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Echocardiography as a guide for fluid management Boyd, John H; Sirounis, Demetrios; Maizel, Julien; Slama, Michel Sep 4, 2016

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REVIEW Open AccessEchocardiography as a guide for fluidmanagementJohn H. Boyd1,2,3*, Demetrios Sirounis1,2, Julien Maizel4,5 and Michel Slama4,5AbstractBackground: In critically ill patients at risk for organ failure, the administration of intravenous fluids has equalchances of resulting in benefit or harm. While the intent of intravenous fluid is to increase cardiac output andoxygen delivery, unwelcome results in those patients who do not increase their cardiac output are tissue edema,hypoxemia, and excess mortality. Here we briefly review bedside methods to assess fluid responsiveness, focusingupon the strengths and pitfalls of echocardiography in spontaneously breathing mechanically ventilated patients asa means to guide fluid management. We also provide new data to help clinicians anticipate bedsideechocardiography findings in vasopressor-dependent, volume-resuscitated patients.Objective: To review bedside ultrasound as a method to judge whether additional intravenous fluid will increasecardiac output. Special emphasis is placed on the respiratory effort of the patient.Conclusions: Point-of-care echocardiography has the unique ability to screen for unexpected structural findings whileproviding a quantifiable probability of a patient’s cardiovascular response to fluids. Measuring changes in stroke volumein response to either passive leg raising or changes in thoracic pressure during controlled mechanical ventilation offergood performance characteristics but may be limited by operator skill, arrhythmia, and open lung ventilation strategies.Measuring changes in vena caval diameter induced by controlled mechanical ventilation demands less training of theoperator and performs well during arrythmia. In modern delivery of critical care, however, most patients are nursedawake, even during mechanical ventilation. In patients making respiratory efforts we suggest that ventilator settingsmust be standardized before assessing this promising technology as a guide for fluid management.Keywords: Shock, Point-of-care ultrasound, Echocardiography, ResuscitationBackgroundA routine but challenging task facing acute care physi-cians is to identify and treat patients at risk for acuteorgan failure as a result of inadequate systemic perfusionand oxygen delivery. The decision to administer supple-mental intravenous fluids to the patient at risk is builtupon the belief that additional volume expansion will, orwill not, increase cardiac output. Although there aremany unknowns in a critically ill patient, fundamentalcardiovascular physiology represents a touchstone fromwhich decisions can be made.One important premise is that during the time it takes toadminister bolus intravenous fluid, one can assume a con-stant cardiac contractility. Changes in stroke volume in re-sponse to intravenous fluids are therefore mainlydetermined by changes in ventricular end-diastolic volume.At constant cardiac contractility, the relationship betweenstroke volume and ventricular end-diastolic volume hasbeen classically described by Patterson and Starling [1],Sarnoff and colleagues [2–5], and Guyton and Coleman [6].At low ventricular end-diastolic volume, the stroke volumeincreases briskly with administration of intravenous fluids.This immediately increases both cardiac output and oxygendelivery. Unfortunately, once the patient reaches their plat-eau ventricular end-diastolic volume, further increasingpreload with intravenous fluids will not improve car-diac output and has been shown to result in clinicalharm [7–13]. It is therefore critical that the clinicianuses the best means at their disposal to judge* Correspondence: John.Boyd@hli.ubc.ca1Critical Care Research Laboratories, Centre for Heart Lung Innovation at St.Paul’s Hospital University of British Columbia, 1081 Burrard Street, Vancouver,BC V6Z 1Y6, Canada2Department of Critical Care Medicine, University of British Columbia,Vancouver, BC, CanadaFull list of author information is available at the end of the article© 2016 The Author(s). Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, andreproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link tothe Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver(http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.Boyd et al. Critical Care  (2016) 20:274 DOI 10.1186/s13054-016-1407-1whether additional intravenous fluids will result inbenefit (increased cardiac output, oxygen delivery, andultimate reversal of impending organ failure) [14] orharm (tissue edema, hypoxemia, and excess mortality).While the clinical effect of fluids in a given patientwill be determined through careful examination and anumber of parameters such as reduction in lactate,urine output, and level of consciousness, in the fol-lowing sections when we refer to the presence of“fluid responsiveness” we refer to a measurable in-crease of 15 % in cardiac output.Is the patient on the steep portion of the Starlingcurve?Clinical prediction of fluid responsiveness was firststudied using single measurements of cardiac fillingvolumes (preload). These include the direct measure-ment of right atrial pressure as a surrogate of volume,also referred to as central venous pressure (CVP) andless commonly as the pulmonary capillary wedgepressure, which in ideal situations is synonymous withleft atrial pressure as a surrogate of left ventricularend-diastolic volume. As has been extensivelyreviewed elsewhere, static measures of preload per-form no better than chance in patients who are critic-ally ill. It is now recognized that bedside maneuverswhich rapidly change preload are more discriminativethan static measures. Currently, passive leg raising(PLR) and respiratory variation in thoracic pressureare the two techniques used to vary preload. Within1 minute of bilateral PLR, there is an effective in-crease in preload through recruitment of bloodpooled in the legs [15]. In the patient not on vaso-pressors, an increase in blood pressure suggests thatthe patient will respond to a fluid bolus, whereas inthose on vasoactive medications there is no detectablechange in blood pressure and the output of interest ischange in cardiac output. This technique is thereforebest suited to patients who are not yet on vasopres-sors, with normal intrathoracic pressures (mechanic-ally ventilated patients often fail to augment theirpreload as definitely), and those without significantabdominal pathology.Variation in intrathoracic pressure during tidal breathingis the other cause of varied right or left cardiac preload. Itis important to recognize that the type of respiration (spon-taneous versus controlled) will determine the resultantphysiology. In mechanically ventilated patients with no re-spiratory effort, the positive inspiratory pressure transfersblood from the lungs to the left heart, resulting in an in-crease in stroke volume. This is seen as a rapid increase inpulse pressure. At high levels of positive intrathoracic pres-sure one can also decrease the venous return, and aftertransit of this reduced blood volume from the right to leftheart there can be a decline in pulse pressure. The largerthe fluctuations in pulse pressure as a result of respiration,the greater the chance that the patient will increase cardiacoutput in response to fluid. This method cannot be usedduring arrhythmias such as atrial fibrillation or with veryrapid heart rates.Respiratory changes in intrathoracic pressure alsooccur in the dimensions of both the inferior and super-ior vena cavae. These changes also depend on the degreeof intrathoracic pressure change and on the complianceof the vena cavae. Positive intrathoracic pressure in-creases the size of the inferior vena cava (IVC), whilenegative intrathoracic breaths reduce its size. When thevena cava is distended, the compliance markedly re-duces. A large, nonfluctuant IVC therefore suggests thatthe patient is not on the steep (volume responsive) por-tion of the Starling curve. The IVC diameter is easilyand reproducibly measured 1–2 cm from the right atrialjunction using transthoracic ultrasound [16–21].The patient following initial resuscitationVenous return, central venous pressure, and cardiac out-put are tightly coregulated as described by Patterson andStarling [1], Sarnoff and colleagues [2–5], and Guytonand Coleman [6]. Highly predictable under normal cir-cumstances, the ability to increase cardiac outputthrough augmentations in venous return and centralvenous pressure changes dramatically in the patient whodevelops shock refractory to intravenous fluids. In 2016,standardized protocols dictate that following the recog-nition of nonhemorrhagic shock the patient will rapidlyreceive at least 20 ml/kg fluid [22]. Fifty percent ofpatients [23] do not achieve adequate perfusion withmodest volume expansion and thus require