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The oxygen supply demand balance:A monitoring challenge

Krisztin Tnczos, MD, Clinical Director of Neuro-traumaIntensive Care Unit, Zsolt Molnr, MD, PhD, Clinical Professorof Anaesthesiology and Critical Care, Head of Department *

Department of Anaesthesia and Intensive Therapy, University of Szeged, 6, Semmelweis St,6725 Szeged, Hungary

Keywords:oxygen deliveryoxygen consumptioncentral venous oxygen saturation

mixed venous oxygen saturation

The principal task of acute critical care is to avoid or correct oxygendebt by increasing oxygen delivery (DO 2) and/or decreasing oxy-gen consumption (VO 2). The most commonly used methods toassess the relationship of adequate delivery and consumption are

mixed venous oxygen saturation and its surrogate, central venousoxygen saturation (ScvO 2). The purpose of this article is to reviewthe values and limitations of the two parameters and evaluate theclinical use of ScvO 2 in certain clinical scenarios, such as anaemiaand transfusion, hypovolaemia, major surgery, septic shock, and indif cult-to-wean patients.

2013 Elsevier Ltd. All rights reserved.

Oxygen is one of the major essentials required for sustaining life. The primary goal of the cardio-respiratory system is to deliver adequate oxygen to the tissues to meet their metabolic re-quirements. The adequacy of tissue oxygenation is determined by the balance between the rate of oxygen transport to the tissues (oxygen delivery, DO 2) and the rate at which the oxygen is used by thetissues (oxygen consumption, VO 2) [1] . Standard formulae to determine DO 2 and VO 2 are:

DO2 [ SV HR Hb 1:34 SaO2 D 0:003 PaO2 [ CO CaO2

VO2 [ CO CaO2 L Hb 1:34 SvO2 D 0:003 PvO2 [ CO CaO2 L CvO2

where DO 2 is oxygen delivery, SV is stroke volume, HR is heart rate, Hb is haemoglobin, SaO 2 is Hbarterial oxygen saturation, PaO 2 is arterial oxygen partial pressure, CO is cardiac output, CaO 2 is arterial

* Corresponding author. Tel.: 36 62545168.E-mail addresses: [email protected] (K. Tnczos), [email protected] , [email protected] (Z. Molnr).

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Best Practice & Research Clinical

Anaesthesiologyj ou rna l homepage : www.e l s ev i e r. com/loca t e /bean

1521-6896/$ see front matter 2013 Elsevier Ltd. All rights reserved.http://dx.doi.org/10.1016/j.bpa.2013.06.001

Best Practice & Research Clinical Anaesthesiology 27 (2013) 201 207
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oxygen content, VO 2 is oxygen consumption, SvO 2 is Hb mixed venous oxygen saturation, PvO 2 isvenous oxygen partial pressure and CvO 2 is venous oxygen content.

From the above formulae, DO 2 at rest can be calculated:

CO [ 70 ml 72 =min [ 5 l min L 1

CaO2 [ 150 g lL 1 1:34 ml 1 D 0:003 100 mmHg [ 201 :3 ml l L 1

DO2 w 1000 ml minL 1

VO2 at rest is:

CvO2 [ 150 g lL 1 1:34 ml 0:75 D 0:003 40 mmHg [ 150 :87

VO2 [ 5 l minL 1 201 :3 ml l L 1 L 150 :87 ml l L 1 w 250 ml min L 1

Oxygenextraction O2ER [ VO2=DO2 100250 ml min L 1 =1000 ml min L 1 100 [ 25%

In the critically ill and in the perioperative period, there is often an imbalance between deliveryandconsumption. DO 2 may be inadequate considering arterial oxygen content and/or CO may be reduced[2,3] . The circulation can compensate to some extent, but after a critical threshold severe oxygen debtand shock may occur [4] . The principal task of acute critical care is to avoid or correct oxygen debt byincreasing DO 2 and/or decreasing VO 2. Furthermore, knowing when increasing DO 2 has restored tissueperfusion and no further increase is necessary is an important question in order to avoid harm that canbe caused by unnecessary over-resuscitation. Perhaps the most commonly used methods to assessglobal VO 2 are SvO 2 and its surrogate, central venous oxygen saturation (ScvO 2).

