Intensive Care Med (2006) 32:48–59DOI 10.1007/s00134-005-2834-7 R E V I E W

S. PriceE. NicolD. G. GibsonT. W. Evans

Echocardiography in the critically ill:current and potential roles

Received: 25 January 2005Accepted: 22 September 2005Published online: 16 November 2005� Springer-Verlag 2005

This article is discussed in the editorialavailable at: http://dx.doi.org/10.1007/s00134-005-2833-8S.P. is the British Heart Foundation JillDando Fellow in Adult Congenital HeartDisease

S. Price · D. G. GibsonDepartment of Cardiology,Royal Brompton Hospital,Sydney Street, London, SW3 6NP, UK

S. Price · E. Nicol · T. W. Evans ())Department of Intensive Care Medicine,Royal Brompton Hospital,Sydney Street, London, SW3 6NP, UKe-mail: t.evans@rbh.nthames.nhs.ukTel.: +44-207-3518523Fax: +44-207-3518524

Abstract Background: The use ofechocardiography in the critically illpresents specific challenges. Howev-er, information of direct relevance toclinical management can be obtainedrelating to abnormalities of structureand function and can be used to es-timate pulmonary arterial and venouspressures. Discussion: Investigationof the consequences of myocardialischaemia, valvular dysfunction andpericardial disease can be facilitated,and changes characteristic of specificconditions (e.g. sepsis, pulmonarythromboembolism) detected. Echo-cardiography can also be used tomonitor the effects of therapeutic in-terventions. Conclusions: The appli-cations of echocardiography in thecritical care setting (excluding stan-dard peri-operative echocardiography

for cardiac surgery) are reviewed,with particular emphasis on the as-sessment of cardiac physiology.

Keywords Echocardiography ·Intensive care · Haemodynamics

Introduction

Historical perspective and aim of the review

The first formal description of the use of ultrasound toassess cardiac function was published 50 years ago [1].Since then echocardiography has allowed an increasinglysophisticated understanding of myocardial structure andfunction. Pulsed Doppler systems were developed in the1970s, followed by phased array scanners in the 1980swhich allowed the accurate display of the temporal andspatial relationships between cardiac structures and theelectrocardiogram (M-mode, Fig. 1a). Improvements inmicroprocessor technology enabled non-invasive assess-ment of intra-cardiac pressures and velocities (Fig. 1b).Eventually, two-dimensional echocardiography coupled

to colour Doppler permitted the real-time imaging ofblood velocities in a picture immediately recognizable asthe heart (Fig. 1c). More recently, ultrasonic contrastagents have been developed that allow improved endo-cardial border definition and bedside assessment ofmyocardial perfusion (Fig. 1d) [2]. Finally, trans-thoracicechocardiography (TTE) has been supplemented by trans-oesophageal imaging (TEE) [3], which has superior res-olution (Fig. 2a) and real-time three-dimensional imaging(Fig. 2b) [4]. Intra-cardiac echocardiography (ICE), withits potential for continuous monitoring at extremely highresolution is under evaluation at present and will furtherexpand the potential of the technique in the ICU setting,although at considerable cost [5] (Fig. 2c).

Although interpretation of echocardiographic findingsin the critically ill is particularly challenging, the expe-

49

rienced operator can gain information regarding cardiacstructure and function of direct relevance to clinicalmanagement, Further, echocardiography can be used tomonitor the effects upon cardiac performance, bothdetrimental and beneficial, of therapeutic interventionsrelevant to the critically ill. The specific objectives of thisreview are to provide an introduction to the current andpotential applications of echocardiography in the ICU.Particular emphasis is placed upon the assessment ofcardiac physiology, and the potential for echocardiogra-phy to complement other investigations and to direct and

monitor therapy. Secondly, we identify fields where moreinformation is required, and speculate briefly on the po-tential clinical value of novel techniques.

Choice of echocardiographic techniques in the ICU

Limitations on the use of echocardiography in the ICUrelate not only to difficulties in image acquisition but alsothe confounding effects on cardiovascular physiology ofpositive pressure ventilation, sedation, changes in arterial

Fig. 1 a M-mode parasternal long-axis trans-thoracic echocardio-gram. The M-mode cursor (dotted line) is shown across the mitralvalve leaflets, demonstrating normal mitral valve leaflet motion.AMVL Anterior mitral valve, leaflet; ECG electrocardiogram; PCGphonocardiogram. b Continuous-wave (CW) Doppler. Trace showstricuspid regurgitation (TR), demonstrating assessment of pulmo-nary arterial pressure from TR velocity. Peak velocity reflects thepeak pressure gradient from right ventricle to right atrium and thusthe right ventricular systolic pressure. TR CW Tricuspid regurgi-tation continuous-wave Doppler. c Apical four-chamber trans-tho-racic echocardiogram, standard 2-D image using colour Doppler.Colour Doppler shows flow across the mitral valve in diastole,

revealing PISA and a degree of mitral stenosis. LA Left atrium; RAright atrium; LV left ventricle; RV right ventricle; TV tricuspidvalve; MV mitral valve. d Myocardial contrast echo (MCE). Trans-thoracic echo following anterior myocardial infarction showingakinetic anterior septum and apex (a, arrows), immediate post-highmechanical index destruction frame on MCE (b); lack of contrastopacification of the dysynergic segments even at 15 cardiac cycles(c, arrows), lack of functional recovery at 12 weeks despiterevascularisation (d, arrows). LV left ventricle; LA left atrium; AVaortic valve; MV mitral valve (broken arrow). (Courtesy of RoxySenior and Raj Janardhanan)

50

carbon dioxide tensions, inotropic and pressor agents andpacing. These, together with variations in loading condi-tions much greater than those seen in standard cardio-logical practice, may radically alter echocardiographicfindings. The experienced critical care echocardiographermust consider all these factors before accurate image in-terpretation is possible. Thus normal values for indicescommonly measured in the non-critical care setting arenot necessarily applicable to the ICU population. More-over, there are few systematic studies in the literatureevaluating echocardiography in detecting the effects ofICU interventions.

