Journal of Cardiology (2009) 54, 347—358

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REVIEW

Doppler echocardiography: A contemporary review

Nandan S. Anavekar (MD)a, Jae K. Oh (MD)a,b,∗

a Division of Cardiovascular Diseases, Mayo Clinic College of Medicine, 200 1st Street SW, Rochester, MN 55905, USAb Cardiac and Vascular Center, Samsung Medical Center, Seoul, Republic of Korea

Received 15 July 2009; received in revised form 14 September 2009; accepted 28 September 2009Available online 22 October 2009

KEYWORDSEchocardiography;Doppler;Systolic function;Diastolic function;Hemodynamics

Summary The 2D echocardiographic examination of the heart provides insight into struc-ture and function, providing a precise anatomical display of the cardiovascular anatomy withhigh temporal resolution. Prior to advances in 2D imaging, Doppler echocardiography had beenthe mainstay of cardiovascular noninvasive assessment. Doppler echocardiography, remainsan integral part of the cardiovascular echocardiographic examination, providing a precisehemodyanamic evaluation of the heart. Both systolic and diastolic function can be quantitated

by blood pool and tissue Doppler. Pressure gradients, intracardiac pressures, valve areas, regur-gitant volume, and shunt volume can be noninvasively determined reliably. Based on Dopplerhemodynamics as well as on 2D echocardiography, most of hemodynamic conditions can be man-aged surgically as well as medically without invasive hemodynamic measurements. We presenta review of these current applications of Doppler echocardiography. © 2009 Published by Elsevier Ireland Ltd on behalf of Japanese College of Cardiology.

Contents

Introduction.............................................................................................................. 348Doppler echocardiography ............................................................................................... 349Color flow imaging ....................................................................................................... 349Applications of Doppler echocardiography to clinical cardiology.......................................................... 349

Transvalvular gradients.............................................................................................. 350Intracardiac pressures............................................................................................... 350

Left ventricular outflow tract obstruction ..................Assessment of systolic function............................Assessment of diastolic function and diastolic heart failureDoppler flow velocities ....................................

∗ Corresponding author at: Division of Cardiovascular Diseases, Mayo CUSA. Tel.: +1 507 284 2511.

E-mail address: oh.jae@mayo.edu (J.K. Oh).

0914-5087/$ — see front matter © 2009 Published by Elsevier Ireland Ltddoi:10.1016/j.jjcc.2009.10.001

......................................................... 351.......................................................... 352......................................................... 352

.......................................................... 353

linic College of Medicine, 200 1st Street SW, Rochester, MN 55905,

on behalf of Japanese College of Cardiology.

348 N.S. Anavekar, J.K. Oh

Transmitral flow .............................................................................................. 353Mitral annular velocities ...................................................................................... 353

Flow within the great vessels ............................................................................ 353Assessment of valve function........................................................................................ 354Continuity equation ................................................................................................. 354Pressure half time................................................................................................... 355

Regurgitant volume, fraction, and orifice area........................................................... 355Volumetric method ...................................................................................... 355

Proximal isovelocity surface area.................................................................................... 356Conclusions .............................................................................................................. 356

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References ...............................................

ntroduction

n 1842, an Austrian professor of mathematics and prac-ical geometry, Christian Doppler, presented results of hisnvestigations in the field of astronomy, without notion thathey would become important principles of modern ultra-ound diagnostics. Almost a century later, at the Universityf Osaka, Japan, S. Satomura first applied these princi-les to measure the blood flow velocities in peripheral andxtracranial brain-supplying vessels [1]. In 1954, Edler andertz [2] of Sweden were the first to record movementsf cardiac structures with ultrasound. In 1956, Japanesenvestigators also observed echoes from heart structures [3].he results were presented at ‘‘The Second Internationalongress on Acoustics’’ in June 1956 in Cambridge, MA, USA.hey used both A-scan and time-position indication. Whenbarium titanate transducer working with a frequency ofMHz was applied to the heart-apex area, they found ‘‘a

pecial echo, which oscillated delicately but rapidly to andro, changing the echo intensity and position of the cathode-ay screen with synchronization to each heart beat.’’ Thischo is doubtless an echo from the heart [3]. In the early960s, Joyner and Reid [4] at the University of Pennsylvaniaere the first Americans to use ultrasound in the examina-

ion of the heart, and shortly thereafter, Feigenbaum et al.5] were responsible for the introduction of echocardiog-aphy into the clinical practice of cardiology by detectingericardial effusion, which was a difficult undertaking athat time. Doppler echocardiography was not used clinicallyntil the late 1970s when two independent groups, Holent al. [6] and Hatle et al. [7] refined the techniques to belinically applicable.

