Hemodynamic Assessmentin the Contemporary

Intensive Care UnitA Review of Circulatory Monitoring Devices

Mohamad Kenaan, MDa,*, Mithil Gajera, MDb,Sascha N. Goonewardena, MDa

KEYWORDS

� Hemodynamic � Circulatory � Monitoring � Critically ill � Intensive care unit

KEY POINTS

� The ideal circulatory monitoring system would be noninvasive, cost-effective and easy touse.

� As understanding of hemodynamics and critical illness has evolved, more sophisticatedcirculatory monitoring technologies have been developed.

� The primary hemodynamic goal in the management of critically ill patients includes theassessment and manipulation of the circulatory system to ensure adequate tissue deliveryof oxygen and essential metabolic substrates.

� Current monitoring devices should continue to be selected on a patient-specific basis,either alone or in combination with other hemodynamic monitors, until the gold standardhemodynamic monitoring tool is developed.

INTRODUCTION

The primary hemodynamic goal in the management of critically ill patients includes theassessment and manipulation of the circulatory system to ensure adequate tissue de-livery of oxygen and essential metabolic substrates. Goals of optimization of the circu-latory system in the ICU have met with mixed results. Traditional methods to assessthe circulatory system can sometimes be inadequate, particularly in the early stagesof shock when compensatory mechanisms may cloud the presentation.1,2

a Division of Cardiovascular Medicine, Department of Internal Medicine, University ofMichigan Medical Center, 1500 East Medical Center Drive, Ann Arbor, MI 48109, USA;b Department of Internal Medicine, Christiana Care Health System, 4755 Ogletown-StantonRoad, Newark, DE 19718, USA* Corresponding author. Division of Cardiovascular Medicine, University of Michigan Cardio-vascular Center, 2381 Cardiovascular Center Spc 5853, 1500 East Medical Center Drive, AnnArbor, MI 48109.E-mail address: mkenaan@med.umich.edu

Crit Care Clin 30 (2014) 413–445http://dx.doi.org/10.1016/j.ccc.2014.03.007 criticalcare.theclinics.com0749-0704/14/$ – see front matter � 2014 Elsevier Inc. All rights reserved.

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As the understanding of hemodynamics and critical illness has evolved, more so-phisticated circulatory monitoring technologies have been developed, including pul-monary artery catheterization (PAC). The introduction of PAC was accompaniedwith great optimism; unfortunately, clinical studies have failed to show a consistentbenefit with routine use of PAC in the ICU. Because of the belief that PAC was inad-equate because of technical problems in interpretation and complications associatedwith its use, a new wave of noninvasive modalities were developed. Traditionalmethods continue to have a role in assessing critically ill patients but newer technol-ogies have greatly expanded circulatory monitoring systems.The ideal circulatory monitoring system would be noninvasive, cost-effective, and

easy to use. Although such a system remains elusive, several circulatory monitorspossess a combination of these characteristics. This article reviews the mostcommonly available technologies and their underlying physiologic principles as wellas their strengths and limitations in the assessment of critically ill patients.

CLINICAL METHODS FOR HEMODYNAMIC ASSESSMENT

Detailed physical examination along with other clinical data provide a framework forassessment of the underlying pathophysiology of the patient against which all informa-tion obtained from hemodynamic monitors can be interpreted. These methods areused to infer data about the two major parameters of the circulatory system: intravas-cular volume and tissue perfusion.

Invasive Blood Pressure Monitoring

Given the unreliability of sphygmomanometers at blood pressure extremes, invasivearterial blood pressure monitoring is often needed in hemodynamically unstable pa-tients. Literature is starting to emerge questioning the use of arterial catheters in crit-ically ill patients. Lakhal and colleagues3 demonstrated that noninvasive bloodpressure monitoring is accurate and reliable compared with invasive monitors. Thisis particularly when assessing mean arterial blood pressure at the arm level, althoughlimitations at extremes of blood pressure or body mass index were still noted.Regardless of the method, a mean arterial pressure (MAP) of 60 to 65 mm Hg is the

normally accepted target for resuscitative efforts. It is necessary to understand thatnormalization of blood pressure does not always indicate microcirculatory sufficiencyand adequate tissue perfusion. This goal should also be adjusted according to theclinical scenario. For example, a higher MAP may be necessary with untreated criticalcoronary artery stenosis or elevated intracranial pressure, whereas a lower MAP in theabsence of significant tissue hypoperfusion may be tolerated in conditions such assevere aortic insufficiency.

Assessment of filling pressures and left ventricular function using arterial pressurevariationPhysiologic variation of arterial blood pressure during the respiratory cycle is driven bythe effect of lung inflation and changes in thoracic or abdominal pressure on ventric-ular loading conditions in the setting of ventricular interdependence. During sponta-neous inspiration, the reduction in left ventricular (LV) stroke volume (SV) causes adecrease in systemic blood pressure and pulse pressure (PP) at end-inspiration(Fig. 1). During positive pressure ventilation, the right ventricular (RV) preload usuallydecreases at end-inspiration, shifting the ventricular septum to the right and improvingLV compliance. LV preload also increases as the alveolar inflation enhances venousreturn to the left atrium (LA). This, coupled with the decrease in LV afterload, producesan increase in systemic blood pressure at end-inspiration. A few heart beats later and

Fig. 1. Physiologic cardiorespiratory interactions in a spontaneously breathing patient.

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during expiration, the propagation of the decreased RV SV reaches the LV output andleads to a decrease in systolic blood pressure and PP.4,5 Appreciating how the venousreturn changes with the various pathologic states, in addition to its alterations in thesetting of positive pressure ventilation, helps in the diagnosis and management ofthe common hemodynamic profiles encountered in shock.6

These variations have been used to predict fluid responsiveness. Michard and col-leagues7 showed that PP variation (PPV) in mechanically ventilated patients was thebestpredictor of fluid responsiveness. In this study, theoptimal cutoff todiscriminate fluid

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responders was a change of 13% in the PP during the respiratory cycle. The respiropha-sicPPVhadasensitivityof 94%, specificity of 96%,anddemonstratedagoodcorrelationwith an increase in cardiac index in response to fluid administration.8 Unfortunately, theusefulness of PPV in spontaneously breathing patients remains unknown.

