acta anaesthesiologica scandinavica291 - 2012 se

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Central venous oxygen saturation is a good indicator of

altered oxygen balance in isovolemic anemia

S. Kocsi1, G. Demeter1, J. Fogas1, D. rces2, J. Kaszaki2 and Z. Molnr11Department of Anaesthesiology and Intensive Therapy, Faculty of Medicine, University of Szeged, Szeged, Hungary, and 2Institute of SurgicalResearch, Faculty of Medicine, University of Szeged, Szeged, Hungary

Background: Red blood cell transfusion is done primarily as ameans to improve oxygen delivery (DO2). Current transfusionguidelines are based solely on hemoglobin levels, regardless ofactual DO2 need. As central venous oxygen saturation (ScvO2)may reflect imbalances in DO2 and consumption (VO2) the aimof this study was to investigate the value of ScvO2 as an indicatorof oxygen balance in isovolemic anemia.Methods: After splenectomy, anesthetized Vietnamese minipigs (n = 13, weight range: 1830 kg) underwent controlledbleeding in five stages (T0T5). During each stage approximately10% of the estimated starting total blood volume was removedand immediately replaced with an equal volume of colloid.Hemodynamic measurements and blood gas analysis were thenperformed.Results: Each stage of bleeding resulted in a significant fall inhemoglobin, T0: 125 (113134) to T5: 49 (4355) g/l [T0: 7.7 (6.98.2) to T5: 3.0 (2.63.4) mmol/l]. The O2-extraction (VO2/DO2)

increased significantly only from T3: 35 (2140) %, P < 0.05. Thechange of ScvO2 showed a similar pattern and dropped belowthe physiological threshold of 70% at T4: 68 (6176) %. At thispoint, hemoglobin was below the recommended transfusiontrigger value, 59 (5367) g/l [3.6 (3.34.1) mmol/l]. There was astrong significant association between ScvO2 (< 70%) and VO2/DO2 (> 30%): r = -0.71, r2 = 0.50, P < 0.001.Conclusion: The results of this study show that ScvO2 reflectschanges of VO2/DO2 in isovolemic anemia better than Hb alone,therefore it may be used as an additional indicator of bloodtransfusion in clinical practice.

Accepted for publication 11 November 2011

2012 The AuthorsActa Anaesthesiologica Scandinavica 2012 The Acta Anaesthesiologica Scandinavica Foundation

The adequacy of tissue oxygenation is deter-mined by the balance between oxygen delivery

(DO2) and consumption (VO2).1 In the critically illthere is often an imbalance between the two arms:DO2 may be too low, frequently to the accompani-ment of an increased VO2. After a critical threshold,severe oxygen debt and shock may occur.2 One ofthe most common causes of inadequate DO2 in theintensive care unit is anemia requiring red bloodcell transfusions.3 Although the prevalence of

anemia among critically ill patients could be as highas 95% by day 3, the transfusion trigger, i.e. theindication and timing of the necessity of bloodtransfusion, is still uncertain, and the detection ofaltered oxygen extraction caused by anemia is there-fore of great clinical importance.4,5

A number of guidelines are of help in transfusionpractice, but the criteria for the optimal manage-ment of anemia are not clearly defined. In mostguidelines the transfusion trigger is a certain level

of hemoglobin (Hb), usually 70100 g/l (4.36.1 mmol/l).6,7 It was recently suggested that Hblevel should not be the only factor on which theindication of the need for transfusion is based.6,7

There is increasing evidence that transfusion is adouble-edged sword: untreated anemia can beassociated with a worse outcome and increasedmortality, whereas transfusion may cause variousinfectious and non-infectious adverse effects.810 Asmacrohemodynamic changes are not informative

enough, there is a clear need for additional quanti-tative parameters that would give information onanemia-related altered oxygen extraction and hencethe need for blood administration.7,11 One of thepotentially useful physiological parameters is thecentral venous oxygen saturation (ScvO2). The ScvO2has been found to be slightly higher than the mixedvenous oxygen saturation (SvO2), with normalvalues 7382%.12 Importantly, the ScvO2 closelytrends the changes in SvO2, and is considered a

Acta Anaesthesiol Scand 2012; 56: 291297Printed in Singapore. All rights reserved