Mixed venous oxygen saturation

Mixed venous sampling is performed by gentle aspiration of blood from the distal port of anunwedged pulmonary artery catheter (PAC). This ensures complete admixture of blood from superiorand inferior venae cavae and the coronary sinus. SvO 2 is measured either intermittently by co-oximetryon mixed venous samples or continuously by bre-optic re ectance oximetry using a modi ed cath-eter. According to the above-speci ed physiological changes, measurement of SvO 2 can be an indirectindex of tissue oxygenation in the entire body [5] . However, the risk/bene t of the placement of a PACremains controversial. Several studies have reported no favourable impact on survival in patients withthis type of catheter; hence, the use of the PAC has become somewhat unpopular [6,7] . By contrast,insertion of a central venous catheter in the superior vena cava via the internal jugular or the sub-clavian vein is considered standard care in critically ill patients. Similar to SvO

2, the measurement of

ScvO2 has been advocated in order to detect global tissue hypoxia [4]. Monitoring of ScvO 2 may betherefore an attractive alternative to that of SvO 2.

Central venous oxygen saturation

ScvO2 is an easily obtained parameter via the central venous catheter already in situ in most crit-ically ill patients and it is often used as a marker of the balance between DO 2 and VO 2. Measurement of ScvO2 indicates the level of venous oxygenation of the brain and the upper part of the body. The normalvalue varies between 73% and 82% [8] .

Because of the different level of measurement (entire body in the case of SvO 2 4 brain and the

upper part of the body with ScvO 2), there has been considerable debate on the interpretation of ScvO 2values as compared to SvO 2. Most of the studies that have analysed the relationship between ScvO 2 andSvO2 have shown that ScvO 2 is an average of 5% higher than SvO 2 and is considered a reasonablesurrogate marker in the clinical setting [9 11] . However, recent clinical trials, mainly on septic patients,were unable to show satisfactory agreement between ScvO 2 and SvO 2. This could in part be explained

K. Tnczos, Z. Molnr / Best Practice & Research Clinical Anaesthesiology 27 (2013) 201 207 202


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by modi cations of blood- ow distribution and oxygen extraction (O 2ER) by brain and splanchnictissues [12] . It appears that ScvO 2 and SvO 2 are not numerically equivalent but the variations in thesetwo parameters usually occur in a parallel manner [13] .

The main factors, which in uence ScvO 2, are haemoglobin (Hb), SaO 2, CO and VO2. Theoretically, if three of these factors are kept constant the value of ScvO 2 re ects the changes of the latter. There aremultiple physiologic, pathologic and therapeutic factors which in uence venous oxygen saturation.These are summarised in Fig.1[14] . One of the important features of venous saturation is that it can bepathologic when it is high and also when it is low. In a recent large cohort of septic patients in theemergency department, it was found that mortality was 40% in patients admitted with an ScvO 2 < 70%but it was almost as high, 34%, in patients with high initial ScvO 2 of > 90% [15] .

Finally, one has to bear in mind that ScvO 2 should be measured in the superior vena cava. In aheterogeneous patient population, it was found that there were very wide limits of agreement betweenScvO2 measured in the superior vena cava as compared to results from the inferior vena cava; therefore,femoral venous oxygen saturation should not be used as a surrogate for ScvO 2 [16] .

The current place of ScvO 2 s in clinical practice

ScvO 2 as a transfusion trigger

One of the most common causes of inadequate DO 2 in the perioperative setting is anaemiarequiring red blood cell transfusions [17] . It has recently been suggested that the Hb level should notbe the only factor on which the indication of the need for transfusion is based [18,19] . According tothe TRICC (Transfusion Requirements in Critical Care) trial, patients with Hb levels above 10 g dl 1

require rarely transfusion while red blood cell donation is usually necessary if the Hb level is below7 mg dl 1 [20] . There is however a clear need for additional parameters in patients with Hb levelsbetween 7 and 10 g dl 1. Clinicians use different tools ranging from simple clinical signs (confusion,tachycardia, ST-segment elevation/depression and diuresis) to invasive haemodynamic measure-ments (ScvO 2, O2ER and central venous-to-arterial carbon dioxide difference) in order to obtain in-formation on anaemia-related altered O 2ER and hence the need for blood administration [21] . One of the potentially useful physiological parameters is ScvO 2. It was found during haemorrhage in animaland human experimental models that ScvO 2 may be useful for the identi cation of patients withoccult or ongoing clinically signi cant blood loss [22,23] . In bleeding conditions, an ScvO 2 value of w 70% has been used as a goal to therapeutic intervention in attempts at improving DO 2 [21] . In a

Fig. 1. Mixed venous saturations in the critically ill. SvO 2, mixed venous saturation; ScvO 2, central venous oxygen saturation; DO 2,oxygen delivery; VO 2, oxygen consumption. See text for explanation.