Central Venous Pressure

Central venous pressure (CVP), a measure of right atrium pressure (RAP), can be esti-mated noninvasively by measuring the jugular venous pressure or invasively by trans-ducing a central venous catheter with its tip placed in the superior vena cava or rightatrium (RA).9 Normal CVP in a spontaneously breathing patient is 0 to 5 mm Hg,whereas the generally accepted normal upper limit in mechanically ventilated patientsis 10 mm Hg. CVP has been suggested as a measure for preload; however, its validityin predicting fluid responsiveness is nonexistent across numerous studies. Except forextremely low values, static levels of CVP are often unreliable in predicting volumeexpansion responders.10,11

Dynamic changes of CVP in response to fluids or in relation to the respiratory cyclehave been investigated in evaluating preload responsiveness with some conflicting ev-idence.12,13 Caution should be used when using CVP variation because it can bealtered by a host of factors independent of volume status, including changes in tidalvolumes, abdominal pressure, and vascular tone.14,15

Passive Leg Raising Test

The passive leg raising (PLR) maneuver (Figs. 2 and 3) returns approximately 200 mLof blood from the lower extremities toward the central circulatory compartment, result-ing in an instantaneous increase in right-sided preload.16 In the setting of fluid respon-siveness, this trial would result in an increased pulmonary capillary wedge pressure(PCWP), early mitral inflow, and a resultant augmentation of LV SV. Given the transientnature of improvement in SV, a PLR test should be coupled with real-time monitoringof the aortic blood flow, frequently using Doppler parameters obtained by echocardi-ography or esophageal Doppler monitor (EDM). A positive PLR test is defined as anincrease in aortic blood flow greater than 10% for at least 30 seconds. It predicts pre-load responsiveness with a sensitivity of 97% and specificity of 94%. Notably, this in-crease in PCWP is immediate and fully reversible when the legs are laid back down.These studies suggest that the PLR test can help predict fluid responsiveness whileavoiding the potentially hazardous effects of unnecessary volume expansion.12,17

Laboratory Studies

B-type natriuretic peptideB-type natriuretic peptide (BNP) is a peptide released by the ventricles when the myo-cytes are stretched in the setting of increased preload. The role of BNP in assessingintravascular volume has been best studied in stable cardiac and heart failure subjects.In critically ill subjects, many noncardiac conditions are known to increase BNP release,

Fig. 2. The PLR maneuver. (From Teboul JL, Monnet X. Prediction of volume responsiveness incritically ill patients with spontaneous breathing activity. Curr Opin Crit Care 2008;14:334–9;with permission.)

Fig. 3. Normal pulmonary artery catheter tracings in various catheter positions. (Courtesy ofUniversity of Michigan Health System. Available at: http://www.pathology.med.umich.edu/gynonc/bluebook/treatment/peri/peri2.htm. Accessed August 28, 2013.)

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including sepsis, acute lung injury, pulmonary embolism, and intracranial hemorrhage.This makes the interpretation of BNP levels highly unreliable in the ICU.18–20

LactateElevated lactate can be caused by a wide range of conditions and medications.Lactate is best used in the ICU as a surrogate of cellular hypoperfusion and is usefulfor risk stratification in critically ill patients, including cardiac patients. There are alsorecent data about using lactate as a target endpoint of resuscitation. In septic shocksubjects, Jones and colleagues21 compared resuscitation protocols guided by lactateclearance to goal-central venous oxygen saturation (ScvO2), as suggested by earlygoal-directed therapy, and found no significant difference in mortality.22,23 Attanaand colleagues24 also examined the prognostic implications of lactate clearance insubjects developing cardiogenic shock after ST-elevation myocardial infarction. Sub-jects with 12-hour lactate clearance of less than 10% had lower survival rates.24 How-ever, clinicians need to be aware of the limitations of monitoring lactate. Not only canlactate be a slowly changing metabolic marker that could lag behind clinical changes,Marik and colleagues25 also argue that high lactate levels in septic subjects is not al-ways an indication of anaerobic metabolism and, therefore, therapies targeted to treata nonexistent oxygen debt may be harmful. Rather than targeting therapy to lactateclearance only, understanding and addressing the hemodynamic derangementsresponsible for elevated lactate levels should be the composite end-point of treat-ment. In the absence of arterial access, the concentration of central venous lactatecan be a reliable substitute for arterial lactate concentration with a good correlation(area under the curve [AUC] 0.98) when lactate concentration is more than 2 mmol/L.26

Mixed venous oximetryMixed venous oxygen saturation (SvO2) refers to the oxygen saturation of hemoglobinin the proximal pulmonary artery. It is influenced by the balance between oxygen sup-ply and demand, and acts as an indirect measure of oxygen delivery and tissueoxygenation. More specifically, rearrangement of the Fick equation illustrates thatvenous oxygen content is determined by the arterial oxygen content, oxygen con-sumption, and cardiac output (CO).

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A change in SvO2 should alert the clinician to a possible alteration in the oxygensupply-demand balance (Table 1). SvO2 values are initially maintained in the normalrange by many compensatory mechanisms aimed at increasing oxygen delivery,including an increase in CO. As these mechanisms are exhausted, the venous oxygenreserve is used by increasing oxygen extraction, resulting in a decrease in SvO2.Beyond this point, when oxygen demand can no longer be met, anaerobic metabolismand lactic acidosis ensues. This point is called critical extraction ratio for oxygen(ERO2). The critical ERO2 decreases in several critical illnesses, including sepsis.Several observational and prospective clinical studies have addressed the diag-

nostic and prognostic significance of SvO2 in a variety of critically ill cohorts.27,28

Despite an extensive amount of research into the clinical usefulness of monitoringSvO2, its use in guiding therapy remains controversial, especially given its level ofinvasiveness.

ScvO2 and its relationship to SvO2

ScvO2 was introduced as a surrogate for mixed venous oximetry with SvO2. ScvO2 is ameasurement of oxygen saturation in the superior vena cava close to or at the RA junc-tion, whereas SvO2 is determined in the pulmonary artery. Normally, ScvO2 is lowerthan SvO2 but this relationship can be reversed in critically ill patients due to redistri-bution of the CO and regional variation in oxygen consumption. Data about the corre-lation between mixed and ScvO2 seem to be highly variable with the greatestdiscordance in patients with low cardiac index.29,30 No conclusive evidence existsto support routine use of ScvO2 as a replacement to SvO2 monitoring and shouldbe used with caution. However, it is clear that, for both markers, recognizing thepatient-specific trend is more important than the absolute value.30,31

INVASIVE HEMODYNAMIC MONITORINGPAC

Following its introduction into clinical practice in the 1970s, bedside PAC using flow-directed balloon-tipped catheters gradually became a standard of care for critically illpatients. During the PAC era, its widespread use significantly improved the under-standing of the physiologic responses and pathophysiologic changes in various con-ditions. Despite the criticism for the use of PAC generated by the lack of evidencesupporting an outcome benefit,32–36 particularly after the PAC-Man (Assessment ofthe Clinical Effectiveness of Pulmonary Artery Catheters in Management of Patientsin Intensive Care)37 and ESCAPE (Evaluation Study of Congestive Heart Failure andPulmonary Artery Catheterization Effectiveness)38 trials, this invasive hemodynamictool continues to find a role in the management of a subset of critically ill patients.39–41

It remains very useful when used for the appropriate indication and interpreted by cli-nicians with adequate expertise in the analysis and application of data obtained from

Table 1Interpreting mixed SvO2

Decreased SvO2 Increased SvO2

� Decreased CO� Hypoxemia� Increased metabolic rate (eg, fever)� Anemia

� High CO states (sepsis, cirrhosis, hyperthyroidism)� Decreased tissue extraction (sepsis)� Left to right intracardiac shunt� Severe mitral regurgitation� Hypothermia� Nitroprusside toxicity or cyanide poisoning� Wedged pulmonary artery catheter

Hemodynamic Assessment in the Contemporary ICU 419

PAC. It also is the benchmark against which all new hemodynamic monitors aretested.