TTE is the imaging technique of choice in the ICUsetting, unless impractical or technically impossible. Al-though the difficulties of obtaining adequate TTE viewsin immobile, ventilated patients are well documented, theuse of the sub-costal window is often helpful. Whereimaging is proving difficult, echocardiographic contrastthat passes through the pulmonary circulation has beenshown to improve the diagnostic yield in the ICU sig-nificantly, even in the hands of inexperienced operatorsand in patients who have poor echocardiographic win-dows [6]. TEE should be used when superior resolution isrequired or TTE views are impossible to obtain.

Fig. 2 a Standard trans-oesophageal view of left ventricular out-flow tract and aortic valve. LVOT Left ventricular outflow tract; AVaortic valve; LA left atrium ascending aorta. b Three-dimensionalechocardiogram of the mitral valve taken from the atrial aspectduring systole. Three-dimensional echocardiograph of an abnormalmitral valve, with a central defect in the posterior mitral valve

leaflet (arrowed), and failure of coaptation during systole, whichwould lead to mitral regurgitation. AMVL Anterior mitral valveleaflet; PMVL posterior mitral valve leaflet. (Courtesy of SiemensMedical Solutions). c Colour Doppler with intra-cardiac echocar-diography (ICE). Intracardiac echocardiograph of a secundum atrialseptal defect. ASD Secundum atrial septal defect; LA left atrium

51

Echocardiography in the ICU:what information can it provide

Probably the commonest reason for requesting an echo-cardiogram in the ICU is to assess left ventricular (LV)function. Congenital abnormalities, significant valve dis-

ease, septal defects, aortic root dilatation, intra-cardiacmasses and disease of the pericardium (pericardial tam-ponade or constriction) should also be specifically ex-cluded. Alternatively, echocardiography may identifysimple underfilling of either ventricle. Only when theseconditions have been excluded should echocardiography

Table 1 Potential clinical and echocardiographic findings on theintensive care unit. (HOCM hypertrophic obstructive cardiomyop-athy, LVH left ventricular hypertrophy, LVOTO left ventricularoutflow tract obstruction, VSD ventricular septal defect, ASD atrialseptal defect, LV left ventricle, RV right ventricle, LA left atrium, RAright atrium, AS aortic stenosis, AR aortic regurgitation, MS mitral

stenosis, MR mitral regurgitation, TR tricuspid regurgitation, TEEtrans-oesophageal echo, 2D two-dimensional echo, PW pulse-waveDoppler, CW continuous-wave Doppler, IVRT isovolumic relaxationtime, RV LAX right ventricular long axis function, CABG coronaryartery bypass graft, PE pulmonary embolus, CVA cerebrovascularaccident, SIRS systemic inflammatory response syndrome)

Clinical finding Cardiac cause Echocardiographic finding Notes

Low cardiac output(unresponsive toinotropes)

Valvular disease Any severe stenoticor regurgitant lesion

Difficult to assess in ICU; sequentialstenotic lesions may mask severityof individual lesions

Intrinsic cardiacdisease

HOCM/lVH with LVOTO See textLarge VSD/ASDSevere LV/RV dysfunction

Extrinsic cardiacdisease

Tamponade, pericardial effusion,pericardial disease

NB: Post-operative cardiac surgicalpatients (see text)

Oliguria Underfilling Low trans-mitral/tricuspidvelocities

If severe LVH papillary apposition maybe unreliable sign

Small ventricular volumesApposition of LV papillarymuscles in systole

Intrinsic cardiacdisease

Poor LV function, severe AS High LA pressure demonstrated

Pericardial disease Pericardial effusion, pericardialtamponade, pericardialconstriction

NB: Post-operative cardiac surgicalpatients (see text)

Increased fillingpressures (left-sided)

Impaired LV Increased E>A ratio(corrected for age), short IVRT

See text for detailed explanation

Mitral valve disease Significant MS or MR MRa: dynamic ventricle, increasedforward velocities (>1m/s), short durationand low velocity (<3m/s) regurgitant jet

Increased fillingpressures (right-sided)

Secondary toleft-sided disease

Significant AS, AR, MS, MRor LV disease

Impaired RV Reduced RV LAX function Any reduction in association withpulmonary hypertension is significant;mild impairment after CABG is normal

Tricuspid regurgitation Annular dilatation or endocarditis If severe, RV dynamic with increasedforward velocities (>1m/s), short durationand low velocity regurgitant jet

Sepsis/SIRS LV/RV dysfunction Systolic/diastolic dysfunction Changes controversial and may bemasked by inotropes

Source of sepsis EndocarditisEndocarditis Native/prosthetic valve,

pacemaker wires, extra-cardiac “endocarditis”

