Advanced(Applicaon(of(Pointof1Care( Echocardiography(in ... · velocity is "1 m/s because squaring a number "1 makes it even smaller. When the proximal velocity is over 1.5 m/s or

Advanced Applica,on of Point-‐of-‐Care Echocardiography in Cri,cal Care

Dr. Mark Tutschka Dr. Rob ArnAield

OBJECTIVES

•  Provide an overview of common “advanced” echocardiographic techniques suitable for use at the point-‐of-‐care with the goal of enhancing hemodynamic assessment and clinical decision-‐making in the ICU or any acute care environment.

Contents

•  Valvular pathology –  Aor,c regurgita,on –  Aor,c stenosis – Mitral regurgita,on – Mitral stenosis

•  RV dysfunc,on / Pulmonary hypertension •  Cardiac tamponade •  Diastolic func,on •  LV systolic func,on

Aor,c Regurgita,on

GOALS: 1.  Determina,on of severity

a.  Color Doppler jet size b.  Vena contracta width c.  Pressure half-‐,me

2.  Integrate in to pa,ent care decision

Aor,c Regurgita,on, cont’d 1.  Regurgitant jet profile –  Easy and effec,ve at point of care –  Color Doppler of AV/LVOT –  Es,mate jet width just below the

level of the aor,c valve in the LVOT –  Jet occupying >65% of LVOT suggests

severe AR –  Important limita,ons: •  Eccentric jets may impinge on LVOT altering their profile

•  Apparent size of jet may be significantly influenced by window (i.e. parasternal vs. apical) and image quality

•  Jet is viewed in 2D – may miss a wider area in 3D space

Aor,c Regurgita,on, cont’d 2. Vena contracta size –  Width of the aor,c jet as it crossed the

aor,c valve orifice •  Closely approximates regurgitant orifice

–  Measure where flow across the valve is preceded by a convergence zone and followed by the widening jet (hourglass appearance)

–  Nyquist at least 50-‐60 cm/s –  <3mm = MILD; ≥7mm = SEVERE –  Limita,ons:

•  Tiny measurement – small errors lead to big discrepancies in severity •  Not useful when mul,ple jets present

Vena Contracta

Aor,c Regurgita,on, cont’d 3.  Pressure-‐half-‐,me (PHT) –  Time for peak transvalvular gradient

to fall to by ½ •  Reflects degree of regurg and LVEDP •  PHT inversely propor,onal to severity – a wider orifice / higher LVEDP cause the gradient to fall more rapidly

–  CW Doppler across Ao valve –  Trace decelera,on slope of the

Doppler signal –  SEVERE = <200msec; MODERATE =

200-‐500msec; MILD = >500 –  Important Considera,ons:

•  PHT will tend to normalize with chronic AR as LV adapts to é LVEDP

•  PHT will be shortened by diastolic dysfunc,on, LV failure / é LVEDP

•  PHT will be increased by hypertension / increased PVR

PHT derived from peak velocity and slope

Aor,c Stenosis


a.  Peak gradient b.  Mean gradient

2.  Integrate into pa,ent care decisions

Aor,c Stenosis, cont’d 1. Peak velocity –  Higher velocity reflects increasing severity –  CW Doppler across Ao valve •  Mul,ple windows to obtain highest velocity •  Measure peak height of velocity curve •  MODERATE = >3m/sec; SEVERE = >4m/sec

–  Limita,ons / caveats •  LV dysfunc,on -‐ may lower peak velocity, interpret with cau,on if EF <40%

•  LV hypertrophy / diastolic dysfunc,on – lowers stroke volume and thereby peak velocity

•  Uncontrolled HTN – will tend to decrease transvalvular flow

•  AR – Will tend to increase measured peak velocity, par,cularly when severe

•  MR – will tend to decrease Ao valve flow veloci,es, par,cularly when severe

•  High cardiac output states – will tend to exaggerate the severity of AS

included in measurements. Some colour scales ‘blur’ the peak veloc-ities, sometimes resulting in overestimation of stenosis severity. Theouter edge of the dark ‘envelope’ of the velocity curve (Figure 2) istraced to provide both the velocity–time integral (VTI) for thecontinuity equation and the mean gradient (see below).

Usually, three or more beats are averaged in sinus rhythm, averag-ing of more beats is mandatory with irregular rhythms (at least 5consecutive beats). Special care must be taken to select representativesequences of beats and to avoid post-extrasystolic beats.

The shape of the CW Doppler velocity curve is helpful in distin-guishing the level and severity of obstruction. Although the timecourse of the velocity curve is similar for fixed obstruction at any level(valvular, subvalvular, or supravalvular), the maximum velocity oc-curs later in systole and the curve is more rounded in shape withmore severe obstruction. With mild obstruction, the peak is in earlysystole with a triangular shape of the velocity curve, compared withthe rounded curve with the peak moving towards midsystole insevere stenosis, reflecting a high gradient throughout systole. Theshape of the CWD velocity curve also can be helpful in determiningwhether the obstruction is fixed or dynamic. Dynamic subaorticobstruction shows a characteristic late-peaking velocity curve, oftenwith a concave upward curve in early systole (Figure 3).

B.1.2. Mean transaortic pressure gradient. The difference in pressurebetween the left ventricular (LV) and aorta in systole, or transvalvularaortic gradient, is another standard measure of stenosis severity.8–10

Gradients are calculated from velocity information, and peak gradientobtained from the peak velocity does therefore not add additionalinformation as compared with peak velocity. However, the calcula-tion of the mean gradient, the average gradient across the valveoccurring during the entire systole, has potential advantages andshould be reported. Although there is overall good correlation be-tween peak gradient and mean gradient, the relationship betweenpeak and mean gradient depends on the shape of the velocity curve,

which varies with stenosis severity and flow rate. The mean transaor-tic gradient is easily measured with current echocardiography systemsand provides useful information for clinical decision-making.

Transaortic pressure gradient (!P) is calculated from velocity (v)using the Bernoulli equation as:

!P " 4v2

The maximum gradient is calculated from maximum velocity:

!Pmax " 4vmax2

and the mean gradient is calculated by averaging the instantaneousgradients over the ejection period, a function included in most clinicalinstrument measurement packages using the traced velocity curve.Note that the mean gradient requires averaging of instantaneousmean gradients and cannot be calculated from the mean velocity.

This clinical equation has been derived from the more complexBernoulli equation by assuming that viscous losses and accelerationeffects are negligible and by using an approximation for the constant thatrelates to themass density of blood, a conversion factor formeasurementunits.

In addition, the simplified Bernoulli equation assumes that theproximal velocity can be ignored, a reasonable assumption whenvelocity is "1 m/s because squaring a number "1 makes it evensmaller. When the proximal velocity is over 1.5 m/s or the aorticvelocity is "3.0 m/s, the proximal velocity should be included in theBernoulli equation so that

!P " 4(vmax2 # vproximal

2 )

when calculating maximum gradients. It is more problematic toinclude proximal velocity in mean gradient calculations as each pointon the ejection curve for the proximal and jet velocities would needto be matched and this approach is not used clinically. In thissituation, maximum velocity and gradient should be used to gradestenosis severity.

