Seediscussions,stats,andauthorprofilesforthispublicationat:https://www.researchgate.net/publication/317153029

Fluidtherapyrecommendationsformajorabdominalsurgery.ViaRICArecommendationsrevisited.PartIII:Goaldi....

Article·May2017

DOI:10.1016/j.redare.2017.03.006

CITATION

1

READS

153

9authors,including:

Someoftheauthorsofthispublicationarealsoworkingontheserelatedprojects:

TissueperfusionViewproject

GOALSTRIALViewproject

JavierRipollés-Melchor

HospitalUniversitarioInfantaLeonor

106PUBLICATIONS160CITATIONS

SEEPROFILE

DanielChappell

Ludwig-Maximilians-UniversityofMunich

135PUBLICATIONS3,605CITATIONS

SEEPROFILE

HollmannAya

StGeorges'sUniversityHospitalsNHSFound…

39PUBLICATIONS328CITATIONS

SEEPROFILE

AngelVicenteEspinosa

ÖrebroUniversityHospital

41PUBLICATIONS113CITATIONS

SEEPROFILE

AllcontentfollowingthispagewasuploadedbyAlfredoAbadGurumetaon25April2018.

Theuserhasrequestedenhancementofthedownloadedfile.

ARTICLE IN PRESS+Model

Rev Esp Anestesiol Reanim. 2017;xxx(xx):xxx---xxx

www.elsevier.es/redar

Revista Española de Anestesiologíay Reanimación

SPECIAL ARTICLE

Fluid therapy recommendations for major abdominalsurgery. Via RICA recommendations revisited. Part III:Goal directed hemodynamic therapy. Rationalefor maintaining vascular tone and contractility�

Recomendaciones de fluidoterapia perioperatoria para la cirugía abdominalmayor. Revisión de las recomendaciones de la Vía RICA. Parte III: Terapiahemodinámica guiada por objetivos. Fundamento para el mantenimientodel tono vascular y la contractilidad

J. Ripollés-Melchor a,∗, D. Chappellb, H.D. Aya c, Á. Espinosad, M.G. Mhytene,A. Abad-Gurumeta a, S.D. Bergese f, R. Casans-Francés g, J.M. Calvo-Vecinoh

a Departamento de Anestesia, Hospital Universitario Infanta Leonor, Universidad Complutense de Madrid, Madrid, Spainb Departamento de Anestesia, Hospital Universitario LMU de Múnich, Múnich, Germanyc Departamento de Cuidados Intensivos, St George’s University Hospitals, NHS Foundation Trust, London, United Kingdomd Departamento de Anestesia Cardiovascular y Torácica, y Cuidados Intensivos, Bahrain Defence Force Hospital, Riffa, Bahraine University College London Hospital, National Institute of Health Research, Biomedical Research Centre, London, United Kingdomf Departamento de Anestesia y Neurocirugía, Wexner Medical Center, The Ohio State University, Columbus, OH, United Statesg Departamento de Anestesia, Hospital Clínico Universitario Lozano Blesa, Zaragoza, Spainh Departamento de Anestesia, Complejo Asistencial Universitario de Salamanca, Universidad de Salamanca (CAUSA), Salamanca,

Spain

Received 30 January 2017; accepted 1 March 2017

� Please cite this article as: Ripollés-Melchor J, Chappell D, Aya HD, Espinosa Á, Mhyten MG, Abad-Gurumeta A, et al. Recomendacionesde fluidoterapia perioperatoria para la cirugía abdominal mayor. Revisión de las recomendaciones de la Vía RICA. Parte III: Terapia hemo-dinámica guiada por objetivos. Fundamento para el mantenimiento del tono vascular y la contractilidad. Rev Esp Anestesiol Reanim. 2017.http://dx.doi.org/10.1016/j.redar.2017.03.002

∗ Corresponding author.E-mail address: ripo542@gmail.com (J. Ripollés-Melchor).

2341-1929/© 2017 Sociedad Espanola de Anestesiologıa, Reanimacion y Terapeutica del Dolor. Published by Elsevier Espana, S.L.U. All rightsreserved.

REDARE-807; No. of Pages 12

Document downloaded from http://www.elsevier.es, day 25/05/2017. This copy is for personal use. Any transmission of this document by any media or format is strictly prohibited.

ARTICLE IN PRESS+Model

2 J. Ripollés-Melchor et al.

Introduction

Non-cardiac surgery in high-risk patients is associated withan increased incidence of postoperative complications1 andmortality,2 with multiple organ failure being a main cause ofdeath in these patients.3 Only about 10% of all anaestheticprocedures are performed in high-risk surgical patients;however, these patients account for more than 80% ofperioperative deaths.4 Poor cardiopulmonary reserves limitthe patient’s ability to respond to the stressful insult andprevent the body compensating for the increased oxygendemand and, in essence, defines the ‘‘high-risk surgicalpatient’’.5

Even though perioperative goal directed hemodynamictherapy (GDHT) has shown improved patient outcomes,6---8

and despite recommendations from experts in the UnitedStates and Europe,9,10 assessment of oxygen delivery (DO2)during high-risk surgery is not widely used.11---13 Althoughmost anaesthetists use some kind of therapeutic goals andhemodynamic interventions, some of those common goalsmay not be appropriate.14 Stroke volume (SV), cardiac out-put (CO), and arterial blood pressure (BP) are the maincomponents of hemodynamic optimization in the operat-ing room.15 Lower SV,16 lower CO,17 or lower BP and itscumulative duration are associated with postoperative mor-bidity and mortality.18 BP and SV are weakly correlated,19

but complement microcirculatory perfusion.20 Insufficienttissue perfusion and cellular oxygenation due to hypo-volaemia, heart dysfunction or both are main determinantsof impaired outcomes.21 GDHT should be used on an indi-vidual basis, always from a physiological point of view,9,22

resulting in a more appropriate use of fluids, vasopressors,and inotropes.23

Rationale for maintaining vascular tone

Hypotension

Hypotension is frequent between the induction of anaes-thesia and the beginning of surgery.24 Disputed definitionsof intraoperative hypotension include systolic BP below80 mmHg, mean arterial pressure (MAP) below 55---60 mmHg,and a 20---25% decrease in systolic or mean BP frombaseline.25 However, there is evidence that intraoperativehypotension is associated with acute kidney injury (AKI),myocardial injury, stroke, and mortality26---30; untreatedhypotension could contribute to increased postoperativemorbidity by damaging major organs, such as the brain,heart, and kidney due to poor organ perfusion andischemia.31 Moreover, prolonged intraoperative hypotensionis associated with a decrease in both short and long-term survival32,33 In critically ill patients, values of MAP of72 mmHg or higher may be essential in order to preventAKI and myocardial injury.34 A case control study conductedin patients undergoing non-cardiac and non-neurologicalsurgeries concluded that a sustained decrease in intraop-erative MAP of more than 30% from baseline values ‘‘wassignificantly associated with postoperative stroke’’.35 Bijkeret al. found that MAP of less than 50 mmHg had the great-est independent association with death in their study in1705 patients undergoing noncardiac surgery.33

Triple low

Sessler et al. discussed the concept of triple low (MAP<75 mmHg, low bispectral index (BIS) <45, and low minimalalveolar concentration (MAC) <0.80) in the context of exces-sive length of stay and increased risk of 30-day mortality. Theauthors concluded that a double combination of low MAP andlow MAC was a strong predictor of mortality, and even moreso when associated with low BIS values.36 Drummond sug-gested considering ‘‘variability in normal population’’ whendiscussing published scientific evidence regarding cerebralblood flow (CBF) autoregulation with ‘‘declining MAP’’ andthe incidence of stroke.37

