders.6 Normally, an acute hemodynamic deterioration leads to an increase in systemic oxygen extraction (decreased Scvo2). When this compensatory mechanism ceases to meet V˙ o2, lactate production occurs. However, the aforementioned comorbidities give rise to “alactemic” patients who can tolerate a pathologically low V˙ o2 before lactate production and are known as “metabolic hibernators.” Thus, lactate production is subject to significant individual variability.

We agree with Dr Manthous that factors other than global Do2 dependency likely contribute to lactic acidosis (Table 1), making it an insensitive real-time indicator of tissue perfusion. It is important to note, however, that global estimates, such as Scvo2 or mixed venous oxygen saturation, may be insensitive to regional imbalances at the microcirculatory level. Nonetheless, the macrocirculation and microcirculation are connected. Early reversible and correctable causes of global tissue hypoxia, such as arterial hypoxia, anemia, myocardial dysfunction, and increased oxygen demands, should be eliminated as early as possible. This physiologic and rational approach has been described for decades. Perhaps the dramatic outcome benefit in the Rivers et al7 trial, acknowledged by Dr Manthous, was at least partially due to this approach leading to recruitment of compromised microcirculatory beds by macrocirculatory resuscitation. In the United States, patients with sepsis wait an average of 5 h in the ED, which is similar to the Early Goal-Directed Therapy study.8 The origin of these patients is the ED for 52.4% (mortality of 27.6%), ICU for 12.8% (mortality of 41.3%), and hospital wards for 34.8% (mortality of 46.8%).9 These data indicate that sepsis is a hospital-wide disease. The mortality rates for acute myocardial infarction, stroke, and trauma were significantly reduced when the “golden hours” were applied. After 1 decade, a similar approach to sepsis, called early-goal directed therapy, has been robustly replicated in >50 publications and thousands of patients. We agree that although pathogenic questions remain, they should not stand in the way of providing today’s best evidence-based care.

Table Graphic Jump Location
Table 1 —Causes of Persistent Lactate Elevation With Normalization of Do2 and Scvo2

Do2 = oxygen delivery; Scvo2 = central venous oxygen saturation.

Rivers EP, Elkin R, Cannon CM. Counterpoint: should lactate clearance be substituted for central venous oxygen saturation as goals of early severe sepsis and septic shock therapy? No. Chest. 2011;1406:1408-1413. [CrossRef] [PubMed]
 
Hanique G, Dugernier T, Laterre PF, Dougnac A, Roeseler J, Reynaert MS. Significance of pathologic oxygen supply dependency in critically ill patients: comparison between measured and calculated methods. Intensive Care Med. 1994;201:12-18. [CrossRef] [PubMed]
 
Rosário AL, Park M, Brunialti MK, et al. SvO(2)-guided resuscitation for experimental septic shock: effects of fluid infusion and dobutamine on hemodynamics, inflammatory response, and cardiovascular oxidative stress. Shock. 2011;366:604-612. [CrossRef] [PubMed]
 
Friedman G, De Backer D, Shahla M, Vincent JL. Oxygen supply dependency can characterize septic shock. Intensive Care Med. 1998;242:118-123. [CrossRef] [PubMed]
 
Kasnitz P, Druger GL, Yorra F, Simmons DH. Mixed venous oxygen tension and hyperlactatemia. Survival in severe cardiopulmonary disease. JAMA. 1976;2366:570-574. [CrossRef] [PubMed]
 
Rady M, Jafry S, Rivers E, Alexander M. Characterization of systemic oxygen transport in end-stage chronic congestive heart failure. Am Heart J. 1994;1284:774-781. [CrossRef] [PubMed]
 
Rivers E, Nguyen B, Havstad S, et al. Early goal-directed therapy in the treatment of severe sepsis and septic shock. N Engl J Med. 2001;34519:1368-1377. [CrossRef] [PubMed]
 
Wang HE, Shapiro NI, Angus DC, Yealy DM. National estimates of severe sepsis in United States emergency departments. Crit Care Med. 2007;358:1928-1936. [CrossRef] [PubMed]
 
Levy MM, Dellinger RP, Townsend SR, et al; Surviving Sepsis Campaign Surviving Sepsis Campaign The Surviving Sepsis Campaign: results of an international guideline-based performance improvement program targeting severe sepsis. Crit Care Med. 2010;382:367-374. [CrossRef] [PubMed]
 

Figures

Tables

Table Graphic Jump Location
Table 1 —Causes of Persistent Lactate Elevation With Normalization of Do2 and Scvo2

Do2 = oxygen delivery; Scvo2 = central venous oxygen saturation.

References

Rivers EP, Elkin R, Cannon CM. Counterpoint: should lactate clearance be substituted for central venous oxygen saturation as goals of early severe sepsis and septic shock therapy? No. Chest. 2011;1406:1408-1413. [CrossRef] [PubMed]
 
Hanique G, Dugernier T, Laterre PF, Dougnac A, Roeseler J, Reynaert MS. Significance of pathologic oxygen supply dependency in critically ill patients: comparison between measured and calculated methods. Intensive Care Med. 1994;201:12-18. [CrossRef] [PubMed]
 
Rosário AL, Park M, Brunialti MK, et al. SvO(2)-guided resuscitation for experimental septic shock: effects of fluid infusion and dobutamine on hemodynamics, inflammatory response, and cardiovascular oxidative stress. Shock. 2011;366:604-612. [CrossRef] [PubMed]
 
Friedman G, De Backer D, Shahla M, Vincent JL. Oxygen supply dependency can characterize septic shock. Intensive Care Med. 1998;242:118-123. [CrossRef] [PubMed]
 
Kasnitz P, Druger GL, Yorra F, Simmons DH. Mixed venous oxygen tension and hyperlactatemia. Survival in severe cardiopulmonary disease. JAMA. 1976;2366:570-574. [CrossRef] [PubMed]
 
Rady M, Jafry S, Rivers E, Alexander M. Characterization of systemic oxygen transport in end-stage chronic congestive heart failure. Am Heart J. 1994;1284:774-781. [CrossRef] [PubMed]
 
Rivers E, Nguyen B, Havstad S, et al. Early goal-directed therapy in the treatment of severe sepsis and septic shock. N Engl J Med. 2001;34519:1368-1377. [CrossRef] [PubMed]
 
Wang HE, Shapiro NI, Angus DC, Yealy DM. National estimates of severe sepsis in United States emergency departments. Crit Care Med. 2007;358:1928-1936. [CrossRef] [PubMed]
 
Levy MM, Dellinger RP, Townsend SR, et al; Surviving Sepsis Campaign Surviving Sepsis Campaign The Surviving Sepsis Campaign: results of an international guideline-based performance improvement program targeting severe sepsis. Crit Care Med. 2010;382:367-374. [CrossRef] [PubMed]
 
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