Sources of error for pressure gradient calculationsIn addition to the above-mentioned sources of error (malalignment

of jet and ultrasound beam, recording of MR jet, neglect of anelevated proximal velocity), there are several other limitations oftransaortic pressure gradient calculations. Most importantly, any un-derestimation of aortic velocity results in an even greater underesti-mation in gradients, due to the squared relationship between velocityand pressure difference. There are two additional concerns whencomparing pressure gradients calculated from Doppler velocities topressures measured at cardiac catheterization. First, the peak gradientcalculated from the maximum Doppler velocity represents the max-imum instantaneous pressure difference across the valve, not thedifference between the peak LV and peak aortic pressure measuredfrom the pressure tracings. Note that peak LV and peak aorticpressure do not occur at the same point in time; so, this differencedoes not represent a physiological measurement and this peak-to-peak difference is less thanthe maximum instantaneous pressuredifference. The second concern is the phenomenon of pressurerecovery (PR). The conversion of potential energy to kinetic energyacross a narrowed valve results in a high velocity and a drop inpressure. However, distal to the orifice, flow decelerates again. Al-though some of the kinetic energy dissipates into heat due toturbulences and viscous losses, some of the kinetic energy will bereconverted into potential energy with a corresponding increase inpressure, the so-called PR. Pressure recovery is greatest in stenoseswith gradual distal widening since occurrence of turbulences is then

Figure 2 Continuous-wave Doppler of severe aortic stenosis jetshowing measurement of maximum velocity and tracing of thevelocity curve to calculate mean pressure gradient.

Journal of the American Society of Echocardiography Baumgartner et al 5Volume 22 Number 1

Height of peak corresponds to peak velocity

Aor,c Stenosis, Cont’d 2. Mean gradient –  Higher gradient reflects increasing severity –  CW Doppler across Ao valve •  Mul,ple windows to obtain highest velocity •  Outline profile of velocity curve

–  Mild = 20-‐30; Moderate 30-‐40, Severe >40-‐50*

–  Limita,ons: •  Mirror those observed in peak velocity

3. Any normal appearing Ao valve cusp in the PSLA view tends to exclude severe AS

included in measurements. Some colour scales ‘blur’ the peak veloc-ities, sometimes resulting in overestimation of stenosis severity. Theouter edge of the dark ‘envelope’ of the velocity curve (Figure 2) istraced to provide both the velocity–time integral (VTI) for thecontinuity equation and the mean gradient (see below).

Usually, three or more beats are averaged in sinus rhythm, averag-ing of more beats is mandatory with irregular rhythms (at least 5consecutive beats). Special care must be taken to select representativesequences of beats and to avoid post-extrasystolic beats.

The shape of the CW Doppler velocity curve is helpful in distin-guishing the level and severity of obstruction. Although the timecourse of the velocity curve is similar for fixed obstruction at any level(valvular, subvalvular, or supravalvular), the maximum velocity oc-curs later in systole and the curve is more rounded in shape withmore severe obstruction. With mild obstruction, the peak is in earlysystole with a triangular shape of the velocity curve, compared withthe rounded curve with the peak moving towards midsystole insevere stenosis, reflecting a high gradient throughout systole. Theshape of the CWD velocity curve also can be helpful in determiningwhether the obstruction is fixed or dynamic. Dynamic subaorticobstruction shows a characteristic late-peaking velocity curve, oftenwith a concave upward curve in early systole (Figure 3).

B.1.2. Mean transaortic pressure gradient. The difference in pressurebetween the left ventricular (LV) and aorta in systole, or transvalvularaortic gradient, is another standard measure of stenosis severity.8–10

Gradients are calculated from velocity information, and peak gradientobtained from the peak velocity does therefore not add additionalinformation as compared with peak velocity. However, the calcula-tion of the mean gradient, the average gradient across the valveoccurring during the entire systole, has potential advantages andshould be reported. Although there is overall good correlation be-tween peak gradient and mean gradient, the relationship betweenpeak and mean gradient depends on the shape of the velocity curve,

which varies with stenosis severity and flow rate. The mean transaor-tic gradient is easily measured with current echocardiography systemsand provides useful information for clinical decision-making.

Transaortic pressure gradient (!P) is calculated from velocity (v)using the Bernoulli equation as:

!P " 4v2

The maximum gradient is calculated from maximum velocity:

!Pmax " 4vmax2

and the mean gradient is calculated by averaging the instantaneousgradients over the ejection period, a function included in most clinicalinstrument measurement packages using the traced velocity curve.Note that the mean gradient requires averaging of instantaneousmean gradients and cannot be calculated from the mean velocity.

This clinical equation has been derived from the more complexBernoulli equation by assuming that viscous losses and accelerationeffects are negligible and by using an approximation for the constant thatrelates to themass density of blood, a conversion factor formeasurementunits.

In addition, the simplified Bernoulli equation assumes that theproximal velocity can be ignored, a reasonable assumption whenvelocity is "1 m/s because squaring a number "1 makes it evensmaller. When the proximal velocity is over 1.5 m/s or the aorticvelocity is "3.0 m/s, the proximal velocity should be included in theBernoulli equation so that

!P " 4(vmax2 # vproximal

2 )

when calculating maximum gradients. It is more problematic toinclude proximal velocity in mean gradient calculations as each pointon the ejection curve for the proximal and jet velocities would needto be matched and this approach is not used clinically. In thissituation, maximum velocity and gradient should be used to gradestenosis severity.

Sources of error for pressure gradient calculationsIn addition to the above-mentioned sources of error (malalignment

of jet and ultrasound beam, recording of MR jet, neglect of anelevated proximal velocity), there are several other limitations oftransaortic pressure gradient calculations. Most importantly, any un-derestimation of aortic velocity results in an even greater underesti-mation in gradients, due to the squared relationship between velocityand pressure difference. There are two additional concerns whencomparing pressure gradients calculated from Doppler velocities topressures measured at cardiac catheterization. First, the peak gradientcalculated from the maximum Doppler velocity represents the max-imum instantaneous pressure difference across the valve, not thedifference between the peak LV and peak aortic pressure measuredfrom the pressure tracings. Note that peak LV and peak aorticpressure do not occur at the same point in time; so, this differencedoes not represent a physiological measurement and this peak-to-peak difference is less thanthe maximum instantaneous pressuredifference. The second concern is the phenomenon of pressurerecovery (PR). The conversion of potential energy to kinetic energyacross a narrowed valve results in a high velocity and a drop inpressure. However, distal to the orifice, flow decelerates again. Al-though some of the kinetic energy dissipates into heat due toturbulences and viscous losses, some of the kinetic energy will bereconverted into potential energy with a corresponding increase inpressure, the so-called PR. Pressure recovery is greatest in stenoseswith gradual distal widening since occurrence of turbulences is then

Figure 2 Continuous-wave Doppler of severe aortic stenosis jetshowing measurement of maximum velocity and tracing of thevelocity curve to calculate mean pressure gradient.

