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CURRENTOPINION Current tools for assessing heart function andperfusion adequacy

Sheldon Magder

Purpose of review

Many devices are currently available for measuring cardiac output and function. Understanding the utilityof these devices requires an understanding of the determinants of cardiac output and cardiac function, andthe use of these parameters in the management of critically ill patients. This review stresses the meaning ofthe physiological measures that are obtained with these devices and how these values can be used.

Recent findings

Evaluation of devices for haemodynamic monitoring can include just measurement of cardiac output, thepotential to track spontaneous changes in cardiac output or changes produced by volume infusions or

vasoactive drugs, or the ability to assess cardiac function. Each of these puts different demands on theneed for accuracy, precision, and reliability of the devices, and thus devices must be evaluated based onthe clinical need.

Summary

Evaluation of cardiac function is useful when first dealing with an unstable patient, but for ongoingmanagement measurement of cardiac output itself is key and even more so the trend in relationship to thepatients overall condition. This evaluation would be greatly benefited by the addition of objectivemeasures of tissue perfusion.

Keywords

cardiac output, central venous pressure, right atrial pressure, stressed volume, venous return

INTRODUCTIONA primary objective in managing critically illpatients is to ensure that tissue perfusion is adequatefor tissue needs. Failure to do so results in multi-organ failure and poor outcomes. It is also axiomaticthat adequate output from the heart is needed toprovide appropriate blood flow to tissues. This inturn requires adequate cardiac function to producethe necessary cardiac output and adequate functionof the return of blood to the heart [1

&

,2]. There aremany new and old tools that assess the componentsof these seemingly obvious statements [3

&&

]. How-

ever, each technology answers different questionsand one needs to consider the clinical requirement.The real value of these tools can only be establishedby outcome studies, but these are difficult to do andcurrently there are few properly powered prospec-tive studies. An important study design problem isthat mortality is low in many common clinicalconditions, such as complex surgical patients, andsofter endpoints have to be used, but there is a lackof consensus about their worth. The emphasis of thischapter is on the physiological implications thatcardiac function and output have on the choice of

tools forclinical assessment. I will primarily deal withthe haemodynamic measurements, for echocardio-graphy and tissue perfusion are covered in otherchapters; but I will make some comments on howthese should be considered in the overall evaluation.My major thesis is that for the management of fluidsand shock the emphasis should be on cardiac outputitself and not cardiac function, and recent advancesin noninvasive measurement of cardiac output makeuse of this measure more feasible.

THE TERMS

Cardiac output is the product of heart rate andstroke volume. Stroke volume is determined by pre-load, the pressure (force) that gives the final stretch

Department of Critical Care Medicine, McGill University Health Centre,

Montreal, Quebec, Canada

Correspondence to Sheldon Magder, MD, Royal Victoria Hospital, 687

Pine Avenue West, Montreal, QC H3A 1A1, Canada. E-mail:sheldon.

[email protected]

Curr Opin Crit Care 2014, 20:294300

DOI:10.1097/MCC.0000000000000100

www.co-criticalcare.com Volume 20 Number 3 June 2014

REVIEW
mailto:[email protected]:[email protected]:[email protected]:[email protected]



to myofibres before the onset of contraction; after-load, the load that shortening muscle faces after itbegins to contract; and contractility, which is basedon the extent and velocity of muscle shortening fora given preload and afterload. Cardiac function iswell described by the volume pressure relationshipsof the ventricles (Fig. 1). At a fixed heart rate, preloadis given by the ventricular end-diastolic volumepressure point, afterload is approximated by thepressure at which the ventriculararterial valveopens after isovolumetric contraction, and con-

tractility is related to the slope of the end-systolicpressurevolume line which is the maximum

ventricular elastance during the cardiac cycle [4].However, volume is not easy to measure accurately,especially changing volumes. As an alternative, Star-ling [5]at the turn of the century assessed cardiacfunction with a plot of cardiac output at differentpreloads and constant heart rate, afterload, andcontractility. Figure 2 gives the derivation of the

