The Value of Venous Oximetry

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The value of venous oximetryKonrad 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 patientswith 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. ª 2005 Lippincott Williams & Wilkins.

Klinik f. Anasthesiologie und Intensivtherapie, Klinikum derFriedrich-Schiller-Universitat, Jena, Germany

Correspondence to Prof. Dr. med. K. Reinhart, Klinikum derFriedrich-Schiller-Universitat Jena, Klinik f. Anasthesiologie und Intensivtherapie,Erlanger Allee 101, 07747 Jena, GermanyTel: +49 3647 932 31 01; fax: +49 3641 932 31 02;

e-mail: [email protected]

Current Opinion in Critical Care 2005, 11:259——263

ª 2005 Lippincott Williams & Wilkins.1070-5295

IntroductionContinuous 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 rou-

tinely measured cardiorespiratory parameters provide in-

formation 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 im-

pending tissue hypoxia. In some situations, tissue

hypoxia may exist despite normal values obtained by con-

ventional hemodynamic monitoring such as arterial blood

pressure, central venous pressure, heart rate, and urineoutput.

Measurement of mixed venous oxygen saturation (SvO2)

from the pulmonary artery has for some time been advo-

cated as an indirect index of tissue oxygenation. In myo-

cardial 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 cardiovas-

cular surgery, a low SvO2 was associated with a poor prog-

nosis [2–4]. 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 ve-

nous 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 ad-

equacy of global oxygen supply in various clinical setting

[1]. However, it has been questioned whether this param-

eter exactly mirrors the SvO2 especially in critically ill

patients. Rivers et al. [6] demonstrated in a recent pro-

spective randomized study in patients with severe sepsisand septic shock that, in addition to maintaining central

venous pressure above 8–12 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 useful-

ness of measuring ScvO2 in clinical practice.

259



Physiologic differences between SvO2

and ScvO2

Mixed venous O2 content (CvO2) is measured in the pul-

monary 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 deter-

mine CvO2 since physically dissolved oxygen reflected by

PvO2 can be neglected and hemoglobin should be con-

stant over a certain period of time in most clinical settings.

Due to this relation, SvO2 has been propagated as a param-

eter describing the adequacy of tissue oxygenation.

SvO2 measurement always necessitates the insertion of a

pulmonary artery catheter, which is a costly and an inva-

sive procedure. Already in 1969, Scheinman et al. [8] in-

vestigated 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 there-fore 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 satura-

tion in the superior vena cava. Most commonly, central ve-

nous 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 10–30% of central ve-nous catheters are inserted into the right atrium. It might

be therefore possible that blood drawn from a central ve-

nous 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

catheter moves upwards away from the right atrium due

to lengthening of mediastinal structures and vice versa.

Difference between SvO2 and ScvO2 in theclinical settingThe 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 pres-

sures where cerebral trauma and barbiturate coma may

decrease cerebral metabolism. Patients with elevated in-

tracranial pressures revealed the highest difference be-tween SvO2 and ScvO2 [11•].

The reversal of the physiologic difference between ScvO2

and SvO2 can also be observed in the state of cardiocircu-

latory shock. During hemodynamic deterioration, mesen-

teric 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 correla-

tion coefficients between ScvO2 and SvO2 under various

conditions have been reported [13]. As in the experimen-

tal 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 informa-

tion about SvO2. However, several conditions such as

shock or general anesthesia (see above) affect the physi-

ologic 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 rea-

sonable that a precise determination of SvO2 by the

Figure 1. Calculation of O2 consumption (VO2) accordingto the Fick principle

The equation can be solved to the mixed venous oxygen content(CvO2). The calculation of CaO2 and CvO2 neglects the physicallydissolved 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, arterialO2 saturation; SvO2, mixed venous O2 saturation.

260 C ardiopulmonary monitoring



measurement of ScvO2 is not possible. However, more im-

portant than the precise prediction of SvO2 is the question

whether changes in SvO2 indicating a hemodynamic de-

rangement 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 re-

liable 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. Al-

though the difference between SvO2 and ScvO2 increasesafter onset of septic shock, the curves of both parameters

change in parallel.

Clinical application of SvO2

Importance of SvO2 monitoring has been originally pro-

posed 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 inju-

ries [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 prob-lems 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

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 pa-

tients after coronary artery bypass grafting. In the treat-

ment 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 hospi-

tal length of stay by one day in the treatment group. Ap-

proximately 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 improve-

ment for this monitoring device [5]. It may well be that

the failure to demonstrate the usefulness of SvO2 moni-

toring in most studies results from the fact that these

studies enrolled patients too late and/or that this monitor-

ing was without clear treatment algorithms and goals.

Clinical application of ScvO2

Since monitoring of SCV O2 looked promising in the exper-

imental setting, several clinical studies including one large

randomized trial have been performed in patients with

different kinds of shock. This included patients with se-

vere sepsis or septic shock, severe trauma, and cardiogenic

shock.

Severe sepsis and septic shock

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

Figure 2. Changes of ScvO2 and SvO2

Changes of ScvO2 and SvO2 caused by several experimentalmanipulations in a dog [14].

Figure 3. Course of mixed venous (SvO2) and centralvenous (ScvO2) oxygen saturations

Course of mixed venous (SvO2) and central venous (ScvO2) oxygensaturations over several days in a septic patient who developed septicshock on day 3. Modified from [7].

The value of venous oximetry Reinhart and Bloos 261



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 hemo-

dynamically 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 patientswith a ScvO2 <65% were in need of further interventions

and demonstrated prolonged cardiac dysfunctions and ele-

vated lactate levels. Although there has been no study that

investigated the validity of ScvO2 to guide hemodynamic

stabilization in polytraumatized patients, there is good ev-

idence 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 trans-

fusion [19]. However, in a similar study, only lactate con-centrations 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 in-

crease 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 corre-

lated with cardiac output and a drop in SvO2 is a good and

early marker of cardiac deterioration [15]. Correlation be-

tween SvO2 and ScvO2 was insufficient in patients withheart failure [8] but was reported to be accurate in pa-

tients with myocardial infarction [21]. Nevertheless, pa-

tients 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 max-

imum O2 extraction resulting in an ScvO2 <20%. Success-

ful 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 circu-

lation 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 in-

dicative of an impairment of tissue O2 utilization probably

due to a prolonged cardiac arrest [25].

ConclusionMeasurement 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 doesnot 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 inten-

sive 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), lac-

tate 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 readingPapers of particular interest, published within the annual period of review, havebeen highlighted as:• of special interest•• of outstanding interest

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262 C ardiopulmonary monitoring



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•

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The value of venous oximetry Reinhart and Bloos 263

The Value of Venous Oximetry

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