Indications and Contraindications

The indications for PAC in critically ill patients include

� Acute myocardial infarction complicated by shock, severe heart failure, ormechanical complications (acute mitral regurgitation, ventricular septal defect)

� Differentiation between various causes of shock� Severe LV failure to guide therapy, including inotropes, vasodilators, and diuretics� Cardiac tamponade when clinical and echocardiographic findings areinconclusive

� Assessment of level and magnitude of intracardiac shunt� Severe acute respiratory distress: to guide the application of positive end-expiratory pressure and use of intravenous fluids

� Severe pulmonary hypertension to guide therapy.

CO Measurements

The PAC provides two methods for the assessment of CO. Thermodilution and Fickprinciple–derived equations are reliable but are not without limitations.

Thermodilution methodThermodilution is based on the indicator dilution principle. It is considered the goldstandard of CO measurement. It involves the injection of a bolus of cold normal salinethrough the most proximal port of the PAC followed by measuring the temperaturechanges by a distal thermistor just proximal to the balloon, allowing the generationof a plot of temperature change against time. CO can then be determined by the modi-fication of the Stewart-Hamilton equation. Measurements obtained by this methodaverage the CO over several cardiac cycles.The thermodilution method assumes three major conditions: complete mixing of the

indicator and blood, constant blood flow, and lack of loss of indicator between the siteof injection andplaceof detection. Theseassumptions introduce thepossibility for inac-curate CO assessment via thermodilution methods with some causes listed in Table 2.

Fick principleCOcalculation using the Fick principle is based on the conservation ofmass so that thetotal uptake or release of a substance by an organ is the product of blood flow to thatorgan multiplied by the arteriovenous concentration difference. Solving for the CO,the equation can be reduced to: CO 5 VO2/[(SpO2�SvO2) � 1.36 � 10 � Hb] in which

Table 2Causes of inaccurate estimation of CO by bolus thermodilution

Related to patient � Tricuspid regurgitation� Arrhythmias� Intracardiac shunts� Extremes of CO (very low CO)

Related to injection � Slow injection (>4 s)� Incorrect volume of injectate� Incorrect temperature of injectate

Related to catheter � Pulmonary artery catheter is in wedge position� Thermistor impinging on vessel wall� Proximal port within venous sheath

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CO is the CO in liters per minute, VO2 is the oxygen consumption, SpO2 is the arterialoxygen saturation, SvO2 is the oxygen saturation of a mixed venous sample obtainedfrom the distal PAC port, and Hb is hemoglobin in grams per deciliter.The inaccuracy of the Fick method is mostly related to the oxygen consumption

parameter that is often estimated using several formulas (125 � body surface area[BSA] for men and 110 � BSA for women, or 3 mL O2/kg � weight). Even when theVO2 is actually measured, subsequent calculations using the same previouslymeasured VO2 do not take into account the considerable change in oxygen consump-tion accompanying the change in clinical status, including fevers, catabolic states, orcooling during induced hypothermia.

Derived Parameters

Once themeasured variables areobtained,PACcanbeuseful in calculating several otherhemodynamicparameters that areshown inTable3. It should, however,benoted that theaccuracyof thesecalculated indices is usually affectedby the inaccuracies of themultiplemeasured parameters. Moreover, when an intracardiac shunt is suspected, a saturationrun can be performed during the insertion of the PAC. Left to right shunt is suggested bysaturation step-up of 7% from an atrial shunt and 5% from a ventricular shunt.

Clinical Scenarios

Using the pressures and CO values obtained from PAC, the data can be integrated intothe overall clinical presentation to help establish the diagnosis in several clinical sce-narios. A summary of the changes in the filling pressures and CO occurring in the settingofmany of various conditions encountered in the critically ill patients is shown inTable 4.

Table 3Measured and derived hemodynamic parameters from pulmonary artery catheter

Measured Hemodynamic Variable Normal Value

RAP 0–7 mm Hg

RV Systolic pressure 15–30 mm HgDiastolic pressure 0–8 mm Hg

Pulmonary artery Systolic pressure 15–30 mm HgDiastolic pressure 4–12 mm HgMean pressure (MPAP) 10–20 mm Hg

PCWP 8–15 mmHg

CO 5.0–8.0 L.min�1

Derived Hemodynamic Variable Normal Value

Cardiac index 5 CO/BSA 2.8–4.2 L.min�1.m�2

SVRSVR 5 [(MAP�RAP) � 80]/CO

700–1600 dyne.s.cm�5

9–20 Wood units

Pulmonary vascular resistance (PVR)PVR 5 [(MPAP�PCWP) � 80]/CO

20–130 dyne.s.cm�5

0.25–1.6 Wood units

Stroke volume index (SVI) 5 cardiac index/heart rate 35–70 mL.m�2 per beat

Left ventricular stroke work index (LVSWI)LVSWI 5 (MAP�PCWP) � SVI � 0.0136

44–68 g-m/m2

RV stroke work index (RVSWI)RVSWI 5 (MPAP�RAP) � SVI � 0.0136

4–8 g-m/m2

Abbreviations: MPAP, mean pulmonary artery pressure; SVR, systemic vascular resistance.

Table 4Changes of pulmonary artery catheter parameters in various clinical scenarios

Condition RA RV PA PCWP CO SVR Comments

Shock Hypovolemic Y Y Y Y Y [ —Cardiogenic -/[ -/[ -/[ [ Y [Distributive Y Y Y Y [/Y Y

RV infarct [ Y RVSP[ RVDP

— -/Y Y [ � RA >PCWP� Steep Y-descent� Square root sign in RV tracing

Acute mitralregurgitation

— — — [ Y [ � Prominent v-wave in PCWPtracing (v-wave >2 PCWP)

Tamponade [ [ [ [ Y [ � Diastolic equalization ofpressure

� RA has steep X-descent andabsent Y-descent

Massive pulmonaryembolism

[ [ RVSP[ RVDP

[ Y Y [ � Ventricularization of PAwaveform with rapiddiastolic descent

� Absent dicrotic notch

Acute VSD [ [ [ [ Y [ � O2 saturation step-up� Prominent v-wave

Constriction [ [ [ [ Y [ � Dip and plateau in RV� M- or W-shaped RA tracing

Abbreviations: PA, pulmonary artery; RVDP, RV diastolic pressure; RVSP, RV systolic pressure; SVR,systemic vascular resistance; VSD, ventricular septal defect.

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MINIMALLY INVASIVE HEMODYNAMIC MONITORING AND IMAGING

The major reservations and concerns about the use of PAC given its level of inva-siveness and the lack of evidence supporting improved outcomes, as well as thedecreased familiarity and training in PAC, have triggered the search for less inva-sive hemodynamic monitoring methods. As a result, many imaging modalitiesand minimally invasive monitors have surfaced as potential alternatives to invasivecatheterization.

Echocardiography

Echocardiography has been established as an essential tool in the evaluation of crit-ically ill patients. It can assist in the rapid, accurate, and noninvasive diagnosis of abroad range of acute cardiovascular diseases. The availability of echocardiographyhas appropriately decreased the need for invasive procedures needed to diagnosislife-threatening conditions such as acute mitral regurgitation and tamponade. Acomprehensive echocardiographic evaluation has a high sensitivity and specificityfor defining cardiac causes of shock when performed by a trained sonographer andinterpreted by an experienced cardiologist.42

General indications in the ICUThe general indications for an echocardiogram in the ICU can be fairly extensive(Table 5). Some of these indications and limitations of transthoracic echocardiog-raphy (TTE) necessitate the performance of transesophageal echocardiography(TEE).