Monk et al. observed that 1-year mortality increased by3.6% for every minute that systolic blood pressure was lessthan 80 mmHg.38 In a retrospective review of perioperativedeaths, Lienhart et al. found that intraoperative hypoten-sion and anaemia were closely associated with postoperativemyocardial ischaemic events.39 Intraoperative hypotensionhas also been linked to non-cardiac complications andadverse outcome after surgery. Episodes (not necessarilycontiguous) of hypotension lasting longer than 15 min havebeen associated with an increase in mortality.36

Rationale for vasopressor therapy

The goal of any hemodynamic perioperative interven-tion is to maintain or improve tissue perfusion. WhenMAP decreases below an autoregulatory threshold ofabout 60---65 mmHg, organ perfusion becomes pressuredependent40 (Fig. 1). Within the microcirculation, the distri-bution and magnitude of blood flow represent a coordinatedinterplay between arteriolar, capillary, and venular seg-ments based on local and regional metabolic demand. Therationale for vasopressor therapy in hypotensive states isbased on the knowledge that in all regional circulations,including the renal, splanchnic, cerebral and coronary beds,blood flow is autoregulated.41 Nonetheless, and contraryto what is often believed, tissue and microcirculatory per-fusion is physiologically regulated by changes in bloodflow, vessel density and local vasomotor responses, and notBP.42 Under physiological conditions, regulation of bloodflow occurs autonomously in the tissues and is driven bymetabolic demand.43 Atasever et al. demonstrated thebiphasic response of the human microcirculatory systemto NTG-induced hypotension in a clinical setting.44 Thisresponse to a relatively large dose of NTG is character-ized by an initial increase in arteriolar diameter and areduction in systemic BP, promoting microcirculatory flow.Then, when BP gets too low, this is followed by a phasein which microcirculatory flow can no longer be sustained.Although severe loss of BP results in alterations in micro-circulatory perfusion,44 within the physiological range ofCO and MAPm the relationship between systemic hemody-namics and microcirculation is relatively loose.45 It is tobe expected that venoconstriction produced by a vasopres-sor allows the transfer of blood from the splanchnic bedsto the heart increasing right ventricular filling and CO.46

Alternatively, this is expected to increase ventricular after-load and thereby decrease SV.47 These two mechanismsare not mutually exclusive, and likely compete against one

Document downloaded from http://www.elsevier.es, day 25/05/2017. This copy is for personal use. Any transmission of this document by any media or format is strictly prohibited.

ARTICLE IN PRESS+Model

Fluid therapy recommendations for major abdominal surgery 3

Vasodilatation

Vasoconstriction

Autoregulation

Perfusion pressure

Blo

od

flo

w

Figure 1 Autoregulation of blood flow to the tissues drivenby the perfusion pressure curve. The red line represents theautoregulatory responses in which flow changes relatively littledespite a major change in perfusion pressure. In situations ofsevere hypotension (mean arterial pressure <50 mmHg), bloodflow to the tissues is decreased, leading to hypoxia. There is apressure below which an organ is incapable of autoregulatingits flow because it is maximally dilated. This perfusion pressuremay be between 50 and 70 mmHg, depending upon the organ.Below this perfusion pressure, blood flow decreases passively inresponse to further reductions in perfusion pressure.

another.48 Together with the complex interaction betweenmany factors regulating splanchnic circulation, they deter-mine the effect of vasopressors on CO49 (Fig. 2). As Maaset al. showed, since stroke volume variation (SVV) is a mea-sure of how SV varies with changes in preload, patients withhigh SVV are operating on the steep portion of the car-diac function curve.50 Because the effect of norepinephrineon mean systemic pressure generally exceeds the effect onvenous vascular resistance, increased preload with norepi-nephrine resulted in a significant increase in CO in this groupof patients. In contrast, patients with low SVV are operat-ing on the flat portion of their cardiac function curves, andthe negative effect of increased afterload likely exceedsthe small benefit of augmented venous return (VR), therebydecreasing CO.51

Recently, Rebet et al. showed similar effects followingadministration of phenylephrine after episodes of hypoten-sion in ventilated patients under general anaesthesia duringsurgery. They found that in preload-dependent patients, car-diac index (CI) and SV remained unchanged; whereas inpreload-independent patients, administration of phenyle-phrine decreased CI and SV.48 Therefore, the response interms of increasing SV and CO following the administrationof vasopressors can be predicted by baseline SVV or PPV,because these give a picture of patient status within theFrank---Starling curve.50

Although the deviating effects of noradrenaline andphenylephrine on MAP and CO are known, SV and COmonitoring will provide crucial information; however,most clinicians still rely on BP, heart rate and oxygensaturation during intraoperative hemodynamic manage-ment of patients undergoing high-risk surgery.52 Thereis some evidence of lack of benefit in increasing MAP

Decreased afterload

Increased afterload

Ventr

icula

r perf

orm

ance

(card

iac o

utp

ut, s

troke v

olu

me)

Myocardial fibre length

ventricular end-diastolic pressure

Figure 2 Stroke volume and afterload. Afterload is the resistance against which the ventricles pump, so greater afterload makesit harder for the ventricles to eject the stroke volume (SV). All else constant, an increase in vascular resistance would decrease SV.This usually does not occur, as contractility increases to maintain SV and thus cardiac output. A decrease in afterload increases SV.

Document downloaded from http://www.elsevier.es, day 25/05/2017. This copy is for personal use. Any transmission of this document by any media or format is strictly prohibited.

ARTICLE IN PRESS+Model

4 J. Ripollés-Melchor et al.

Eadyn

Eadyn

Eadyn

Stroke volume variation

Pu

lse

pre

ssu

re v

aria

tio

n

Figure 3 Effect of changes in arterial tone on the ratiobetween PPV and the SVV. Eadyn, dynamic arterial elastance;PPV, pulse pressure variation; SVV, stroke volume variation.

with noradrenaline53 or phenylephrine54 without clinicalimprovement of CO in terms of organ perfusion in preload-dependent patients, which is the ultimate determinantof GDHT; therefore, complex hemodynamic monitoring isessential. Interestingly, the PPV/SVV ratio (Eadyn) definescentral arterial stiffness or dynamic elastance,55,56 and canbe used as a functional assessment of arterial load (Fig. 3).The question of whether vasoconstrictors or volume expan-sion should be used in the setting of a hypotensive state stillremains.57

Vasodilatation after anaesthesia induction

Anaesthesia induction causes vasodilatation that reducesVR, causing SV and CI to decrease, accompanied by a sig-nificant decrease in BP and HR. Fluid volume optimizationperformed in this setting merely serves to counteract thedecrease in SV that occurs in response to induction. The highefficiency of fluid infused after the induction of anaesthe-sia must be matched by a strong increase in CO to maintainDO2. When CO does not increase, as in fluid non-responders,DO2 decreases. This response must be considered as a riskwhen infusing fluid without SV monitoring.58 In this setting,instead of volume therapy patients may require a thera-peutic strategy that is aimed more at restoring vasomotortone instead of one that is driven by volume therapy, inso-far as the primary defect is poor vasomotor tone resultingin an enlarged vascular space.59 This is especially rele-vant in patients on chronic angiotensin-converting enzymeinhibitor and angiotensin receptor blocker therapy, whohave a dampened sympathetic response,60 and in patientswith preoperative predictors of hypotension after inductionof anaesthesia24 or evidence of dehydration.58 In patientsat high risk of complications resulting from intra-operativehypovolaemia and hypotension, and in those suspected ofhypovolaemia, ultrasound measurement of the inferior venacava and collapsibility index may provide clinically usefulinformation, as it would identify patients who could benefitfrom preoperative fluid load.61