2012 The Authors

Acta Anaesthesiologica Scandinavica

2012 TheActa Anaesthesiologica Scandinavica Foundation

ACTA ANAESTHESIOLOGICA SCANDINAVICA

doi: 10.1111/j.1399-6576.2011.02622.x

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reasonable surrogate marker of mixed venous satu-ration in the clinical setting.12 As such ScvO2, whichis easily measured at the bedside, has been foundreflect the balance between DO2 and VO2 in manyclinical settings.11,12

DO2 is dependent on in part of the concentrationof Hb. The value of using changes in ScvO2 to detectanemia-related changes in oxygen balance in clinicalpractice is still unclear. The aim of our study there-fore was to monitor the changes of ScvO2 in isovo-lemic anemia using a large animal model, and testwhether an altered VO2/DO2 balance, which is duesolely to a decreased Hb level, can be detected byScvO2.

Materials and methods

The study protocol was approved by the local ethicscommittee at the University of Szeged, and thestudy was carried out in the research laboratory ofthe Institute of Surgical Research.

Animals and instrumentationVietnamese mini pigs (n = 13) weighing 24 3 kgunderwent a 24-h fast preoperatively but withwater ad libitum. Anesthesia was induced with anintramuscular injection of a mixture of ketamine(20 mg/kg) and xylazine (2 mg/kg) and main-tained with a continuous infusion of propofol(6 mg/kg/h i.v.). A tracheal tube was inserted andthe animals lungs were ventilated mechanically.

The tidal volume was set at 13

2 ml/kg, and therespiratory rate was adjusted to maintain the end-tidal carbon dioxide and the partial pressure ofarterial carbon dioxide in the range of 3545 mmHg(4.65.9 kPa) and the arterial pH between 7.35 and7.45. The adequacy of the depth of anesthesia wasassessed by monitoring the jaw tone. After the ini-tiation of anesthesia, the right carotid artery andjugular vein and the right femoral artery and veinwere dissected and catheterized. The animalsunderwent suprapubic urinary catheter placementand laparotomy for splenectomy. Splenectomy in

swine hemorrhage models are performed becauseof the distensibility of the spleen and the resultantvariation in the amounts of sequestered blood.13

The core temperature was maintained at 37 1 Cthrough use of an external warming device.

For invasive hemodynamic monitoring, atranspulmonary thermodilution catheter (PiCCO,PULSION Medical Systems AG, Munich, Germany)was placed in the femoral artery and a pulmonaryartery catheter (PV2057 VoLEF Catheter, PULSION

Medical Systems AG) by pressure tracings via thefemoral vein. The latter was also used to draw mixedvenous blood gas samples. The femoral arteryserved as the site of arterial blood gas samples andthe central venous line was used for central venous blood gas sampling and for the injection of coldsaline boluses for thermodilution measurements.Central venous catheter was positioned by usingguidewire attached intracavital ECG. During theexperiment blood was drained from the catheter inthe right carotid artery, which was also used toreplace the blood loss with the same amount ofcolloid, in order to avoid a sudden increase in rightventricular preload.

Experimental protocolThe most important steps in the experiment areoutlined in Fig. 1. At baseline (T0) hemodynamicand blood gas parameters were recorded, and

heparin sulfate (200 IU/kg) was administeredthrough the central venous line. Isovolemic anemiawas achieved in five intervals (T1T5). During eachinterval 10% of the estimated total blood volumewas withdrawn over a 5- to 10-min period. Hemo-dynamic parameters were recorded and the amountof blood drained off was immediately replaced byan equal volume of colloid (hydroxyethyl starch130 kDa/0.4, 6%, Voluven, Fresenius, Germany). Toachieve a steady state, the animals were allowed torest for 10 min between intervals. At the end of eachcycle, hemodynamic and blood gas parameters were

measured. At the end of the experiment the animalswere humanely euthanized.