vasopressorsto maintain circulatory tone. In these patients, intraven-ous volume expansion during the first 6–12 hours fol-lowing admission increases dramatically to 50–70 ml/kg[23, 24]. Norepinephrine, the vasopressor of choice inmost circumstances [25], will not only increase arterialblood pressure through increased systemic vascular re-sistance but has a significant effect upon capacitancevessels, both arterial and venous, resulting in effectivefluid loading to the right heart [26]. It is evident that in-fusion of an entire blood volume of new fluid into thecirculation, along with recruitment of circulatory capaci-tance, results in an extreme change to venous return,central venous pressure, and cardiac output.In addition to the direct influence of the cardiovascu-lar system, cardiopulmonary interactions play a crucialrole in establishing the equilibrium of venous return,central venous pressure, and cardiac output. This isbecause 70–90 % of patients with shock require mechan-ical ventilation [25, 27]. In the early phase of resuscita-tion during which patients are sedated to facilitateBoyd et al. Critical Care  (2016) 20:274 Page 2 of 7investigations and treatment, mean airway pressures ofup to 24 cmH2O/18 mmHg [28] have significant but un-predictable effects. These high thoracic pressures causea decline in venous return and/or a functional unloadingof the left ventricle through pressurization of the heartand thoracic aorta.What can the clinician expect to find on clinicalexamination and echocardiography followinginitial volume resuscitation?Central venous pressure in health is tightly governed at 0–5 mmHg [1–6], resulting in an IVC diameter of 13–21 mmwhen supine, and a collapse of more than 50 % upon quietinspiration [16, 17, 19]. In patients who have received thecurrent aggressive early volume expansion we know thenewly established value for central venous pressure will be9–15 mmHg [12, 24]. This change in venous pressure ishighly influential upon the vena caval diameter as measuredby transthoracic echocardiography. In our recentlypublished study into the utility of ultrasound following vol-ume expansion to guide therapy in nonhemorrhagic shock[14] we went back to review the impact of 30 ml/kg intra-venous fluid resuscitation upon the IVC diameter and fluc-tuation. In 110 subjects the IVC diameter followingintravenous volume expansion was increased by 35 % fromnormal values to 17–29 mm. Furthermore, in nearly half(45 %) of the patients there was no variation in diameter ac-cording to respiration. In a further 20 % of patients therewas >0 but <15 % variability (the median cutoff point ofIVC collapse which defines fluid responsiveness). This in-formation may be of utility for the clinician without accessto ultrasound, who may choose to restrict further fluidsbased upon a pretest probability of 0.65 that their fluid-resuscitated patient on vasopressors will not augment car-diac output as a result of further fluids.Summary of what the clinician can expect whenusing central venous pressure and ultrasound toguide fluid therapy in the ventilated critically illpatient following resuscitation for shock1. A central venous pressure of 9–15 mmHg.2. Maximum IVC diameter of 17–29 mmHg3. According to the increase in IVC diameter uponmandated inspiration, 2/3 patients will be deemednonresponsive to fluid.Clinical methods at the bedside to assess volumeresponseUsing ultrasound to monitor stroke volume whileperforming the passive leg raising maneuverPassive leg raising (PLR) is one of the most versatiletechniques to assess fluid needs in ICU patients.PLR can be performed at the bedside in bothmechanically ventilated patients and in spontan-eously breathing patients [15, 29–31]. Meta-analysisof 23 studies with a combined total of 1013 patientsfrom a wide range of clinical settings demonstratedthat the global predictive value of PLR was strong.The test performed very well with a pooled sensitiv-ity of 86 %, specificity of 92 %, and a summaryAUROC of 0.95 [30]. In another meta-analysis, 21studies were analyzed and the pooled correlation be-tween the PLR-induced versus fluid-induced in-creases in cardiac output was 0.76. The pooledsensitivity was 0.85, the pooled specificity was 0.91,and the pooled AUROC was 0.95 [15]. This maneu-ver is easy to perform at the bedside. The patient isplaced in a semirecumbent position with the head ofthe bed 30–45° above the horizontal. The maneuverconsists of rapidly moving the bed to simultaneouslyelevate the lower limbs to 