Journal of the American Society of Echocardiography Baumgartner et al 5Volume 22 Number 1

Area under curve (VTI) reflects mean gradient

*severity cut-‐offs are different for AHA (lower) and ESC (higher)

Sonosite Machine Use: Calcs -‐> AV -‐> VTI

Mitral Regurgita,on


a.  Regurgitant jet profile b.  Vena contracta width


Mitral Regurgita,on, cont’d 1. Regurgitant jet profile rela,ve to LA

–  Subjec,ve assessment of mitral regurgita,on – more useful for detec,on of MR than quan,fica,on of severity

–  Loose criterion for severe MR •  “Large central jet or eccentric jet adhering,

swirling and reaching posterior LA wall” •  MILD – jet occupies <20% of LA, SEVERE – jet

occupies >40% of LA

–  Limita,ons: •  Jet size subject to Doppler seqngs (set Nyquist

to 50-‐60) •  Elevated LAP reduces jet size – oren a

significant factor in acute MR •  Appearance of eccentric jets altered

significantly when they impinge on LA walls

depends on many technical and haemodynamic factors. For a similarseverity, patients with increased LA pressure or with eccentric jetsthat hug the LA wall or in whom the LA is enlarged may exhibitsmaller jets area than those with normal LA pressure and size orwith central jets (Figure 15).15 In acute MR, even centrally directedjets may be misleadingly small. Furthermore, as this method is asource of many errors, it is not recommended to assess MR severity.Nevertheless, the detection of a large eccentric jet adhering, swirlingand reaching the posterior wall of the LA is in favour of significantMR. Conversely, small thin jets that appear just beyond the mitralleaflets usually indicate mild MR.Key point

The colour flow area of the regurgitant jet is not rec-ommended to quantify the severity of MR. The colourflow imaging should only be used for diagnosing MR.

A more quantitative approach is required when morethan a small central MR jet is observed.

Vena contracta widthThe vena contracta is the area of the jet as it leaves the regurgitantorifice; it reflects thus the regurgitant orifice area.16–18 The venacontracta is typically imaged in a view perpendicular to the com-missural line (e.g. the parasternal long-axis or the apical four-chamber view) using a careful probe angulation to optimize theflow image, an adapted Nyquist limit (colour Doppler scale)(40–70 cm/s) to perfectly identify the neck or narrowest portionof the jet and the narrowest Doppler colour sector scancoupled with the zoom mode to improve resolution and measure-ment accuracy (Figure 16). Averaging measurements over at leasttwo to three beats and using two orthogonal planes wheneverpossible is recommended. A vena contracta ,3 mm indicatesmild MR whereas a width !7 mm defines severe MR. Intermediatevalues are not accurate at distinguishing moderate from mild orsevere MR (large overlap); they require the use of anothermethod for confirmation.

The concept of vena contracta is based on the assumption thatthe regurgitant orifice is almost circular. The orifice is roughly cir-cular in organic MR; although in functional MR, it appears to berather elongated along the mitral coaptation line and non-circular.19,20 Thus, the vena contracta could appear at the sametime narrow in four-chamber view and broad in two-chamberview. Moreover, conventional 2D colour Doppler imaging doesnot provide appropriate orientation of 2D scan planes to obtainan accurate cross-sectional view of the vena contracta. The venacontracta can be classically well identified in both central andeccentric jets. In case of multiple MR jets, the respective widthsof the vena contracta are not additive. Such characteristics maybe better appreciated and measured on 3D echocardiography. Infunctional MR, a mean vena contracta width (four- and two-chamber views) has been shown to be better correlated withthe 3D vena contracta. A mean value .8 mm on 2D echo(Figure 17) has been reported to define severe MR for all

Figure 15 Visual assessment of mitral regurgitant jet usingcolour-flow imaging. Examples of two patients with severemitral regurgitation. (A) Large central jet. (B) Large eccentric jetwith a clear Coanda effect. CV, four-chamber view.

Figure 16 Semi-quantitative assessment of mitral regurgitationseverity using the vena contracta width (VC). The three com-ponents of the regurgitant jet (flow convergence zone, vena con-tracta, jet turbulence) are obtained. CV, chamber view; PT-LAX,parasternal long-axis view.

Table 2 Unfavourable TTE characteristics for mitralvalve repair in functional mitral regurgitation11

Mitral valve deformation

Coaptation distance !1 cm

Tenting area .2.5–3 cm2

Complex jets

Posterolateral angle .458Local LV remodelling

Interpapillary muscle distance .20 mm

Posterior papillary-fibrosa distance .40 mm

Lateral wall motion abnormality

Global LV remodelling

EDD. 65 mm, ESD. 51 mm (ESV. 140 mL)

Systolic sphericity index .0.7

EDD, end-diastolic diameter; ESD, end-systolic diameter; ESV, end-systolicvolume; LV, left ventricle.

P. Lancellotti et al.314

Mitral Regurgita,on, cont’d 2. Vena contracta width –  Simplest and most effec,ve method of

assessing MR severity –  Jet width at level of regurgitant orifice

•  Measure at narrowest point, preceded by a convergence zone and followed by the expanding jet

•  Helpful to use zoom func,on •  Ideally, should be assessed in mul,ple views (i.e.

parasternal long and apical 2 or 4)

–  MILD = <3MM; SEVERE = >7MM –  Limita,ons:

•  Minor miscalcula,ons can drama,cally influence severity assessment

•  Intermediate values non-‐diagnos,c for severity Convergence zone

Regurgitant jet

Mitral Stenosis


a.  Mean pressure gradient b.  Pressure half ,me


Mitral Stenosis, cont’d 1. Mean pressure gradient

–  Es,mate of pressure gradient derived from CW Doppler velocity across valve •  Based on simplified version of Bernoulli equa,on ΔP = 4v2

–  Mild = <5; MODERATE = 5-‐10; SEVERE >10

–  Gradient highly dependent on hemodynamics: •  Overes,mate gradient: MR, tachcardia •  Underes,mate gradient: bradycardia, poor EF, AR

Sonosite Machine Use: Calcs -‐>MV -‐> VTI – trace Doppler profile

Mitral Stenosis, cont’d 3.  Pressure half-‐,me (PHT): ,me for peak

transvalvular gradient to fall to by ½ –  Inversely propor,onal to MV orifice area –  Trace decelera,on of mitral inflow E wave to

characterize peak velocity and slope using PW Doppler •  Ignore the ini,al peak if slope is bimodal •  MILD: PHT = <150; MODERATE: PHT 150-‐219; SEVERE: PHT >220

–  Perturba,ons in LAP or LV compliance or pressure will alter the PHT •  Diastolic dysfunc,on and/or calcified mitral disease have variable effects on PHT rendering it less reliable for assessment of MS •  Severe AR shortens PHT •  Difficult to assess PHT in tachycardic pa,ents

PHT derived from peak velocity and slope

Sonosite Machine Use: Calcs -‐> MV -‐> PHT

RV Dysfunc,on / Pulmonary HTN


a.  RV : LV size b.  Short-‐axis D-‐septum


RV Dysfunc,on / Pulmonary HTN, cont’d

1. RV : LV size –  RV assessment is largely qualita,ve –  Normal RV size 2/3 that of LV –  Increased RV size rela,ve to LV suggests RV

dysfunc,on or overload

2. Short-‐axis D-‐septum –  Normal appearing LV cavity is round

throughout the cardiac cycle –  In RV pressure or volume overload, LV will

take on a “D” shape due to septal flavening •  RV pressure over-‐load is most evident during systole •  RV volume over-‐load most evident during diastole •  In the POCUS seqng dis,nguishing pressure versus volume overload of the RV of minimal clinical u,lity

of pooled studies using these methods for the measurement of RV EFis 44%, with a 95% confidence interval of 38% to 50% (Table 4).

