The value of venous oximetry

Konrad Reinhart and Frank Bloos

Purpose of review
Maintenance of adequate tissue oxygenation is an
important task in intensive care units. In this context, venous
oximetry by obtaining mixed venous oxygen saturation or
central venous oxygen saturation has been discussed as
useful monitoring parameters. This review discusses the
physiology and clinical application of these parameters.
Recent findings
No study has so far demonstrated that venous oxygen
saturation monitoring can reduce mortality in critically ill
patients although length of stay has been decreased in
cardiac surgery patients. Furthermore, pulmonary artery
catheter usage does not affect outcome in critically ill
patients. In contrast, early goal directed therapy for patients
with severe sepsis or septic shock, which includes
treatment goals for mean arterial pressure, central venous
pressure, and central venous oxygen saturation, was able to
increase survival in these patients. There is also evidence
that central venous oxygen saturation measurement is
beneficial in other types of shock.
Summary
Early goal directed therapy should be implemented in the
initial resuscitation of septic patients. Measurement of
central venous oxygen saturation can easily be applied in
intensive care unit patients and offers a useful indirect
indicator for the adequacy of tissue oxygenation.
Keywords
central venous oxygen saturation, hemodynamic
monitoring, mixed venous oxygen saturation, oxygen
transport, tissue oxygenation
Curr Opin Crit Care 11:259
263. 2005 Lippincott Williams & Wilkins.
Klinik f. Anasthesiologie und Intensivtherapie, Klinikum der
Friedrich-Schiller-Universitat, Jena, Germany
Correspondence to Prof. Dr. med. K. Reinhart, Klinikum der
Friedrich-Schiller-Universitat Jena, Klinik f. Anasthesiologie und Intensivtherapie,
Erlanger Allee 101, 07747 Jena, Germany
Tel: +49 3647 932 31 01; fax: +49 3641 932 31 02;
e-mail: Konrad.Reinhart@med.uni-jena.de
Current Opinion in Critical Care 2005, 11:259
263
2005 Lippincott Williams & Wilkins.
1070-5295

Introduction
Continuous measurement of the systemic blood pressure
and heart rate are routinely obtained in critically ill
patients. It is a very basic question to what extent the routinely measured cardiorespiratory parameters provide information about the adequacy of oxygen transport and,
more importantly, on the quality of tissue oxygenation.
Recognition, prevention, and treatment of tissue hypoxia
play a key role in intensive care medicine. The aim of
cardiovascular monitoring is the early recognition of impending tissue hypoxia. In some situations, tissue
hypoxia may exist despite normal values obtained by conventional hemodynamic monitoring such as arterial blood
pressure, central venous pressure, heart rate, and urine
output.
Measurement of mixed venous oxygen saturation (SvO2)
from the pulmonary artery has for some time been advocated as an indirect index of tissue oxygenation. In myocardial infarction, decreased SvO2 was found to be
indicative of current or imminent cardiac failure [1]. In
several diseases such as cardiopulmonary disease, septic
shock, cardiogenic shock, and in patients after cardiovascular surgery, a low SvO2 was associated with a poor prognosis [24]. Based on these findings, fiberoptic pulmonary
artery (PA) catheters for continuous SvO2 measurement
have been developed. However, PA catheterization is costly
and includes inherent risks. Furthermore, its usefulness in
various clinical conditions remains under debate due to
a lack of convincing data [5]. In comparison, central venous catheterization via the superior vena cava is part of
standard care for critically ill patients and is easier and
safer to perform. Similar to the SvO2, the measurement
of the central venous oxygen saturation (ScvO2) has been
advocated as a simple method to assess changes in the adequacy of global oxygen supply in various clinical setting
[1]. However, it has been questioned whether this parameter exactly mirrors the SvO2 especially in critically ill
patients. Rivers et al. [6] demonstrated in a recent prospective randomized study in patients with severe sepsis
and septic shock that, in addition to maintaining central
venous pressure above 812 mm Hg, mean arterial pressure
above 65 mm Hg, and urine output above 0.5 mL/kg/h, the
maintenance of a ScvO2 above 70% resulted in an absolute
reduction of mortality by 15%. These findings refueled
the interest in the measurement of ScvO2 in critically
ill patients. The purpose of this review is to discuss the
differences and the similarities between mixed and central
venous oxygen saturation as well as the potential usefulness of measuring ScvO2 in clinical practice.
259