The Doppler principle was initially applied to determineow velocities, flow direction, and flow characteristics inhe heart and great vessels and is based on the Dopplerffect (Fig. 1), which was described by Christian Doppler1].

It was more recently applied to determine the veloc-ty of myocardial tissue using tissue Doppler imaging [8,9].he Doppler effect is the increase in sound frequency as aound source moves toward the observer and the decreasen sound frequency as the source moves away from the

bserver. In the circulatory system, the red blood cell is theoving target and in tissue Doppler Imaging, myocardial tis-

ue or structure is the target. When an ultrasound beam isirected toward moving targets, the transducer determineshe frequency shift (�f) which is the difference between

F(

.......................................................... 356

he transmitted frequency of the transducer (ft) and theeceived frequency (fr). The frequency shift is related tohe velocity of the moving target (v), transmitted frequencyft), and the angle between the direction of ultrasound beamnd the direction of the moving target as shown by theoppler equation.

f = 2ftv cos �

c

By determination of blood flow velocities, the Dopplerchocardiography allows various hemodynamic determina-ions in the heart and the vascular system. There are twoasic equations needed to determine pressure gradients,troke volume, and orifice area using Doppler echocardio-raphy. First, the modified Bernoulli equation is used tostimate pressure gradients.

P = 4v2

igure 1 Diagram of the Doppler effect. RBCs, red blood cells.Reproduced with permission from Oh et al. [44].)

Doppler echocardiography: a contemporary review

Figure 2 Drawing of pulsed wave and continuous wave

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Tiasgosures and shunts; measures of systolic cardiac performance

Doppler echocardiography from the apical view. Ao, aorta; LA,left atrium; LV, left ventricle; RA, right atrium; RV, right ventri-cle. (Reproduced with permission from Oh et al. [44].)

or

SV = A × TVI

Doppler echocardiography

The spectral Doppler display shows blood flow velocitiesplotted against time. The information that can be obtainedfrom a spectral Doppler trace includes flow velocity, direc-tion of flow (that above the baseline is toward the transducerand that below the baseline is away from the transducer),the timing of the signal with cardiac events, and intensityof the flow signal. There are two different forms of Dopplerechocardiography: the continuous wave and pulsed waveDoppler (Fig. 2). Continuous wave Doppler refers to contin-uous transmission of the Doppler signal toward the movingred blood cells and the continuous reception of the return-ing signals reflected from the moving red blood cells. In thecontinuous wave mode the transducer uses two crystals;one to send and the other to receive the reflected ultra-sound waves continuously. Blood flow along the entire beamis observed. Therefore there is no range resolution, whichmeans no indication of the depth from which the signalshave been generated. The principal advantage of continuouswave Doppler is in its ability to display high velocity Dopplersignals. Continuous wave Doppler is usually performed witheither an image guided or non-imaging transducer. In thepulsed wave mode, a single ultrasound crystal sends andreceives sound beams. The ultrasound signals are sent outin short bursts or pulses. Through range gating, pulse waveDoppler has the ability to select Doppler information froma particular location within the heart or great vessels utiliz-

ing a sample volume. The pulse repetition frequency (PRF),refers to the frequency at which the pulse wave transducerpulses and thus determines when the next burst of soundwaves are emitted. The Nyquist limit is the maximum veloc-

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349

ty that can be measured by pulse wave Doppler, and thisimit is determined by the PRF.

yquist limit = PRF

2

If the frequency shift is higher than the calculatedyquist frequency, aliasing occurs, that is, the Doppler spec-rum is cut off at the Nyquist frequency, and the remainingrequency shift is recorded on the top or bottom of thepposite side of the baseline. The PRF varies inversely withhe depth of the sample volume, the shallower the loca-ion of the sample volume, the higher the PRF and Nyquistrequency. In other words, higher velocities can be recordedithout aliasing by pulsed wave Doppler, the closer the sam-le volume is to the transducer.