Vasopressors in goal directed hemodynamictherapy

Wuethrich et al. compared a liberal maintenance fluidtherapy versus a restrictive fluid therapy accompanied bycontinuous infusion of norepinephrine in patients under-going planned open cystectomy with thoracic epidural. Inthe norepinephrine group, postoperative zero fluid balance,lower in-hospital and 90-day postoperative complicationrates, and reduced hospitalization time were observed.Remarkably, only a slight increase in serum lactate wasfound in the restrictive group; there were no differences inother tissue perfusion parameters or hemodynamic indicesat the end of the intervention. Unfortunately, the authorsdid not compare a GDHT group versus control. However,they showed that administration of norepinephrine coun-teracts the decrease in sympathetic tone and vasodilatationinduced by epidural analgesia, anaesthetics, and analgesics,and may be more physiologic at compensating for a plegicvascular system than the liberal use of intravenous fluids.62

The induced reduction in enlarged unstressed blood vol-umes caused by norepinephrine, and the restoration ofstressed blood volumes can maintain an adequate hemody-namic balance.63

In spite of the positive results obtained by Wuethrichet al.,62 it seems more physiological to base vasopres-sor administration on hemodynamic algorithms, rather thanon continuous infusion. Salzwedel et al. randomized 160patients undergoing elective major abdominal surgery andshowed that GDHT using PPV, CI trending and MAP thatinvolved the use of fluids, vasopressors and inotropes,reduced the total number of complications and the numberof patients with complications.64 The benefits of such algo-rithms have been widely demonstrated.6,65 Although GDHTprotocols aim to optimize tissue perfusion, it is currentlyunclear whether systemic hemodynamic parameters accu-rately reflect the final impact on perfusion at local tissuelevel. Interestingly, Stens et al. investigated whether GDHTbased on PPV, MAP and CI (similar to Salzwedel et al.64)improves microcirculatory perfusion when compared to aMAP-based strategy in patients undergoing elective abdomi-nal surgery. The authors found that although the GDHT groupshowed an improvement in hemodynamic parameters, thisdid not correlate with an improvement in microcirculationor lactate measurements on the first postoperative day.66

These findings suggest that the relation between systemichemodynamics and microcirculation is not fixed, especiallywhen CO and BP values are within normal ranges.45 How-ever, high-risk surgery is associated with microvasculardysfunction, and these alterations may play a role in thedevelopment of postoperative organ dysfunction.21,45 Defin-ing the adequacy of GDHT requires attention to both globaland regional perfusion.67

Rationale for maintaining contractility

‘‘Normal’’ cardiac output

Cardiac output is one of the most important physiologicalparameters, as it directly and proportionally reflects the

Document downloaded from http://www.elsevier.es, day 25/05/2017. This copy is for personal use. Any transmission of this document by any media or format is strictly prohibited.

ARTICLE IN PRESS+Model

Fluid therapy recommendations for major abdominal surgery 5

Normal

Heart failure

Increased contractility

Myocardial fibre length

ventricular end-diastolic pressure

Ventr

icula

r perf

orm

ance

(card

iac o

utp

ut,

str

oke v

olu

me)

Figure 4 The Frank---Starling curves. Increasing EDV is equivalent to pre-extension of the muscle heart muscle, which will affectcontraction tension through the length---force relation. However, as increased diameter also increases total load, the effect onstroke volume may be somewhat less than the effect seen in isolated muscles. Contractility increases with inotropic stimuli anddecreases with heart failure, being a state of reduced contractility.

metabolism of the entire organism. It is the primary determi-nant of global oxygen transport from the heart to the tissues,since it is the main contributor to DO2. Cardiac output is thesum of the systemic flow per minute, and is the product ofSV and HR. The ability of the body to adapt to increasedworkload and hence metabolism is the result of the abil-ity of the heart to increase HR and SV. The normal CO valuedepends on metabolic demand and individual characteristics(Fig. 4). Cardiac index (CI) is the ratio of left ventricular COin 1 min to body surface area (BSA), thus relating heart per-formance to the size of the individual. The mean CI valuesreported are 3.1 ml/min/m2 for women and 3.2 ml/min/m2

for men.68 Interestingly, Carlsson et al. found no differencebetween the CI at rest in normal individuals and elite ath-letes, showing that CI is primarily dependent on the basalmetabolism.68 The fundamental characteristic of elite ath-letes is an increase in basal SV, due to a higher total heartvolume (THV),69 due to either an increase in ventricular sizeor improved pumping mechanics, and a decrease in HR. Thissupports the higher reserve capacity of athletes for increas-ing CI through HR increase during stress. The larger THVof athletes can generate greater CO due to higher SV atsimilar HR.68 In patients with congestive heart failure, CIis lower compared to the healthy population, primarily dueto a lower SV. At rest, heart failure patients often main-tain a normal CO until later stages of the disease, whenCO becomes too low to meet the metabolic demands ofthe body.70 Ageing is associated with a sedentary lifestylewhich decreases metabolism, so CI decreases with age.71

Age-associated changes in cardiac and vascular function are

identified as a major risk factor for cardiovascular morbid-ity and mortality, with older patients having a higher risk ofmorbidity and mortality.72,73 At rest DO2 exceeds the oxy-gen consumption of all tissues (VO2) combined. The optimallevel of DO2 varies according to metabolic demands, butan inadequate DO2 increases the oxygen extraction ratio(OER), thereby maintaining aerobic metabolism. Physiolog-ically, every time there is a reduction in DO2, there will bean increase in tissue oxygen extraction in order to stabi-lize VO2. The OER will keep increasing up to a critical DO2

below which VO2 becomes supply-dependent and anaerobicmetabolism will occur.74 When this process begins, DO2 iscalled critical DO2 and VO2/DO2 dependence is established75

(Fig. 5).

Perioperative oxygen requirements

Oxygen absorption during exercise is not directly compa-rable with oxygen absorption in the perioperative patient.However, as with exercise, oxygen consumption dur-ing and after major surgery is high.76 Major surgicaltrauma increases oxygen requirements from an average of110 ml/min/m2 at rest to an average of 170 ml/min/m2 inthe postoperative period.77 Anaesthesia is associated withcardiovascular depression and delay or failure to respond tofluid and blood loss, anaemia, and pre-existing comorbidi-ties, such as cardiac, pulmonary or renal insufficiencies. Theactivation of an inflammatory response to surgery result-ing in hemodynamic active substances such as cytokines is a

Document downloaded from http://www.elsevier.es, day 25/05/2017. This copy is for personal use. Any transmission of this document by any media or format is strictly prohibited.