30–45° above the horizon-tal while lowering the head of the bed to 0o (supine).This maneuver transfers blood from the legs and thesplanchnic reservoir to the intrathoracic compart-ment, rapidly increasing the preload, thereby testingthe preload dependency of the heart. Using PLR,250–350 ml of blood is transferred from the legs tothe heart and this method is entirely reversible [30].It is essential that this maneuver should be donefrom the semirecumbent position because this in-creases the blood shift and accentuates the changein cardiac output compared with a supine start [32].Cardiac output changes can be detected 1–2 minutesafter the PLR maneuver using echocardiography [31].It is useful to note that there is a close correlationbetween the changes in cardiac output or stroke vol-ume induced by the PLR and that achieved throughequivalent intravenous volume expansion. In otherwords, the change is not simply a threshold effect,and the greater the increases in cardiac output andstroke volume during PLR, the greater will be theincrease in these parameters after fluid infusion.Arrhythmia should have no effect on the diagnosticperformance because the effect of PLR is measuredover multiple heartbeats and multiple breaths, likelynullifying potential distorting effects of arrhythmiaand spontaneous breathing, respectively [30], but thishas yet to be confirmed by a large prospective studyin this population. The PLR maneuver seemsinaccurate in patients with very significant intra-abdominal hypertension, as demonstrated by Mahjoubet al. [33].Advantages of the passive leg raising maneuver1. PLR can be performed regardless of arrhythmia ormode of ventilation.Boyd et al. Critical Care  (2016) 20:274 Page 3 of 72. The PLR is not simply “positive” versus “negative”;the degree of increase in stroke volume to PLRpredicts the increase in these parameters to fluids.Disadvantages of the passive leg raising maneuver1. The interobserver and intraobserver reliability ofmeasurements in cardiac output is highly operatordependent. A skilled operator is required to achievehigh-quality measures of aortic blood flow.Using ultrasound to monitor stroke volume whilereceiving controlled mechanical ventilationAortic flow variations during mechanical ventilationmay be a superior measure of what is observed clinic-ally as stroke volume variation (SVV), a parametercorrelated with fluid responsiveness [34]. Feissel et al.[35] assessed the variation of the maximal velocityduring the respiratory cycle and found that variationgreater than 12 % accurately predicted fluid respon-siveness of ICU patients. The aortic blood flow is re-corded from an apical five-chamber view using pulsedDoppler imaging. Aortic blood flow variation sharesthe same limitations as pulse pressure variation.These two parameters may be used only in patientswithout arrhythmia and seem invalid in patients withright ventricular dilation or dysfunction [36]. Thepathophysiology of these parameters is based on theeffects of mechanical ventilation, which induces trans-pulmonary and intrathoracic pressure change. Themagnitude of these effects depends mainly on thetransmission of airway pressure variations to theheart. Open chest conditions therefore make all ofthese parameters invalid to assess fluid need. Simi-larly, protective mechanical ventilation (in which alow tidal volume is used to decrease the plateau pres-sure and driving pressure) is now widely used forARDS patients, in whom the low tidal volume de-creases airway pressure variations and may dramatic-ally decrease the hemodynamic effects of mechanicalventilation [37]. De Baker and Scolletta [38] demon-strated that low tidal volume (<8 ml/kg) invalidatesthe cutoff value of 12 % for pulsed pressure variation(PPV) (a surrogate of stroke volume variation). In anattempt to solve this problem, Liu et al. [39] sug-gested estimating pleural pressure variations as a sur-rogate of thoracic pressure variations in ARDSpatients and then adjusting the PPV accordingly in orderto improve prediction and prevent false negatives for fluidresponsiveness. This approach, however, requires measure-ment of esophageal pressure using a balloon catheter, in-creasing the complexity of care, and is therefore usedclinically in a small number of centers.Advantages of measuring aortic blood flow duringmechanical ventilation1. No additional maneuvers are required; standardmechanical ventilation provides the dynamicchanges in preload.Disadvantages of measuring aortic blood flow duringmechanical