260 Cardiopulmonary monitoring

Physiologic differences between SvO2

and ScvO2
Mixed venous O2 content (CvO2) is measured in the pulmonary artery and reflects the relation between whole body
O2 need and cardiac output under conditions of a constant
CaO2 (Fig. 1). SvO2 is the most important factor to determine CvO2 since physically dissolved oxygen reflected by
PvO2 can be neglected and hemoglobin should be constant over a certain period of time in most clinical settings.
Due to this relation, SvO2 has been propagated as a parameter describing the adequacy of tissue oxygenation.
SvO2 measurement always necessitates the insertion of a
pulmonary artery catheter, which is a costly and an invasive procedure. Already in 1969, Scheinman et al. [8] investigated whether the central venous oxygen saturation
(ScvO2) reflects changes in SvO2.
Venous O2 saturations differ among several organ systems
since they extract different amounts of oxygen. It is therefore reasonable that venous oxygen saturation depends on
the site of measurement. In healthy humans, the oxygen
saturation in the inferior vena cava is higher than in the
superior vena cava. Since the pulmonary artery contains
a mixture of blood from both the superior as well as the
inferior vena cava, SvO2 is greater than the oxygen saturation in the superior vena cava. Most commonly, central venous catheters are inserted via a jugular vein or subclavian
vein. Thus, central venous blood sampling should reflect
the venous blood of the upper body only. However, the tip
of the catheter may not only be located in the superior
vena cava but also at the superior vena caval/atrial junction
or inside the right atrium [9]. About 1030% of central venous catheters are inserted into the right atrium. It might
be therefore possible that blood drawn from a central venous catheter also to some degree contains blood from the
inferior vena cava. Furthermore, the catheter tip may be
moved depending on the position of the patient. When
a patient is moved from a supine to upright position, the
Figure 1. Calculation of O2 consumption (VO2) according
to the Fick principle

The equation can be solved to the mixed venous oxygen content

(CvO2). The calculation of CaO2 and CvO2 neglects the physically
dissolved oxygen, which affects the oxygen content only little. CO,
cardiac output; avDO2, difference of arterio-venous O2 content; CaO2,
arterial oxygen content; Hb, hemoglobin concentration; SaO2, arterial
O2 saturation; SvO2, mixed venous O2 saturation.

catheter moves upwards away from the right atrium due

to lengthening of mediastinal structures and vice versa.

Difference between SvO2 and ScvO2 in the

clinical setting
The physiologic difference between ScvO2 and SvO2 is
not constant and may be affected by several conditions.
These conditions include general anesthesia, severe head
injury, redistribution of blood flow as it occurs in shock,
and microcirculatory shunting or cell death.
During anesthesia, ScvO2 may exceed SvO2 by up to 6%
[10]. This observation may be explained by the effect of
inhalation anesthetics to increase cerebral blood flow and
therefore reducing cerebral O2 extraction. This leads to a
higher SO2 in the superior vena cava. A similar effect can
be observed in patients with elevated intracranial pressures where cerebral trauma and barbiturate coma may
decrease cerebral metabolism. Patients with elevated intracranial pressures revealed the highest difference between SvO2 and ScvO2 [11].
The reversal of the physiologic difference between ScvO2
and SvO2 can also be observed in the state of cardiocirculatory shock. During hemodynamic deterioration, mesenteric blood flow decreases followed by an increase of O2
extraction in these organs [12]. Naturally, this goes along
with venous desaturation in the lower body. On the other
hand, cerebral blood flow is maintained over some period
in shock causing a delayed drop of ScvO2 in comparison to
SvO2. This effect can be demonstrated in several types of
shock [11].
Theoretically, the physiologic difference between SvO2
and ScvO2 may also be altered if the regional O2 extraction
of a certain organ decreases. This may be due to increased
shunting in the microcirculation. Progressive cell death
would also decrease oxygen extraction in the affected
organ.