ARTICLE IN PRESS+Model

6 J. Ripollés-Melchor et al.

Physiological dependencePathological dependence

DO2

Critical

DO2

VO

2

SvO2

O2ER

Lactate

Figure 5 Relationship between oxygen delivery, oxygen consumption, oxygen uptake rate and lactate. Initially, as metabolicdemand (VO2) increases or DO2 diminishes, O2ER increases to maintain aerobic metabolism and consumption remains independentof delivery. However, maximum O2ER is reached at a point called critical DO2 (cDO2). This is believed to be ∼70%. Beyond cDO2, anyfurther increase in VO2 or decline in DO2 must lead to tissue hypoxia and anaerobic metabolism (lactate production is a surrogatefor this).

contributing factor that alters tissue oxygenation and nor-mal values. Compromised physiologic reserves and multiplecomorbidities in combination with extensive surgery seemto be a hallmark of high complication and mortality rates,78

because these patients are less likely to meet the increasedoxygen demand that occurs during major surgery.79 Whilehealthy or older individuals or patients with heart failureare able to maintain adequate DO2 at rest, this parameteris compromised in stressful situations such as exercise, orsurgery, which is associated with significant systemic inflam-matory response which is in turn associated with increasedoxygen demand.

The supranormal oxygen delivery approach

Alterations in oxygen transport leading to tissue hypoxiaand impaired microvascular flow are associated with thedevelopment of organ failure and death.3,21,80 The lack ofan early marker for tissue hypoxia coupled with the factthat pioneering studies in which normal DO2 goals wereused found no benefit21,81 suggests that normal values maynot be adequate during surgical trauma; therefore, treat-ing patients to achieve a high DO2 was seen as an attractivealternative. This prompted Shoemaker to hypothesize thatdeliberately increasing DO2 may prevent the developmentof organ failure.82,83 The ultimate aim of GDHT is still toprevent tissue oxygen debt by maintaining tissue perfusion.Supranormal DO2I has been shown to reduce both morbid-ity and mortality in the perioperative period.7,84,85 However,the clinically important question is whether there is an

identifiable subset of patients who may benefit from supra-normal DO2I targets.86

Certain authors have studied survival rates in patientswith a high CI and high DO2.87 The suggested DO2 valueof 600 ml/min/m2 has yet to be confirmed.88 Nevertheless,when absolute values of CI or DO2 are used as therapeutictargets, they are often predefined. The use of individ-ual goals instead of a pre-established arbitrary value of>600 ml/min/m2 is more rational and would avoid potentialadverse events related to the GDHT. There is widespreadcontroversy at to which values are the most suitable, andfor which patients.15,88 Supra-normal values of DO2 shouldbe defined in relation to pre-operative (i.e. normal) val-ues of DO2 and not in relation to the ‘‘magic number’’ of600 ml/min/m2.89 From an ‘‘energy debt’’ perspective, itis certainly much more important to consider the DO2---VO2

relationship than to indicate a specific value of DO2 or CI asa goal.90

The oxygen supply

The most commonly used methods to assess global VO2/DO2

are mixed venous oxygen saturation (SvO2) and its surrogate,central venous oxygen saturation (ScvO2). During anaesthe-sia, it is reasonable to assume that ScvO2 reflects CO andoxygen supply. ScvO2 may therefore be a useful physiologicindicator to guide fluid responsiveness and administration.The main factors that influence ScvO2 are haemoglobin,arterial oxygen saturation of haemoglobin, CO, and oxy-gen consumption, or SvO2 = SaO2 − (VO2/[CO × Hb × 1.34]).

Document downloaded from http://www.elsevier.es, day 25/05/2017. This copy is for personal use. Any transmission of this document by any media or format is strictly prohibited.

ARTICLE IN PRESS+Model

Fluid therapy recommendations for major abdominal surgery 7

Individual

Assessment of patient riskASA classification, POSSUM, RCRI, ACSRC calculators

facilitate preoperative estimation of surgical risk

80% of the perioperative deaths occur in a small subset of

high risk surgical procedures. This subgroup constitutes

only 12% of surgical population`

Goal settingHemodynamic goals should be

predefined according to patient

characteristics. Keep in mind that

these can change during surgery,

depending on the events

Creating a planWhile for low-risk patients conventional

monitoring is usually sufficient, in

order to maintain zero balance, in

high-risk patients it is necessary to set

hemodynamic goals

1

2

3

4

5

ExecutionNo monitoring per se will improve

postoperative outcomes!

Keep it!The ERAS protocols try to maintain an

euvolemic status throughout their

hospital stay, avoiding situations of

hypoperfusion and volume overload.

This applies to all patients

Re

vie

w

Low risk High risk

Fluids

for

hypovolaemia

Vasopressor

for

vasodilation

Inotropy for

decreased

contractility

COSVSVVCIMAPScvO2

Advanced hemodynamic monitoring in

the medium-high risk surgical patient

Individualizes the goals to each

patient

Pre.....Intra.....Postoperative

Hypo o

r hyper

ERAS Pathway

Hemodynamic plan

Usual care

Figure 6 Infographic summary.

Theoretically, if three of these factors remain constant(SaO2, SvO2 and VO2) the ScvO2 value will reflect the changesin VO2. There are multiple physiologic, pathologic, andtherapeutic factors that influence ScvO2, such as anaemia,hypovolaemia, contractility and bleeding.91 More impor-tantly, both low and high levels of ScvO2 can be pathologic.

The normal range for SvO2 is 65---75%.92 Although SvO2 above70% does not necessarily reflect adequate tissue oxygen-ation, a persistently low SvO2 (>30%) is associated withtissue ischemia93 and bad outcome,92,94 whereas normalor supranormal ScvO2 values do not guarantee adequatetissue oxygenation.91 Therefore, additional hemodynamic

Document downloaded from http://www.elsevier.es, day 25/05/2017. This copy is for personal use. Any transmission of this document by any media or format is strictly prohibited.

ARTICLE IN PRESS+Model

8 J. Ripollés-Melchor et al.

measures are needed to evaluate ScvO2 values,95 since asingle ScvO2 value will not indicate which interventions willbe most effective in achieving the target ScvO2 or how longthis value should be maintained.96

Inotropics in GDHT

Fluid boluses alone may be sufficient to achieve CI, ScvO2

and DO2 goals, and GDHT using only fluids has beenshown to improve outcomes in certain groups of surgicalpatients.7,8,97,98 Nonetheless, fluids are often not enoughto achieve these goals, and inotropics and vasodilatorsmay be necessary. Jhanji et al. highlighted the impor-tant pathophysiological mechanisms underlying the benefitof GDHT. They showed that SV-targeted colloid adminis-tration coupled with a fixed infusion rate of dopexamineimproved oxygen DO2, central ScvO2, micro-vascular bloodflow, and tissue oxygenation, and that fluid therapy aloneled to additional modest improvements.99 However, theOPTIMISE trial, which examined the effect of GDHT (algo-rithm based on intravenous fluid boluses and an inotrope)in high-risk gastrointestinal surgical patients on outcomesfollowing surgery84 did not confirm previous data suggest-ing the benefit of GDHT. Although a decrease was foundin the primary outcome --- a composite of predefined mod-erate or major postoperative complications and mortalityat 30 days following surgery (OR 0.73; 95% CI, 0.53---1.00;p = 0.05) and cumulative mortality at 180 days (OR 0.61; 95%CI, 0.36---1.04; p = 0.07), these reductions were not signifi-cant. However, the study was underpowered, as the samplesize was calculated based on an expected 30-day compli-cation incidence of 50% in the control group and a 37.5%incidence in the GDHT group, whereas the incidence ofcomplications was only 43.4% in the control group and 36.6%in the GDHT group (p = 0.07). Thus, the initial sample sizecalculation was based on a much higher incidence of post-operative complications than expected. Interestingly, in thepre-specified adherence-adjusted analysis conducted usingestablished methods, the observed treatment effect wasstrengthened when the 65 patients whose care was non-adherent were assumed to experience the same outcomeas if they had been allocated to the alternative group (RR,0.80; 95% CI, 0.61---0.99; p = 0.04). Moreover, a significantinteraction (p = 0.02) was found for timing of recruitment;the intervention was associated with a reduction in the pri-mary outcome for patients recruited later (RR, 0.59; 95%CI, 0.41---0.84) compared with earlier at each site (RR, 1.51;95% CI, 0.75---3.01). This shows that when the GDHT pro-tocol was consistently applied, the treatment effect wasstrengthened. Arulkumaran et al. found a reduction in mor-bidity in patients who were treated to achieve supranormalDO2 targets with the use of fluids and inotropes, withoutfinding an increase in cardiac complications due to the useof inotropes.100