Hemodynamic measurementsCardiac output (CO), global end-diastolic volume,intrathoracic blood volume, extravascular lungwater, stroke volume (SV), SV variation (SVV), indexof left ventricular contractility (dPmx), heart rate(HR), and mean arterial pressure (MAP) were meas-ured by transpulmonary thermodilution and pulsecontour analysis at baseline and at the end of eachinterval. Detailed description of transpulmonary

thermodilution and pulse contour analysis are pro-vided elsewhere.13,14 All hemodynamic parameterswere indexed for body surface area. The averages ofthree random measurements following 10 ml bolusinjections of ice-cold 0.9% saline were recorded.Continuous variables of invasive blood pressuremeasurements and pulse contour analysis, such asCO, MAP, HR, SV, SVV, and dPmx, were measuredand recorded at the end of each bleeding episodeand at the same times as the other hemodynamic

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variables. The central venous pressure (CVP) wasdetermined by the pulmonary artery catheter at theend of each bleeding episode and at the same timesas the other hemodynamic variables.

Arterial, central venous, and mixed venous bloodgas samples (Cobas b 221, Roche Ltd., Basel, Swit-zerland) were drawn and analyzed by cooximetrysimultaneously at baseline and at the end of eachcycle (Fig. 1).

From these parameters the following variableswere calculated according to standard formulas:

DO SV HR Hb SaO PaOCO CaO

2 2 2

2

1 34 0 003= + ( )[ ]= [ ]

. .

VO CO CaO Hb SvO

PvO CO CaO CvO2 2 2

2 2 2

1 34

0 003

= ([+ ( ))] = [ ]

.

.

Oxygen extraction VO DO CO CaO CvOCO CaO

2 2 2 2

2 100( ) = [ ]

[ ]

Simplified oxygen extraction O ERSaO ScvO SaO

2

2 2 2

( )

= ( )

Data analysis and statisticsData are reported as medians (interquartile ranges)or means standard deviations, unless indicated

otherwise. To test for normal distribution, theKolmogorov-Smirnov test was used. The changes inall parameters throughout the experiment weretested by repeated measures analysis of variance(ANOVA); and the number of degrees of freedomwas adjusted to GreenhouseGeisser epsilon whenneeded. For pairwise comparisons, Pearsons corre-lation was used. To evaluate the performance ofScvO2 in the detection of altered oxygen extractionwith a threshold of 30% of VO2/DO2, receiver oper-ating characteristics (ROC) curve analysis was per-formed, and sensitivity, specificity, and positive

predictive (PPV) and negative predictive values(NPV) were also determined. To model the linearrelationship between VO2/DO2 and the possibleindicator of altered oxygen extraction, linear regres-sion model was used. Post hoc calculation showed apower of 86% with an effect of 25% increase in VO2/DO2, for a sample size of 13 and a = 0.05. For statis-tical analysis SPSS version 18.0 for Windows (SPSS,Chicago, IL, USA) was used and P < 0.05 was con-sidered statistically significant.

Oneintervaloftheexperiment(T0T1)

T0

T1

Baselinemeasurement:

1)Bloodsamples

2)Themodilution

3)Registration

Measurement:

1)Blood

samples

2)Themodilution

3)Registration

B

leeding

Continuoushemodynamicdataregistration

10minforrestorationofsteadystate

Bloodreplacementwithcolloid

Fig

.1

.Schemat

icdiagram

illustrat

ingone

intervalof

theexper

imen

talpr

otocol

.Afterrecord

ing

theresu

ltsof

theb

asel

inemeasuremen

ts,1

0%of

thees

tima

tedtotalbloo

dvolumewas

withdrawn

from

thean

imals.

Im

med

iatelyaf

terrecord

ing

thecon

tinuous

hemodynam

icvar

iables

,thew

ithdrawn

bloo

dwasrep

lace

dw

iththesameamoun

tofco

lloi

d.

After

10m

in

forrestorat

ionofstea

dystate,anot

herse

tofmeasuremen

tswererecorde

d.

Monitoring oxygen imbalance in anemia

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Results

Hemodynamic effects of isovolemic anemiaAll 13 animals survived the study. The blood losswas on average 150 33 ml in each phase. Hemo-dynamic data are presented in Table 1.

The bleeding caused a gradual decrease in Hblevel after each phase and by the end of the experi-ment it had fallen by 61% of the baseline value. Thepreload as indicated by global end-diastolic volumeindex (GEDI), intrathoracic blood volume index

(ITBI), and CVP values did not change significantly.HR, dPmx, and CI were increased significantly afterthe first bleeding and remained so for the rest of theexperiment. Only CI changed significantly until T3when comparing the values at each interval with theprevious one. MAP decreased significantly from T2,but the median remained > 70 mmHg throughout.Other macrohemodynamic variables did not changesignificantly during the experiment.