olor flow imaging

olor flow imaging is based on pulsed wave Doppler princi-les and displays intracavitary blood flow using a color map,epending on the speed, direction and extent of turbulence.t uses multiple sampling sites along multiple ultrasoundeams (multigated). At each sampling gate, the frequencyhift is measured, converted to a digital format, automati-ally correlated with a preset color scheme, and displayeds color flow superimposed on 2-dimensional imaging. Bloodow directed toward the transducer has a positive frequencyhift and is color coded in shades of red; blood flow directedway from the transducer has a negative frequency shiftnd is color coded in shades of blue. Each color has multi-le shades, and the lighter shades within each primary colorre designated to higher velocities within the Nyquist limit.hen flow velocity is higher than the Nyquist limit, color

liasing occurs and is depicted as color reversal. With eachultiple of the Nyquist limit, the color repeatedly reverts

o the opposite color. Turbulence is characterized by theresence of variance which is the difference between theean velocity of flow and individual flow velocities. Since

urbulent flow has increased flow velocity differences, theariance is shown as green color. Color flow imaging has aole in semi quantification of the degree of valvular regur-itation or intracardiac shunting as well as quantification ofther Doppler-derived information, such as calculation ofegurgitant volumes using the proximal isovelocity surfacerea (PISA) technique [10].

pplications of Doppler echocardiography tolinical cardiology

he most important role of any clinical tool is in its abil-ty to answer clinical questions that will ultimately guide

clinician to formulate the most appropriate therapeutictrategy for their patients. In this way, Doppler echocardio-raphy has developed its niche in hemodynamic evaluationf the heart: transvalvular gradients and intracardiac pres-

y stroke volume and cardiac output; severity of valvularesions be it regurgitant or stenotic in nature; measures ofiastolic cardiac performance; and differentiation betweenyocardial and pericardial diseases. Currently, most of

3 N.S. Anavekar, J.K. Oh

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Figure 3 (a) A diagram of simultaneous left ventricular (LV)and aortic (Ao) pressures in aortic stenosis. The correspondingcontinuous Doppler recording is shown below. The mean gra-dient is delineated by the shaded area. (b) A still frame ofcsa(

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ntracardiac hemodynamic assessments required for clinicalanagement of cardiac patients are performed noninva-

ively by 2-dimensional and Doppler echocardiography.

ransvalvular gradients

ased on the Doppler shift, Doppler echocardiography mea-ures blood flow velocities in the cardiac chambers and greatessels. Blood flow velocities can be converted into pres-ure gradients using the modified Bernoulli equation. Bloodow velocity measured with Doppler echocardiography isn instantaneous event, and the pressure gradients derivedrom Doppler velocities are instantaneous gradients. Whenhe maximal Doppler velocity is converted to pressure gra-ient using the simplified Bernoulli equation, it representshe maximal instantaneous gradient. The mean gradient ishe average of the pressure gradients during the entire floweriod (Fig. 3a and b), and the mean gradient obtained withoppler echocardiography has been shown to correlate wellith one measured in the catheterization laboratory. From

he Doppler tracing, the mean gradient can be obtained byracing the velocity signal and using the built-in calculationackage.

ntracardiac pressures

fundamental principle is that the velocity across an ori-ce in the cardiovascular system is related directly to theressure difference between the proximal and distal por-ions of the orifice, according to the Bernoulli equation.sing this principle several key intracardiac pressures cane calculated.

Tricuspid regurgitation (Fig. 4) occurs during the systolichase of the cardiac cycle and the tricuspid regurgitantelocity reflects the systolic pressure difference betweenhe right ventricle (RVSP) and the right atrium (RAP)11—13].

VSP = RAP + 4(vTR)2

If there is no obstruction at the right ventricular outflowract (RVOT) then the pulmonary artery systolic pressurePASP) will be the same as the calculated RVSP. The RVOTnd pulmonary valve velocities should be measured in allatients who have an increased tricuspid regurgitant veloc-ty to ensure there is no RVOT obstruction.