cardiac function curve from the volumepressurerelationship. If cardiac output is measured, this plotcan be used to determine where the heart is on thecardiac function curve. An increase in heart rate,decrease in afterload, increase in contractility, orincrease in ventricular diastolic compliance all shiftthe cardiac function curve upwards and they cannotbe distinguished from one another. However, heartrate is easily measured and so is a change in afterloadbased on the changes in arterial pressure. If thesehave not changed, and it is thought that diastoliccompliance did not change, a change in cardiacoutput for a given preload must be because ofa change in contractility. Diastolic compliance isdifficult to assess because this requires knowledge ofthe pressure across the ventricular wall. Standardpressure measurements are made relative to atmos-pheric pressure, but the pressure outside the heartis pleural and not atmospheric pressure. At endexpiration of a spontaneous breath, pleural pressureis slightly below the atmospheric pressure andbecomes more negative during inspiration. Withpositive pressure ventilation and positive end-expir-atory pressure (PEEP), pleural pressure is positive.For this reason, intrathoracic vascular pressures

should always be made at end expiration, whichis when pleural pressure is closest to atmospheric

KEY POINTS

Cardiac function needs to be distinguished fromcardiac output.

A reliable measure of cardiac output combined with acentral venous pressure is the useful measure for theinitial diagnostic evaluation and response to therapy.

Trends in cardiac output generally are more useful thansingle measures, especially when predicting whether toinfuse volume or use vasoactive drugs.

A responsive protocol rather than goal-directedprotocol may reduce the amount of unnecessaryinterventions.

Reliability of devices that measure cardiac outputincreases with the degree of invasiveness and thusmore invasive devices still should be considered for themost unstable patients.

Pressure-time

P

V

Aortic

opening

Arterial

Atrium

Ventricular

Mitral

closure

Mitral

opening

1

2

3

3

4

4

(ESV,ESP)

(EDV,EDP)

1

2

Aortic

closure

Contractility

Preload

Afterload

Pressure-volume

FIGURE 1.Pressure vs. time (left) and volumepressure (right) relationships. The numbers indicate events on the pressuretimerelationship and where they are on the volumepressure plot. In the pressuretime plot, the dotted line is arterial pressure,dark grey line is atrial pressure, and the solid light grey line is ventricular pressure. The passive-filling curve is given by theplot of end-diastolic volume (EDV) and end-diastolic pressure (EDP); note the steep break in this curve. Contractility isrepresented by the line representing end-systolic volume (ESV) and end-systolic pressure (ESP).

Assessing heart function and perfusion adequacyMagder

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pressure [6,7]. An increase in pleural pressure orpericardial pressure can raise cardiac pressuresrelative to atmosphere even though the transmuralpressure is decreased. This will look like a decrease incardiac function, when in reality the problem isdecreased preload[8]. It is also important to makesure that the measure of preload is made at a fixed

reference level, so that a change in preload is not anartefact because of change in the transducer position[9,10].

The cardiac function curve treats the right andleft ventricles and the pulmonary arteries and veinsas a single unit. Under steady-state conditions, thisis not a problem for left and right ventricularoutputs must be the same. The right atrial pressure(Pra) or central venous pressure (CVP), for they areusually essentially the same, indicate the preload forthe heart as a whole and the output from the leftventricle the output from the heart. There are some

important limitations to the use of the simpleStarling analysis. When cardiac function is decreased,the analysis does not indicate where the problem lies.To do so, one must know the pulmonary arterial andleft atrial pressures or have some other measure suchas a chest radiograph or echocardiogram to localizethe problem. On the other hand, imaging techniquessuch as echocardiography or magnetic resonancehave a narrower perspective on function and aremore weighted to assessing cardiac contractility byexamining volumes, velocity of shortening, and theejection fraction.