Table 5ICU indications for echocardiographic examination

Indication Assessment

Hemodynamiccompromise

� Ventricular function� Valvular function� Hemodynamically significant pericardial effusion� Volume status� Findings suggestive of pulmonary embolism� Cardiothoracic surgical complications

Unexplained hypoxemia � Shunt� Ventricular function� Findings suggestive of pulmonary embolism

Infective endocarditis � Valves� Hardware

Source of emboli � LV function� LV apical thrombi� Atrial appendage and atrial body thrombi� Shunt

Aortic dissection � Diagnosis of dissection flap and aortic enlargement� Complications of dissection including pericardial effusion and

aortic regurgitation

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Echocardiographic assessment of hemodynamic parametersSeveral hemodynamic parameters can be evaluated using the different modalities ofechocardiography, including two-dimensional (2D)-echo, color, and spectral Dopplerinterrogation.

Assessment of preload and volume responsiveness Accurate estimation of preload,volume status, and fluid responsiveness is essential for the proper management of pa-tients with circulatory insufficiency. Using filling pressures to infer LV preload can beinaccurate in conditions that affect LV compliance or in the presence of dynamic LVoutflow obstruction. Defining preload as LV end-diastolic volume (EDV) establishesechocardiography as a potentially useful tool in assessing preload.Subjective assessment of LV volume by visual inspection may be helpful at ex-

tremes of cardiac filling. Systolic obliteration of a small LV cavity is often suggestiveof hypovolemia. More quantitative measures are usually available by using endocar-dial border tracing. LV end-diastolic area (EDA) and EDV are commonly used to es-timate LV preload.43,44 Such findings should be interpreted within the clinical contextbecause a large EDA or EDV would not necessarily equate to adequate preload inpatients with chronic severe LV dysfunction and dilation. As a result, single-point es-timations of LV dimensions have, at best, a modest correlation to fluid responsive-ness.45–47 Alternatively, changes in EDA can be better at predicting changes in COin response to fluid challenges. This parameter should be used judiciously becauseit has been validated in small studies and can be affected by multiple factors that canrender it less useful.48

Echocardiograms also provide estimates of right-sided and left-sided filling pres-sures. Several echocardiogram-derived parameters have also been assessed in pre-dicting volume responsiveness.

RAP� Measuring inferior vena cava (IVC) diameter and its respirophasic response canbe used to estimate RA pressure as shown in Table 6.49,50

Table 6Echocardiographic estimation of RA pressure

IVC Size (cm) Respiratory Collapsibility of IVCa Estimated RA Pressure (mm Hg)

<2.1 >50% collapse 0–5<50% collapse 5–10

>2.1 >50% collapse<50% collapse >15

a (maximum expiratory diameter�minimum inspiratory diameter)/maximum diameter � 100%.

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� IVC is best viewed in the subcostal or subxiphoid window and is usuallymeasured at 2 cm from its junction with the RA, usually at the level of the hepaticvein.

� This technique faces many limitations, including unpredictable variation withpositive pressure ventilation and questionable reliability in patients with elevatedright heart pressures, intra-abdominal pressures, or pulmonary hypertension.

LA pressure� Spectral Doppler used to determine mitral valve inflow variables and pulmonaryvein flow patterns in addition to tissue Doppler imaging (TDI) and LA volume canbe used to help estimate LA pressure (LAP) (Fig. 4).

Fig. 4. Echocardiographic assessment of left atrial pressure (LAP).

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� In hypovolemia, the LV early diastolic filling (mitral inflow E wave) decreases incomparison to the late LV filling during atrial contraction (mitral inflow A wave)leading to a lower E to A ratio, as does the systolic phase of pulmonary vein flow.

� As LAP becomes significantly elevated, the E wave increases out of proportion tothe A wave leading to an increased E/A ratio together with elevated E/E0 (E0 beingthe early diastolic mitral annular displacement velocity obtained using TDI) andpredominance of diastolic pulmonary vein blood flow (in the absence of mitralregurgitation). Specific thresholds that have been found to be supportive ofelevated LAP include E/E0 greater than 15, E/A greater than 2, and pulmonaryvein systolic to diastolic wave ratio of less than 1, especially if they occur inthe setting of LA dilation. Other supportive but more technically difficult and,therefore, less commonly preformed measures include (1) a color M-modeDoppler flow propagation velocity through the mitral valve (Vp) less than 45 cmper second, (2) E/Vp greater than 2.5 (in patients with depressed LV ejection frac-tion), and (3) the time difference between the duration of the atrial reversal waveof pulmonary vein flow and the mitral inflow A-wave duration (Ar-A) greater than30 milliseconds. These variables are illustrated in Fig. 4.

� The reliability of these measures decrease in the setting of positive pressureventilation by altering venous pulmonary return to the LA and affecting early pas-sive filling. They can also be difficult to assess in the setting of tachyarrhythmia,along with other limiting factors.

Volume responsiveness� IVC dispensability index defined as (IVC maximum diameter�IVC minimumdiameter) per IVC minimum diameter has been evaluated in small studies. Inmechanically ventilated patients, an IVC dispensability index in excess of 12% to18% has been suggested to predict volume responsiveness, as would a valueexceeding 40% in spontaneously breathing patients.51–53 This parameter shouldbe used cautiously in the appropriate clinical setting because it remains subjectto many of the limitations encountered with CVP measurements and has notbeen validated in large trials.

� A more promising dynamic measure for assessing fluid responsiveness is therespiratory variation of peak aortic velocity by more than 12% indicating preloadresponsiveness. This measure is most reliable in mechanically ventilated patientswithout asynchrony or arrhythmias.54,55

Cardiac outputSeveral methods to measure the CO using 2D and Doppler echocardiography havebeen described. These techniques focus on combining Doppler-derived instanta-neous blood flow velocity through a conduit with a cross-sectional area (CSA) of theconduit to obtain an estimate of the SV fromwhichCO can be deduced. Of these struc-tures, the LV-outflow tract (LVOT) conduit and aortic valve measurements are the mostcommonly used. The LVOT CSA is calculated from the LVOT diameter assuming a cir-cular shape of the LVOT. Multiplying this CSA with the LVOT flow velocity time integralfrom spectral Doppler tracings will yield SV (Fig. 5), which is then multiplied by heartrate to obtain CO with good correlation with thermodilution-obtained CO.56–58

Ventricular functionClinical examination is often insufficient to provide adequate assessment of biventric-ular function in the ICU where timely and accurate estimation of systolic function is anintegral part of the management of most patients:

Fig. 5. Echocardiographic estimation of SV using LVOT flow. (From Otto CM. Textbook ofclinical echocardiography. 3rd edition. Philadelphia: Elsevier Saunders, 2004; with permission.)

