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Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited. C URRENT O PINION Current tools for assessing heart function and perfusion adequacy Sheldon Magder Purpose of review Many devices are currently available for measuring cardiac output and function. Understanding the utility of these devices requires an understanding of the determinants of cardiac output and cardiac function, and the use of these parameters in the management of critica
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  Copyright © Lippincott Williams Wilkins. Unauthorized reproduction of this article is prohibited.   C URRENT O PINION  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 of the 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 orvasoactive 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 thepatient’s 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 INTRODUCTION A primary objective in managing critically illpatientsistoensurethattissueperfusionisadequatefor tissue needs. Failure to do so results in multi-organfailureandpooroutcomes.Itisalsoaxiomaticthat 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, and‘softer’ endpoints have to be used, but there is a lackofconsensusabouttheirworth.Theemphasisofthischapter is on the physiological implications thatcardiac function and output have on the choice of toolsforclinicalassessment.Iwillprimarilydealwiththe haemodynamic measurements, for echocardio-graphy and tissue perfusion are covered in otherchapters; but I will make some comments on howtheseshouldbeconsideredintheoverallevaluation.Mymajorthesis isthatforthe managementoffluidsand shocktheemphasisshouldbeoncardiacoutputitself and not cardiac function, and recent advancesinnoninvasivemeasurementofcardiacoutputmakeuse 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, CanadaCorrespondence to Sheldon Magder, MD, Royal Victoria Hospital, 687Pine Avenue West, Montreal, QC H3A 1A1, Canada. E-mail: Curr Opin Crit Care  2014, 20:294–300DOI:10.1097/MCC.0000000000000100  Volume 20    Number 3    June 2014 REVIEW  Copyright © Lippincott Williams Wilkins. Unauthorized reproduction of this article is prohibited. 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 iswelldescribedbythevolume–pressurerelationshipsoftheventricles(Fig.1).Atafixedheartrate,preloadis given by the ventricular end-diastolic volume–pressure point, afterload is approximated by thepressure at which the ventricular–arterial valveopens after isovolumetric contraction, and con-tractility is related to the slope of the end-systolicpressure–volume line which is the maximumventricular elastance during the cardiac cycle [4].However, volume is not easy to measure accurately,especiallychangingvolumes.Asanalternative,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 thecardiac function curve from the volume–pressurerelationship. 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 shiftthecardiacfunctioncurveupwardsandtheycannotbe distinguished from one another. However, heartrateiseasilymeasuredandsoisachangeinafterloadbased 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 of a change in contractility. Diastolic compliance isdifficult to assess because this requires knowledge of the 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. Withpositivepressureventilationandpositiveend-expir-atory pressure (PEEP), pleural pressure is positive.For this reason, intrathoracic vascular pressuresshould 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-timePV Aorticopening ArterialAtriumVentricular MitralclosureMitralopening123344 (ESV,ESP)(EDV,EDP) 12AorticclosureContractilityPreload“Afterload” Pressure-volume FIGURE 1.  Pressure vs. time (left) and volume–pressure (right) relationships. The numbers indicate events on the pressure–timerelationship and where they are on the volume–pressure plot. In the pressure–time 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 adequacy  Magder 1070-5295    2014 Wolters Kluwer Health | Lippincott Williams & Wilkins  295  Copyright © Lippincott Williams Wilkins. Unauthorized reproduction of this article is prohibited. pressure [6,7]. An increase in pleural pressure orpericardial pressure can raise cardiac pressuresrelative to atmosphere even though the transmuralpressureisdecreased.Thiswilllooklikeadecreaseincardiac function, when in reality the problem isdecreased preload [8]. It is also important to makesure that the measure of preload is made at a fixedreference level, so that a change in preload is not anartefactbecauseofchangeinthetransducerposition[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 areusuallyessentiallythesame,indicatethepreloadforthe heart as a whole and the output from the leftventricle the output from the heart. There are someimportant limitations to the use of the simpleStarlinganalysis.Whencardiacfunctionisdecreased,theanalysisdoesnotindicatewheretheproblemlies.Todoso,onemustknowthepulmonaryarterialandleftatrialpressuresorhavesome othermeasure suchas a chest radiograph or echocardiogram to localizetheproblem.Ontheotherhand,imagingtechniquessuch 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 of the 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 preventsheartmuscle from reaching the downward part of themusclelength–tensionrelationship[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 around10mmHg if the transducer is referenced to 5cmbelow the sternal angle or 12–14mmHg 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. Theheart should only be called ‘dysfunctional’ if theplateau of the function curve occurs with aninadequate cardiac output. I say inadequatebecauseitispossibletohaveapatientwhoisvolumelimitedwith cardiac index of 4.5l/min/m 2 , 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’, VQP Pressure-volume 11223344 Cardiac function curve“Starling curve”Filling pressure(Pra or Pla) Change in preload FIGURE 2.  Derivation of cardiac function from the volume–pressure plot. The ventricular volume–pressure relationship is onthe left and cardiac function curve on the right. The numbers from 1 to 4 indicate increases in preload (volume–pressurepoints). The afterload is constant (dotted line) as is the contractility (end-systolic pressure–volume – 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 296  Volume 20    Number 3    June 2014  Copyright © Lippincott Williams Wilkins. Unauthorized reproduction of this article is prohibited. 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 theplateau 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 inpulmonaryvesselsandproducepulmonaryoedema,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 generaldecreaseincardiacfunction.Thisscenarioshouldbeobvious 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 outputin 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(venousreturncurve)[1 & ,2].Thedeterminantsof venous return are the stressed volume, which isthe 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,andtheoutf lowpressureforvenousdrainage,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 lowerPra and CVP to atmospheric pressure, orin a patienton PEEP, to lower Pra and CVP below the pleuralpressure.Oncethisoccurs,floppyveinscollapseandproduceflow limitation, andfurther lowering of Praand CVP by an increase in cardiac function cannotincrease venous return or cardiac output. Only anincrease in volume or decrease in venous resistancecan 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 bemistakenforadecreaseincardiac function[14].Thetissues see cardiac output and not stroke volume,andsoIalwaysusecardiacoutputratherthanstrokevolume.If cardiac output and Pra and CVP are known,thedependenceofcardiacoutputontheinteractionof pump and return functions provides a simpleguide to the diagnosis and management of shock[1 & ]. Asarterialpressureisdeterminedbythecardiacoutput 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 andCVPindicatesthattheprimaryproblemisadecreasein cardiac function, and low Pra and CVP indicatesthat the primary problem is a decrease in the returnfunction, which most often is inadequate volume.Thisapproachisevenmoreusefulfortrackingtreadsby observing the changes in these variables [1 & ]. IMPLICATIONS OF THE PHYSIOLOGY FOR PROTOCOLS Goal-directed protocols often include reducing vol-ume responsiveness [15 && ]. However, this approachcan lead to excess volume use and recent trials haveshown worse outcomes in patients treated with thisapproach [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. Assessing heart function and perfusion adequacy  Magder 1070-5295    2014 Wolters Kluwer Health | Lippincott Williams & Wilkins  297
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