Right heart limitation is common in the ICU,especially after cardiac surgery and in septicpatients. I use the broader term limitation ratherthan dysfunction. Everyone has a limit to diastolicfilling of their ventricles, which occurs because ofthe steep portion of the ventricular passive-fillingcurve (Fig. 1). This limit normally is because of

restraint by the pericardium, but even without apericardium the cardiac cytoskeleton prevents heartmuscle from reaching the downward part of themuscle length tension relationship [11]. Limitationto filling of the right heart occurs at much lowerfilling pressures than that of the left heart. In mostpeople, this occurs at a Pra or CVP of around10 mmHg if the transducer is referenced to 5 cmbelow the sternal angle or 1214 mmHg if refer-enced to the mid-axillary line [12]. Importantly,protocols that aim to eliminate volume responsive-ness do so by creating right heart limitation. The

heart should only be called dysfunctional if theplateau of the function curve occurs with aninadequate cardiac output. I say inadequate becauseit is possible to have a patient who is volume limitedwith cardiac index of 4.5 l/min/m2, but is markedlyhypotensive because of a low vascular resistance.

When right ventricular limitation is present,signs of underfilling of the left heart, such as alow pulmonary artery occlusion pressure or a smallhypercontractile ventricle on echocardiography,cannot be corrected by giving volume. There isno left-sided success without right-sided success,

V

QP

Pressure-volume

1

12

2

3

3

4

4

Cardiac function curve

Starling curve

Filling pressure

(Pra or Pla)

Change in preload

FIGURE 2. Derivation of cardiac function from the volumepressure plot. The ventricular volumepressure relationship is on

the left and cardiac function curve on the right. The numbers from 1 to 4 indicate increases in preload (volumepressurepoints). The afterload is constant (dotted line) as is the contractility (end-systolic pressurevolume solid line). Increasingpreload increases cardiac output on the function curve until a plateau is reached, which is because of the steep part of thediastolic-filling curve.

Cardiopulmonary monitoring

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and only an increase in cardiac function canincrease the output when there is right heart limita-tion.

Although end-diastolic volume (EDV) is linearlyrelated to stroke volume, whereas the Pra and CVPrelationship is curvilinearly related, Pra and CVP isthe better measure to follow. This is because the

plateau of the cardiac function curve can be recog-nized by an increase in Pra and CVP without achange in cardiac output, but not with a volumemeasurement because volume does not change. Onechocardiography, volume limitation is only appa-rent when there is an observable distortion of theright ventricle, which is after the fact. Right ven-tricular limitation also limits the usefulness of totalintrathoracic blood volume measurements, for thevolume outside the right heart is irrelevant for thedetermination of cardiac output.

The cardiac function curve is less helpful whenthere is a pure left heart problem, for the right heartcan maintain a low Pra and CVP and normal cardiacoutput whilst left-sided filling pressure is very high.Initially, the imbalance only moderately decreasesthe cardiac output because output only falls whenPra and CVP increases and venous return decreases.For this to happen, volume must accumulate inpulmonary vessels and produce pulmonary oedema,and the patient essentially drowns from the con-tinued success of the right ventricle without leftventricular success. When severe hypoxaemia andhypercarbia eventually develop, there is a generaldecrease in cardiac function. This scenario should be

obvious by the presence of pulmonary oedema onthe chest radiograph. It occurs more often in cor-onary care units than in general ICUs, and was therationale for the development of the flow-directedpulmonary artery catheter by Swan and Ganz[13].

So far, I have considered cardiac output in termsof the cardiac function curve, but as described byArthur Guyton, cardiac output itself is determinedby the interaction of cardiac function and by afunction that defines the return of blood to theheart (venous return curve) [1

&

,2]. The determinantsof venous return are the stressed volume, which is

the blood volume that actually distends the vascu-lature, the compliance of small venules and veinswhich contain the greatest percentage of bloodvolume, resistance in the veins draining this region,and the outflow pressure for venous drainage, whichis Pra/CVP [1