Vegetations, paraprosthetic leaks,aortic root abscess

Vegetations rare in prosthetic valveendocarditis

Pulmonaryhypertension

Acute PE Dilated RV, severe TR May rarely demonstrate intra-cardiacthrombus

Post-pneumonectomy Displaced heart, Increasedpulmonary acceleration time

Views often difficult even with TEE

Mitral valve disease Significant MS or MR(2D, PW, CW and colour Doppler)

Severe MR in ICU may be difficult todiagnose (see text and superscript a, above)

Failure to weanfrom ventilator

Intrinsic cardiacdisease

Ischaemia, severe MR, HOCM,LV/RV dysfunction

Stress echo may be necessary to makediagnosis

CVA, embolic event Intra-cardiac thrombus LA appendage, RA, apical LVthrombus

Exclude intra-cardiac shunt with contraststudy

EndocarditisCyanosis Intra-cardiac shunting Positive contrast study Use agitated blood/saline; perform Valsalva

manoeuvre

52

be employed to provide information concerning abnormalventricular function and to guide the application of ther-apeutic interventions, affecting the heart both directly andindirectly (Table 1).

Exclusion of structural abnormalities

Mitral and aortic incompetence

Echocardiographic quantification of mitral regurgitation(MR) can be difficult in the ICU as intermittent positivepressure ventilation (IPPV) and vasoactive medications

can influence the extent of valvular incompetence. Fur-ther, where MR is suspected in patients who fail to weanfrom mechanical ventilation, sedation to allow cardiaccatheterization or TEE significantly reduces the degree ofregurgitation [7]. Here a targetted TTE study at the timewhen the patient is haemodynamically compromised iscrucial in establishing the diagnosis [8]. In severe MR thecharacteristic regurgitant jet recorded on continuous-wave(CW) Doppler may be short and of low velocity (<3m/s).In the most severe cases atrio-ventricular regurgitationmay not be visualized using colour flow, and pulsed-wave(PW) recording across the valve shows sinusoidal laminarflow (Fig. 3a). Acute MR may result from myocardial

Fig. 3 a PW Doppler showing free (very severe) atrio-ventricularvalvar regurgitation: Sinusoidal laminar flow is shown both insystole and diastole across the valve demonstrated using Note thereis no regurgitant (systolic) murmur demonstrated on phonocardi-ography. ECG Electrocardiogram; PCG phonocardiogram. b Aorticregurgitation. Spectral velocity flow profile of continuous-waveDoppler from the apical five-chamber position across a regurgitantaortic valve in an ICU patient. Diastolic flow (towards the trans-ducer) has a peak velocity of approx. 4m/s. The deceleration slope

of the aortic regurgitation envelope is approx. 400 cm/s, consistentwith severe regurgitation. X End-diastolic velocity; AR aortic re-gurgitation continuous-wave Doppler, ECG electrocardiogram;PCG phonocardiogram. c Calcific aortic stenosis: two-dimensionalechocardiogram from the parasternal short-axis views of calcificaortic stenosis, taken in an intensive care patient. The bodies of theleaflets as well as the commisures are calcified. AV Aortic valve;RVOT right ventricular outflow tract; PA main pulmonary artery

53

ischaemia/infarction, papillary muscle rupture, infectiveendocarditis and trauma. Where severe MR of any causeis suspected, TEE should be performed to confirm anyanatomical abnormalities, and prompt discussion withsurgical colleagues is essential.

Aortic regurgitation is readily detectable using CWDoppler, even in patients with sub-optimal echo windows[8] (Fig. 3b). Severe aortic regurgitation (AR) results inhigh forward velocities across the aortic valve and dia-stolic regurgitant velocities falling to less than 2 m/s atend-diastole. Where AR is catastrophic, aortic velocitiesreach zero before end-diastole, followed by diastolic MR,and flow reversal may be visualized on Doppler in thedescending aorta. Here M-mode of the mitral valvedemonstrates premature closure. Common causes of se-vere acute AR include fulminating infective endocarditis(vegetations) and aortic dissection, where a dissectionflap and pericardial blood may also be visible. TEEshould be performed in all cases in which significantvalvular regurgitation is diagnosed with TTE, followed byearly surgical referral.

Mitral and aortic stenosis

Valvular stenosis as an unsuspected pathology in the ICUis uncommon but may be equally challenging to theechocardiographer where cardiac output (CO) is markedlyreduced, as echocardiographic trans-valvular velocitiesare low [8]. Thus as the diagnosis of valvular stenosisrelies upon demonstrating increased velocities across avalve, haemodynamically important disease may remainundetected. Aortic stenosis (AS) is increasingly commonin the elderly. The diagnosis is suggested from calcifi-cation of the aortic valve and immobile cusps (visibleeven with limited TTE views; Fig. 3c). There are noagreed values for what constitutes significant AS in thecritically ill patient. Where LV function is poor and COlow, any pressure drop across the aortic valve may becorrespondingly small, obscuring significant AS. Wherepossible, peak velocity below the valve should also bemeasured by PW Doppler. We consider a four-fold step-up in velocity across the aortic valve to be indicative ofsevere AS.