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� LV function: Echocardiography can provide adequate information of LV functionin most ICU patients. Global ventricular function can be reliably qualitatively as-sessed by visual inspection. Several quantitative measures could be used to es-timate LV systolic function, including fractional shortening percentage andTeichholz equation (only reliable in the absence of focal wall motion abnormal-ities), the modified Simpson method, and wall motion score.43,44,59,60

� RV function: Another essential part of ventricular assessment is the RV function,which can be compromised in a variety of conditions. Echocardiographic evalu-ation of the RV requires an assessment of size, kinetics of the cavity, septal inter-action, and other sequelae of RV disease.61,62

� Assessment of RV function is primarily subjective by visual inspection. Mea-sures of tricuspid annular plane systolic excursion less than 1.6 cm and useof TDI can be helpful in quantitative measures of RV function.

� RV size is often evaluated by visual comparison to LV. Quantitatively, the ratioof diastolic RV area to that of the LV can be used to assess RV dilation withmoderate enlargement suggested by a ratio greater than 0.6 and severe RVdilation when the ratio is greater than 1.

� Septal motion: Systolic septal flattening (D-sign) is consistent with RV pressureoverload and diastolic septal bowing into the LV implies RV volume overload(Fig. 6).

� RA-IVC dilation, opening of the foramen ovale as the RA pressure exceeds thatof the LA, and presence of TR are all useful in the assessment of the RV.

Assessment of pulmonary artery pressurePulmonary hypertension is common in critically ill patients and is defined as restingpulmonary systolic pressure of greater than 30 mm Hg, diastolic pressure of 15 mmHg, or a mean of 25 mm Hg. Using continuous wave spectral Doppler, an

Fig. 6. Echocardiographic D-sign consistent with RV pressure overload. Ventricular short axisview. Right panel shows a normal circular left ventricle with crescenteric right ventricularshape during ventricular systole. Left panel shows a D-shaped left ventricle due to septalflattening and shift (blue arrow) to the left caused by right ventricular pressure overloadduring ventricular systole. (Data from Goldhaber Z. Echocardiography in the managementof pulmonary embolism. Ann Intern Med 2002;136:691–700.)

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echocardiogram can estimate pressures using the modified Bernoulli equation, whichis simplified to63

� Systolic pressure 5 4(VTR max)2 1 RAP, where VTR max is the maximum tricuspid

regurgitant velocity� Diastolic pressure 5 4(VPI end-diastolic)

2 1 RAP, where VPI end-diastolic is the end-diastolic pulmonary regurgitant velocity.

To calculate the systolic and diastolic pulmonary artery pressures, tricuspid andpulmonary regurgitation, respectively, must be present. Some investigators havequestioned the accuracy of pulmonary artery pressure estimation by echocardiogra-phy in patients with underlying WHO Group III pulmonary hypertension.64,65 Thiscan partially be attributed to the difficulty in obtaining an accurate Doppler signal inthe setting of pulmonary abnormalities.

Evaluation of cardiac tamponadeRecognizing cardiac tamponade in the critically ill patients is necessary. Most intensiv-ists rely on echocardiography as the primary diagnostic tool. The parasternal and api-cal windows will usually show the effusion but it is not uncommon for critically illpatients to have suboptimal image quality with the only adequate images throughthe subcostal windows. The subcostal window is also useful in assessing the feasi-bility of pericardiocentesis because the needle will follow a similar tract.Several parameters are used to assess for echocardiographic evidence of

tamponade59:

� RV diastolic collapse is highly specific for cardiac tamponade. M-mode in theparasternal windows can make it easier to detect diastolic collapse of the RV.

� RA collapse is less specific and should not be confused with RA systolic contrac-tion. The specificity of RA collapse improves if it last for more than one-third thePR interval.

� It is important to recognize that these findings can be absent in the setting ofcompartmentalized effusions or hematomas, particularly in poststernotomy pa-tients with localized chamber compression.

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� Doppler evaluation of atrioventricular valve inflow respiratory variation is theechocardiographic equivalent of pulsus paradoxus. It is based on the exagger-ated interventricular dependence and can be helpful in confirming the hemody-namic significance of an effusion (Fig. 7). Mitral valve E wave respiratory variationby more than 25% and, to a lesser extent, tricuspid valve variation of 40% can besuggestive of hemodynamic compromise. These parameters should be usedmore cautiously in patients on positive pressure mechanical ventilators and inpatients with arrhythmias or significant bronchospasm.

� Evidence of filling pressure elevation suggested by a distended IVC withminimal respirophasic collapse is a prerequisite for tamponade. Conditionscausing significantly decreased right-sided filling pressures can be associatedwith right atrial collapse in the absence of actual tamponade. In these circum-stances, a fluid challenge followed by repeating the echocardiogram would behelpful.

Other applications of echocardiography in the hemodynamically unstable patientIn addition to the usefulness of echocardiography in providing discrete hemodynamicmeasures related to filling pressure and perfusion, it is also useful in establishing thecause of circulatory insufficiency in some patients. Echocardiography can provide in-formation about valvular dysfunction. It is also useful in assessing for postmyocardialinfarction or cardiac surgery mechanical complications as causes of shock or intracar-diac shunts as causes of refractory hypoxemia.

Fig. 7. Echocardiographic pulsus paradoxus in cardiac tamponade. (Adapted from StanfordUniversity. Echocardiography in the ICU. Available at: http://www.stanford.edu/group/ccm_echocardio/cgi-bin/mediawiki/index.php/Tamponade. Accessed September 15, 2013.)

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Comparison to PAC and Effects of Echocardiography on Management

In critically ill patients, echocardiography is useful in clarifying the diagnosis anddefining the underlying pathophysiologic process in a different and complementaryway to other circulatory monitoring modalities. The correlation between hemody-namic parameters assessed by PAC and echocardiography can be variable.54–57,63

Available evidence suggests that bedside echo is of considerable benefit in manage-ment of patients with unexplained hemodynamic instability. Several studies haveshown that either formal TTE or TEE can result in a change in the management ofup to 50% of the study population.42,66,67 Poelaert and colleagues68 showed that44% of subjects with a PAC underwent therapeutic changes after a TEE was per-formed in both cardiac and septic groups. However, there have been no convincingdata to demonstrate that echocardiographic-guided management improves clinicaloutcomes.

Emerging Trends in ICU Echocardiography

The role of goal-directed echocardiography performed by intensivists who are nottrained in cardiology is constantly growing due to its immediate availability and diag-nostic value. The literature continues to confirm that brief, goal-directed TTE per-formed by intensivists are feasible and reliable in assessing some causes ofshock.69–71 Vieillard-Baron and colleagues72 also demonstrated that qualitativeassessment of hemodynamics using TEE can be accurate and useful in managing cir-culatory failure in septic shock. The development of a new generation of portable,lightweight, battery-powered, hand-carried ultrasound (HCU) has further strength-ened this role of echocardiography. The accuracy of images created by these deviceshas shown good agreement with standard echocardiography when using standard 2Dimaging.71,73–76 Nevertheless, intensivist-performed, brief echocardiographic exami-nations using HCU should not be used to replace formal echocardiograms but,instead, as an adjunct to physical examination.77 One of the current limitations ofechocardiography compared with the other commonly used circulatory monitoringdevices is that it does not provide continuous data. A single-use, miniaturized,indwelling 2D-TEE has been developed to allow continuous hemodynamic assess-ment with good promise in improving the usefulness of echocardiography in moni-toring the response to therapy in the ICU.78 With the decreased use of PAC and theobvious value of echocardiography in critically-ill patients, many training programshave already started shifting some attention to provide trainees sufficient educationand experience with using this modality.