Parallel tracking of SvO2 and ScvO2

Several animal studies have been performed to prove the
reliability of ScvO2 as a substitute for SvO2. High correlation coefficients between ScvO2 and SvO2 under various
conditions have been reported [13]. As in the experimental setting, a good correlation between ScvO2 and SvO2
could be found in critically ill patients [1,11]. It was
therefore concluded that ScvO2 yields adequate information about SvO2. However, several conditions such as
shock or general anesthesia (see above) affect the physiologic difference between SvO2 and ScvO2. It might be
therefore argued that the correlation between ScvO2 and
SvO2 is clinically unacceptable in critically ill patients.
According to the physiologic properties of ScvO2, it is reasonable that a precise determination of SvO2 by the

The value of venous oximetry Reinhart and Bloos 261

measurement of ScvO2 is not possible. However, more important than the precise prediction of SvO2 is the question
whether changes in SvO2 indicating a hemodynamic derangement or a treatment effect are mirrored by changes
in the ScvO2. In a dog model, various clinical conditions
such as hypoxia and hemorrhagic shock were investigated
regarding their effects on these parameters [14]. This
study confirmed that ScvO2 differed from SvO2 but
changes in SvO2 were accompanied by parallel changes
in ScvO2 (Fig. 2).
This could also be demonstrated in the clinical setting
where 32 critically ill surgical patients were monitored
for a total of 1097 hours. A good agreement between
SvO2 and ScvO2 was shown [11]. The authors concluded
that the continuous measurement of ScvO2 might be a reliable and convenient tool to monitor the adequacy of the
oxygen supply/demand ratio. Figure 3 shows an example of
a septic patient who developed septic shock on day 3. Although the difference between SvO2 and ScvO2 increases
after onset of septic shock, the curves of both parameters
change in parallel.

Clinical application of SvO2

Importance of SvO2 monitoring has been originally proposed in cardiology patients [15]; however, indications
for this monitoring technique have been extended to other
areas. One small study demonstrated that maintaining a
normal SvO2 is beneficial in patients with multiple injuries [16]. As this was a non-randomized study, this trial
is of low-grade evidence only. Large controlled trials failed
to demonstrate an outcome improvement when SvO2 was
used as a treatment goal. One of the most important problems was the fact that a considerable amount of patients
did not reach the treatment target.
Gattinoni et al. [17] could not find any difference in
morbidity and mortality in a large multicenter trial where

Figure 3. Course of mixed venous (SvO2) and central

venous (ScvO2) oxygen saturations

Course of mixed venous (SvO2) and central venous (ScvO2) oxygen

saturations over several days in a septic patient who developed septic
shock on day 3. Modified from [7].

critically ill patients were resuscitated to an SvO2 >70%.

However, the anticipated goal was only achieved in one
third of the patients.
Polonen et al. [2] undertook a goal-oriented trial in patients after coronary artery bypass grafting. In the treatment group, SvO2 was maintained >70% and lactate
<2 mmol/l while there was standard care provided to the
control group. There was a significant reduction of hospital length of stay by one day in the treatment group. Approximately half of the patients did not achieve the target.
Although the study by Polonen et al. gave a hint that SvO2
monitoring might be beneficial for critically ill patients,
trials about the PAC failed to show an outcome improvement for this monitoring device [5]. It may well be that
the failure to demonstrate the usefulness of SvO2 monitoring in most studies results from the fact that these
studies enrolled patients too late and/or that this monitoring was without clear treatment algorithms and goals.

Figure 2. Changes of ScvO2 and SvO2

Clinical application of ScvO2

Since monitoring of SCVO2 looked promising in the experimental setting, several clinical studies including one large
randomized trial have been performed in patients with
different kinds of shock. This included patients with severe sepsis or septic shock, severe trauma, and cardiogenic
shock.
Severe sepsis and septic shock

Changes of ScvO2 and SvO2 caused by several experimental

manipulations in a dog [14].