Effects on oxygen balanceVariables relating to the oxygen balance are listed in

Table 2.SaO2 remained in the normal range throughoutthe experiment. DO2 fell significantly from T2, VO2 atT4, VO2/DO2 increased significantly from T3, andexceeded the physiologic threshold of 30%. Thechange in ScvO2 displayed a similar pattern as VO2/DO2 and changed significantly and also fell below70% only at T4. The other parameters did not changesignificantly. The pattern of changes of VO2/DO2and ScvO2 over time is demonstrated in Fig. 2. Only

arterial oxygen partial pressure increased signifi-cantly by the end of the experiment, other blood gasparameters did not change significantly.

We determined the association between VO2/DO2and ScvO2, and found a strong, negative correlation(r = -0.71, P < 0.001) (Fig. 3).

ROC analysis revealed the same tendency asthe correlation. With 30% taken as the physiologicthreshold for VO2/DO2, the area under thecurve (AUC), its standard error and that of the 95%confidence interval were > 0.5 for ScvO2 [AUC =

0.768 0.056 (0.6570.878) P < 0.001]. It was alsoimportant to determine the best cut-off for ScvO2 todetect the significant increase in VO2/DO2, there-fore, sensitivity, specificity, PPV, and NPV for ScvO2levels of 70% and 75% were calculated. An ScvO2level of 70% had better specificity and PPV, whereasa ScvO2 level of 75% had better sensitivity andNPV (sensitivity: 45%, specificity: 97%, PPV: 95,NPV: 58; sensitivity: 68%, specificity: 77%, PPV:79, NPV: 65, respectively). Furthermore, linearregression revealed a significant relationship between ScvO2 (r = 0.71, r2 = 0.50, P < 0.001) and

VO2/DO2.

Discussion

Maintaining adequate tissue oxygenation byimproving DO2 is the rational for blood transfusion.Despite this fact, treatment of anemia with bloodtransfusion in the absence of acute bleeding is rec-ommended at certain levels of Hb, regardless ofactual DO2 and need, thus resulting in possible

Table 1

Hemodynamic effects of isovolemic anemia.

T0 T1 T2 T3 T4 T5

Hb (g/l) 125 (113134) 102 (90109)* 79 (7393)* 68 (6076)* 59 (5367)* 49 (4355)*(mmol/l) 7.7 (6.98.2) 6.3 (5.56.7) 4.8 (4.55.7) 4.2 (3.74.7) 3.6 (3.34.1) 3.0 (2.63.4)

HR (beats/min) 125 (91135) 119 (100138)* 123 (102146)* 129 (110159)* 139 (118179)* 147 (131177)*MAP (mm Hg) 91 (79105) 89 (79101) 83 (7598)* 82 (6890)* 72 (5985)* 72 (6386)*CVP (mm Hg) 6 (58) 8 (59) 7 (49) 7 (59) 7 (59) 7 (310)

CI (L/min/m2

) 2.6 (2.32.8) 3.3 (2.73.6)* 3.6 (2.93.8)* 3.6 (3.34.1)* 3.5 (3.24.0)* 3.9 (3.64.1)*GEDI (ml/m2) 270 (243284) 271 (245320) 276 (248298) 274 (236305) 268 (227302) 261 (232298)ITBI (ml/m2) 335 (307352) 335 (305400) 343 (303373) 342 (295383) 334 (282375) 333 (285375)ELWI (ml/kg) 9 (910) 10 (1010) 9 (910) 10 (910) 10 (910) 10 (911)SVI (ml/m2) 21 (1829) 26 (2331) 27 (2431) 28 (2531) 25 (2133) 28 (2231)SVV (%) 17 (1421) 15 (1221) 19 (921) 15 (1120) 19 (1125) 14 (1127)dPmx (mm Hg/s) 540 (485790) 700 (540985)* 800 (5701075)* 810 (5401480)* 880 (5601360)* 975 (5621275)*

GLM repeated measures ANOVA.*P< 0.05 compared with T0.P< 0.05 compared with previous.Hb, hemoglobin; HR, heart rate; MAP, mean arterial pressure; CVP, central venous pressure; CI, cardiac index; GEDI, globalend-diastolic volume index; ITBI, intrathoracic blood volume index; ELWI, extravascular lung water index; SVI, stroke volume index;SVV, stroke volume variation; dPmx, index of left ventricular contractility; T 0, baseline measurement; T1T5, five intervals of bleeding.