ESOPHAGEAL DOPPLER MONITOR

EDM was initially introduced in 1971 by Side and Gosling and subsequently modifiedby Singer in 1998. An esophageal Doppler monitor is a minimally invasive hemody-namic device that evaluates the CO and fluid status based on the assessment ofdescending aortic blood flow.79–81 Using a Doppler probe inserted into the esoph-agus, the velocity of the descending aortic blood flow can be determined by the fre-quency shift as the waves get reflected of the moving red blood cells. The spectralanalysis of the Doppler shift provides the velocity waveforms. This waveform isused to estimate SV and CO.

Insertion and Placement

The EDM probe is about 6 to 7 mm in diameter. Two types of probes are available:CardioQ (Deltex Medical, Chichester, UK) probe and HemoSonic (Arrown

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International, USA) probe, the latter of which has M-mode capabilities. The probe isinserted orally or nasally in intubated patients. The probe is usually inserted to thedistal esophagus where it is closest and most parallel to the aorta. Contraindicationsto EDM placement include pharyngeal and esophageal disease (pharyngeal pouch,esophageal stent, cancer, stricture, surgery) or significant systemic coagulopathy.

Safety and advantages� Ease of use� Speed: it requires about 5 minutes to place and obtain a clear signal82,83

� Absence of major complications associated with other invasive techniques� Provides continuous monitoring� Short period of training for the operator to develop efficiency and accuracy.84

Measured Parameters and Waveform Analysis

The pulsatile blood flow in the aorta translates to a change in velocity over time, allow-ing the calculation of a stroke distance in the descending aorta (SDa). SDa is the dis-tance a column of blood travels along the aorta with each ventricular systole. The SDais estimated by integrating the derivative of the velocity over time from the start of ejec-tion to the end of flow that equates to the AUC of the velocity-time curve. The shape ofthe waveform and several other parameters obtained from the velocity-time curveallow the assessment of preload, afterload, and contractility (Fig. 8).

Corrected flow timeFlow time (FT) in milliseconds, equivalent to LV-ejection time, is measured from thebase of the waveform starting from the beginning of the aortic pulse upstroke to its re-turn to baseline. Corrected FT (FTc) is calculated by correcting for a heart rate of 60beats per minute using the Bazzett correction formula. The normal range of FTc isgenerally 330 to 360ms.82 EDM uses FTc as a measure of LV preload. Some data sug-gest using SV, as opposed to FTc, as a more reliable indicator for preload becauseFTc can be directly affected by changes in afterload and contractility. Other factors,such as left bundle branch block, can affect LV-ejection time independent of hemody-namics. It is important to recognize conditions when the patient may be volume over-loaded and yet have a low FTc due to pathologic limitation to LV preload (pulmonaryembolism, mitral stenosis, tamponade).

Mean acceleration and peak velocityMean acceleration (MA) is the slope of the upstroke of the aortic pulse velocity wave-form. MA, often used as a surrogate for peak acceleration which in turn, is a goodmeasure of LV contractility independent of afterload. The height of the velocity curveis the peak velocity (PV), calculated as centimeters per second that, together with MA,can be used to infer information about LV contractility and afterload. The normal PVnormally declines with age and a good estimate of the lower end of normal PV in adultsis 120 minus age.

COThe SDa is estimated by the area under the velocity-time curve. Using a built-in nomo-gram for age, height, and weight or using the M-mode capabilities of the HemoSonicprobe, the distal aortic CSA (A) is obtained. The product of these two parameters pro-vides the aortic SV (SVa 5 SDa � A), which is multiplied by a correction factor, to ac-count for the cephalic circulation, to estimate the SV (SV). The CO is calculated as COequals SV multiplied by heart rate.

Fig. 8. EDM-measured parameters and their change in various clinical scenarios. (Modifiedfrom King SL, Lim MS. The use of the esophageal Doppler monitor in the intensive care unit.Crit Care Resusc 2004;6:113–22.)

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Additional hemodynamic measuresThe force and kinetic energy associated with each cardiac cycle have been assessedas potential contractility indices and seem to have a more discriminative powercompared with MA and PV.85 Similarly, the total systemic vascular resistance indexand compliance can also be calculated and could be useful in patients being treatedwith vasoactive agents.

Clinical Scenarios

The EDM waveform shape and the measured or derived parameters are often helpfulin identifying the various hemodynamic profiles encountered in the ICU, particularly inthe setting of intravascular hypovolemia. These various profiles are summarized inTable 7 and Fig. 8.

Table 7EDM profiles in various hemodynamic states

Clinical Scenario FTc PV MA Comments

Hypovolemia Y Normal Normal � Narrower waveform

LV failure -/[ Y Y � Dome-shaped as opposed totriangular waveform

� FTc >360 ms

Vasoconstriction Y Y -/[ � Shorter and narrower waveform

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Assumptions and Limitations of EDM

Two major assumptions are the basis of CO measurements using EDM. Because theprobe measures blood flow in the descending aorta, it presumes a fixed percentage ofCO to supply the coronary, cerebral, and brachiocephalic circulation, and adjusts for itwith a correction factor. This percentage is reliable in young healthy patients but canbe highly variable depending on the metabolic activity of different organs or the path-ologic state. The second assumption is the cross-sectional area of the descendingaorta because using the nomogram might not be applicable to all patients. TheM-mode option does not completely resolve this problem because the diameter ofthe aorta is dynamic and changes with alterations in vascular tone, volume status,and PP.86,87

Other limitations in the use of EDM include

� Operator dependence, accurate probe position, and issues with dislodgement� Inaccurate in aortic regurgitation, aneurysm, or coarctation, and in patients withIABP

� Cannot provide SvO2

� Most studies were done in subjects with hypovolemic shock (it is less extensivelystudied in cardiogenic and distributive shocks).

Validity and Clinical Evidence

There has been a sizable body of evidence to evaluate the validity of EDM-derivedmeasures and to support their clinical value in critically ill patients. Most of the studieswere performed in hemodynamically stable patients. More recent data have providedevidence for its use in hemodynamically unstable cohorts.80,88–90

Several studies have compared FTc to other measures of preload, including PCWPand LV EDA index, with good agreement.91–94 One study followed FTc and PCWP insubjects whose ventricular preload was being manipulated.95 The results showedmatched changes in FTc and PCWP in hypovolemic and normovolemic subjects. Inhypervolemic subjects receiving nitrates PCWP decreased, whereas FTc initiallyincreased, reflecting optimal CO before decreasing. This showed that FTc is a usefulmeasure to direct optimal ventricular loading.91,92 Ventilator-induced variations in PVand SV accurately correlate with fluid responsiveness.96,97

In contrast, reviews on the ability of EDM to accurately assess CO and contractilityhave been variable in hemodynamically unstable subjects. Some studies have showna good correlation between the CO derived from EDM compared with thermodilution(r as high as 0.89), whereas other trials have demonstrated EDM can underestimateCO by as much as 40%.83,89,98–100 Most of these studies found a good agreement be-tween changes in CO noticed on EDM and thermodilution with correlation coefficientsof 0.90 to 0.94, with significantly lower interobserver variability in EDM CO comparedwith thermodilution.80,84,98 This suggests that EDM is highly useful in accurately

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reflecting the direction and magnitude of change in CO over time but less useful inmeasuring absolute CO. The data on the use of EDM-derived measures to guidethe administration and titration of inotropes remain limited.101

Effect on Outcomes

Numerous studies have appraised the effect of EDM-guided fluid management on out-comes. Those trials have primarily included surgical subjects with fluid replenishmentusing EDM, resulting in improved outcomes varying from shorter ICU stay, ability totolerate diet earlier, and shorter hospital stays.102–104 On closer examination of thedata, it seems that EDM subjects received more fluids, which might explain the effecton outcome. These studies were not completely blinded and were restricted to thesurgical cohort. Further studies to determine the effect on other outcomes, includingmortality, that examine medical and cardiac ICU subjects with vasoactive medicationsare necessary.