ventilation1. The interobserver and intraobserver reliability ofmeasurements in cardiac output is highly operatordependent. A skilled operator is required to achievehigh-quality measures of aortic blood flow.2. Not accurate during arrhythmia.3. Of limited utility with “open lung” ventilatorstrategies which reduce pleural pressure swings.Mechanical ventilation induced variations in vena-caval diameterControlled ventilationUnder controlled mechanical ventilation, positive pressureis applied into the thorax. The superior vena cava (SVC) istherefore subjected to this positive pressure during mech-anical insufflation. Vieillard-Baron et al. [40] demon-strated that respiratory variation of the superior vena cavaanalyzed using transesophageal echocardiography accur-ately predicts fluid responsiveness of ICU patients with acutoff value of 36 %. Following this study there was arevolution in ultrasound technology which facilitated aless invasive approach, and in 2016 most clinicians prefertransthoracic echocardiography rather than the trans-esophageal approach to assess the IVC. Multiple studiesanalyzed the IVC in ICU patients under controlled mech-anical ventilation [41–44]. Together these studies demon-strated that, like static measures of central venouspressure, the absolute size of the IVC was not able to ac-curately predict the effect of fluid infusion on cardiac out-put. In contrast, the change in IVC diameter induced byintrathoracic pressure swings during mechanical ventila-tion is useful. Using the ratio between maximal size minusminimum size to the average of these two values, Feisselet al. [43] found that a variation higher than 12 % was as-sociated with an increase of cardiac output after fluid infu-sion. Barbier et al. [41] found that 18 % was the cutoffvalue by using the ratio of the maximal size minus theminimum size to the minimum size. All of these measure-ments were made on M-mode images of a longitudinalview of the IVC obtained from a subcostal window. Intra-abdominal hypertension, the tidal volume, and the pa-tient’s inspiratory efforts in spontaneous breathing may bepossible limitations of this approach [45].Boyd et al. Critical Care  (2016) 20:274 Page 4 of 7Spontaneously breathing patientsFollowing the initial resuscitation, most patients inthe modern era are nursed while awake and are en-couraged to breathe in collaboration with the ventila-tor. This means that in awake, spontaneouslybreathing patients the swings in pleural pressures dur-ing inspiration which are transmitted to the IVC canvary from deeply negative (in those ventilated onCPAP only, as in a spontaneous breathing trial) toneutral/positive in cases with high levels of pressuresupport or neuromuscular weakness. It has recentlybeen shown in healthy volunteers that the change inIVC diameter is highly correlated with respiratory ef-fort [46]. In our center we have found that the degreeof additional pressure support applied in a spontan-eously breathing patient on mechanical ventilationwill dramatically change both the IVC diameter andthe degree of IVC collapse we observe. Figure 1shows IVC tracings in a patient who was firstscanned while they were assisted with pressure sup-port of 8 cmH2O above PEEP. Immediately followingthis scan the patient began a spontaneous breathingtrial with 0 cmH2O additional support. Clearly boththe IVC diameter and fluctuation are highly influ-enced even at modest levels of pressure support. Thisintuitive but under-recognized fact has important im-plications when interpreting the results of an ultra-sound examination in awake patients with the intentof guiding fluid therapy. Reports of changes in IVCdiameter in spontaneously breathing patients havefound that these failed to accurately predict fluid re-sponsiveness. For instance, IVC respiratory variations>42 % in spontaneously breathing patients demonstrated ahigh specificity (97 %) and a positive predictive value (90 %)to predict an increase in CO after fluid infusion with a cut-off value >42 % [47] but a low sensitivity and negative pre-dictive value. A recently published physiology-basedopinion suggests that IVC respiratory variations are in factprone to both false negatives and positives due to five majorcategories: ventilator settings, patient’s inspiratory efforts,lung hyperinflation, cardiac conditions impeding venousreturn, and high intra-abdominal pressures [45].Advantages of measuring vena caval diameter as asurrogate of volume responsiveness during mechanicalventilation1. No additional