Cardiac tamponade

Tamponade is suggested by a combination of clinical andechocardiographic features, each of which depends uponthe rate of accumulation of pericardial fluid and thepresence or absence of cardiac disease. Diagnosis in theICU setting presents particular challenges. First, althougha large pericardial effusion is easy to visualize, whereimaging is limited, small but haemodynamically signifi-cant effusions may be missed. Second, many of the di-

agnostic echocardiographic features that alter with respi-ration are affected by IPPV. Third, in the period imme-diately following cardiac surgery pericardial collectionswith no classical echocardiographic features of tampon-ade may cause significant adverse haemodynamic effects.Thus where a large effusion is visualized on TTE togetherwith clinical and echocardiographic features of tampon-ade, the diagnosis is straightforward. By contrast, if suchfeatures are absent, a haemodynamically significantpericardial collection cannot be excluded, especially fol-lowing cardiac surgery [9], and clinicians should have alow threshold for early re-exploration.

Assessment of ventricular function

Left ventricular function

Although requests for echocardiographic assessment ofLV function are common in the ICU, it remains chal-lenging. LV function may be assessed using a combina-tion of techniques including assessment of ejection frac-tion/fractional shortening, Doppler patterns of ventricularfilling and ventricular long axis function/tissue Dopplerimaging (TDI) [8]. The measures of LV systolic functionmost commonly employed (ejection fraction, fractionalshortening) are based on assumptions regarding ventric-ular morphology and load independence that may be in-valid. The same constraints of loading and geometry alsoapply to newer modalities such as three-dimensionalechocardiography and the Tei index (total isovolumictime/filling time plus ejection time) [10]. Further, therelevance of normal values of LV size and function(measured in outpatients) to the critically ill is question-able. Although changes in LV function may even so beuseful in monitoring therapy, more useful informationrelating to ventricular function (and the potential to im-prove myocardial performance) may be obtained frommeasurements that also take into account the timing ofevents within the cardiac cycle such as ventricular filling,ventricular long axis function and TDI.

Although the majority of myocardial fibres are ar-ranged circumferentially, longitudinal fibres situated inthe subepicardium and subendocardium of the free wallsof the LV and right ventricle (RV) play a major role inmaintaining normal function [11, 12, 13]. These fibresaccount for long axis (LAX) movement of the septal, RVand LV free wall with respect to the apex of the heart.LAX function has three components: amplitude, velocityand timing (Fig. 4a). Assessment of LAX function pro-vides a simple, fast and reproducible assessment of LV/RV systolic function, even where imaging is sub-optimal[8]. TDI shows the differential of LAX motion with re-spect to the displacement) and thus provides similar in-formation (Fig. 4b) [8].

54

Assessment of function must also include measure-ment of the LV filling pattern, as an abnormal patternmay be present despite normal ejection fraction/fractionalshortening [13]. Trans-mitral Doppler is also easily ob-tained even with sub-optimal echo windows. Identifica-tion of normal/abnormal LV filling patterns is possibletherefore, even in the ventilated patient. The normalpattern of LV filling is shown in Fig. 5a. In healthy youngpatients about 70% of blood enters the LV during earlydiastole (E-wave) after the isovolumic relaxation time(IVRT, period from A2 to mitral leaflet opening). Sub-sequently the remaining 30% of blood enters the ventriclelate in diastole as a result of atrial contraction (A-wave).

In the absence of ventricular disease E-wave velocity fallswith increasing age, such that in the elderly atrial filling(A-wave) is dominant [13]. At higher heart rates there issummation of ventricular filling. In the ICU population E/A ratios may therefore not be measurable. Despite theseconcerns demonstration of an abnormal LV filling patternin the ICU may indicate significant LV restriction(shortened E wave deceleration time and increased ve-locity), abnormal LV filling pressures (a short IVRT anddominant E wave; Fig. 5b) or be indicative of cardiacdisease not demonstrable by measurement of ejectionfraction/fractional shortening (see below, ‘ Coronary ar-tery disease: ischaemia and infarction’).

Fig. 4 a i M-mode of left-sided long-axis trace demonstrating themagnitude and velocity of annular movement in systole and dia-stole. The third component (timing) is of annular movement mea-sured with respect to timing during the cardiac cycle: the onset ofsystole (ECG) and aortic valve closure (A2 timed with phonocar-diogram). PCG Phonocardiogram; A2 aortic component of secondheart sound. ii M-mode of right-sided long-axis trace demonstratingthe magnitude and velocity of annular movement in systole anddiastole: The third component (timing) is of annular movement

measured with respect to timing during the cardiac cycle: the onsetof systole (ECG) and aortic valve closure (A2 timed with phono-cardiogram). Note increased excursion compared with left-sidedlong-axis motion (i). PCG Phonocardiogram; A2 aortic componentof second heart sound. b i Left ventricle; ii right ventricle. TissueDoppler imaging (TDI). Rates of the differential of annularmovement are shown with respect to displacement. PCG Phono-cardiogram; S systolic movement; E early diastolic movement; Alate diastolic movement

55

Right ventricular function

Measurement of the annular movement of the RV freewall (RVLAX) has been shown to be well correlated withradionuclide and cardiac magnetic resonance assessmentsof RV function [14]. As with the LV, both the timing andamplitude of annular motion are indicators of RV dys-function, and therefore RVLAX as well as TDI should beobtained (Fig. 4a ii, 4b ii). Normal RVLAX amplitude is2 cm, falling after cardiac surgery to 1.5 cm or less. Anyreduction in RVLAX amplitude in the setting of PHTindicates significant RV dysfunction; an amplitude lessthan 1 cm suggests severe RV impairment. The principlesof assessment of diastolic function used for the left side ofthe heart apply equally to the right, although the isovo-lumic phases of the cardiac cycle are shorter and thetrans-tricuspid velocities lower. The presence of an Awave throughout the respiratory cycle on pulmonary ar-terial Doppler is suggestive of RV restriction, a cause ofright-sided failure (and prolonged ICU admission) even inthe absence of systolic RV dysfunction [15].

