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George Washington University, Washington, DC
Correspondence to: Vinayak Jha, MD, George Washington University, 2150 Pennsylvania Ave, Suite 5–425, Washington, DC 20037; email: vjha{at}mfa.gwu.edu
To the Editor:
We share the sentiments expressed by Otero et al1 (November 2006) regarding the importance of reducing mortality from severe sepsis, and applaud their efforts to develop early intervention strategies. While agreeing on the salutary effects of early and vigorous fluid resuscitation, we question the focus on mixed venous oxygen saturation (SvO2) as a centerpiece of the early goal-directed therapy (EGDT) algorithm. Specifically, we add a cautionary note against using blood transfusions to raise SvO2 > 70%.
In the study by Rivers et al,2 basal hematocrit was almost 35% in both groups, which would argue against transfusion. However, 64.1% of the EGDT subjects received transfusions. This we believe was the consequence of two interacting factors related to the study itself. Firstly, the larger volume of IV fluids received in the EGDT group caused greater hemodilution. Secondly, the intervention protocol dictated SvO2 > 70%. According to the Fick principle, SvO2 varies directly with arterial oxygen saturation, cardiac output, and hemoglobin concentration and inversely with oxygen consumption. Hemodilution-induced decreases in hemoglobin concentration would have had a depressing effect on SvO2. Since blood transfusion is the most energy-efficient way to raise SvO2, more so than the administration of dobutamine, which increases both cardiac output and oxygen consumption, it is not surprising that transfusion became the workhorse with which to achieve SvO2 > 70%. The unanswered issue is whether a transfusion-induced increase in SvO2 is tantamount to improved cellular oxygen utilization. We think not.
Otero et al1 assert that transfusions had a "physiologic effect." Indeed they did, but that effect was the expected increase in SvO2, not necessarily improved cellular bioenergetics. Transfusion at similar hemoglobin concentrations has been found not to increase tissue oxygen utilization in septic patients3 or in trauma patients.4 In addition to these physiologic considerations, the large-scale clinical trials5 suggesting harm associated with transfusions remain concerning.
Footnotes
The authors have no conflicts of interest to disclose.
Dr. Otero has received a research grant from Biosite, Inc., which ran the assays cited in the abstract reference 9. Dr. Rivers has spoken on behalf of Edwards Lifesciences and donates his honorarium to the research fund.
References
Henry Ford Hospital, Detroit, MI
Correspondence to: Ronny M. Otero, MD, Henry Ford Hospital, Emergency Medicine, 2799 West Grand Blvd, CFP-259, Detroit, MI 48202; e-mail: rotero1{at}hfhs.org
To the Editor:
We would like to thank Drs. Jha and Gutierrez for emphasizing the importance of evaluating more than a single parameter, such as central venous oxygen saturation (ScvO2), as the centerpiece of decisions regarding resuscitation of patients with severe sepsis, especially in the use of transfusion therapy.
Our recent article in CHEST (November 2006)1 was aimed at elucidating the rationale behind the stratified treatment strategy of early goal-directed therapy (EGDT).2 EGDT includes optimization of preload, afterload, arterial oxygen content, and subsequently contractility using a serial sequence of end points that incorporates ScvO2 among other important end points.
Although it is true that ScvO2 alone cannot be used as the only indicator of oxygen delivery, patients in the control and treatment arms were also monitored with serial assessments of various metabolic parameters including repeated measurements of lactate and base deficit. Although oxygen extraction ratios were not calculated in the original study, one can conceive that the improvement in ScvO2 in combination with the decrease in lactate level may signify an improvement in the imbalance between systemic oxygen demands and delivery.
As Dr. Jha points out, the baseline hematocrit was not the basis for transfusing a patient 3 h into the resuscitation. It was a uniform observation that the volume provided during the resuscitative course decreased the hematocrit by 30% at 3 h. The hematocrit value in the presence of a decreased ScvO2 and an increased lactate level signifies supply dependency and inadequate oxygen delivery. This has pathologic consequences in patients with cardiopulmonary comorbidities.345
Dr. Jha also indicated that the Fick equation suggests a direct correlation between oxygen consumption and arterial oxygen content. Previous studies678 are inconsistent on whether RBC transfusion increases tissue oxygen utilization. These studies reflect the presence of patients who were in the later stages of ICU admissions and who did not have the same degree of global tissue hypoxia as the patients in the EGDT study.2 If one concedes that the resolution of hypoperfusion at a local tissue level is clinically suggested by an increase in lactate clearance, as seen in the EGDT arm, then it logically proceeds that there must be improved perfusion at a cellular level.9 While animal and human data indicate deranged rheologic characteristics of RBCs in the setting of sepsis,10 which may impair microcirculatory flow,11 the outcome implications of these findings remain to be determined in this specific patient population.
One must remember that every component of EGDT has been part of critical care management for > 25 years. The relative contribution of each of these components is difficult to fully quantify, but the absolute consistent benefit of mortality reduction is the most important end point until we come up with something better.
References
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