Pulmonary regurgitation occurs during the diastolic phasef the cardiac cycle and the pulmonary regurgitant veloc-ty represents the diastolic pressure difference between theulmonary artery and the right ventricle:

AEDP = RAP + 4(vPR)2

Mitral regurgitation occurs during the systolic phase of

he cardiac cycle and the mitral regurgitant velocity rep-esents the systolic pressure difference between the leftentricle and the left atrium. In patients without left ven-ricular outflow tract (LVOT) obstruction, the systolic bloodressure is practically the same as the left ventricular sys- p

ontinuous wave Doppler recording for the apex in aortic steno-is, the border of the velocity display is traced and entered intobuilt-in calculation package to determine the mean gradient.

Reproduced with permission from Oh et al. [44].)

olic pressure.

SBP = LASP + 4(vMR)2

∴ LASP = SBP − 4(vMR)2

Aortic regurgitation (Fig. 5) occurs during the diastolichase of the cardiac cycle and the aortic regurgitant veloc-ty represents the diastolic pressure difference between theorta and the left ventricle.

DBP = LVEDP + 4(vAR)2

∴ LVEDP = DBP − 4(vAR)2

In Fig. 5 we present the spectral Doppler display of aatient with aortic regurgitation. The diastolic blood pres-

Doppler echocardiography: a contemporary review 351

Figure 4 Simultaneous right ventricular (RV) and right atrial

Figure 6 Simultaneous Doppler and cardiac pressure record-

pressure tracings and tricuspid regurgitant velocity recording bycontinuous wave Doppler echocardiography. (Reproduced withpermission from Oh et al. [44].)

sure is 60 mmHg and the end-diastolic aortic regurgitationvelocity is 2.5 m/s which corresponds to 25 mmHg gradientbetween the aortic pressure and LV pressure at end-diastole.Therefore, using the equation LV end-diastolic pressure(LVEDP) is 60—25 mmHg which is 35 mmHg.

The left ventricular end-diastolic pressure and left atrialpressures can also be estimated by various diastolic fillingvariables from the mitral inflow, pulmonary venous flow, andtissue Doppler velocities.

Intracardiac pressure measurements obtained by Dopplerechocardiography correlate well with pressures derived bycatheter techniques (Fig. 6), and thus may mitigate the needfor extensive invasive measurements in patients with com-plex hemodynamic problems [14].

Figure 5 Aortic regurgitation velocity recording in a patientwith heart failure. (Reproduced with permission from Oh et al.[44].)

ings show an excellent correlation between Doppler- andc(w

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atheter-derived pressure gradients in (a) mitral stenosis andb) aortic stenosis. Ao, aorta; LV, left ventricle. (Reproducedith permission from Oh et al. [44].)

eft ventricular outflow tract obstruction

ynamic left ventricular outflow tract (LVOT) obstructions classically described in hypertrophic obstructive car-iomyopathy. However, it must be appreciated that not allynamic LVOT obstruction is due to the former [15]. If ven-ricular systolic function becomes hyperdynamic in a patientith basal septal hypertrophy, the LVOT becomes obstructed

n a dynamic fashion, and the hemodynamic profile is similaro that observed in hypertrophic obstructive cardiomyopa-hy. This is most often seen in elderly patients with a clinicalistory of hypertension, however the latter is not a pre-equisite [16]. Clinical presentation includes dyspnea, chestain, hypotension, or a combination of these. Similar toypertrophic obstructive cardiomyopathy, the hemodynamiconditions are negatively affected by agents that produce a

ow volume state or peripheral vasodilation. Another clinicalcenario associated with dynamic LVOT obstruction can bebserved in surgical patients in the postoperative period whoay be intravascularly volume depleted and who are receiv-

352

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atient with dynamic LVOT obstruction in the setting of hyper-rophic obstructive cardiomyopathy. Note the dagger-shapedrofile. (Reproduced with permission from Oh et al. [44].)