Clinical Value

Comparedwith PAC, EDM is aminimally invasive, safe, and easymeans to continuous,real-time circulatory monitoring that requires minimal training and can safely be usedfor a prolonged period of time without significant complications. In clinical practice,EDM has been best studied and shown to be most useful in goal-directed optimizationof preload84,91,95 in intravascularly volume-depleted patients. This is especially truewhen emphasis is placed on the trend of change in SV and CO as opposed to absolutevalues. Further studies are needed to confirm the same level of reliability in cardiacpatients and its usefulness in guiding vasoactive and inotropic agents use.

PULSE CONTOUR ANALYSIS OR PULSE WAVE ANALYSIS

Newly emerging technologies based on pulse wave analysis (PWA) can be helpful inthe measurement and optimization of flow. These devices have gained attentionbecause they are relatively less invasive. They are all based on a similar basic principleof continuously estimating SV by analyzing arterial pressure waveforms but they usedifferent techniques with varying proprietary algorithms. Understanding the physi-ology and technology used in PWA is important for the correct measurement andinterpretation of the hemodynamic variables obtained.

Principles

The Windkessel effect describes the interaction between SV and the compliance ofthe arterial tree and can be evaluated using the shape of the arterial pressure wave-form. In 1974, Wesseling and colleagues105,106 developed a basic algorithm for moni-toring SV by measuring the area under the systolic portion of the arterial pressurewaveform and then dividing the area by aortic impedance. CO is calculated by multi-plying the derived SV by the heart rate (Fig. 9). A modification to the formula, adding acorrection factor for individual aortic impedance that was lacking in the earlier formula,remains in use today.

Devices

Several devices, available commercially, use the PWA for continuous CO measure-ment. Three are most commonly used and are the focus of this review. These systemscan be broadly divided into two groups, those requiring calibration (PiCCO and lithiumdilution CO [LiDCO]) and the uncalibrated systems (Flo-Trac).

Fig. 9. Principle of PW analysis using the PiCCO system.

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PiCCO system (Pulsion Medical Systems, Germany)� PiCCO requires a thermistor-tipped arterial line to measure downstream tem-perature changes after the injection of a cold indicator via a central venouscatheter.

� It uses PWA according to a modified Wesseling algorithm with periodic thermo-dilution calibration to continuously measure SV and calculate the CO, SV varia-tion (SVV), PPV, and systemic vascular resistance.

� It is useful in periodically measuring several other parameters, includingintrathoracic blood volume (ITBV), global EDV (GEDV), and extravascularlung water (EVLW), all of which are measures of cardiac preload, pulmonaryedema, and contractility that together provide a global indication of cardiacperformance.

LiDCO system (LiDCO Ltd, UK)� LiDCO uses PWA along with dye dilution (lithium) calibration to measure CO.� For calibration, a small dose of lithium is injected into a vein, where an ion selec-tive electrode sensor mounted on a peripheral arterial line plots the concentrationof lithium over time to calculate the CO.

� For PWA, this system uses an algorithm based on the law of conservation of po-wer for continuous CO calculations. It assumes that the net power change in thearterial tree is equal to the amount of blood entering (SV) minus that of blood leav-ing. Once calibrated for compliance, the linear relationship between power andflow can be obtained and converted to nominal SV that is then converted to anactual SV.

Flo-Trac or Vigileo system (Edwards Lifesciences, California, USA)� Flo-Trac is designed around the application of advanced statistical principles tothe arterial pressure tracing, resulting in the creation of a proprietary algorithmthat recalibrates itself constantly, rending external calibration unnecessary.

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� It is based on a principle of the linear relation between PP and SV. The arterialpressure waveform is sampled every 20 seconds at 100 Hz, allowing the arterialpulsatility to be derived from the standard deviation of the pressure wave over20 seconds, which is then multiplied by the patient-specific aortic complianceto obtain SV.

� It can be unreliable with arterial waveform artifact, aortic regurgitation, intenseperipheral vasoconstriction, severe cardiac dysfunction, and irregular pulse ortachycardia.

Clinical Value and Reliability

Literature about the reliability and clinical value of PWA monitors has been variable. Ahigh degree of correlation between CO obtained by the PWA method and PAC hasbeen demonstrated in different clinical settings, including cardiac surgery, burn sur-gery, neurosurgery, and septic patients.107–112 In a study by Hamzaoui and col-leagues,113 the reliability of PiCCO in subjects with rapidly changing vascular tonewas found to be good with frequent calibrations. Similar results have been demon-strated for the LiDCO system.111,114,115 In contrast, the earlier generation of Flo-Trac was associated with significant bias with a percentage error of greater than30% compared with PAC. The third generation of Flo-Trac claims to have overcomethese problems but the literature supporting this claim is conflicting.116–119 There is asizable body of evidence suggesting that, although PAC, Flo-Trac, LiDCO, and PiCCOdisplay similar mean CO values, they often trend differently in response to therapy andshow different interdevice agreement.120

Besides CO monitoring, PWA methods can be used for evaluating volume statusand fluid responsiveness. Although GEDV and ITBV have some value,121–123 SVVand PPV during the inspiratory and expiratory phases of mechanical ventilation arethe most promising dynamic variables to optimize fluid therapy. Applicable thresh-olds of this parameter differ depending on the device used. The PiCCO technicalspecifications list SVV and PPV of less than 10% as being normal, with an optimalthreshold values greater than 12% for SVV and greater than 13.5% for PPV for pre-dicting a 25% increase in SV when assessing fluid responsiveness. The LiDCO prod-uct information states that an SVV or PPV less than 10% is normal, whereas valuesgreater than 13% to 15% predict fluid responsiveness. The major limitation withthese dynamic variables is the limited trials regarding their usefulness in spontane-ously breathing patients. To reliably use these parameters in clinical practice, pa-tients need to be synchronous on mechanical ventilation with tidal volume greaterthan 8 mL/kg.124–126

Effect on Outcomes

Regarding its effect on clinical outcomes, trials supporting PWA methods to guidegoal-directed therapy are limited and variable. A prospective study comparing PiCCOwith PAC showed no effect on mortality but an association with greater positive fluidbalance and fewer ventilator-free days. After the correction for confounders, thechoice of the monitoring system had no influence on the major outcomes, whereasa positive fluid balance was a significant independent predictor of examined out-comes.127,128 On the other hand, the use of PiCCO-based hemodynamic optimizationwas found to be associated with improved outcomes in decompensated liver cirrhosisand subjects with subarachnoid hemorrhage.128,129 Hemodynamic optimization withLiDCO was also associated with improved outcomes in high-risk surgical and criticallyill patients. Nevertheless, these systems should be used cautiously in hemodynami-cally unstable patients.