Recommendations: Two dimensionally derived estima-tion of RV EF is not recommended, because of the heteroge-neity of methods and the numerous geometricassumptions.

C. Three-Dimensional Volume Estimation

The accuracy of RV volumes on 3D echocardiography has beenvalidated against animal specimens,45,46 animal cast models ofthe right ventricle,46-48 and human intraoperative RV volumemeasurements.49 At present, the disk summation and apicalrotational methods for RV volume and EF calculation are most com-monly used in 3D echocardiography. Images may be acquired bytransesophageal echocardiography49-51 as well as transthoracicechocardiography. The methodology is complex and beyond thescope of this document, and interested readers are referred toa recent report by Horton et al52 for a discussion of methodology.Compared in vitro, the 3D apical rotational method was most accu-rate when $8 equiangular planes were analyzed.46 Three-dimensional apical rotation using 8 imaging planes provided similarresults to the 3D disk summation method in a mixed adult patientgroup.53 In a variety of clinical settings, both methods have shownto correlate well with MRI-derived RV volumes in children54-56 andadults.51,57-63

With 3D echocardiography, there is less underestimation of RVend-diastolic and end-systolic volumes and improved test-retest vari-ability compared with 2D echocardiography.43,60 Pooled data fromseveral small studies and one larger study64 indicate that the upperreference limit for indexed RV end-diastolic volume is 89 mL/m2

and for end-systolic volume is 45 mL/m2, with indexed volumes be-ing 10% to 15% lower in women than in men (Table 2). The lowerreference limit for RV EF is 44% (Table 4).

Advantages:RV volumes and EFmay be accurately measured by3D echocardiography using validated real-time 3D algorithms.

Disadvantages: Limited normative data are available, with stud-ies using different methods and small numbers of subjects. RV vol-umes by both 2D and 3D echocardiography tend to underestimateMRI-derived RV volumes, although 3D methods are more accurate.Moreover, the 3D disk summation method is a relatively time-consuming measurement to make. Finally, fewer data are availablein significantly dilated or dysfunctional ventricles, making the accu-racy of 3D volumes and EFs less certain.

Recommendations: In studies in selected patients withRV dilatation or dysfunction, 3D echocardiography usingthe disk summation method may be used to report RVEFs. A lower reference limit of 44% has been obtainedfrom pooled data. Until more studies are published, itmay be reasonable to reserve 3Dmethods for serial volumeand EF determinations.

THE RIGHT VENTRICLE AND INTERVENTRICULAR SEPTALMORPHOLOGY

Chronic dilatation of the right ventricle such as may occur with iso-lated RV volume overload (eg, TR) results in progressive lengtheningof the base to apex as well as the free wall to septum dimensions ofthe right ventricle, with the RV apex progressively replacing the leftventricle as the true apex of the heart. In the PSAX, the left ventricleassumes a progressively more D-shaped cavity as the ventricular sep-tum flattens and progressively loses its convexity with respect to thecenter of the RV cavity during diastole.65-67 RV pressure overloadalso distorts the normal circular short-axis geometry of the left ventri-cle by shifting the septum leftward away from the center of the rightventricle and toward the center of the left ventricle, resulting in

Figure 10 Serial stop-frame short-axis two-dimensional echocardiographic images of the left ventricle at the mitral chordal level withdiagrams from a patient with isolated right ventricular (RV) pressure overload due to primary pulmonary hypertension (left) and froma patient with isolated RV volume overload due to tricuspid valve resection (right). Whereas the left ventricular (LV) cavity maintainsa circular profile throughout the cardiac cycle in normal subjects, in RV pressure overload there is leftward ventricular septal (VS) shiftand reversal of septal curvature present throughout the cardiac cycle with most marked distortion of the left ventricle at end-systole.In the patient with RV volume overload, the septal shift and flattening of VS curvature occurs predominantly in mid to late diastole withrelative sparing of LV deformation at end-systole. Reproduced with permission from J Am Coll Cardiol.69

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Rudski et al 697

of pooled studies using these methods for the measurement of RV EFis 44%, with a 95% confidence interval of 38% to 50% (Table 4).

Recommendations: Two dimensionally derived estima-tion of RV EF is not recommended, because of the heteroge-neity of methods and the numerous geometricassumptions.

C. Three-Dimensional Volume Estimation

The accuracy of RV volumes on 3D echocardiography has beenvalidated against animal specimens,45,46 animal cast models ofthe right ventricle,46-48 and human intraoperative RV volumemeasurements.49 At present, the disk summation and apicalrotational methods for RV volume and EF calculation are most com-monly used in 3D echocardiography. Images may be acquired bytransesophageal echocardiography49-51 as well as transthoracicechocardiography. The methodology is complex and beyond thescope of this document, and interested readers are referred toa recent report by Horton et al52 for a discussion of methodology.Compared in vitro, the 3D apical rotational method was most accu-rate when $8 equiangular planes were analyzed.46 Three-dimensional apical rotation using 8 imaging planes provided similarresults to the 3D disk summation method in a mixed adult patientgroup.53 In a variety of clinical settings, both methods have shownto correlate well with MRI-derived RV volumes in children54-56 andadults.51,57-63

With 3D echocardiography, there is less underestimation of RVend-diastolic and end-systolic volumes and improved test-retest vari-ability compared with 2D echocardiography.43,60 Pooled data fromseveral small studies and one larger study64 indicate that the upperreference limit for indexed RV end-diastolic volume is 89 mL/m2

and for end-systolic volume is 45 mL/m2, with indexed volumes be-ing 10% to 15% lower in women than in men (Table 2). The lowerreference limit for RV EF is 44% (Table 4).

Advantages:RV volumes and EFmay be accurately measured by3D echocardiography using validated real-time 3D algorithms.

Disadvantages: Limited normative data are available, with stud-ies using different methods and small numbers of subjects. RV vol-umes by both 2D and 3D echocardiography tend to underestimateMRI-derived RV volumes, although 3D methods are more accurate.Moreover, the 3D disk summation method is a relatively time-consuming measurement to make. Finally, fewer data are availablein significantly dilated or dysfunctional ventricles, making the accu-racy of 3D volumes and EFs less certain.

Recommendations: In studies in selected patients withRV dilatation or dysfunction, 3D echocardiography usingthe disk summation method may be used to report RVEFs. A lower reference limit of 44% has been obtainedfrom pooled data. Until more studies are published, itmay be reasonable to reserve 3Dmethods for serial volumeand EF determinations.