ng inotropic agents thereby creating the perfect stormor dynamic outflow tract obstruction [17,18]. Acute LVOTbstruction may occur in the setting of acute anterior api-al myocardial infarction, especially if there is pre-existingasal septal hypertrophy [19,20]. In this setting there isyperdynamic function of the non infarcted myocardium,pecifically the inferobasal region, which results in systolicnterior motion of the mitral valve. In this setting hemody-amic compromise may be dramatic necessitating treatmentith intravenous fluids, �-blockade, or even a pure �-agonist

uch as phenylephrine.The degree of left ventricular outflow obstruction is

eadily assessed with continuous wave Doppler echocardio-raphy. Increased flow velocity across the left ventricularutflow tract is optimally detected from the apical acousticindow. The resulting Doppler spectrum has a characteristic

ate-peaking dagger-shaped appearance (Fig. 7). The peakelocity detected can be used to calculate the maximumnstantaneous pressure gradient across the LVOT. The corre-ation between the Doppler-derived and catheter-derivedressure gradients is good [21]. The dynamic nature ofVOT obstruction can be documented with continuous waveoppler echocardiography during the Valsalva maneuver orith the inhalation of amyl nitrate. It has been shown

hat the LVOT velocity also increases after a meal or afterngestion of alcohol due to afterload reduction that occursecondary to peripheral vasodilation [22,23].

ssessment of systolic function

he echocardiographic examination has been integral tohe current evaluation of cardiac systolic function. Muchf this assessment is based on 2-dimensional echocardio-raphic imaging and calculation of left ventricular ejection

raction. In this regard, parameters such as left ventric-lar wall thickness, presence or absence of regional wallotion abnormalities, and calculation or estimation of the

eft ventricular ejection fraction, combined, can be a usefulssessment of global systolic function. Additional parame-

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N.S. Anavekar, J.K. Oh

ers such as stroke volume and cardiac output can also bebtained with the Doppler echocardiographic assessment.he latter is based on the principle that flow rate is equalo the cross-sectional area of flow multiplied by the velocityf the moving fluid.

= Av

Because flow velocity varies during ejection in a pulsatileystem, individual velocities of the Doppler spectrum needo be summed to measure the total volume of flow duringgiven ejection period. The sum of velocities is called the

ime velocity integral (TVI), and is calculated as the areanclosed by the baseline and the Doppler spectrum. Thenits ascribed to this parameter is a distance and repre-ents the distance a column of blood travelling in a cylinderith cross-sectional area ‘‘A’’ would travel during the stroke

ime. As such, the stroke volume (SV) can be extrapolateds the multiplication of the stroke distance by the cross-ectional area of the containing cylinder.

V = A × TVI

The location most frequently used to determine thetroke volume is the left ventricular outflow tract. The areaf the orifice is assumed to be circular.

A = �r2

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2

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= 0.785d2

∴ SV = 0.785d2 × TVI

CO = SV × HR

CI = CO

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ssessment of diastolic function and diastolic heartailure

n half of patients, the primary cause of heart failure is dias-olic dysfunction, with preservation of the left ventricularjection fraction [24,25]. Abnormal myocardial relaxationnd increased filling pressures have to be present to estab-ish the diagnosis of diastolic heart failure [26]. Dopplerchocardiography is the most practical method for assessinglling patterns and myocardial relaxation and for estimating

eft ventricular filling pressures at rest and with exertion byecording flow velocities from the atrioventricular valves,entral veins, and myocardial tissue.

Normal diastolic function allows adequate filling of theentricles during rest and with exercise, without an abnor-al increase in diastolic pressures. With active myocardial

elaxation, left ventricular pressure becomes less than lefttrial pressure, and when this occurs the mitral valve opensnd early rapid diastolic filling begins. Normally, the pre-ominant determinant of the driving force of early diastolic

lling is the elastic recoil and the normal relaxation of the

eft ventricle; the left atrial pressure is less important in theormal state. Approximately 80% of left ventricular fillingccurs during this phase. As a result of rapid filling, left ven-ricular pressure increases and momentarily may exceed left

Doppler echocardiography: a contemporary review

Figure 8 Left ventricular (LV) and atrial (LA) pressures as seenin cardiac catheterization correlated to various mitral inflow

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Doppler patterns. In this diagram, impaired relaxation, nor-mal filling, and restrictive filling patterns are demonstrated.(Reproduced with permission from Oh et al. [44].)