Supportive interventions in the critically ill:effects on echocardiography

The effects of intermittent positive pressure ventilation

During IPPV the interpretation of echocardiographic im-ages requires modification. Specifically, ventilation mayincrease pulmonary vascular resistance (PVR) by raisingRV afterload. Studies manipulating tidal volume (VT)without changing airway pressure (PAW) or changing PAW

but not VT have demonstrated that that the latter, mani-

fested via modifications to the distending pressure of thelung (alveolar pressure minus pleural pressure), is themain factor determining RV afterload during mechanicalventilation [16]. Secondly, venous return is concomitantlyreduced through increased intrathoracic pressure. Bycontrast, increasing PEEP during volume-controlled me-chanical ventilation leads to respiration-phase-specificreduction in RV output, especially pronounced during theinspiratory phase [17].

The effects of volume resuscitation

Haemodynamic manipulation of patients with cardiovas-cular insufficiency or septic shock often requires con-trolled volume expansion, and in these cases echocardi-ography may be utilized to identify unexpectedly highventricular filling pressures or to direct therapy. Whenconsidering the left heart, the pattern of LV filling can beused to exclude or diagnose abnormally high LA fillingpressures that may suggest cardiac disease [18]. IVRTincreases with age, coronary artery disease, LV hyper-trophy and diabetes. By contrast, as left atrial pressurerises, the IVRT shortens such that at LV end-diastolicpressure of around 30 mmHg the IVRT is zero. As withmany indices of cardiac function, however, the validity ofthese measurements in the ventilated, inotrope-dependentpatient has not been determined. Additionally, the valueof flow measurements across the aortic valve [includingaortic velocity-time integral, VTI(a)] in the assessment offlow velocity variation with cyclic altering of intratho-racic pressures has been assessed at different volumeloads. In an animal setting the VTI(a) has been shown todecrease progressively with graded and controlled blood

Fig. 5 a Normal left ventricular filling pattern. Trans-mitral PWDoppler showing a biphasic pattern (diastolic E and A waves) in ayoung patient with a normal heart. E Early diastolic filling; A late(atrial) diastolic filling; PCG phonocardiogram; A2 aortic compo-

nent second heart sound. b Restrictive filling pattern (left-sided).Doppler trace of mitral inflow showing a monophasic E wave (earlydiastolic filling) with rapid acceleration and deceleration due toventricular restriction

56

loss. Thus respiratory variations in VTI(a) may be used asan index of fluid loading, compatible with the findings ofsystolic pressure variation, stroke volume (SV) variation,and pulse pressure variation [19].

Right heart filling in ventilated patients has been as-sessed by employing beat-to-beat changes in superiorvena caval (SVC) diameter and Doppler RV outflow tocalculate an index for volume resuscitation (index=max-imal expiratory SVC diameter minus minimal inspiratorySVC diameter, divided by maximal expiratory diameter)[20]. Here a low collapsibility index was associated with amoderate inspiratory decrease in RV outflow. By contrast,a high collapsibility index was associated with a majorinspiratory decrease in RV outflow and reduced pulmo-nary artery flow period. A high SVC collapsibility indexcan predict a positive response to volume expansion,marked by a 15% or greater increase in Doppler flow[21].

Echocardiographic findings in critical illness

The sepsis syndromes

Sepsis and septic shock are characterized by a markedloss of peripheral vascular tone and alterations in regionalblood flow. Over the past three decades studies of ven-tricular performance in patients with sepsis have beenperformed using radionuclide assessment of biventricularfunction and invasive haemodynamic monitoring, with orwithout echocardiography, and using such techniquesvarying changes in LV and RV function have been de-scribed [22, 23, 24]. Thus although septic shock has longbeen considered to be characterized by a normal or in-creased cardiac output [25], with hyperkinetic LV onechocardiography and/or a high forward flow estimatedby Doppler techniques, in a recently published series only65% of patients with septic shock had an elevated cardiacindex (>3 l min�1 m�2) at admission [26, 27, 28]. Bycontrast, 35% of the same patient population presentedwith a low cardiac index (<3 l min�1 m�2) and marked LVhypokinesis (mean LV ejection fraction: 38€17%) mea-sured echocardiographically [21]. Such a low output statewas also demonstrated in early investigations using ra-dionuclide angiography, revealing an ejection fractionless than 45% in 55% of the study population [24]. Thisso-called hypodynamic sepsis may be associated with aparticularly poor prognosis [29].

The range of LV ejection fraction observed at the onsetof septic shock is therefore wide. However, LVEF is af-fected not only by contractility (and therefore the use ofinotropes) but also by preload and afterload (and thereforefilling state, and the use of pressors and IPPV). Thus lowsystemic vascular resistance (SVR) may mask depressedmyocardial contractility, which is only revealed whenrestoring arterial pressure through the administration of

pressors. Further, whilst the concept of acute LV dilata-tion in septic shock has gained some credence [24], thishas not been documented using echocardiography in pa-tients with septic shock. Finally, authorities in this areahave shown that LV systolic function rather than di-mensions are the main determinant of LV stroke indexafter optimal volume expansion.