The ideal CO monitoring system should fulfil the follow-ing requirements: presentation of non-invasive, continuous,real-time data, easy to apply, easy to operate, non-operator dependent, accurate and reliable, and easy tointerpret.101

There is currently no monitoring system that meetsthis ideal. Selecting the most appropriate hemodynamic

monitoring device may be an important first step in reducingthe risk of complications.102 However, no single hemody-namic goal or monitoring method has been accepted inthe literature,103 and all variables measured must be cor-rectly interpreted and applied to the individual patient104

(Fig. 6).

Conclusions

The concept of GDHT is based on anticipation. Predefinedinterventions with pre-specified goals are organized in aspecific fashion in order to provide the best possible careto patients undergoing a high-risk intervention. Fluid load-ing, vasopressor or inotropic therapy could be adapted toeach patient and each situation using comprehensive hemo-dynamic monitoring. Local algorithms should be available tooptimize all hemodynamic components during this high-riskperiod.

Conflict of interest

JRM: received travel funding from Deltex Medical and hono-raria for lectures from Fresenius Kabi, Edwards Lifesciences,Deltex Medical and Merck Sharp & Dohme.

DC: received honoraria for lectures and academic studiesfrom BBraun, Fresenius Kabi, Grifols, and LFB Biomedika-ments.

HA: received financial support for educational programsand for attending symposia from Applied Physiology andLiDCO.

AE: not stated.MM: is a member of the Editorial Board of the BJA;

Co-Editor-in-Chief of Perioperative medicine and a paidConsultant for Deltex Medical and Edwards Lifesciences. MMhas held educational meetings that have received grantsfrom Deltex Medical, Edwards Lifesciences, LidCo, Chee-tah and Pulsion (www.ebpom.org). MM’s University Chair isSponsored by Smiths Medical. MM is a Director of The Blooms-bury Innovation Group.

AAG: not stated.SB: not stated.RCF: JRM received travel funding from Fresenius Kabi and

honoraria for lectures from Edwards Lifesciences, DeltexMedical and Merck Sharp & Dohme.

JMCV: received honoraria and travel funding for lecturesfrom Merck Sharp & Dohme, Deltex Medical and FreseniusKabi.

Acknowledgements

Professor Jean-Louis Vincent, Professor of Intensive CareMedicine (Université Libre de Bruxelles), Dept. of IntensiveCare, Erasme University Hospital, Brussels, Belgium. Pro-fessor Can Ince, Dept. of Intensive Care, Erasmus MedicalCenter Erasmus University of Rotterdam, the Netherlands.Bernard M. van den Berg, Ph.D. Dept. of Internal Medicine(Nephrology) Leiden University Medical Center, Leiden, theNetherlands. Professor Hans Vink, CArdiovascular ResearchInstitute Maastricht (CARIM), Dept. of Vascular Medicine atthe Academic Medical Center, Amsterdam, the Netherlands.

Document downloaded from http://www.elsevier.es, day 25/05/2017. This copy is for personal use. Any transmission of this document by any media or format is strictly prohibited.

ARTICLE IN PRESS+Model

Fluid therapy recommendations for major abdominal surgery 9

Professor Ignacio García Monge, Dept. of Intensive Care,Hospital SAS de Jerez, Experimental Research Unit of Hospi-tal SAS de Jerez, Spain. Professor Susana González Suárez,Dept. of Anaesthesiology, Vall d’Hebrón University Hospital,Barcelona, Spain. Eugenio Martínez Hurtado, Infanta LeonorUniversity Hospital, Madrid, Spain. Professor Vladimir Cerny,Dept. of Anaesthesiology, Perioperative Medicine and Inten-sive Care J.E. Purkinje University, Masaryk Hospital Ustinad Labem, Czech Republic. Professor José Manuel RamírezRodríguez, Dept. of Colorectal Surgery, Lozano Blesa Univer-sity Hospital, Zaragoza, Spain. Alix Zuleta-Alarcón, Dept. ofAnaesthesiology and Critical Care, The Ohio State Univer-sity Hospital, Columbus, USA. Teresa de la Torre Aragonés,professional librarian, Infanta Leonor University Hospital,Madrid, Spain. GERM: Grupo Espanol de Rehabilitación Mul-timodal; Enhanced Recovery After Surgery (ERAS) SpainChapter; and EAR Group (Evidence Anaesthesia ReviewGroup).

References

1. The International Surgical Outcomes Study Group. Globalpatient outcomes after elective surgery: prospective cohortstudy in 27 low-, middle- and high-income countries. Br JAnaesth. 2016;117:601---9.

2. Pearse RM, Moreno RP, Bauer P, Pelosi P, Metnitz P, Spies C,et al. Mortality after surgery in Europe: a 7 day cohort study.Lancet. 2012;380:1059---65.

3. Lobo SM, Rezende E, Knibel MF, Silva NB, Paramo JA, NaculFE, et al. Early determinants of death due to multiple organfailure after noncardiac surgery in high-risk patients. AnesthAnalg. 2011;112:877---83.

4. Pearse RM, Harrison DA, James P, Watson D, Hinds C, RhodesA, et al. Identification and characterisation of the high-risksurgical population in the United Kingdom. Crit Care. 2006;10:R81.

5. Lees N, Hamilton M, Rhodes A. Clinical review: goal-directedtherapy in high risk surgical patients. Crit Care. 2009;13:231.

6. Ripollés J, Espinosa A, Martínez-Hurtado E, Abad-Gurumeta A,Casans-Francés R, Fernández-Pérez C, et al. [Intraoperativegoal directed hemodynamic therapy in noncardiac surgery:a systematic review and meta-analysis]. Rev Bras Anestesiol.2016;66:513---28 [Portuguese].

7. Ripolles-Melchor J, Espinosa A, Martinez-Hurtado E, Abad-Gurumeta A, Casans-Frances R, Fernandez-Perez C, et al.Perioperative goal-directed hemodynamic therapy in noncar-diac surgery: a systematic review and meta-analysis. J ClinAnesth. 2016;28:105---15.

8. Cecconi M, Corredor C, Arulkumaran N, Abuella G, Ball J,Grounds RM, et al. Clinical review: goal-directed therapy ---what is the evidence in surgical patients? The effect on differ-ent risk groups. Crit Care. 2013;17:209.

9. Miller TE, Roche AM, Mythen M. Fluid management and goal-directed therapy as an adjunct to Enhanced Recovery AfterSurgery (ERAS). Can J Anaesth. 2015;62:158---68.