maneuvers are required; the standardmechanical ventilation provides the dynamicchanges in preload.Fig. 1 A 57-year-old male patient admitted with septic shock 18 hours before imaging required 0.2 μg/kg/minute of norepinephrine to maintaina mean arterial blood pressure of 70 mmHg. Central venous pressure via the right internal jugular catheter was 13 mmHg and he was in atrialfibrillation, rate of 100 beats/minute. Sedation had been discontinued and the patient was awake and spontaneously breathing on a mechanicalventilator. Using a subcostal approach the IVC was imaged using M-mode at 1.5 cm from the IVC–right atrial junction. The patient then began aspontaneous breathing trial, with some translational movement of the IVC noted, and imaging continued. In this case the IVC diameter duringinspiration did not change according to the level of pressure support, whereas the end-expiratory IVC diameters were markedly greater withpositive pressure applied. Thus the delta IVC during usual mechanical ventilation was 29 %, while during his spontaneous breathing trial the deltaIVC was only 11 %. A CardioQ™ esophageal Doppler probe was in place and an optimal descending aortic blood flow was calculated. In thispatient the stroke volume increased from 49 to 65 ml (33 % increase) with a 500 ml bolus of plasmalyte™, and thus was truly volume responsive.IVC inferior vena cava, PEEP positive end-expiratory pressureBoyd et al. Critical Care  (2016) 20:274 Page 5 of 7Disadvantages of measuring vena caval diameter as asurrogate of volume responsiveness during mechanicalventilation1. Of limited utility in controlled modes of ventilationusing “open lung” strategies which reduce pleuralpressure swings.2. In awake patients, the IVC diameter and collapse arehighly dependent upon the patient’s respiratoryeffort and levels of ventilatory support.3. While echocardiography is of great value in thediagnosis of right ventricular failure, more directmeasures of left ventricular performance such asdescending aortic Doppler flow are required in thispopulation.Future directionsLeft ventricular outflow tract obstructionIn a recent study, Chauvet et al. [48] found that 22 % pa-tients in the early phase of septic shock presented withfunctional left ventricular outflow tract obstruction(LVOTO). In most of these patients, fluid infusion de-creased this obstruction, increased cardiac output, andclinically improved the patient [48]. Pending confirm-ation and prospective validation, LVOTO may be con-sidered a new fluid-responsiveness parameter.ConclusionUltrasound imaging of vena caval diameter fluctuationwith respiration is a safe, noninvasive method to assessfluid responsiveness in apneic patients on controlledmechanical ventilation. Two-thirds of patients will not befluid responsive following an initial volume resuscitationof 30 ml/kg. In spontaneously breathing patients thedegree of IVC fluctuation is a function of both respiratoryeffort and the pressure applied to assist ventilation, andwithout standardized ventilator settings it has not beenproven a reliable indicator of fluid responsiveness.AbbreviationsAUROC, area under the receiver operator curve; IVC, inferior vena cava;LVOTO, left ventricular outflow tract obstruction; PLR, passive leg raising;PPV, pulsed pressure variationFundingThis work was supported by the Canadian Institutes of Health Research.Authors’ contributionsAll authors contributed equally to the conception, preparation, analysis andreview of this work. All authors read and approved the final manuscript.Competing interestsThe authors declare that they have no competing interests.Ethics approval and consent to participateAll new (unpublished) patient data presented in this manuscript wereobtained with informed consent under the University of British ColumbiaEthics Protocol H12-01542, which allows for publication of anonymized data.Author details1Critical Care Research Laboratories, Centre for Heart Lung Innovation at St.Paul’s Hospital University of British Columbia, 1081 Burrard Street, Vancouver,BC V6Z 1Y6, Canada. 2Department of Critical Care Medicine, University ofBritish Columbia, Vancouver, BC, Canada. 3Faculty of Medicine, University ofBritish Columbia, Vancouver, BC, Canada. 4Réanimation médicale, CHU Sud,Amiens, France. 5Unité INSERM 1088, UPJV, Amiens, France.References1. Patterson SW, Starling EH. On the mechanical factors which determine theoutput of the ventricles. J Physiol. 1914;48:357–79.2. 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