Severe sepsis and septic shock are frequently complicated

by the development of the multiple organ dysfunction
syndrome (MODS). Tissue hypoxia is believed to be one
of the most important mechanisms for the onset of MODS.
However, treatment concepts favoring the achievement of
a maximum O2 delivery proved to be of no benefit to these

262 Cardiopulmonary monitoring

patients [17]. Furthermore, it is very difficult to define

goals for cardiovascular resuscitation in these patients.
In this context, Rivers et al. demonstrated in patients with
severe sepsis or septic shock that an early and aggressive
resuscitation guided by the ScvO2 additionally to central
venous pressure and mean arterial pressure reduced the
28-day mortality rates from 46.5% to 30.5% (P = 0.009)
[6]. Compared with the conventionally treated group,
the ScvO2 group received more fluids, more frequently
dobutamine, and more blood transfusion during the first
6 hours. This resulted in a faster and better improvement
of organ functions in the ScvO2 group.
Severe trauma and hemorrhagic shock

The care of severely traumatized patients is defined by

early and aggressive resuscitation followed by early surgical
intervention. Patients with shock, who have been hemodynamically stabilized according to vital signs such as heart
rate, blood pressure, and central venous pressure, had an
insufficient ScvO2 in 50% of the cases [18]. These patients
with a ScvO2 <65% were in need of further interventions
and demonstrated prolonged cardiac dysfunctions and elevated lactate levels. Although there has been no study that
investigated the validity of ScvO2 to guide hemodynamic
stabilization in polytraumatized patients, there is good evidence from patients with severe sepsis or septic shock
that the ScvO2 is a good parameter in the resuscitation
of hemodynamically unstable patients [6].
In initially hemodynamically stable patients after trauma,
an ScvO2 below 65% was able to detect those patients who
suffered from blood loss and were in need of blood transfusion [19]. However, in a similar study, only lactate concentrations and arterial base deficit but not ScvO2 was
able to distinguish patients with delayed blood loss from
patients without bleeding prior to surgery [20].
Heart failure and cardiac arrest

Heart failure is characterized by a limited cardiac output.

Therefore, such patients are unable to sufficiently increase cardiac output during a rise of O2 need. Changes
in need of O2 can therefore only be covered by changes
in O2 extraction. In these patients, SvO2 is tightly correlated with cardiac output and a drop in SvO2 is a good and
early marker of cardiac deterioration [15]. Correlation between SvO2 and ScvO2 was insufficient in patients with
heart failure [8] but was reported to be accurate in patients with myocardial infarction [21]. Nevertheless, patients with congestive heart failure, who present high serum
lactate levels and a low ScvO2, require a more aggressive
management in the emergency department than patients
with normal ScvO2 and normal lactate levels [22]. Patients
with an ScvO2 below 60% were in cardiogenic shock.
During cardiac arrest, cardiopulmonary resuscitation
(CPR) is applied to the patient with the goal to reestab-

lish the circulation by the use of standardized procedures.

In this setting, continuous ScvO2 measurement can be
helpful in the management during CPR. Venous blood
is massively desaturated during cardiac arrest due to maximum O2 extraction resulting in an ScvO2 <20%. Successful chest compression leads to an immediate increase of
ScvO2 above 40% [23]. In all patients who reached an
ScvO2 >72% during CPR, a return of spontaneous circulation was observed [24]. On the other hand, a very high
ScvO2 (>80%) in the presence of a very low O2 delivery
after successful CPR is also an unfavorable predictor of
outcome. It has been argued that a very high ScvO2 is indicative of an impairment of tissue O2 utilization probably
due to a prolonged cardiac arrest [25].

Conclusion
Measurement of ScvO2 is simple and does not necessitate
additional invasive techniques. There is a good correlation
between ScvO2 and SvO2 under non-shock conditions.
During the state of circulatory shock, however, ScvO2 does
not always exactly mirror SvO2. However, changes of both
parameters occur in a parallel manner. Furthermore,
changes in SvO2 due to therapeutic interventions are well
reflected in changes of ScvO2. This holds true especially
in patients with severe sepsis/septic shock and patients
with cardiac arrest. In critically ill patients, ScvO2 is higher
than SvO2. This implies that a pathologic ScvO2 indicates
an even lower SvO2. As many other parameters in intensive care medicine, ScvO2 should not be used as the only
measure in the assessment of the cardiocirculatory system
but should be combined with standard vital parameters
(heart rate, blood pressure, central venous pressure), lactate measurement, and parameters of organ function (urine
output, gastric tonometry). Combining several parameters
for a goal-oriented therapy should increase the reliability to
achieve stable hemodynamic conditions without evidence
of tissue hypoxia.

References and recommended reading

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of special interest
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