atrial pressure, and this loss of positive driving force resultsin deceleration of mitral inflow. A positive transmitralpressure gradient and flow are created again by atrial con-traction during late diastole and this accounts for 15—20% ofleft ventricular filling in normal subjects. With myocardialrelaxation, the left ventricular cavity elongates and expandslaterally. The longitudinal motion of the mitral annulus hasbeen shown to reflect the rate of myocardial relaxation [27].In most patients, the left ventricular diastolic filling patternscan be determined by 2-dimensional echocardiography andmitral inflow characteristics. However, a definitive assess-ment of diastolic filling and estimation of filling pressuresmay require tissue Doppler imaging [28—30], pulmonary andhepatic venous Doppler imaging, and color-M-mode imagingof the mitral inflow

Doppler flow velocities

Transmitral flowThe transmitral flow comprises three parts that are delin-eated on the spectral Doppler display (Fig. 8). The E wavecorresponds to the early diastolic flow, the A wave corre-sponds to transmitral flow during atrial contraction, and theflow period between the E and A wave is the period of dias-tasis where left atrial and left ventricular pressures begin toequalize. However, despite the equilibrium achieved duringdiastasis, blood continues to flow from left atrium to leftventricle due to inertial forces. The time taken for the peakE velocity to reach zero velocity is referred to as the decel-eration time, and is a useful parameter in the assessment ofdiastolic function. In patients with a relaxation abnormalityas the predominant diastolic dysfunction, the decelerationtime is prolonged, because with a slower and continueddecrease in left ventricular pressure until mid to late dias-tole, it takes longer for the left atrial and left ventricular

pressures to equilibrate. The isovolumic relaxation time par-allels the changes in deceleration times, being prolonged inabnormal relaxation and shortened with rapid relaxation orincreased filling pressure or both.

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353

The transmitral flow profile can be significantly influ-nced by the presence of left-sided valvular abnormalities.n patients with severe aortic regurgitation, there may be

rapid increase in LVEDP due to the increase in left ven-ricular volume from the additional regurgitant volume.his rapid increase in LVEDP results in a rapid equilibra-ion between the left atrium and left ventricle, creating ahortened deceleration time. In mitral regurgitation, theres an increase in the transmitral E velocity due to an increasen forward flow across the mitral valve. Additionally whenhere is severe mitral regurgitation, the left atrial pressure isncreased and may produce a restrictive filling profile (Fig. 8)ith shortened isovolumic relaxation time, an increasedeak E velocity and a shortened deceleration time.

In the presence of mitral stenosis, significant mitral annu-ar calcification or prosthetic mitral valves, the transmitraloppler assessment is hindered and as such precludes anyonclusions regarding diastolic filling and annular motion.dditionally, the peak early diastolic annular velocity (Em)erived at either the lateral or medial mitral annulus, inhe presence of abnormal septal motion caused by recentardiac operation, left bundle branch block, or right ven-ricular pacing, has been found to correlate poorly with leftentricular filling pressures.

itral annular velocitieshe mitral annular velocities are measured using tis-ue Doppler imaging technique [28]. Measurements madeegarding mitral annular velocities reflecting the statusf myocardial relaxation can be used independently andn combination with information obtained with transmitraloppler assessment, in the evaluation of diastolic function.here are three components of the tissue Doppler profilehat are routinely measured: the systolic myocardial veloc-ty (S′); the early diastolic myocardial velocity (E′); and theate diastolic myocardial velocity (A′). E′ is essential forlassifying the diastolic filling pattern and estimating fillingressures. In normal subjects, E′ increases as the transmitralradient increases with exertion or with increased preload.owever, in patients with impaired myocardial relaxation,′ reduces at baseline and does not increase as much as inormal subjects with increased preload [27]. A decrease in′ is one of the earliest markers for diastolic dysfunction,nd this decrease is present in all stages of diastolic dys-unction [28,31]. Because the E′ velocity remains reducedegardless of preload, and the mitral E velocity increasesith higher filling pressure, the ratio between the peak Eelocity measured on the transmitral velocity profile and theeak E′ velocity measured on tissue Doppler imaging corre-ates well with left ventricular filling pressure. E′ velocity islso helpful in distinguishing restrictive myocardial diseaserom constrictive pericarditis (Fig. 9) in patients with heartailure and normal ejection fraction. Mitral lateral annulus′ velocity is usually higher than medial annulus E′, but inonstrictive pericarditis, medial E′ is frequently higher thanateral E′ and is usually preserved or augmented while E′ iseduced in patients with myocardial disease.