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THORACIC ELECTRICAL BIOIMPEDANCE OR IMPEDANCE CARDIOGRAPHY

Impedance cardiography (thoracic electrical bioimpedance [TEB]) in the measurementof cardiovascular performance was introduced in the late 1960s.90 Its appeal was thatis was the least invasive method to continuously monitor SV and CO. It is based on themeasurement of changes in the thoracic impedance to an electrical current that is pro-duced by the fluctuations in thoracic blood volume with each cardiac cycle.Depending on the equation used, the theory behind impedance cardiography

models the thorax as a cylinder130 or a truncated cone131 that is homogenouslyperfused with blood of a specific resistivity based on the hematocrit. The thoraxhas a steady state mean base impedance. Spot or band electrodes placed on the pa-tient’s thorax are used to emit and sense a low-voltage (2.5–4.0 mA), high-frequency(70–100 kHz), alternating electrical current through the thorax.90 The electrical imped-ance is inversely proportional to the volume of thoracic fluids, implying that the pulsa-tile decrease in total thoracic impedance can be used in several mathematical modelsto estimate the beat-to-beat SV as well as CO.

Limitations and Pitfalls

The models used for estimating hemodynamic parameters from impedance cardiog-raphy are based onmultiple assumptions that introduce amargin of inaccuracy. Theselimitations, and other pitfalls of impedance cardiography, are summarized in Table 8.Newer generation TEB methods have overcome some of these limitations by havingfaster signal processing,132 better signal filters, improved EKG triggering, and respira-tory filtering.

Clinical Value

The apparent advantages offered by TEB when it comes to noninvasiveness and easeof use have resulted in extensive testing to establish its effectiveness and applicability.Trials using TEB, in comparison with thermodilution133–136 and direct and indirect Fickmethods,137–139 have shown TEB to be reliable in young healthy volunteers. Resultshave been highly inconsistent in the critically ill population with problems including

Table 8Limitation and pitfalls of impedance cardiography

Limitations and Pitfalls Examples

Ignores the effects of other factors besideaortic blood flow on thoracicbioimpedance

� Changes in tissue fluid volume� Respiratory-induced changes in

pulmonary and venous blood flow� Pulmonary edema� Pleural effusion� Chest wall edema

Alteration in electrode position candrastically change CO measurements

—

Bases the measurement of ventricularejection time on distance between QRSon EKG

� Precludes use in patients with arrhythmias.

Subject to interference from mechanicalventilation

—

Uses nomograms based on age, height,weight, and gender to estimate thevolume of electrically participating tissue

� Inaccurate in patients who do not fitnomogram criteria

� Inaccurate with sternal wire or othercases of presence of metal in the chest

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underestimation of high CO and overestimation of low CO, particularly in the setting ofpositive pressure ventilation, arrhythmias, and pulmonary disorders (due to changes inthoracic cavity configuration and surface area). It is also highly unreliable in the pres-ence of valvular disease and intracardiac shunts.As a result, ICG remains controversial with regard to its accuracy and use in clinical

practice. However, many investigators who question its ability to estimate absoluteCO values, suggest usefulness in following hemodynamic trends within individ-uals.140–143 Without further improvements in signal processing and accuracy in hemo-dynamically unstable patients, it is unlikely that TEB will become a standard monitor inthe critical care setting. New advancements have produced three new monitors thatshow some promise in the unstable patients (Table 9).

Indirect Fick Method

A new noninvasive monitor called the NICO system (Novametrix Medical Systems,Wallingford, CT) can be used in mechanically ventilated patients to estimate pulmo-nary artery blood flow that, in the absence of a significant shunt, should be equal tothe CO. The NICO system is based on carbon dioxide (CO2) elimination by the lungsusing a technique called the differential CO2 Fick partial rebreathing method. It in-volves adding 150 mL of dead space to the ventilator circuit by opening a rebreathingvalve and then measuring the change in CO2 elimination and end-tidal CO2 made dur-ing a period of no rebreathing and a subsequent rebreathing period. This allows thecalculation of CO.Promising advantages of the NICO systems include its noninvasiveness, ease of

use, and the ability to provide capillary blood flow and several other ventilation param-eters. It is constructed on several assumptions that can affect its accuracy in COmea-surement. This system is less reliable in patients with diffusion abnormalities or in thesetting of pulmonary shunting144 and heterogeneous ventilation encountered in acutelung injury.145,146 Changes in ventilation affecting dead space can have significant arti-ficial effects on CO estimations. Another important limitation of the NICO system is theinability to assess volume status and fluid responsiveness. It can only be used inmechanically ventilated patients.

FUTURE DIRECTIONS FOR HEMODYNAMIC MONITORING IN THE ICU

Despite all the controversy regarding the use of PAC, there has been no argumentagainst the limitations of physical examination in critically ill patients and the need

Table 9Thoracic electrical bioimpedance monitors

Aesculon (Osypka Medical,LA Jolla, CA, USA)

� Uses electrical velocimetry� Interprets maximum rate of change in TEB to

calculate CO

ECOM (CONMED, Utica, NY, USA) � Places electrode on endotracheal tube cuff due toproximity to aorta eliminating many assumptions

� Preliminary data suggest adequate reliability

Bioreactance (NICOM, Cheetah TEB,Vancouver, WA, USA)

� Analyzes frequency variations of the deliveredoscillating current

� Higher signal-to-noise ratio resulting in improvedperformance

� High agreement with other monitors (PAC, PiCCO,Flo-Trac)

Hemodynamic Assessment in the Contemporary ICU 437

for better hemodynamic assessment to provide a better understanding of the under-lying pathophysiologic state and, as important, help in the development of goal-directed management strategies. To achieve these goals and to overcome theperceived limitations of PAC, alternative hemodynamic assessments have evolved.These new technologies have their own strengths and limitations and patient-specific variables cannot be ignored with the use of these technologies.The noninvasive, easy-to-use, cost-effective, and reliable hemodynamic monitor re-

mains elusive. Perhaps, just as important, there is paucity of large, clinical studiescomparing these newer modalities with each other and traditional hemodynamic as-sessments, making it difficult to define the patient populations that clearly wouldbenefit from these technologies. Correspondingly, more trials are constantly beingperformed to validate promising parameters such as ITBV, GEDV, and EVLW in clinicaluse. Further studies to assess the effect of current and developing devices on clinicaloutcomes remain in progress. Likewise, data on the efficacy and outcome improve-ment using a combination of twomodalities seem to be lacking and need further inves-tigation, which could be the focus of future studies. In the meantime, currentmonitoring devices should continue to be selected on a patient-specific basis, eitheralone or in combination with other hemodynamic monitors, until the gold standardhemodynamic monitoring tool is developed.

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