10. Camacho Navarro LH, Bloomstone JA, Costa Auler JO Jr,Cannesson M, Della Rocca G, Gan TJ, et al. Perioperative fluidtherapy: a statement from the international Fluid Optimiza-tion Group. Perioper Med (Lond). 2015;4:3.

11. Srinivasa S, Kahokehr A, Soop M, Taylor M, Hill AG. Goal-directed fluid therapy --- a survey of anaesthetists in theUK, USA, Australia and New Zealand. BMC Anesthesiol. 2013;13:5.

12. Ahmad T, Beilstein CM, Aldecoa C, Moreno RP, Molnar Z, Novak-Jankovic V, et al. Variation in haemodynamic monitoring formajor surgery in European nations: secondary analysis of theEuSOS dataset. Perioper Med (Lond). 2015;4:8.

13. Suehiro K, Tanaka K, Mukai A, Joosten A, Desebbe O,Alexander B, et al. Hemodynamic monitoring and managementin high-risk surgery: a survey among Japanese anesthesiolo-gists. J Anesth. 2016;30:526---9.

14. Ripolles-Melchor J, Casans-Frances R, Abad-Gurumeta A,Suarez-de-la-Rica A, Ramirez-Rodriguez JM, Lopez-TimonedaF, et al. Spanish survey on enhanced recovery after surgery.Rev Esp Anestesiol Reanim. 2016;63:376---83.

15. Ripolles Melchor J, Espinosa A. Goal directed fluid therapy con-troversies in non-cardiac surgery. Rev Esp Anestesiol Reanim.2014;61:477---80.

16. Hamilton MA, Cecconi M, Rhodes A. A systematic reviewand meta-analysis on the use of preemptive hemodynamicintervention to improve postoperative outcomes in moder-ate and high-risk surgical patients. Anesth Analg. 2011;112:1392---402.

17. Shoemaker WC, Wo CC, Thangathurai D, Velmahos G, BelzbergH, Asensio JA, et al. Hemodynamic patterns of survivorsand nonsurvivors during high risk elective surgical operations.World J Surg. 1999;23:1264---70, discussion 1270---1.

18. Mascha EJ, Yang D, Weiss S, Sessler DI. Intraoperativemean arterial pressure variability and 30-day mortality inpatients having noncardiac surgery. Anesthesiology. 2015;123:79---91.

19. Le Manach Y, Hofer CK, Lehot JJ, Vallet B, Goarin JP, Tav-ernier B, et al. Can changes in arterial pressure be usedto detect changes in cardiac output during volume expan-sion in the perioperative period? Anesthesiology. 2012;117:1165---74.

20. Fischer MO, Cannesson M. The veno-ventricular-arterial cou-pling during anaesthesia. Anaesth Crit Care Pain Med.2015;34:315---6.

21. Jhanji S, Lee C, Watson D, Hinds C, Pearse RM. Microvascularflow and tissue oxygenation after major abdominal surgery:association with post-operative complications. Intensive CareMed. 2009;35:671---7.

22. Chappell D, Jacob M, Hofmann-Kiefer K, Conzen P, Rehm M.A rational approach to perioperative fluid management. Anes-thesiology. 2008;109:723---40.

23. Lobo SM, Mendes CL, Rezende E, Dias FS. Optimizing peri-operative hemodynamics: what is new? Curr Opin Crit Care.2013;19:346---52.

24. Reich DL, Hossain S, Krol M, Baez B, Patel P, Bernstein A, et al.Predictors of hypotension after induction of general anesthe-sia. Anesth Analg. 2005;101:622---8.

25. Bijker JB, van Klei WA, Kappen TH, van Wolfswinkel L, MoonsKG, Kalkman CJ. Incidence of intraoperative hypotension as afunction of the chosen definition: literature definitions appliedto a retrospective cohort using automated data collection.Anesthesiology. 2007;107:213---20.

26. Walsh M, Devereaux PJ, Garg AX, Kurz A, Turan A, RodsethRN, et al. Relationship between intraoperative mean arte-rial pressure and clinical outcomes after noncardiac surgery:toward an empirical definition of hypotension. Anesthesiology.2013;119:507---15.

27. Sun LY, Wijeysundera DN, Tait GA, Beattie WS. Associa-tion of intraoperative hypotension with acute kidney injuryafter elective noncardiac surgery. Anesthesiology. 2015;123:515---23.

28. Van Waes JA, van Klei WA, Wijeysundera DN, van WolfswinkelL, Lindsay TF, Beattie WS. Association between intraopera-tive hypotension and myocardial injury after vascular surgery.Anesthesiology. 2016;124:35---44.

Document downloaded from http://www.elsevier.es, day 25/05/2017. This copy is for personal use. Any transmission of this document by any media or format is strictly prohibited.

ARTICLE IN PRESS+Model

10 J. Ripollés-Melchor et al.

29. Hallqvist L, Martensson J, Granath F, Sahlen A, Bell M. Intraop-erative hypotension is associated with myocardial damage innoncardiac surgery: an observational study. Eur J Anaesthesiol.2016;33:450---6.

30. Wesselink EM, Kappen TH, van Klei WA, Dieleman JM, vanDijk D, Slooter AJ. Intraoperative hypotension and delir-ium after on-pump cardiac surgery. Br J Anaesth. 2015;115:427---33.

31. Lima EQ, Zanetta DM, Castro I, Massarollo PC, Mies S, MachadoMM, et al. Risk factors for development of acute renal failureafter liver transplantation. Ren Fail. 2003;25:553---60.

32. Monk TG, Bronsert MR, Henderson WG, Mangione MP, Sum-Ping ST, Bentt DR, et al. Association between intraoperativehypotension and hypertension and 30-day postoperativemortality in noncardiac surgery. Anesthesiology. 2015;123:307---19.

33. Bijker JB, van Klei WA, Vergouwe Y, Eleveld DJ, van Wolf-swinkel L, Moons KG, et al. Intraoperative hypotension and1-year mortality after noncardiac surgery. Anesthesiology.2009;111:1217---26.

34. Badin J, Boulain T, Ehrmann S, Skarzynski M, BretagnolA, Buret J, et al. Relation between mean arterial pres-sure and renal function in the early phase of shock: aprospective, explorative cohort study. Crit Care. 2011;15:R135.

35. Bijker JB, Persoon S, Peelen LM, Moons KG, Kalkman CJ, Kap-pelle LJ, et al. Intraoperative hypotension and perioperativeischemic stroke after general surgery: a nested case-controlstudy. Anesthesiology. 2012;116:658---64.

36. Sessler DI, Sigl JC, Kelley SD, Chamoun NG, Manberg PJ, SaagerL, et al. Hospital stay and mortality are increased in patientshaving a ‘‘triple low’’ of low blood pressure, low bispectralindex, and low minimum alveolar concentration of volatileanesthesia. Anesthesiology. 2012;116:1195---203.

37. Drummond JC. Stroke and intraoperative hypotension: tosleep, perchance to stroke-ay, there’s the rub. Anesth Analg.2016;123:814---5.

38. Monk TG, Saini V, Weldon BC, Sigl JC. Anesthetic managementand one-year mortality after noncardiac surgery. Anesth Analg.2005;100:4---10.

39. Lienhart A, Auroy Y, Pequignot F, Benhamou D, WarszawskiJ, Bovet M, et al. Survey of anesthesia-related mortality inFrance. Anesthesiology. 2006;105:1087---97.