low within the great vesselshe pulmonary and hepatic venous Doppler profile parallelshe transmitral and transtricuspid inflow patterns respec-

354

Figure 9 Tissue Doppler assessment of the medial annulus. (a)In restrictive disease E′ is reduced; (b) in constrictive disease E′

is supranormal and varies with respiration. S′, systolic myocar-dd(

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ial velocity; E′, early diastolic myocardial velocity; A′, lateiastolic myocardial velocity; Insp, inspiration; Exp, expiration.Reproduced with permission from Oh et al. [44].)

ively. The pulmonary venous flow is continuous throughouthe cardiac cycle. Systolic forward flow (S) occurs as aesult of atrial relaxation and descent of the mitral annu-us toward the left ventricular apex with ventricular systolend corresponds to the x-descent. The systolic forward flows biphasic in one third of patients; S1 is related to atrialelaxation, S2 occurs in mid to late systole as the mitralnnulus descends toward the cardiac apex. When left atrialressures are elevated, systolic filling from the pulmonaryeins is reduced. Diastolic forward flow (D) occurs duringiastole when there is an open conduit between the pul-onary veins, the left atrium, the open mitral valve, and the

eft ventricle, and corresponds to the y-descent. Atrial floweversal refers to the retrograde flow of blood back into theulmonary veins secondary to atrial contraction. With atrialontraction, blood is ejected from the left atrium into theeft ventricle and also backward into the pulmonary veins.he magnitude and duration of this flow reversal is deter-ined by the transmitral and atriovenous pressure gradientshich are determined by left atrial systolic function and lefttrial and ventricular compliance. The pulmonary venousiastolic flow complements the information obtained onhe transmitral inflow Doppler profile [32]. The pulmonaryenous diastolic flow essentially parallels that of the trans-itral E velocity and deceleration time, so that when peakvelocity is decreased, the peak pulmonary venous dias-

olic velocity is also decreased. Additionally the atrial flow

eversal into the pulmonary veins occurs with atrial con-raction and reflects the pressure gradient between the lefttrium and the pulmonary vein following atrial contraction.hus, measurement of the peak atrial reversal velocity andhe duration of atrial reversal flow into the pulmonary veins

N.S. Anavekar, J.K. Oh

ompared to the mitral A wave duration is also a usefuliastolic parameter used in diastolic assessment.

Hepatic vein velocities reflect changes in pressure, vol-me and compliance of the right atrium. In normal subjects,epatic vein flow velocities consist of four components:ystolic forward flow (S); diastolic forward flow (D), sys-olic flow reversal (SR), and diastolic flow reversal (DR).nder normal hemodynamic conditions, systolic forwardow exceeds diastolic forward flow and there are noajor reversal velocities. Timing and respiratory changes

n forward and reversal velocities of hepatic vein flowre important in the assessment of tricuspid regurgita-ion, constriction, tamponade, restriction, and pulmonaryypertension. As right ventricular filling pressure increases,epatic systolic flow velocity decreases and diastolic flowelocity increases. With marked increase in right ventric-lar filling pressures, a prominent flow reversal occursuring systole and diastole, or both. Diastolic flow rever-al in the hepatic veins is seen in patients with pulmonaryypertension or constrictive pericarditis. It is characteristi-ally augmented with expiration in constriction and remainsonstant without respiratory variation in pulmonary hyper-ension. Severe tricuspid regurgitation produces a typicalystolic flow reversal, but a systolic flow reversal does notlways indicate severe tricuspid regurgitation.