&

]. An increase in stressed volume,decrease in venous compliance (which is unusual),or decrease in venous resistance increase venousreturn. In this analysis, the heart regulates cardiacoutput by regulating Pra and CVP, and thus howmuch blood comes back and not by regulatingarterial pressure. The best the heart can do is lower

Pra and CVP to atmospheric pressure, or in a patienton PEEP, to lower Pra and CVP below the pleuralpressure. Once this occurs, floppy veins collapse andproduce flow limitation, and further lowering of Praand CVP by an increase in cardiac function cannotincrease venous return or cardiac output. Only anincrease in volume or decrease in venous resistance

can alter the cardiac output. When venous return islimited, cardiac output does not increase withincreasing cardiac function and an increase in heartrate will decrease the stroke volume. This can bemistaken for a decrease in cardiac function [14]. Thetissues see cardiac output and not stroke volume,and so I always use cardiac output rather than strokevolume.

If cardiac output and Pra and CVP are known,the dependence of cardiac output on the interactionof pump and return functions provides a simpleguide to the diagnosis and management of shock[1

&

]. As arterial pressure is determined by the cardiacoutput and systemic vascular resistance, a low arte-rial pressure must be due to either a decrease incardiac output or a decrease in systemic vascularresistance. As resistance is calculated from cardiacoutput and blood pressure, the question becomeswhat is the cardiac output? If cardiac output isnormal or elevated, the problem is a decrease insystemic vascular resistance as, for example, septicshock. If the cardiac output is decreased, the nextquestion is what is the Pra and CVP? A high Pra andCVP indicates that the primary problem is a decreasein cardiac function, and low Pra and CVP indicates

that the primary problem is a decrease in the returnfunction, which most often is inadequate volume.This approach is even more useful for tracking treadsby observing the changes in these variables [1

&

].

IMPLICATIONS OF THE PHYSIOLOGY FOR

PROTOCOLS

Goal-directed protocolsoften include reducing vol-ume responsiveness [15

&&

]. However, this approachcan lead to excess volume use and recent trials haveshown worse outcomes in patients treated with this

approach [16,17&&

]. Importantly, volume respon-siveness does not mean volume need. I preferinstead, what I call a responsive treatment algor-ithm for managing fluids. In this approach, volumeis given based on the trigger values such as cardiacindex, blood pressure, CVP, and urine output. Aftera volume bolus is given, the change in cardiacoutput and Pra and CVP are assessed. If cardiacoutput improves but does not correct the triggervalue, further boluses can be given. If the bolus failsto increase Pra and CVP and does not increasecardiac output, something else should be done.





We recently successfully implemented such anapproach in a study on postcardiac surgery [18

&

,19&

].Oxygen delivery is based on the product of

cardiac output, haemoglobin concentration, andarterial oxygen saturation. Gains from increasinghaemoglobin and oxygen saturation usually aresmall, so that cardiac output is the primary variable

that can be manipulated to increase the deliveryof oxygen.Furthermore, in the supine position, reserves in

EDV are small, and unless there has been a majorvolume loss, the benefits from giving volume are notlarge [20]. When a patient is right ventricular lim-ited, giving nonblood solutions actually decreasesoxygen delivery by diluting the haemoglobin con-centration and only an increase in cardiac functioncan increase oxygen delivery.

CENTRAL ROLE OF CARDIAC OUTPUT

Even though I have argued that a cardiac outputmeasurement is central in the management of hae-modynamic problems, it too is not sufficient andmust be evaluated in the clinical context. Forexample, septic patients have high cardiac outputs,yet have signs of inadequate oxygen i n t issues. Someassessment of tissue perfusion [21,22