40. Johnson PC. Autoregulation of blood flow. Circ Res.1986;59:483---95.

41. Bellomo R, Giantomasso DD. Noradrenaline and the kidney:friends or foes? Crit Care. 2001;5:294---8.

42. Dunser MW, Takala J, Brunauer A, Bakker J. Re-thinking resus-citation: leaving blood pressure cosmetics behind and movingforward to permissive hypotension and a tissue perfusion-based approach. Crit Care. 2013;17:326.

43. Segal SS. Regulation of blood flow in the microcirculation.Microcirculation. 2005;12:33---45.

44. Atasever B, Boer C, van der Kuil M, Lust E, Beishuizen A,Speekenbrink R, et al. Quantitative imaging of microcircu-latory response during nitroglycerin-induced hypotension. JCardiothorac Vasc Anesth. 2011;25:140---4.

45. De Backer D, Ortiz JA, Salgado D. Coupling microcirculationto systemic hemodynamics. Curr Opin Crit Care. 2010;16:250---4.

46. Nouira S, Elatrous S, Dimassi S, Besbes L, Boukef R, Mohamed B,et al. Effects of norepinephrine on static and dynamic preloadindicators in experimental hemorrhagic shock. Crit Care Med.2005;33:2339---43.

47. Cannesson M, Jian Z, Chen G, Vu TQ, Hatib F. Effects ofphenylephrine on cardiac output and venous return depend onthe position of the heart on the Frank---Starling relationship. JAppl Physiol (1985). 2012;113:281---9.

48. Rebet O, Andremont O, Gerard JL, Fellahi JL, Hanouz JL,Fischer MO. Preload dependency determines the effects ofphenylephrine on cardiac output in anaesthetised patients:a prospective observational study. Eur J Anaesthesiol.2016;33:638---44.

49. Gelman S, Mushlin PS. Catecholamine-induced changes inthe splanchnic circulation affecting systemic hemodynamics.Anesthesiology. 2004;100:434---9.

50. Maas JJ, Pinsky MR, de Wilde RB, de Jonge E, JansenJR. Cardiac output response to norepinephrine in postop-erative cardiac surgery patients: interpretation with venousreturn and cardiac function curves. Crit Care Med. 2013;41:143---50.

51. Pearl RG. Understanding the divergent effects of norepi-nephrine on cardiac output: go with the flow. Crit Care Med.2013;41:352---4.

52. Cannesson M, Pestel G, Ricks C, Hoeft A, Perel A. Hemody-namic monitoring and management in patients undergoing highrisk surgery: a survey among North American and Europeananesthesiologists. Crit Care. 2011;15:R197.

53. LeDoux D, Astiz ME, Carpati CM, Rackow EC. Effects of per-fusion pressure on tissue perfusion in septic shock. Crit CareMed. 2000;28:2729---32.

54. Meng L, Cannesson M, Alexander BS, Yu Z, Kain ZN, CerussiAE, et al. Effect of phenylephrine and ephedrine bolus treat-ment on cerebral oxygenation in anaesthetized patients. Br JAnaesth. 2011;107:209---17.

55. Cecconi M, Monge Garcia MI, Gracia Romero M, MellinghoffJ, Caliandro F, Grounds RM, et al. The use of pulse pres-sure variation and stroke volume variation in spontaneouslybreathing patients to assess dynamic arterial elastance andto predict arterial pressure response to fluid administration.Anesth Analg. 2015;120:76---84.

56. Garcia MI, Romero MG, Cano AG, Aya HD, Rhodes A, GroundsRM, et al. Dynamic arterial elastance as a predictor of arterialpressure response to fluid administration: a validation study.Crit Care. 2014;18:626.

57. Pinsky MR. Functional hemodynamic monitoring. Crit Care Clin.2015;31:89---111.

58. Li Y, He R, Ying X, Hahn RG. Dehydration, hemodynamics andfluid volume optimization after induction of general anesthe-sia. Clinics (Sao Paulo). 2014;69:809---16.

59. Chawla LS, Ince C, Chappell D, Gan TJ, Kellum JA, Mythen M,et al. Vascular content, tone, integrity, and haemodynamicsfor guiding fluid therapy: a conceptual approach. Br J Anaesth.2014;113:748---55.

60. Licker M, Neidhart P, Lustenberger S, Valloton MB, KalonjiT, Fathi M, et al. Long-term angiotensin-converting enzymeinhibitor treatment attenuates adrenergic responsivenesswithout altering hemodynamic control in patients undergoingcardiac surgery. Anesthesiology. 1996;84:789---800.

61. Zhang J, Critchley LA. Inferior vena cava ultrasonographybefore general anesthesia can predict hypotension after induc-tion. Anesthesiology. 2016;124:580---9.

62. Wuethrich PY, Burkhard FC, Thalmann GN, Stueber F,Studer UE. Restrictive deferred hydration combined withpreemptive norepinephrine infusion during radical cystec-tomy reduces postoperative complications and hospitalizationtime: a randomized clinical trial. Anesthesiology. 2014;120:365---77.

63. Gelman S. Is norepinephrine infusion during intraoperativeperiod justified? Anesthesiology. 2014;121:433---4.

64. Salzwedel C, Puig J, Carstens A, Bein B, Molnar Z, Kiss K,et al. Perioperative goal-directed hemodynamic therapy basedon radial arterial pulse pressure variation and continuous car-diac index trending reduces postoperative complications aftermajor abdominal surgery: a multi-center, prospective, ran-domized study. Crit Care. 2013;17:R191.

Document downloaded from http://www.elsevier.es, day 25/05/2017. This copy is for personal use. Any transmission of this document by any media or format is strictly prohibited.

ARTICLE IN PRESS+Model

Fluid therapy recommendations for major abdominal surgery 11

65. Benes J, Chytra I, Altmann P, Hluchy M, Kasal E, Svitak R, et al.Intraoperative fluid optimization using stroke volume variationin high risk surgical patients: results of prospective randomizedstudy. Crit Care. 2010;14:R118.

66. Stens J, de Wolf SP, van der Zwan RJ, Koning NJ, DekkerNA, Hering JP, et al. Microcirculatory perfusion during differ-ent perioperative hemodynamic strategies. Microcirculation.2015;22:267---75.

67. Harrois A, Dupic L, Duranteau J. Targeting the microcirculationin resuscitation of acutely unwell patients. Curr Opin Crit Care.2011;17:303---7.

68. Carlsson M, Andersson R, Bloch KM, Steding-Ehrenborg K,Mosen H, Stahlberg F, et al. Cardiac output and cardiac indexmeasured with cardiovascular magnetic resonance in healthysubjects, elite athletes and patients with congestive heartfailure. J Cardiovasc Magn Reson. 2012;14:51.

69. Steding K, Engblom H, Buhre T, Carlsson M, Mosen H, WohlfartB, et al. Relation between cardiac dimensions and peak oxygenuptake. J Cardiovasc Magn Reson. 2010;12:8.

70. Williams SG, Jackson M, Cooke GA, Barker D, Patwala A, WrightDJ, et al. How do different indicators of cardiac pump functionimpact upon the long-term prognosis of patients with chronicheart failure? Am Heart J. 2005;150:983.

71. Kaess BM, Rong J, Larson MG, Hamburg NM, Vita JA, Levy D,et al. Aortic stiffness, blood pressure progression, and incidenthypertension. JAMA. 2012;308:875---81.

72. Shih H, Lee B, Lee RJ, Boyle AJ. The aging heart and post-infarction left ventricular remodeling. J Am Coll Cardiol.2011;57:9---17.