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prospective human interventional study, it was found that acute isovolaemic anaemia of Hb of 50 g l 1 in conscious healthy resting humans did not produce haemodynamic instability, but oxygenimbalance was accompanied by a signi cant drop in mixed venous saturation [24] . These results werereinforced by a retrospective analysis of a prospective observational study in which ScvO 2 was foundto be a good indicator of transfusion [25] . The results of our animal study on isovolaemic haemo-dilution gave further evidence that anaemia-induced change in oxygen balance can be monitored byScvO2 [26] .

According to the above-mentioned studies, it seems that ScvO 2 better identi es the point whencompensatory mechanisms fail and DO 2 begins to decline, as compared to the Hb concentrationalone. A low level of Hb does not necessarily lead to oxygen debt in haemodynamically stable,anaesthetised, ventilated patients, while oxygen imbalance may occur in agitated, pyrexial patientswith normal Hb level. These ndings are in accord with the idea that compensatory changes in COand other parameters of DO 2 make Hb concentration alone a less sensitive marker of oxygen balanceand for the need for therapeutic intervention to increase DO 2. ScvO2 could therefore be important inhelping to avoid hypoxia and tissue injury under such circumstances, while helping to more accu-rately guide blood transfusions. Therefore, we believe that not only the Hb level but also ScvO 2 and

other physiological signs of oxygen debt (confusion, angina, low diuresis, serum lactate level, etc.)should be taken into account before using red blood cells in order to reduce the number of unnec-essary transfusions. Protocolising transfusion and adopting protocols for every patient are thereforedif cult, because of its multimodal features. Nevertheless, applying the above-mentioned approach of including physiological indicators of oxygen debt in the decision making may help us in individu-alising transfusion therapy.

ScvO 2 as an indicator of hypovolaemia

A common cause for decreased CO in the intensive care unit (ICU) is hypovolaemia. Diagnosinghypovolaemia is an everyday challenge in critical care. Although diagnosis may prove dif cult, earlyrecognition of hypovolaemia is of utmost importance. By the time macro-haemodynamic changesmanifest, the microcirculation may already be damaged [3] . Furthermore, on the one hand early uidresuscitation can save lives, but on the other hand a cumulative positive uid balance is an indepen-dent factor of mortality [27] . Up until now, there has been no consensus either on the most accuratehaemodynamic indicator of hypovolaemia, or on the end points for optimal uid therapy [28,29] .Many recent studies have suggested that uid therapy should be based on dynamic (such as CO, pulsepressurevariation and SV variation) rather than static haemodynamic variables (such as central venouspressure (CVP) and pulmonary artery occlusion pressure), because they are better predictors of uidresponsiveness in ICU patients. However, pulse pressure variation and SV variation are limited topatients who are fully ventilated and have no arrhythmias [22,30] . Although it is not strictly a hae-modynamic variable, in certain clinical conditions a ScvO 2 value of w 70% has been used as a thera-peutic end point to improve DO 2 [23] . In a recent study, it was found that a 4% increase in ScvO 2 after

uid challenge had > 80% sensitivity and speci city in predicting volume responsiveness at the bedsidein critically ill patients [31] .

ScvO 2 and major surgery

As the two most common complications in the perioperative setting are bleeding/anaemia andhypovolaemia, it seems logical to assume that ScvO 2 may be a good resuscitation end point during andafter major surgery. In a single-centre study, patients in the ScvO 2-directed therapy group had fewerpostoperative complications and were hospitalised for shorter periods than the patients in the control

group [32] . In a prospective, randomised controlled trial, a therapeutic strategy designed to detect andreverse tissue hypoxia (diagnosed by an increase of O 2ER) was used after major abdominal surgery. Theintervention group received therapy to maintain O 2ER < 27% after prede ned goals for arterial pres-sure, urine output and CVP had been achieved. Early treatment according to O 2ER reduced organfailures and hospital stay [33] .