THE RIGHT VENTRICLE AND INTERVENTRICULAR SEPTALMORPHOLOGY

Chronic dilatation of the right ventricle such as may occur with iso-lated RV volume overload (eg, TR) results in progressive lengtheningof the base to apex as well as the free wall to septum dimensions ofthe right ventricle, with the RV apex progressively replacing the leftventricle as the true apex of the heart. In the PSAX, the left ventricleassumes a progressively more D-shaped cavity as the ventricular sep-tum flattens and progressively loses its convexity with respect to thecenter of the RV cavity during diastole.65-67 RV pressure overloadalso distorts the normal circular short-axis geometry of the left ventri-cle by shifting the septum leftward away from the center of the rightventricle and toward the center of the left ventricle, resulting in

Figure 10 Serial stop-frame short-axis two-dimensional echocardiographic images of the left ventricle at the mitral chordal level withdiagrams from a patient with isolated right ventricular (RV) pressure overload due to primary pulmonary hypertension (left) and froma patient with isolated RV volume overload due to tricuspid valve resection (right). Whereas the left ventricular (LV) cavity maintainsa circular profile throughout the cardiac cycle in normal subjects, in RV pressure overload there is leftward ventricular septal (VS) shiftand reversal of septal curvature present throughout the cardiac cycle with most marked distortion of the left ventricle at end-systole.In the patient with RV volume overload, the septal shift and flattening of VS curvature occurs predominantly in mid to late diastole withrelative sparing of LV deformation at end-systole. Reproduced with permission from J Am Coll Cardiol.69

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Pressure Overload

Volume Overload

RV Dysfunc,on / Pulmonary HTN, Cont’d

3.  Right ventricular systolic pressure (RVSP) – CW Doppler interroga,on of tricuspid regurgitant jet •  Possible from short axis, apical 4-‐chamber or subxyphoid

•  Normal peak TR gradient <2.9 m/s, translates into a PA pressure of <36

•  U/S machine provides RVSP assuming RAP of 5mmHg

– Note that elevated RVSP is not, in and of itself, indica,ve of tricuspid valve disease

Cardiac Tamponade

GOALS: 1.  Evalua,on

a.  IVC assessment b.  RV and RA collapse c.  Mitral or tricuspid valve respiratory inflow varia,on


Cardiac Tamponade, cont’d

Tamponade is a CLINICAL diagnosis!

1. Absence of a dilated IVC effec,vely excludes tamponade physiology

2. Early RV collapse during ventricular diastole and / or RA collapse during ventricular systole are signs of tamponade physiology

–  Results from elevated intrapericardial pressures and impaired RV filling

Cardiac Tamponade, cont’d

3.  Exaggerated respiratory mitral or tricuspid valve inflow varia,on –  Sonographic “pulsus paradoxus” –  PW mitral or tricuspid valve inflow to

LV / RV –  Respiratory varia,on >25% = important

Diastolic Dysfunc,on GOALS: 1.  Determina,on of severity

a.  Mitral valve inflow velocity b.  Tissue Doppler of MV annulus


Diastolic Func,on, cont’d 1. Mitral inflow velocity –  E wave – passive flow of blood from LA to LV

•  Reflects preload and effec,veness of LV relaxa,on –  A wave – contribu,on of diastolic filling from atrial

kick •  Reflect LA func,on and LV compliance

–  E/A ra,o >2.0 suggests significant diastolic dysfunc,on

–  Moderate dysfunc,on may exhibit pseudonormaliza,on •  Compensatory LA pressure increase “normalizes” rela,ve contribu,on of “passive” LV filling

–  E/A < 1 suggests mild diastolic dysfunc,on

In pathologically hypertrophied myocardium, LV relax-ation is usually slowed, which reduces early diastolicfilling. In the presence of normal LA pressure, this shifts agreater proportion of LV filling to late diastole after atrialcontraction. Therefore, the presence of predominant earlyfilling in these patients favors the presence of increasedfilling pressures.

B. LA Volume

The measurement of LA volume is highly feasible andreliable in most echocardiographic studies, with themost accurate measurements obtained using the apical4-chamber and 2-chamber views.10 This assessment is clini-cally important, because there is a significant relationbetween LA remodeling and echocardiographic indices ofdiastolic function.11 However, Doppler velocities and timeintervals reflect filling pressures at the time of measure-ment, whereas LA volume often reflects the cumulativeeffects of filling pressures over time.

Importantly, observational studies including 6,657patients without baseline histories of atrial fibrillation andsignificant valvular heart disease have shown that LAvolume index !34 mL/m2 is an independent predictor ofdeath, heart failure, atrial fibrillation, and ischemicstroke.12 However, one must recognize that dilated leftatria may be seen in patients with bradycardia and4-chamber enlargement, anemia and other high-outputstates, atrial flutter or fibrillation, and significant mitralvalve disease, in the absence of diastolic dysfunction. Like-wise, it is often present in elite athletes in the absence ofcardiovascular disease (Figure 2).Therefore, it is importantto consider LA volume measurements in conjunction with apatient’s clinical status, other chambers’ volumes, andDoppler parameters of LV relaxation.

C. LA Function

The atrium modulates ventricular filling through its reser-voir, conduit, and pump functions.13 During ventricular

systole and isovolumic relaxation, when the atrioventricular(AV) valves are closed, atrial chambers work as distensiblereservoirs accommodating blood flow from the venous circu-lation (reservoir volume is defined as LA passive emptyingvolume minus the amount of blood flow reversal in the pul-monary veins with atrial contraction). The atrium is also apumping chamber, which contributes to maintainingadequate LV end-diastolic volume by actively emptying atend-diastole (LA stroke volume is defined as LA volume atthe onset of the electrocardiographic P wave minusLA minimum volume). Finally, the atrium behaves as aconduit that starts with AV valve opening and terminatesbefore atrial contraction and can be defined as LV strokevolume minus the sum of LA passive and active emptyingvolumes. The reservoir, conduit, and stroke volumes of theleft atrium can be computed and expressed as percentagesof LV stroke volume.13

Impaired LV relaxation is associated with a lowerearly diastolic AV gradient and a reduction in LA conduitvolume, while the reservoir-pump complex is enhanced tomaintain optimal LV end-diastolic volume and normalstroke volume. With a more advanced degree of diastolicdysfunction and reduced LA contractility, the LA contri-bution to LV filling decreases.

Aside from LA stroke volume, LA systolic function can beassessed using a combination of 2D and Doppler measure-ments14,15 as the LA ejection force (preload dependent, cal-culated as 0.5 " 1.06" mitral annular area" [peak Avelocity]2) and kinetic energy (0.5 " 1.06 " LA strokevolume" [A velocity]2). In addition, recent reports haveassessed LA strain and strain rate and their clinical associationsin patients with atrial fibrillation.16,17 Additional studies areneeded to better define these clinical applications.

D. Pulmonary Artery Systolic and DiastolicPressures

Symptomatic patients with diastolic dysfunction usuallyhave increased pulmonary artery (PA) pressures. Therefore,in the absence of pulmonary disease, increased PA pressures

Figure 2 (Left) End-systolic (maximum) LA volume from an elite athlete with a volume index of 33 mL/m2. (Right) Normal mitral inflowpattern acquired by PW Doppler from the same subject. Mitral E velocity was 100 cm/s, and A velocity was 38 cm/s. This athlete hadtrivial MR, which was captured by PW Doppler. Notice the presence of a larger LA volume despite normal function.