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excess blood administration.6,7 In our study in iso-volemic anemia, we found that ScvO2 is a sensitiveindicator of oxygen balance and may thus serve as arational guide to therapy in this all too commonproblem.

Oxygen balance and ScvO2In certain clinical conditions, an ScvO2 value of~70% has been used as a goal to therapeutic inter-vention in attempts at improving DO2.1518 In onestudy in septic patients goal-directed therapy

Table 2

Effects of isovolemic anemia on oxygen balance.

T0 T1 T2 T3 T4 T5

SaO2 (%) 95 (9297) 96 (9497) 96 (9597) 96 (9597) 97 (9797) 97 (9797)

DO2 (ml/min/m2) 431 (362474) 438 (323524) 378 (302412)* 344 (252376)* 284 (236333)* 247 (216292)*

VO2 (ml/min/m2) 119 (82139) 130 (77151) 93 (66136) 113 (67141) 98 (72120) 105 (70120)

VO2/DO2 (%) 29 (1833) 29 (1733) 29 (1832) 35 (2140)* 37 (2643)* 41 (2747)*

ERO2 (%) 19 (1326) 19 (1424) 20 (1422) 21 (1628) 30 (2237)* 32 (2139)*

SvO2 (%) 68 (6477) 67 (6477) 68 (6379) 64 (5876) 62 (5572)* 58 (5272)*ScvO2 (%) 76 (6983) 73 (72 (82) 77 (7583) 77 (6881) 68 (6176)* 66 (6076)*

Lactate (mmol/l) 4.5 (3.25.3) 4.2 (3.05.1) 5.0 (3.26.0) 4.1 (2.96.0) 4.2 (2.96.5) 4.0 (3.06.4)

pH 7.44 (7.407.50) 7.43 (7.407.50) 7.43 (7.417.50) 7.43 (7.397.49) 7.44 (7.427.49) 7.44 (7.407.47)

PaO2 (mm Hg) 76 (6680) 75 (7280) 76 (7380) 77 (7282) 79 (7585)* 81 (7790)*

(kPa) 10.1 (8.810.7) 10.0 (9.610.7) 10.1 (9.710.7) 10.3 (9.610.9) 10.5 (10.011.3) 10.8 (10.312.0)

PaCO2 (mm Hg) 39 (3544) 38 (3543) 37 (3445) 39 (3446) 37 (3442) 38 (3541)

(kPa) 5.2 (4.75.9) 5.1 (4.75.7) 4.9 (4.56.0) 5.2 (4.56.1) 4.9 (4.55.6) 5.1 (4.75.5)

aHCO3 (mmol/l) 25 (2427) 24 (2426) 25 (2327) 25 (2327) 25 (2227) 25 (2125)

aBE (mmol/l) 0.90 (-0.052.50) 0.40 (-0.852.25) 0.60 (-0.92.45) 0.80 (-0.453.15) 0.90 (-1.452.35) 0.70 (0.431.08)

GLM repeated measures ANOVA.*P< 0.05 compared with T0.P < 0.05 compared with previous.SaO2, arterial oxygen saturation; DO2, oxygen delivery; VO2, oxygen consumption; VO2/DO2, oxygen extraction ratio; ERO2, simplified oxygen extractionratio; SvO2, mixed venous oxygen saturation; ScvO2, central venous oxygen saturation; PaO2, arterial oxygen partial pressure; PaCO2, arterial carbondioxide partial pressure; aHCO3, arterial bicarbonate; aBE, arterial base excess; T0, baseline measurement; T1T5, five intervals of bleeding.