&&

] thus isnecessary to provide a calibration of the appropri-ateness of the measured cardiac output. This can beas simple as observing the level of wakefulness andresponsiveness, but most often mental status isaltered by the underlying disease or drugs and is

not a useful guide to tissue perfusion. The kidney is asensitive monitor of the adequacy of tissue per-fusion, but renal function, too, often is directlyaltered by the underlying disease. When present,acrocyanosis and cool clammy skin indicateinadequate tissue perfusion, but likely are not sen-sitive indicators. Although lactate rises with somedelay after the reduction of tissue perfusion, it is akey indicator of inadequate tissue perfusion [23] andlactate clearance is a good guide to the efficacy oftherapy [2426]. Central or mixed venous satur-ation provide useful information about the tissue

utilization of oxygen, but excess reliance on this cancause problems [27]. For example, giving fluidboluses on the basis of low central venous saturationcan paradoxically lower central venous oxygen if thefluid fails to increase cardiac output and just dilutesthe haemoglobin. Very high central venous satur-ations are actually a bad sign[26,28]. What are notuseful guides to tissue perfusion are heart rate andblood pressure.

Techniques are evolving to assess peripheral per-fusion, including direct visualization of the micro-vasculature, continuous transcutaneous oxygen and

carbon dioxide tension, near-infrared spectroscopy,and a peripheral perfusion index derived from thepulse-oximetry signal [22

&&

,29,30,31&&

]. These are dis-cussed in another chapter, but a few limitations needto be discussed. It must be known how perfusion ofthe vascular bed being studied compares to that ofvital organs such as the brain, heart, and kidney as

well as other tissues. It appears that the peripheralvessels and the gastrointestinal vasculature behavesimilarly but differently from vital organs [22

&&

,30].Decreased perfusion of these tissues predicts pooroutcome, but this does not mean that they shouldbe used as the targets for resuscitation, for perhapsthey are just markers and targeting them will lead tooverresuscitation. Furthermore, flow in the micro-circulation does not mean that there is actualnutrient exchange.

A recent systematic review examined the evi-dence and goals of methods for monitoring goal-directed fluid therapy [3

&&

]. Central venous lactateand stroke volume index had the highest quality ofevidence; cardiac output was only moderate. How-ever, this only indicatesthe status of current evidenceand the lack of evidence does not mean that othermeasures are not useful. The most important con-clusion was that there is scant high-quality evi-dence.

CONSIDERATIONS IN THE USE OF

MONITORING TOOLS

Issues that need to be considered when choosing

tools for cardiac parameters include the following: Isthe purpose to assess cardiac function or output? Is asingle measure needed for diagnosis or trends? Hasthe reliability of trends been evaluated properly[32,33

&&

]? What is the inaccuracy, imprecision,and bias of the device [34]? What is the ease ofuse? What is the cost? What are the risks and harm?

Echocardiography can be used to evaluate rightand left heart function, and thus has an importantdiagnosticrole.IntheICU,oesophagealechocardiog-raphy is usually more dependable than the trans-thoracic approach, but is no longer completely

noninvasive. Cardiac output can be measured andused to differentiate a primary resistance problemfrom a cardiac output problem, but most oftencardiac output is not obtained and it is not clearin what percentage of patients this can be doneaccurately. Probes also rarely are left in place toallow a responsive approach, for they are expens-ive and fragile. Without pressure measurements, itis difficult to know wherethe heart is on its functioncurve.

Thermodilution techniques, whether acrossthe right heart or transpulmonary, give accurate





and relatively calibrated measurements of cardiacoutput when less-invasive techniques cannot, suchas in aortic insufficiency [35]. As a central venouscatheter is needed, Pra and CVP can be measuredand cardiac function assessed. If the catheter is inthe pulmonary artery, right and left heart functionscan be assessed. The price paid is increased risk, even

with transpulmonary methods, for a femoral orbrachial arterial line is needed. Continuous measure-ments can be obtained with some devices includingmixed venous saturation, but the measurements areout of phase with real time because of averagingfunctions in the algorithms[36], and normal fluctu-ations in mixed venous saturations sometimes makethe treating team overreact.

Oesophageal Doppler provides a visual signalwhich gives it a quasi calibration. It has a low biasand high clinical agreement with the pulmonaryartery catheter [37], and its usefulness has beenshown in many studies [3840]. Limitations are thatit requires skill to place it and interpret the signals. Itcan be left in place, but often has to be adjusted. Itcannot be used easily in nonintubated patients. Asnoted above, right ventricular limitation can com-plicate the interpretation.