RV dysfunction has also been demonstrated in septicshock using both radionuclide and echocardiographictechniques [26]. Indeed, in one of the few recent studiesin this area using TEE [30] RV dysfunction was observedin 32% of patients. In the clinical setting echocardiogra-phy may be usefully used to identify the presence of LV/RV failure, optimize fluid replacement, and guide thera-pies used to alter pulmonary and systemic vascular re-sistance.

Acute cor pulmonale

RV dysfunction may be related not only to intrinsic de-pression in contractility but also through increased PVR.When an increase in afterload is marked and sudden inonset, such as occurs in massive pulmonary embolism and(less commonly) acute respiratory distress syndrome,acute cor pulmonale occurs (for review see [31]). Undersuch conditions, RV outflow impedance suddenly in-creases, and septal dyskinesia (characterizing systolicoverload), associated with RV enlargement (characteriz-ing diastolic overload) may be seen on echocardiography[32, 33].

Where there is tricuspid regurgitation (TR), the ve-locities can be employed to estimate pulmonary arterial(PA) systolic pressure (DP=4 V2, where DP=pressure dropand V=velocity, modified Bernoulli equation; seeFig. 1b). Thus monitoring serial TR velocities can de-termine changes in peak PA pressure and provide an in-dication as to the success of any intervention applieddesigned to reduce PVR, such as inhaled nitric oxide(iNO). In these circumstances iNO has been shown usingTEE to increase RV ejection fraction significantly (from32€5 to 36€6% before and after iNO) with associatedtrends toward decreased RV end-systolic and end-dia-stolic volumes and right atrial pressures [34]. Care isneeded in severe RV failure, in which PA pressure mayfall due to progressive RV dysfunction, and estimated PApressure falls as RA pressure rises, rather than in responseto successful therapy.

Ventricular failure

Where the LV is dilated, LAX amplitude is reduced andhas been shown to be well correlated with measuredejection fraction. In the presence of left bundle branchblock (€the presence of long aortic valve delay) the

57

timing of long axis movement becomes abnormal, suchthat shortening and tension persist beyond A2 into theperiod of isovolumic relaxation (Fig. 6a) [35]. This limitsearly diastolic filling (visualized using trans-mitralDoppler), stroke volume and hence CO. In the non-ICUsetting biventricular pacing (resynchronization therapy)has been shown to be of significant benefit in some pa-tients, resulting in an acute increase in cardiac index of upto 25% [36]. Although not yet investigated, the identifi-cation of such abnormalities in patients with borderlineCO in the ICU has clear implications for potential ther-apeutic intervention.

The identification of hypertrophic cardiomyopathy(HCM) or admission of a patient with known HCM (orsignificant LV hypertrophy) to the ICU is crucial in di-recting management, as interventions may result in re-versible adverse haemodynamics that may be identifiedwith echocardiography. Here, positive inotropy (eitherendogenous or exogenous), vasodilatation and underfill-

ing may all result in increase in LV outflow tract ob-struction (LVOTO) (Fig. 6b), a reduction in CO, andeventually progressive myocardial ischaemia. In certainpatients these changes are associated with worsening MR.Prompt recognition of HCM (or LV hypertrophy) withsignificant LVOTO with the echocardiographic featuresdescribed above should lead the intensivist to ensure thepatient is adequately filled, to reduce and stop positiveinotropic agents, and if possible introduce beta-blockade.

Coronary artery disease: ischaemia and infarction

In the out-patient setting, regional reductions in LAXmagnitude and velocity have been shown to be correlatedwith infarction demonstrated on myocardial perfusionimaging [37]. Moreover, regional asynchronous LAXcontraction correlates with myocardial ischaemia. Here,the onset of LAX shortening is delayed but the duration

Fig. 6 a Septal motion in left bundle branch block shown fromparasternal short axis (left), and apical septal long-axis (right)views. In the short axis view note the abnormal late inwardmovement of the interventricular septum (arrowed). This corre-sponds on septal long-axis movement to late annular movementpersisting after A2 into the period of diastole (arrowed). Q Q waveon electrocardiogram; A2 aortic component second heart sound. bLeft ventricular outflow tract obstruction (LVOTO). Trans-oe-sophageal echocardiogram showing increased velocities in the leftventricular outflow tract (demonstrated by the narrow outflow tract

and aliasing of the colour Doppler, arrowed) due to a hypertrophiedinter-ventricular septum and systolic anterior motion of the mitralvalve. The magnitude of the outflow tract obstruction can bemeasured using continuous-wave Doppler across the left ventricu-lar outflow tract. LA Left atrium; LV left ventricle; LVOT leftventricular outflow tract; AA ascending aorta. c Left ventricularlong-axis motion in a patient following anterior myocardial in-farction. Note the abnormal septal motion such that tension persistsbeyond A2 into the period of isovolumic relaxation. A2 Aorticcomponent second heart sound

58

References

1. Edler I, Hertz CH (1954) The use ul-trasonic reflectoscope for the continu-ous recording of movements of heartwalls. Kungl Fysiogr Sallsk I LundForhandl 24

