Authors’ Disclosure Statement: The authors report no actual or potential conflict of interest in relation to this article. The opinions expressed in this paper do not reflect those of the Veteran’s Healthcare administration.
Dr Brant is a critical care fellow, department of critical care, multidisciplinary critical care training program, University of Pittsburgh Medical Center, Pennsylvania. Dr Niehaus is a critical care fellow, department of critical care, multidisciplinary critical care training program, University of Pittsburgh Medical Center, Pennsylvania. Dr Kobzik is a critical care fellow, department of critical care, multidisciplinary critical care training program, University of Pittsburgh Medical Center, Pennsylvania. Dr Goodmanson is a critical care fellow, department of critical care, multidisciplinary critical care training program, University of Pittsburgh Medical Center, Pennsylvania. Dr Skolnik is a critical care fellow, department of critical care, multidisciplinary critical care training program, University of Pittsburgh Medical Center, Pennsylvania. Dr Hamade is a critical care fellow, department of critical care, multidisciplinary critical care training program, University of Pittsburgh Medical Center, Pennsylvania. Dr Schott is an assistant professor, department of critical care medicine and emergency medicine, University of Pittsburgh and University of Pittsburgh Medical Center, Pennsylvania, and director of critical care ultrasonography, VA Pittsburgh Health Care Systems, Pennsylvania.
The traditional two assumptions in CVP monitoring are CVP value represents the overall volume status of the patient, and the LV is able to utilize additional preload volume. The latter assumption, however, may be hampered by the presence of sepsis-induced myocardial dysfunction, which may be present in up to 40% of critically ill patients.34 The former assumption does not always hold true due to processes that change filling pressures independent of intravascular volume—eg, acute or chronic pulmonary hypertension, cardiac tamponade, intra-abdominal hypertension, or LV failure. Even before the landmark EGDT study, available data suggested that CVP was not a reliable marker for resuscitation management.35 A recent systematic review by Gottlieb and Hunter36 showed that the area under the receiver-operator curve for low, mid-range, or high CVPs was equivocal at best. In addition to its unreliability and lack of specificity, another significant drawback to using CVP to guide resuscitation therapy in the ED is that it necessitates placement of a CVC, which can be time-consuming and, if not otherwise indicated, lead to complications of infection, pneumothorax, and/or thrombosis.37
Mixed Venous Oxygen
Background
Most EPs are familiar with the use of ScvO2 in EGDT protocols to guide volume resuscitation of septic patients.2 A patient’s ScvO2 represents the O2 saturation of venous blood obtained via a CVC at the confluence of the superior vena cava and the RA, and thus it reflects tissue O2 consumption as a surrogate for tissue perfusion. The measurement parallels the SvO2 obtained from the pulmonary artery. In a healthy patient, SvO2 is around 65% to 70% and includes blood returning from both the superior and inferior vena cava (IVC). As such, ScvO2 values are typically 3% to 5% lower than SvO2 owing to the lower O2 extracted by tissues draining into the IVC compared to the mixed venous blood sampled from the pulmonary artery.38
Though a debate over the benefit of EGDT in treating sepsis continues, understanding the physiology of ScvO2 measurements is another potential tool the EP can use to guide the resuscitation of critically ill patients.39 A patient’s SvO2 and, by extension, ScvO2 represents the residual O2 saturation after the tissues have extracted the amount of O2 necessary to meet metabolic demands (Figure 2).
Figure 2.
If tissue O2 consumption increases, the ScvO2 is expected to decrease as more O2 is extracted from the blood. Additionally, if tissue O2 delivery decreases, the ScvO2 is expected to decrease. Examples of these occur in patients with hypoxemia, anemia, decreased CO due to decreased LV systolic contractility, decreased heart rate, decreased pre-load/stroke volume from intravascular hypovolemia, or decreased perfusion pressures. Treatment therefore can be targeted at each of these etiologies by providing supplemental O2, blood transfusion, inotropic medications, chronotropic medications or electrical pacing, IVFs, or vasoconstrictor drugs, respectively.
Conversely, cellular dysfunction, which can occur in certain toxicities or in severe forms of sepsis, can lead to decreased tissue O2 consumption with a concomitant rise in ScvO2 to supernormal values.38 The EP should take care, however, to consider whether ScvO2 values exceeding 80% represent successful therapeutic intervention or impaired tissue O2 extraction and utilization. There are data from ED patients suggesting an increased risk of mortality with both extremely low and extremely high values of ScvO2.40
Benefits
A critically ill patient’s ScvO2 can potentially provide EPs with insight into the patient’s global tissue perfusion and the source of any mismatch between O2 delivery and consumption. Using additional tools and measurements (physical examination, serum Hgb levels, and pulse oximetry) in conjunction with an ScvO2 measurement, assists EPs in identifying targets for therapeutic intervention. The effectiveness of this intervention can then be assessed using serial ScvO2 measurements, as described in Rivers et al2 EGDT protocol. Importantly, EPs should take care to measure serial ScvO2 values to maximize its utility.38 Similar to a CVP measurement, ScvO2is easily obtained from blood samples for serial laboratory measurements, assuming the patient already has a CVC with the distal tip at the entrance to the RA (ScvO2) or a pulmonary artery catheter (PAC) (SvO2).
Limitations
Serial measurements provide the most reliable information, which may be more useful in patients who spend extended periods of their resuscitation in the ED. In comparison to other measures of global tissue hypoxia, work by Jones et al41 suggests non-inferiority of peripherally sampled, serial lactate measurements as an alternative to ScvO2. This, in conjunction with the requirement for an internal jugular CVC, subclavian CVC, or PAC with their associated risks, may make ScvO2 a less attractive guide for the resuscitation of critically ill patients in the ED.