A

50

40

30

20

10T0 T1 T2 T3 T4 T5 T0 T1 T2 T3 T4 T5

55

60

65

70

75

80

85

B

VO

2/DO

2(%)

ScvO

2(%)

Time intervals Time intervals

Fig. 2. Changes of VO2/DO2 (A) and ScvO2 (B) over time (T0T5). Data are presented as median (interquartile range). *P


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according to ScvO2 values, saw an absolute 16%reduction in in-hospital mortality as compared withconventional therapy.15 Two recent studies have alsodemonstrated that a low ScvO2 predicts peri- andpost-operative morbidity and complications inhigh-risk surgery.16,17 It may also serve as a usefultool to assist the weaning process in mechanicallyventilated patients.18

In our experiment, despite a continuous and sig-

nificant drop in Hb levels, the value of VO2/DO2increased significantly only from T3, and exceededthe physiologic threshold of 30%. The change inScvO2 displayed a similar pattern as VO2/DO2 andfell below 70% only at T4. If we translate that intoclinical practice, the reduced Hb concentrationscould have indicated blood transfusion from T2;however, we found no evidence of impaired VO2/DO2 until the Hb was well below the current recom-mended transfusion threshold.

About two decades ago it was found during hem-orrhage in animal and human experimental models

that ScvO2 may be useful for the identification ofpatients with occult or ongoing clinically significant blood loss.19,20 In a prospective human interven-tional study it was found that in acute isovolemicanemia of Hb 50 g/l (3.1 mmol/l) in conscioushealthy resting humans did not produce evidence ofinadequate systemic DO2 and oxygen imbalance wasaccompanied by a significant drop in SvO2.21 Theseresults were reinforced by a retrospective analysis ofa prospective observational study in which ScvO2

was found to be a good indicator of transfusion. 22

Our results give further evidence that anemia-induced change in oxygen balance can be monitoredby ScvO2.

Hemodynamic effects of isovolaemic anemiaOur goal of maintaining isovolemia was achieved as

parameters of preload and central blood volume,such as GEDI, ITBI, CVP did not change throughoutthe experiment. A significant increase in cardiacindex was found, caused by increased HR, as SV didnot change significantly over time. This increase wasin agreement with the hemodynamic changes of arecent study by Krantz et al. with a similar experi-mental setting, but with a different hypothesis.23

Myocardial contractility as indicated by dPmxvalues, also increased significantly, most likely inresponse to isovolemic anemia. Although we didnot measure catecholamine levels, a theoretical

explanation could be that the bleeding caused anenhanced stress response resulting in the observedpositive inotropic effect.24,25

Limitations of the studyOne of the possible limitations of our study is thatthe length of the preparation of the animals mayhave been too long, which resulted in persistenttachycardia and increased levels of lactate frombaseline to the end of the experiment. The steady-state periods may also have been relatively short,although, the same time intervals have been used

previously.26 Another concern might be the type offluid replacement, as one cannot exclude the possi-bility that the use of different types of colloid solu-tions would affect these results. Furthermore, thesedata were obtained in anesthetized animals, andmay not be the same in conscious animals. Finally,our results cannot be applied directly in those clini-cal conditions where other confounding factors arepresent, which may affect ScvO2, such as severesepsis, septic shock, multiple trauma, etc.

Conclusions

In conclusion, our results show that ScvO2 reflectschanges in oxygen extraction in isovolemic anemia.Furthermore in isovolemic anemia, ScvO2 betteridentifies the point when compensatory mecha-nisms fail and DO2 begins to decline, as comparedwith the Hb concentration alone. These findings arein accord with the idea that compensatory changesin CO and other parameters of DO2 make Hb con-centration alone a less sensitive marker of oxygen

1030

40

50

60

80

90

70

20 30 6040VO2/DO2 (%)

50 70

ScvO2(%)

Fig. 3. Correlation between VO2/DO2 and ScvO2. Data are pre-sented as scatter with a linear regression line and its means 95%confidence interval. VO2/DO2: oxygen extraction, ScvO2: centralvenous oxygen saturation.

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balance and for the need for therapeutic interven-tion to increase DO2. ScvO2 could therefore beimportant in helping to avoid hypoxia and tissueinjury under such circumstances, while helping tomore accurately guide blood transfusions. Thisremains to be confirmed in the clinical setting.

AcknowledgementsThe authors would like to thank the assistants, medical studentsand staff at the Institute of Surgical Research for their help.

Conflicts of interest: The authors have no conflicts of interest.

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Address:Szilvia Kocsi

Department of Anaesthesiology and Intensive TherapyUniversity of SzegedSemmelweis st. 6H-6725 SzegedHungarye-mail: [email protected]

Monitoring oxygen imbalance in anemia

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