Nagueh et al.168

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PW Doppler of MV Inflow

Diastolic Func,on, cont’d 2. Tissue Doppler of MV annulus –  Measures speed of relaxa,on –  Septal or lateral wall –  Measure ,ssue veloci,es ~1cm from

mitral valve inser,on sites on the septum or lateral wall •  Septal e’ <8-‐10 and/or lateral < e’10-‐12 m/s

sugges,ve of impaired relaxa,on •  Normal values vary with age

–  Grading from ra,o of mitral inflow or from the decelera,on ,me (DT) of the E wave •  E/A <0.8 – grade I (mild) •  E/A 0.8 -‐ 1.5 – grade II (mod) •  E/A >1.5 – 2.0 – grade III (severe)

B. Measurements

Primary measurements include the systolic (S), early dias-tolic, and late diastolic velocities.90 The early diastolicannular velocity has been expressed as Ea, Em, E, or e,and the late diastolic velocity as Aa, Am, A, ora. Thewriting group favors the use of e and a, because Ea is com-monly used to refer to arterial elastance. The measurementof e acceleration and DT intervals, as well as accelerationand deceleration rates, does not appear to contain incre-mental information to peak velocity alone91 and need notbe performed routinely. On the other hand, the time inter-val between the QRS complex and e onset is prolongedwith impaired LV relaxation and can provide incrementalinformation in special patient populations (see the follow-ing). For the assessment of global LV diastolic function, itis recommended to acquire and measure tissue Dopplersignals at least at the septal and lateral sides of the mitralannulus and their average, given the influence of regionalfunction on these velocities and time intervals.86,92

Once mitral flow, annular velocities, and time intervalsare acquired, it is possible to compute additional time inter-vals and ratios. The ratios include annular e/a and the mitralinflow E velocity to tissue Doppler e (E/e) ratio.90 The latterratio plays an important role in the estimation of LV fillingpressures. For time intervals, the time interval betweenthe QRS complex and the onset of mitral E velocity is sub-tracted from the time interval between the QRS complexand e onset to derive (TE-e), which can provide incrementalinformation to E/e in special populations, as outlined in thefollowing discussion. Technically, it is important to matchthe RR intervals for measuring both time intervals (time toE and time to e) and to optimize gain and filter settings,because higher gain and filters can preclude the correctidentification of the onset of e velocity.

C. Hemodynamic Determinants

The hemodynamic determinants of e velocity include LVrelaxation (Figure 8), preload, systolic function, and LVminimal pressure. A significant association between e andLV relaxation was observed in animal93,94 and human95–97

studies. For preload, LV filling pressures have a minimaleffect on e in the presence of impaired LV relaxation.87,93,94

On the other hand, with normal or enhanced LV relaxation,preload increasese.93,94,98,99 Therefore, in patients withcardiac disease, e velocity can be used to correct for theeffect of LV relaxation on mitral E velocity, and the E/eratio can be applied for the prediction of LV filling pressures(Figure 9). The main hemodynamic determinants of ainclude LA systolic function and LVEDP, such that an increasein LA contractility leads to increased a velocity, whereas anincrease in LVEDP leads to a decrease ina.93

In the presence of impaired LV relaxation and irrespectiveof LA pressure, the e velocity is reduced and delayed, suchthat it occurs at the LA-LV pressure crossover point.94,100

On the other hand, mitral E velocity occurs earlier withPNF or restrictive LV filling. Accordingly, the time intervalbetween the onset of E and e is prolonged with diastolic dys-function. Animal94,100 and human100 studies have shown that(TE-e) is strongly dependent on the time constant of LV relax-ation and LV minimal pressure.100

D. Normal Values

Normal values (Table 1) of DTI-derived velocities are influ-enced by age, similar to other indices of LV diastolic func-tion. With age, e velocity decreases, whereas a velocityand the E/e ratio increase.101

E. Clinical Application

Mitral annular velocities can be used to draw inferencesabout LV relaxation and along with mitral peak E velocity(E/e ratio) can be used to predict LV filling press-ures.86,90,97,102–106 To arrive at reliable conclusions, it isimportant to take into consideration the age of a givenpatient, the presence or absence of cardiovasculardisease, and other abnormalities noted in the echocardio-gram. Therefore, e and the E/e ratio are important variablesbut should not be used as the sole data in drawing con-clusions about LV diastolic function.

It is preferable to use the average e velocity obtainedfrom the septal and lateral sides of the mitral annulus for

Figure 8 Tissue Doppler (TD) recording from the lateral mitral annulus from a normal subject aged 35 years (left) (e ! 14 cm/s) and a58-year-old patient with hypertension, LV hypertrophy, and impaired LV relaxation (right) (e ! 8 cm/s).

Recommendations for the Evaluation of Left Ventricular Diastolic Function by Echocardiography 175


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B. Measurements

Primary measurements include the systolic (S), early dias-tolic, and late diastolic velocities.90 The early diastolicannular velocity has been expressed as Ea, Em, E, or e,and the late diastolic velocity as Aa, Am, A, ora. Thewriting group favors the use of e and a, because Ea is com-monly used to refer to arterial elastance. The measurementof e acceleration and DT intervals, as well as accelerationand deceleration rates, does not appear to contain incre-mental information to peak velocity alone91 and need notbe performed routinely. On the other hand, the time inter-val between the QRS complex and e onset is prolongedwith impaired LV relaxation and can provide incrementalinformation in special patient populations (see the follow-ing). For the assessment of global LV diastolic function, itis recommended to acquire and measure tissue Dopplersignals at least at the septal and lateral sides of the mitralannulus and their average, given the influence of regionalfunction on these velocities and time intervals.86,92

Once mitral flow, annular velocities, and time intervalsare acquired, it is possible to compute additional time inter-vals and ratios. The ratios include annular e/a and the mitralinflow E velocity to tissue Doppler e (E/e) ratio.90 The latterratio plays an important role in the estimation of LV fillingpressures. For time intervals, the time interval betweenthe QRS complex and the onset of mitral E velocity is sub-tracted from the time interval between the QRS complexand e onset to derive (TE-e), which can provide incrementalinformation to E/e in special populations, as outlined in thefollowing discussion. Technically, it is important to matchthe RR intervals for measuring both time intervals (time toE and time to e) and to optimize gain and filter settings,because higher gain and filters can preclude the correctidentification of the onset of e velocity.