Devices that derive cardiac output from thearterial waveform have the advantage of being lessinvasive and give a continuous measure, but theycannot be calibrated so that they are generally lessreliable and accurate than thermodilution methods[35,41]. Depending on the conditions and algor-ithms, their precision and bias may change with

changes in vascular resistance[4144].Devices that rely on changes in impedance or

plethysmography have the advantage of being com-pletely noninvasive and can be rapidly applied toalmost all patients. Unfortunately, their accuracy islimited in shock conditions [4547] and theyshould be reserved for managing fluids in relativelystable patients.

CONCLUSION

Assessment of cardiac function is important for

diagnosis, but cardiac output itself is the importantmeasure for ongoing management of haemody-namic problems. Measurement of cardiac outputhas become increasingly possible to obtain withnewer technologies, but reliability decreases the lessinvasive the device is. However, less-invasive devicesmay have a place in lower risk situations if they canreliably indicate the response to a fluid bolus, asmanagement of fluids remains a difficult clinicaldecision. Addition of a Pra and CVP measurementhelps separate primarily cardiac problems fromvenous return problems. Cardiac output values need

to be put in the context of signs or measures of tissueperfusion and a complete management plan mustintegrate all these measures.

Acknowledgements

None.

Conflicts of interestThe author has no conflicts of interest to declare inrelation to this study.

REFERENCES AND RECOMMENDED

READINGPapers of particular interest, published within the annual period of review, havebeen highlighted as:& of special interest&& of outstanding interest

1.

&

Magder S. An approach to hemodynamic monitoring: Guyton at the bedside.Crit Care 2012; 16:236243.

This study presents the use of Pra and CVP with a measurement of cardiac output

for the management of haemodynamic abnormalities.2. Guyton AC. Determination of cardiac output by equating venous return curves

with cardiac response curves. Physiol Rev 1955; 35:123129.3.

&&

Wilms H, Mittal A, Haydock MD, et al. A systematic review of goal directedfluid therapy: rating of evidence forgoals andmonitoring methods. J Crit Care2014; 29:204209.

The authors review an extensive number of studies looking for evidence that ameasure was associated with an outcome measure. The major limitations are thatclinical efficacy of the measure is not assessed and the power of studies todetermine a benefit is not evaluated.4. Sagawa K. The ventricular pressurevolume diagram revisited. Circ Res

1978; 43:677687.5. Starling EH. The Linacre Lecture of the law of the heart. London: Longmans,

Green & Co; 1918.6. Magder S. Hemodynamic monitoring in the mechanically ventilated patient.

Curr Opin Crit Care 2011; 17:3642.7. Magder S. Invasive intravascular hemodynamic monitoring: technical issues.

Crit Care Clin 2007; 23:401414.

8. Marini JJ, Culver BH, Butler J. Mechanical effect of lung distention withpositive pressure on cardiac function. Am Rev Respir Dis 1981; 124:382386.

9. Magder S. Central venous pressure: a useful but not so simple measurement.Crit Care Med 2006; 34:22242227.

10. Magder S. Is all on the level? Hemodynamics during supine versus proneventilation. Am J Respir Crit Care Med 2013; 188:13901391.

11. Katz AM. Ernest Henry Starling, his predecessors, and the Law of the Heart.Circulation 2002; 106:29862992.

12. Magder S, Bafaqeeh F. The clinical role of central venous pressure measure-ments. J Intensive Care Med 2007; 22:4451.

13. Forrester JS, Diamond G, McHugh TJ, Swan HJ. Filling pressures in theright and left sides of the heart in acute myocardial infarction. A reappraisalof central-venous-pressure monitoring. N Engl J Med 1971; 285:190193.

14. Magder SA. The ups and downs of heart rate. Crit Care Med 2012; 40:239245.

15.