73. McEniery CM, Yasmin, Hall IR, Qasem A, Wilkinson IB,Cockcroft JR. Normal vascular aging: differential effectson wave reflection and aortic pulse wave velocity: theAnglo-Cardiff Collaborative Trial (ACCT). J Am Coll Cardiol.2005;46:1753---60.

74. Leach RM, Treacher DF. The pulmonary physician andcritical care. 6. Oxygen transport: the relation betweenoxygen delivery and consumption. Thorax. 1992;47:971---8.

75. Vincent JL. Determination of oxygen delivery and consumptionversus cardiac index and oxygen extraction ratio. Crit CareClin. 1996;12:995---1006.

76. Older P. Anaerobic threshold, is it a magic number to determinefitness for surgery? Perioper Med (Lond). 2013;2:2.

77. Older P, Hall A, Hader R. Cardiopulmonary exercise testing as ascreening test for perioperative management of major surgeryin the elderly. Chest. 1999;116:355---62.

78. Pearse R, Dawson D, Fawcett J, Rhodes A, Grounds RM,Bennett ED. Early goal-directed therapy after major surgeryreduces complications and duration of hospital stay. A ran-domised, controlled trial [ISRCTN38797445]. Crit Care. 2005;9:R687---93.

79. Shoemaker WC, Appel PL, Kram HB. Role of oxygen debt in thedevelopment of organ failure sepsis, and death in high-risksurgical patients. Chest. 1992;102:208---15.

80. Bland RD, Shoemaker WC, Abraham E, Cobo JC. Hemo-dynamic and oxygen transport patterns in surviving andnonsurviving postoperative patients. Crit Care Med. 1985;13:85---90.

81. Berlauk JF, Abrams JH, Gilmour IJ, O’Connor SR, KnightonDR, Cerra FB. Preoperative optimization of cardiovascu-lar hemodynamics improves outcome in peripheral vascularsurgery. A prospective, randomized clinical trial. Ann Surg.1991;214:289---97.

82. Shoemaker WC, Appel PL, Waxman K, Schwartz S, Chang P.Clinical trial of survivors’ cardiorespiratory patterns as ther-apeutic goals in critically ill postoperative patients. Crit CareMed. 1982;10:398---403.

83. Lobo SM, Salgado PF, Castillo VG, Borim AA, Polachini CA,Palchetti JC, et al. Effects of maximizing oxygen delivery onmorbidity and mortality in high-risk surgical patients. Crit CareMed. 2000;28:3396---404.

84. Pearse RM, Harrison DA, MacDonald N, Gillies MA, Blunt M,Ackland G, et al. Effect of a perioperative, cardiac output-guided hemodynamic therapy algorithm on outcomes followingmajor gastrointestinal surgery: a randomized clinical trial andsystematic review. JAMA. 2014;311:2181---90.

85. Rhodes A, Cecconi M, Hamilton M, Poloniecki J, Woods J, BoydO, et al. Goal-directed therapy in high-risk surgical patients:a 15-year follow-up study. Intensive Care Med. 2010;36:1327---32.

86. Boyd O, Jackson N. How is risk defined in high-risk surgicalpatient management? Crit Care. 2005;9:390---6.

87. Hayes MA, Timmins AC, Yau EH, Palazzo M, Hinds CJ, WatsonD. Elevation of systemic oxygen delivery in the treatment ofcritically ill patients. N Engl J Med. 1994;330:1717---22.

88. Lobo SM, de Oliveira NE. Clinical review: what are the besthemodynamic targets for noncardiac surgical patients? CritCare. 2013;17:210.

89. Serrano AB, Candela-Toha AM, Zamora J, Vera J, Muriel A,del Rey JM, et al. Preoperative hydration with 0.9% normalsaline to prevent acute kidney injury after major elective openabdominal surgery: a randomised controlled trial. Eur J Anaes-thesiol. 2016;33:436---43.

90. Vallet B, Futier E. Perioperative oxygen therapy and oxygenutilization. Curr Opin Crit Care. 2010;16:359---64.

91. Van Beest P, Wietasch G, Scheeren T, Spronk P, Kuiper M. Clin-ical review: use of venous oxygen saturations as a goal --- a yetunfinished puzzle. Crit Care. 2011;15:232.

92. Collaborative Study Group on Perioperative ScvO2 Monitoring.Multicentre study on peri- and postoperative central venousoxygen saturation in high-risk surgical patients. Crit Care.2006;10:R158.

93. Rady MY, Rivers EP, Martin GB, Smithline H, Appelton T, NowakRM. Continuous central venous oximetry and shock index inthe emergency department: use in the evaluation of clinicalshock. Am J Emerg Med. 1992;10:538---41.

94. Donati A, Loggi S, Preiser JC, Orsetti G, Munch C, Gabbanelli V,et al. Goal-directed intraoperative therapy reduces morbidityand length of hospital stay in high-risk surgical patients. Chest.2007;132:1817---24.

95. Tanczos K, Nemeth M, Molnar Z. The multimodal concept ofhemodynamic stabilization. Front Public Health. 2014;2:34.

96. Pearse RM, Hinds CJ. Should we use central venous saturationto guide management in high-risk surgical patients? Crit Care.2006;10:181.

97. Ripolles-Melchor J, Casans-Frances R, Espinosa A, Abad-Gurumeta A, Feldheiser A, López-Timoneda F, et al.Goal directed hemodynamic therapy based in esophagealDoppler flow parameters: a systematic review, meta-analysisand trial sequential analysis. Rev Esp Anestesiol Reanim.2016;63:384---405.

98. Dalfino L, Giglio MT, Puntillo F, Marucci M, Brienza N.Haemodynamic goal-directed therapy and postoperative infec-tions: earlier is better. A systematic review and meta-analysis.Crit Care. 2011;15:R154.

99. Jhanji S, Vivian-Smith A, Lucena-Amaro S, Watson D,Hinds CJ, Pearse RM. Haemodynamic optimisation improvestissue microvascular flow and oxygenation after majorsurgery: a randomised controlled trial. Crit Care. 2010;14:R151.

100. Arulkumaran N, Corredor C, Hamilton MA, Ball J, GroundsRM, Rhodes A, et al. Cardiac complications associated withgoal-directed therapy in high-risk surgical patients: a meta-analysis. Br J Anaesth. 2014;112:648---59.

Document downloaded from http://www.elsevier.es, day 25/05/2017. This copy is for personal use. Any transmission of this document by any media or format is strictly prohibited.

ARTICLE IN PRESS+Model

12 J. Ripollés-Melchor et al.

101. Renner J, Scholz J, Bein B. Monitoring cardiac function:echocardiography, pulse contour analysis and beyond. BestPract Res Clin Anaesthesiol. 2013;27:187---200.

102. Vincent JL, Pelosi P, Pearse R, Payen D, Perel A, Hoeft A, et al.Perioperative cardiovascular monitoring of high-risk patients:a consensus of 12. Crit Care. 2015;19:224.

103. Wilms H, Mittal A, Haydock MD, van den Heever M, Devaud M,Windsor JA. A systematic review of goal directed fluid therapy:rating of evidence for goals and monitoring methods. J CritCare. 2014;29:204---9.

104. Vincent JL. Measure, interpret, apply --- the MIA rule in criticalcare monitoring. Br J Anaesth. 2016;117:557---8.

Document downloaded from http://www.elsevier.es, day 25/05/2017. This copy is for personal use. Any transmission of this document by any media or format is strictly prohibited.

View publication statsView publication stats