2. Cate FJ ten, Cornel JH, Serruys PW,Vletter WB, Roelandt J, MittertreinerWH (1987) Quantitative assessment ofmyocardial blood flow by contrast two-dimensional echocardiography: initialclinical observations. Am J PhysiolImaging 2:56–60

3. Hisanga K, Hisanga A, Nagata K et al(1972) A new transesophageal real timetwo-dimensional echocardiographicsystem using a flexible tube and itsclinical application. Proc Jpn Soc Ul-trasonic Med 32:43–44

4. Wang X-F, Deng Y-B, Nanda NC,Deng J, Miller AP, Xie MX (2003) Livethree-dimensional echocardiography:imaging principles and clinical appli-cation. Echocardiography 20:593–604

5. Schwartz SL, Gillam LD, WientraubAR, Sanzobrino BW, Hirst JA, Hsu TL,Fisher JP, Marx G, Fulton D, McKayRG et al (1993) Intracardiac echocar-diography in humans using a small-sized (6F), high frequency (12.5 MHz)ultrasound catheter. Methods, imagingplanes and clinical experience. J AmColl Cardiol 21:189–198

6. Nguyen TT, Dhond M, Sabapathy R,Bommer WJ (2001) Contrast mi-crobubbles improve diagnostic yield inICU patients with poor echocardio-graphic windows. Chest 120:1287–1292

7. Pieper EP, Hellemans IM, Hamer HP,Ravelli AC, Cheriex EC, Tijssen JG,Lie KI, Visser CA (1996) Value ofsystolic pulmonary venous flow rever-sal and color Doppler jet measurementsassessed with transesophageal echocar-diography in recognizing severe puremitral regurgitation. Am J Cardiol78:444–450

8. Feigenbaum H, Armstrong WF, Ryan T(2004) Feigenbaum’s echocardiogra-phy, 6th edn. Lippincott, Williams &Wilkins, Philadelphia

9. Price S, Prout J, Jaggar SI, Gibson DG,Pepper JR (2004) ‘Tamponade’ fol-lowing cardiac surgery: terminologyand echocardiography may both mis-lead. Eur J Cardiothorac Surg 26:1156–1160

10. Lutz JT, Giebler R, Peters J (2003) The‘TEI-index’ is preload dependent andcan be measured by transoesophagealechocardiography during mechanicalventilation. Eur J Anaesthesiol2011:872–877

11. Henein MY, Gibson DG (1999) Normallong axis function. Heart 81:111–113

12. Miyatake K, Yamagishi M, Tanaka N,Uematsu M, Yamazaki N, Mine Y,Sano A, Hirama M (1995) New methodfor evaluating left ventricular wall mo-tion by color-coded tissue Doppler im-aging: in vitro and in vivo studies, J AmColl Cardiol 25:717–724

13. Gibson DG, Francis DP (2003) Clinicalassessment of left ventricular diastolicfunction. Heart 89:231–238

14. Carr-White GS, Kon M, Koh TW,Glennan S, Ferdinand FD, De SouzaAC, Pepper JR, Pennell DJ, Gibson DG,Yacoub MH (1999) Right ventricularfunction after pulmonary autograft re-placement of the aortic valve. Circula-tion 100:1136–1141

15. Cullen S, Shore D, Redington A (1995)Characterization of right ventriculardiastolic performance after completerepair of tetralogy of Fallot. Restrictivephysiology predicts slow postoperativerecovery. Circulation 91:1782–1789

16. Vieillard Baron A, Loubieres Y,Schmitt JM, Page B, Dubourg O, JardinF (1999) Cyclic changes in right ven-tricular afterloading during mechanicalventilation. J Appl Physiol 87:1644–1650

remains unchanged, persisting into the period of isovo-lumic relaxation (Fig. 6c). In association, early trans-mi-tral filling is suppressed. These changes, a sensitive non-invasive diagnostic test of myocardial ischaemia, areexaggerated by dobutamine and may occur in the absenceof ECG changes or symptoms [18]. In the ICU setting, thedevelopment of new regional asynchrony at rest withincreasing inotropic support or when attempting ventila-tory weaning suggests myocardial ischaemia and the needto intervene. In the immediate post-operative period in ageneral ICU the finding of regional wall motion abnor-mality in the absence of any cardiac history should raisethe question of intra-operative myocardial infarction or animpending significant ischaemic event. Where significantLV hypertrophy exists, the use of inotropes can result inmyocardial ischaemia, identified by incoordinate LAXfunction. Here, reduction in inotropic support can result inthe resolution of asynchronous changes and increase inCO.

TEE can be used to visualize the first 1–2 cm of thecoronary arteries. Its use in demonstrating significantcoronary artery disruption has been validated in the car-diac peri-operative setting, but not in the general ICU

population. However, in a ventilated patient with bor-derline CO or an abnormal ECG, abnormal coronaryDoppler flow patterns and velocities seen in associationwith a corresponding regional wall motion abnormalitysuggest significant coronary artery disease.

Conclusion

The critically ill present a challenging population for theechocardiographer: from limitations in image acquisition,to interpretation in the context of rapidly changingphysiology and interventions. Echocardiography canprovide important and relevant information, although thismust be interpreted in the context of each individual pa-tient and their current therapy. Careful application of thenewer echocardiographic techniques, together with anappreciation of physiological as well as anatomical ab-normalities may give information of critical value in themanagement of individual cases. It is clear, however, thatsystematic clinical research could revolutionize theamount of useful information available to the critical carephysician.