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ScvO 2 and severe sepsis/septic shock

Global tissue hypoxia as a result of an overwhelming systemic in ammatory response is a frequentand important complication of sepsis and may lead to multiple organ dysfunction syndrome [34] .Treatment strategies that are aimed at restoring tissue perfusion by improving the balance betweenDO2 and VO2 may prevent the development of organ dysfunction syndrome and thus improve theoutcome of septic patients. Rivers and his colleagues reported that in patients with severe sepsis, earlygoal-directed intervention guided by continuous monitoring of ScvO 2, CVP and mean arterial pressure(MAP) reduced mortality from 46.5% to 30.5% at the 28th day [35] . Several studies using early goal-directed therapy (EGDT) end points (CVP 8 12 mmHg, MAP 65 mmHg and ScvO 2 70%) suggestthat this multimodal approach is a useful strategy in the treatment of sepsis [36,37] . However, theEGDT-based protocol aimingat correcting lowScvO 2 levels through a titrated resuscitation has recentlybeen criticised. Recent data suggest that patients with initially high ScvO 2 values mayalso have adverseoutcomes [15,38] , probably due to impaired oxygen utilisation. High ScvO 2 values may thus representan inability of the cells to extract oxygen or microcirculatory shunting in sepsis [39] . Therefore,additional measures are necessary to help evaluate high ScvO 2 values, such as central venous-to-

arterial CO 2 gap, or by applying advanced invasive haemodynamic monitoring. Discussing these is-sues is beyond the scope of this article.

ScvO 2 in dif cult-to-wean patients

During the weaning procedure, the increased respiratory workload (due to the increased respira-tory muscle oxygen consumption) may lead to an imbalance between DO 2 and VO 2. The consequentiallow ScvO 2 can indicate the exhaustion of the patient and thus may predict extubation failure. The aimof a multicentre, clinical study performed in three medical surgical ICUs was to evaluate the predictivevalue of ScvO 2 to detect extubation failure in dif cult-to-wean patients. A signi cant lower centralvenous saturation was found during the spontaneous breathing trial in patients with extubationfailure.

According to this trial, ScvO 2 may be a valuable parameter to be included in weaning protocols of dif cult-to-wean patients and may also serve as a useful tool to assist the weaning process in me-chanically ventilated patients [40] .

Summary

Avoiding and treating oxygen debt in critically ill patients is without doubt one of the mostimportant tasks of our work. Unfortunately, there is no gold standard for the assessment of oxygendebt. Although ScvO 2 is not a perfect surrogate of SvO 2, it is easy to measure and can be of great value inseveral clinical settings. Interpretationof ScvO 2 may be more complicated when its value is high, whichmay require its evaluation together with other measures of anaerobic metabolism and might also be anindication for advanced haemodynamic monitoring. Nevertheless, it can be measured easily andquickly and can be an early warning sign of oxygen debt; therefore, its routine measurement should beincluded in our everyday practice.

Practice points

ScvO2 correlates well with oxygen demand/supply (VO 2/DO2). Low values mean impaired DO 2. Low values may help in decision-making in transfusion and uid therapy.

High values should be taken seriously in septic shock and may necessitate the commence-ment of invasive haemodynamic monitoring. Dynamic changes in ScvO 2 (i.e., during a spontaneous breathing trial) may refer to the pa-tients reserves.



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Con ict of interest

None.

References

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Research agenda

In haemodynamically stable brain-injured patients, the role of ScvO 2 in monitoring theseverity of brain damage and as a prognostic factor has rationale, but very limited data areavailable.

The relationship between high ScvO 2 and measures of anaerobic metabolism (such asvenous-to-arterial CO 2-gap, lactate, etc.) should be studied further.

< XS _FFU > The dynamic changes of ScvO 2 during increased oxygen demand (such asweaning, mobilisation, etc.) as a measure of the patient s DO2 reserves are another veryinteresting eld that deserves further studies.

The value of the continuous measurement of ScvO 2 in certain clinical scenarios such as high-risk surgery and suspected bleeding (gastrointestinal, postoperative, etc.) should also beinvestigated in clinical trials.

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