&&

Lobo SM, de Oliveira NE. Clinical review: what are the best hemodynamictargets for noncardiac surgical patients? Crit Care 2013; 17:210. [Epubahead of print]

A comprehensive review of the measures used for goal-directed management innonsurgical management.16. Lobo SM, Lobo FR, Polachini CA, et al. Prospective, randomized trial

comparing fluids and dobutamine optimization of oxygen delivery in high-risksurgical patients [ISRCTN42445141]. Crit Care 2006; 10:R72.

17.

&&

Challand C, Struthers R, Sneyd JR, et al. Randomized controlled trial ofintraoperative goal-directed fluid therapy in aerobically fit and unfit patientshaving major colorectal surgery. Br J Anaesth 2012; 108:5362.

An example of a study which showedthat optimizing strokevolume didnot improveoutcome, and led to more fluid use and detrimental effects in the aerobically fitsubgroup.18.

&

Magder S, Potter BJ, Varennes BD, et al.Fluids after cardiac surgery: a pilotstudy of the use of colloids versus crystalloids. Crit Care Med 2010;38:21172124.

An example of a responsive protocol that used Pra and CVP and cardiac outputfor the management of fluids in patients after cardiac surgery.





19.

&

PotterBJ, DeverenneB, Doucette S, et al. Cardiac outputresponses in a flow-driven protocol of resuscitation following cardiac surgery. J Crit Care 2013;28:265269.

A detailed analysis of the haemodynamic changes in response to fluids in Ref.[18

&

].20. Magder SA, Daughters GT, Hung J,et al.Adaptation of human left ventricular

volumes to the onset of supine exercise. Eur J Appl Physiol 1987; 56:467473.

21. LimaA, JansenTC, van Bommel J, et al. Theprognostic value of thesubjectiveassessment of peripheral perfusion in critically ill patients. Crit Care Med2009; 37:934938.

22.

&& Donati A, Tibboel D, Ince C. Towards integrative physiological monitoring ofthe critically ill: from cardiovascular to microcirculatory and cellular functionmonitoring at the bedside. Crit Care 2013; 17 (Suppl. 1):S5.

This study reviews the use of monitoring measures of microcirculatory and cellfunction in critically ill patients.23. Jansen TC, van Bommel J, Woodward R, et al. Association between blood

lactate levels, sequential organ failure assessment subscores, and 28-daymortality during early and late intensive care unit stay: a retrospectiveobservational study. Crit Care Med 2009; 37:23692374.

24. Bakker J, de Lima AP. Increased blood lactate levels: an important warningsignal in surgical practice. Crit Care 2004; 8:9698.

25. Jansen TC, van Bommel J, Schoonderbeek FJ, et al. Early lactate-guidedtherapy in intensive care unit patients: a multicenter, open-label, randomizedcontrolled trial. Am J Respir Crit Care Med 2010; 182:752761.

26. Rivers EP, Ander DS, Powell D. Central venous oxygen saturationmonitoring in the critically ill patient. Curr Opin Crit Care 2001; 7:204211.

27. Gattinoni L, Brazzi L, Pelosi P, et al. A trial of goal-oriented hemodynamictherapy in criticallyill patients. SvO2 Collaborative Group.N Engl J Med1995;

333:10251032.28. Perz S, Uhlig T, Kohl M, et al. Low and supranormal central venous

oxygen saturation and markers of tissue hypoxia in cardiac surgerypatients: a prospective observational study. Intensive Care Med 2011;37:5259.

29. Lima A, van Bommel J, Sikorska K,et al.The relation of near-infrared spectro-scopy with changes in peripheral circulation in critically ill patients. Crit CareMed 2011; 39:16491654.

30. Lima A, Bakker J. Clinical monitoring of peripheral perfusion: there is more tolearn. Crit Care 2014; 18:113.

31.

&&

He HW, Liu DW, Long Y, Wang XT. The peripheral perfusion index andtranscutaneous oxygen challenge test are predictive of mortality in septicpatients after resuscitation. Crit Care 2013; 17:R116.