59

17. Schmitt JM, Vieillard Baron A, Au-garde R, Prin S, Page B, Jardin F (2001)Positive end expiratory pressure titra-tion in acute respiratory distress syn-drome patients: impact on right ven-tricular outflow impedence evaluatedby pulmonary artery Doppler flow ve-locity measurements. Crit Care Med29:1154–1158

18. Henein MY, Gibson DG (1999) Longaxis function in disease. Heart 81:229–231

19. Slama M, Masson H, Teboul JL, ArnoutML, Susic D, Frohlich E, Andrejak M(2002) Respiratory variations of aorticVTI: a new index of hypovolemia andfluid responsiveness. Am J PhysiolHeart Circ Physiol 283:H1729–H1733

20. Vieillard Baron A, Augarde D, Prin S,Page B, Beauchet A, Jardin F (2001)Influence of superior vena caval zoneconditions on cyclic changes in rightventricular outflow during respiratorysupport. Anesthesiology 95:1083–1088

21. Vieillard Baron A, Prin S, Chergui K,Dubourg O, Jardin F (2003) Hemody-namic instability in septic shock: besideassessment by Doppler echocardiogra-phy. Am J Respir Crit Care Med168:1270–1276

22. Ozier Y, Gueret P, Jardin F, Farcot JC,Bourdarias JP, Margairaz A (1984) Twodimensional echocardiographic demon-stration of acute myocardial depressionin septic shock. Crit Care Med 12:596–599

23. Kimchi A, Ellrodt GA, Berman DS,Riedinger MS, Swan HJC, Murata GH(1984) Right ventricular performance inseptic shock: a combined radionuclideand hemodynamic study. J Am CollCardiol 4:945–951

24. Parker MM, Shelhamer JH, BacharachL, Green MV, Natanson C, FrederickTM, Damske BA, Parillo JE (1984)Profound but reversible myocardial de-pression in patients with septic shock.Ann Intern Med 100:483–490

25. Parillo J (1993) Pathogenetic mecha-nisms of septic shock. N Engl J Med328:1471–1477

26. Jardin F, Brun-Ney D, Auvert B,Beauchet A, Bourdarias JP (1990)Sepsis related cardiogenic shock. CritCare Med 18:1055–1060

27. Jardin F, Valtier B, Beauchet A, Du-bourg O, Bourdarias JP (1994) Invasivemonitoring combined with two-dimen-sional echocardiographic study in septicshock. Intensive Care Med 20:550–554

28. Jardin F, Fourme T, Page B, LoubieresY, Vieillard Baron A, Beauchet A,Bourdarias JP (1999) Persistent preloaddefect in severe sepsis despite fluidloading: a longitudinal echocardio-graphic study in patients with sepsisshock. Chest 116:1354–1359

29. Watson D, Grover R, Anzueto A, Lor-ente J, Smithies M, Bellomo R, Gun-tupalli K, Grossman S, Donaldson J, LeGall JR; Glaxo Wellcome InternationalSeptic Shock Study Group (2004) Car-diovascular effects of the nitric oxidesynthase inhibitor NG-methyl-L-argi-nine hydrochloride (546C88) in patientswith septic shock: results of a random-ized, double-blind, placebo-controlledmulticenter study. Crit Care Med32:13–20

30. Vieillard Baron A, Schmitt JM, Beau-chet A, Augarde R, Prin S, Page B,Jardin F (2001) Early preload adapta-tion in septic shock? A trasesophagealechocardiographic study. Anesthesiolo-gy 95:1083–1088

31. Vieillard Baron A, Prin S, Chergui K,Dubourg O, Jardin F (2002) EchoDoppler demonstration of acute corpulmonale at the bedside in the medicalintensive care unit. Am J Respir CritCare Med 166:1310–1319

32. Jardin F, Dubourg O, Bourdarias JP(1997) Echocardiographic pattern ofacute cor pulmonale. Chest 111:209–217

33. Jardin F, Dubourg O, Gueret P, De-lorme G, Bourdarias JP (1987) Quanti-tative two dimensional echocardiogra-phy in massive pulmonary embolus:emphasis on ventricular interdepen-dence and leftward septal displacement.J Am Coll Cardiol 101:1201–1206

34. Fierobe L, Brunet F, Dhainaut JF,Monchi M, Belghith M, Mira JP, Dal-l’ava-Santucci J, Dinh-Xuan AT (1995)Effect of inhaled nitric oxide on rightventricular function in adult respiratorydistress syndrome. Am J Respir CritCare Med 151:1414–1419

35. Henein MY, Gibson DG (1999) Longaxis function in disease. Heart 81:229–231

36. Leclercq C, Cazeau S, Le Breton H,Ritter P, Mabo P, Gras D, Pavin D,Lazarus A, Daubert JC (1998) Acutehemodynamic effects of biventricularDDD pacing in patients with end-stageheart failure J Am Coll Cardiol32:1825–1831

37. Shuhaiber HJ, Juggi JS, John V, YousofAM, Braveny P (1990) Differences inthe recovery of right and left ventricularfunction after ischaemic arrest and car-dioplegia. Eur J Cardiothorac Surg4:435–40