C. Hemodynamic Determinants

The hemodynamic determinants of e velocity include LVrelaxation (Figure 8), preload, systolic function, and LVminimal pressure. A significant association between e andLV relaxation was observed in animal93,94 and human95–97

studies. For preload, LV filling pressures have a minimaleffect on e in the presence of impaired LV relaxation.87,93,94

On the other hand, with normal or enhanced LV relaxation,preload increasese.93,94,98,99 Therefore, in patients withcardiac disease, e velocity can be used to correct for theeffect of LV relaxation on mitral E velocity, and the E/eratio can be applied for the prediction of LV filling pressures(Figure 9). The main hemodynamic determinants of ainclude LA systolic function and LVEDP, such that an increasein LA contractility leads to increased a velocity, whereas anincrease in LVEDP leads to a decrease ina.93

In the presence of impaired LV relaxation and irrespectiveof LA pressure, the e velocity is reduced and delayed, suchthat it occurs at the LA-LV pressure crossover point.94,100

On the other hand, mitral E velocity occurs earlier withPNF or restrictive LV filling. Accordingly, the time intervalbetween the onset of E and e is prolonged with diastolic dys-function. Animal94,100 and human100 studies have shown that(TE-e) is strongly dependent on the time constant of LV relax-ation and LV minimal pressure.100

D. Normal Values

Normal values (Table 1) of DTI-derived velocities are influ-enced by age, similar to other indices of LV diastolic func-tion. With age, e velocity decreases, whereas a velocityand the E/e ratio increase.101

E. Clinical Application

Mitral annular velocities can be used to draw inferencesabout LV relaxation and along with mitral peak E velocity(E/e ratio) can be used to predict LV filling press-ures.86,90,97,102–106 To arrive at reliable conclusions, it isimportant to take into consideration the age of a givenpatient, the presence or absence of cardiovasculardisease, and other abnormalities noted in the echocardio-gram. Therefore, e and the E/e ratio are important variablesbut should not be used as the sole data in drawing con-clusions about LV diastolic function.

It is preferable to use the average e velocity obtainedfrom the septal and lateral sides of the mitral annulus for

Figure 8 Tissue Doppler (TD) recording from the lateral mitral annulus from a normal subject aged 35 years (left) (e ! 14 cm/s) and a58-year-old patient with hypertension, LV hypertrophy, and impaired LV relaxation (right) (e ! 8 cm/s).

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Tissue Doppler

Normal

Impaired Relaxa,on

EAE/ASE RECOMMENDATIONS

Recommendations for the Evaluation of Left VentricularDiastolic Function by Echocardiography

Sherif F. Nagueh, MD, Chair†, Christopher P. Appleton, MD†, Thierry C. Gillebert, MD*,Paolo N. Marino, MD*, Jae K. Oh, MD†, Otto A. Smiseth, MD, PhD*, Alan D. Waggoner, MHS†,Frank A. Flachskampf, MD, Co-Chair*, Patricia A. Pellikka, MD†, and Arturo Evangelisa, MD*

Houston, Texas; Phoenix, Arizona; Ghent, Belgium; Novara, Italy; Rochester, Minnesota; Oslo, Norway; St. Louis, Missouri;Erlangen, Germany; Barcelona, Spain

KEYWORDSDiastole;Echocardiography;Doppler;Heart failure

Table of Contents

Preface . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 166I. Physiology . . . . . . . . . . . . . . . . . . . . . . . . 166II. Morphologic and Functional Correlates of Diastolic

Dysfunction . . . . . . . . . . . . . . . . . . . . . . . 167A. LV Hypertrophy . . . . . . . . . . . . . . . . . . . 167B. LA Volume . . . . . . . . . . . . . . . . . . . . . . 168C. LA Function . . . . . . . . . . . . . . . . . . . . . 168D. Pulmonary Artery Systolic and Diastolic Pressures 168

III. Mitral Inflow . . . . . . . . . . . . . . . . . . . . . . . 169A. Acquisition and Feasibility . . . . . . . . . . . . . 169B. Measurements . . . . . . . . . . . . . . . . . . . . 170

C. Normal Values . . . . . . . . . . . . . . . . . . . . 170D. Inflow Patterns and Hemodynamics . . . . . . . . 170E. Clinical Application to Patients With Depressed

and Normal EFs . . . . . . . . . . . . . . . . . . . 170F. Limitations . . . . . . . . . . . . . . . . . . . . . . 171

IV. Valsalva Maneuver. . . . . . . . . . . . . . . . . . . . 171A. Performance and Acquisition. . . . . . . . . . . . 171B. Clinical Application . . . . . . . . . . . . . . . . . 171C. Limitations . . . . . . . . . . . . . . . . . . . . . . 171

V. Pulmonary Venous Flow . . . . . . . . . . . . . . . . 172A. Acquisition and Feasibility . . . . . . . . . . . . . 172B. Measurements . . . . . . . . . . . . . . . . . . . . 172C. Hemodynamic Determinants . . . . . . . . . . . . 172D. Normal Values . . . . . . . . . . . . . . . . . . . . 172E. Clinical Application to Patients With Depressed


VI. Color M-Mode Flow Propagation Velocity . . . . . . . 173A. Acquisition, Feasibility, and Measurement . . . . 173B. Hemodynamic Determinants . . . . . . . . . . . . 174C. Clinical Application . . . . . . . . . . . . . . . . . 174D. Limitations . . . . . . . . . . . . . . . . . . . . . . 174

VII. Tissue Doppler Annular Early and Late DiastolicVelocities. . . . . . . . . . . . . . . . . . . . . . . . . 174A. Acquisition and Feasibility . . . . . . . . . . . . . 174B. Measurements . . . . . . . . . . . . . . . . . . . . 175C. Hemodynamic Determinants . . . . . . . . . . . . 175D. Normal Values . . . . . . . . . . . . . . . . . . . . 175E. Clinical Application . . . . . . . . . . . . . . . . . 175F. Limitations . . . . . . . . . . . . . . . . . . . . . . 177

†Writing Committee of the American Society of Echocardiography.

*Writing Committee of the European Association of Echocardiography.From the Methodist DeBakey Heart and Vascular Center, Houston, TX

(S.F.N.); Mayo Clinic Arizona, Phoenix, AZ (C.P.A.); the University of Ghent,Ghent, Belgium (T.C.G.); Eastern Piedmont University, Novara, Italy(P.N.M.); Mayo Clinic, Rochester, MN (J.K.O., P.A.P.); the University of Oslo,Oslo, Norway (O.A.S.); Washington University School of Medicine, St Louis,MO (A.D.W.); the University of Erlangen, Erlangen, Germany (F.A.F.); and Hos-pital Vall d’Hebron, Barcelona, Spain (A.E.).Reprint requests: American Society of Echocardiography, 2100 Gateway

Centre Boulevard, Suite 310, Morrisville, NC 27560 (E-mail: [email protected]).Disclosures: Thierry C. Gillebert: Research Grant – Participant in compre-

hensive research agreement between GE Ultrasound, Horten, Norway andGhent University; Advisory Board – Astra-Zeneca, Merck, Sandoz.The following stated no disclosures: Sherif F. Nagueh, Frank

A. Flachskampf, Arturo Evangelista, Christopher P. Appleton, ThierryC. Gillebert, Paolo N. Marino, Jae K. Oh, Patricia A. Pellikka, OttoA. Smiseth, Alan D. Waggoner.Conflict of interest: The authors have no conflicts of interest to disclose

except as noted above.