The authors show that these tools predicted mortality which is an important firststep. However, this does not mean that targeting these measures improves theoutcome. Furthermore, central lactate wasequally effective as a predictorand a lotsimpler to obtain.32. CritchleyLA, Yang XX,Lee A. Assessment of trending ability of cardiacoutput

monitors by polar plot methodology. J Cardiothorac Vasc Anesth 2011;25:536546.

33.

&&

Critchley LA, Lee A, Ho AM. A critical review of the ability of continuouscardiac output monitors to measure trends in cardiac output. Anesth Analg2010; 111:11801192.

This study lays out the methodology for use of polar plots to evaluation of trends incontinuous measurements of cardiac output and applies it to the previous pub-lications evaluating this technology.34. Chatburn RobertL. Principlesof measurement. In: TobinMJ, editor. Principles

and practice of intensive care monitoring. New York: McGraw-Hill, Inc; 1997.pp. 4561.

35. Petzoldt M, Riedel C, Braeunig J, et al. Stroke volume determination usingtranscardiopulmonary thermodilution and arterial pulse contour analysis in

severe aortic valve disease. Intensive Care Med 2013; 39:601611.36. Fischer MO, Balaire X, Le Mauff de KC, et al. The diagnostic accuracy ofestimated continuous cardiac output compared with transthoracic echocar-diography. Can J Anaesth 2014; 61:1926.

37. Dark PM,SingerM. The validity of trans-esophageal Dopplerultrasonographyas a measure of cardiac outputin criticallyill adults. IntensiveCare Med2004;30:20602066.

38. Bundgaard-Nielsen M, Holte K, Secher NH, Kehlet H. Monitoring of peri-operative fluid administration by individualized goal-directed therapy. ActaAnaesthesiol Scand 2007; 51:331340.

39. Abbas SM, Hill AG. Systematic review of the literature for the use ofoesophageal Doppler monitor for fluid replacement in major abdominalsurgery. Anaesthesia 2008; 63:4451.

40. Walsh SR, Tang T, Bass S, Gaunt ME. Doppler-guided intra-operative fluidmanagement during major abdominal surgery: systematic review and meta-analysis. Int J Clin Pract 2008; 62:466470.

41. MonnetX, AnguelN, NaudinB, et al. Arterial pressure-based cardiac outputinsepticpatients:differentaccuracy of pulse contour and uncalibrated pressurewaveform devices. Crit Care 2010; 14:R109.

42. Meng L, Tran NP,Alexander BS,et al. The impact of phenylephrine, ephedrine,and increased preload on third-generation Vigileo-FloTrac and esophagealDoppler cardiac output measurements. Anesth Analg 2011; 113:751757.

43. Fischer MO,Pelissier A, Bohadana D, et al. Predictionof responsiveness to anintravenous fluid challenge in patients after cardiac surgery with cardiopul-monary bypass: a comparison between arterial pulse pressure variation anddigital plethysmographic variability index. J Cardiothorac Vasc Anesth 2013;27:10871093.

44. Monnet X, Anguel N, Jozwiak M, et al.Third-generation FloTrac/Vigileo doesnot reliably track changes in cardiac output induced by norepinephrine incritically ill patients. Br J Anaesth 2012; 108:615622.

45. Kupersztych-Hagege E, TeboulJL, Artigas A, et al. Bioreactance is not reliablefor estimating cardiac output and the effects of passive leg raising in criticallyill patients. Br J Anaesth 2013; 111:961966.

46. Taton O, Fagnoul D, De BD,VincentJL. Evaluation of cardiac output in intensivecare using a noninvasive arterial pulse contour technique (Nexfin((1))) com-pared with echocardiography. Anaesthesia 2013; 68:917923.

47. Fischer MO, Coucoravas J, Truong J, et al.Assessment of changes in cardiac

index and fluid responsiveness: a comparison of Nexfin and transpulmonarythermodilution. Acta Anaesthesiol Scand 2013; 57:704712.



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