Reprinted from the Journal of the American Society of Echocardiography 22 (2):107–133, February 2009.With permission from and copyright 2009 by the American Society of Echocardiography.

European Journal of Echocardiography (2009) 10, 165–193doi:10.1093/ejechocard/jep007

at St. Joseph's Health Care London on December 16, 2013

http://ehjcimaging.oxfordjournals.org/

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Sonosite Machine Use: PW Doppler -‐>TDI on

Diastolic Func,on, cont’d

EAE/ASE RECOMMENDATIONS

Recommendations for the Evaluation of Left VentricularDiastolic Function by Echocardiography

Sherif F. Nagueh, MD, Chair†, Christopher P. Appleton, MD†, Thierry C. Gillebert, MD*,Paolo N. Marino, MD*, Jae K. Oh, MD†, Otto A. Smiseth, MD, PhD*, Alan D. Waggoner, MHS†,Frank A. Flachskampf, MD, Co-Chair*, Patricia A. Pellikka, MD†, and Arturo Evangelisa, MD*

Houston, Texas; Phoenix, Arizona; Ghent, Belgium; Novara, Italy; Rochester, Minnesota; Oslo, Norway; St. Louis, Missouri;Erlangen, Germany; Barcelona, Spain

KEYWORDSDiastole;Echocardiography;Doppler;Heart failure

Table of Contents

Preface . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 166I. Physiology . . . . . . . . . . . . . . . . . . . . . . . . 166II. Morphologic and Functional Correlates of Diastolic

Dysfunction . . . . . . . . . . . . . . . . . . . . . . . 167A. LV Hypertrophy . . . . . . . . . . . . . . . . . . . 167B. LA Volume . . . . . . . . . . . . . . . . . . . . . . 168C. LA Function . . . . . . . . . . . . . . . . . . . . . 168D. Pulmonary Artery Systolic and Diastolic Pressures 168

III. Mitral Inflow . . . . . . . . . . . . . . . . . . . . . . . 169A. Acquisition and Feasibility . . . . . . . . . . . . . 169B. Measurements . . . . . . . . . . . . . . . . . . . . 170

C. Normal Values . . . . . . . . . . . . . . . . . . . . 170D. Inflow Patterns and Hemodynamics . . . . . . . . 170E. Clinical Application to Patients With Depressed


IV. Valsalva Maneuver. . . . . . . . . . . . . . . . . . . . 171A. Performance and Acquisition. . . . . . . . . . . . 171B. Clinical Application . . . . . . . . . . . . . . . . . 171C. Limitations . . . . . . . . . . . . . . . . . . . . . . 171

V. Pulmonary Venous Flow . . . . . . . . . . . . . . . . 172A. Acquisition and Feasibility . . . . . . . . . . . . . 172B. Measurements . . . . . . . . . . . . . . . . . . . . 172C. Hemodynamic Determinants . . . . . . . . . . . . 172D. Normal Values . . . . . . . . . . . . . . . . . . . . 172E. Clinical Application to Patients With Depressed


VI. Color M-Mode Flow Propagation Velocity . . . . . . . 173A. Acquisition, Feasibility, and Measurement . . . . 173B. Hemodynamic Determinants . . . . . . . . . . . . 174C. Clinical Application . . . . . . . . . . . . . . . . . 174D. Limitations . . . . . . . . . . . . . . . . . . . . . . 174

VII. Tissue Doppler Annular Early and Late DiastolicVelocities. . . . . . . . . . . . . . . . . . . . . . . . . 174A. Acquisition and Feasibility . . . . . . . . . . . . . 174B. Measurements . . . . . . . . . . . . . . . . . . . . 175C. Hemodynamic Determinants . . . . . . . . . . . . 175D. Normal Values . . . . . . . . . . . . . . . . . . . . 175E. Clinical Application . . . . . . . . . . . . . . . . . 175F. Limitations . . . . . . . . . . . . . . . . . . . . . . 177

† Writing Committee of the American Society of Echocardiography.

*Writing Committee of the European Association of Echocardiography.From the Methodist DeBakey Heart and Vascular Center, Houston, TX

(S.F.N.); Mayo Clinic Arizona, Phoenix, AZ (C.P.A.); the University of Ghent,Ghent, Belgium (T.C.G.); Eastern Piedmont University, Novara, Italy(P.N.M.); Mayo Clinic, Rochester, MN (J.K.O., P.A.P.); the University of Oslo,Oslo, Norway (O.A.S.); Washington University School of Medicine, St Louis,MO (A.D.W.); the University of Erlangen, Erlangen, Germany (F.A.F.); and Hos-pital Vall d’Hebron, Barcelona, Spain (A.E.).Reprint requests: American Society of Echocardiography, 2100 Gateway

Centre Boulevard, Suite 310, Morrisville, NC 27560 (E-mail: [email protected]).Disclosures: Thierry C. Gillebert: Research Grant – Participant in compre-

hensive research agreement between GE Ultrasound, Horten, Norway andGhent University; Advisory Board – Astra-Zeneca, Merck, Sandoz.The following stated no disclosures: Sherif F. Nagueh, Frank

A. Flachskampf, Arturo Evangelista, Christopher P. Appleton, ThierryC. Gillebert, Paolo N. Marino, Jae K. Oh, Patricia A. Pellikka, OttoA. Smiseth, Alan D. Waggoner.Conflict of interest: The authors have no conflicts of interest to disclose

except as noted above.

Reprinted from the Journal of the American Society of Echocardiography 22 (2):107–133, February 2009.With permission from and copyright 2009 by the American Society of Echocardiography.

European Journal of Echocardiography (2009) 10, 165–193doi:10.1093/ejechocard/jep007


are London on Decem



ownloaded from

MV Tissue Doppler Septal e’ Lateral e’

Septal e’ ≥ 8 m/s Lateral e’ ≥ 10 m/s

Normal

Septal e’ ≤ 8 m/s Lateral e’ ≤ 10 m/s

E/A <0.8 E/A 0.8-‐1.5 E/A ≥ 2

Mild dyfunc,on

Moderate dyfunc,on

Severe dyfunc,on

MV Inflow E/A Ra,o

Prac,cal Approach to Assessment of Diastolic Func,on

LV Systolic Func,on GOALS: 1.  Determina,on of Func,on

a.  Qualita,vely b.  Time-‐velocity integral of LVOT flow to determine stroke volume


Ler Ventricular Systolic Func,on 1. Qualita,ve func,on assessment – Simple and effec,ve – Pay aven,on to

•  Inward mo,on of the myocardium •  Thickening of the myocardium •  Mitral valve excursion (PSLAX)

2. Es,ma,on of stroke volume by measuring flow through LVOT –  PW Doppler in LVOT –  Calcs >>> Ao valve >>> LVOT VTI –  Normal ~>18 •  Corresponds to a stroke volume of ~60mL

assuming an LVOT radius of 1

–  Confounded by MR, but s,ll provides informa,on regarding forward flow

LVOT VTI

Documents

Advanced(Applicaon(of(Pointof1Care( Echocardiography(in ... · velocity is "1 m/s because squaring a number "1 makes it even smaller. When the proximal velocity is over 1.5 m/s or