Superior vena caval flow also has a characteristic pat-ern. Systolic forward flow velocity is normally greater thaniastolic forward flow. As right atrial pressure increases,iastolic forward flow becomes more dominant becauseight atrial pressure is reduced with opening of the tricuspidalve. The superior vena caval velocities are accentuated innspiration and attenuated with expiration. This respiratoryariation becomes less prominent with higher right atrialressures and less respiratory effort.

ssessment of valve function

ssessment of valve function involves a combination of a-dimensional evaluation and a Doppler evaluation. Whenvaluating the cardiac valves, the 2-dimensional examina-ion provides information regarding structure and motion.he Doppler echocardiographic examination involves botholor flow imaging and continuous and pulse wave Dopplerxamination.

ontinuity equation

he continuity equation is the Gorlin formula of echocar-iography and is used to calculate the area of a stenotic oregurgitant valve [33]. It uses the concept of conservation ofow. This principle states that the flow in any part of a closedircuit must be equal regardless of varying cross-sectionalreas of the circuit (Fig. 10). Therefore, as area changes,elocity of flow must change to preserve the equilibrium ofow.

SV1 = SV2

A1 × TVI1 = A2 × TVI2

∴ A2 = A1 ×(

TVI1

TVI2

)

Doppler echocardiography: a contemporary review

Figure 10 Schematic of conservation of flow in a closedsystem using the continuity principle. A, area; LVOT, left ven-

bid

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tricular outflow tract; SV, stroke volume; TVI, time velocityintegral. (Reproduced with permission from Oh et al. [44].)

Pressure half time

The pressure half time (PHT) is the time interval for thepeak pressure gradient to reach its half level [34]. Itsderivation is best illustrated by application of Bernoulli’sprinciple:

PPHT = PPEAK

2

4(vPHT )2 = 4(vPeak)2

2

∴ vPHT = vPeak√2

The PHT is proportional to deceleration time such that[35]:

PHT = 0.29DT

Pressure half time can be used to estimate the mitralvalve area with the empiric formula [36]:

MVA = 220PHT

Substituting 0.29DT for PHT

MVA = 759DT

The PHT is not affected by the angle between the direc-tion of the ultrasound beam and blood flow. However, itoverestimates the area of normal prosthetic mitral valves.Another important clinical application of PHT is to assess theseverity of aortic regurgitation. The PHT of aortic regurgita-

tion Doppler velocity becomes significantly shorter (<250 ms)with severe aortic regurgitation (usually in an acute or semi-acute setting) because of a rapid increase in left ventriculardiastolic pressure and decrease in aortic pressure [37,38].However, it is also affected by LV diastolic pressure and can

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e quite reduced without severe aortic regurgitation if theres severe diastolic dysfunction with marked elevation of LViastolic pressure.

egurgitant volume, fraction, and orifice area

egurgitant volume can be estimated in two different wayssing Doppler echocardiography: by the volumetric methodnd by the proximal isovelocity surface area (PISA) method.oth of these methods adhere to the fundamental principlef conservation of flow in a closed circuit.

olumetric methodhe volumetric method of regurgitant volume calculation isased on the principle that the total forward volume acrossregurgitant valve is equal to the sum of the systemic strokeolume and regurgitant volume [39].

V = QTOT − QS

In mitral regurgitation, the total forward flow (QTOT) ishe mitral inflow volume, calculated as the product of theitral valve annulus area and the mitral inflow time velocity

ntegral (TVI). The mitral inflow TVI is obtained by placingsample volume at the center of the mitral annulus dur-

ng diastole. The systemic stroke volume (QS) is obtained byultiplying the LVOT area by the LVOT TVI. The mitral valve

egurgitant volume is then estimated as the mitral inflowolume subtracting the LVOT volume.

QTOT = Mitral inflow

∴ QTOT = 0.785(dMV )2 × TVIMV

QS = LVOT forward outflow

∴ QS = 0.785(dLVOT )2 × TVILVOT

RV = QTOT − QS

This calculation is not accurate in the presence of severeortic regurgitation (the regurgitant volume is underesti-ated).In aortic regurgitation the systemic forward flow is equiv-

lent to the mitral inflow and the total forward flow is thatcross the LVOT.

Mitral inflow = QS

∴ QS = 0.785(dMV )2 × TVIMV

LVOT forward flow = QTOT

∴ QTOT = 0.785(dLVOT )2 × TVILVOT

RV = QTOT − QS

The regurgitant fraction is simply the fraction of the total

orward flow that culminates in regurgitant volume.

egurgitant fraction (%) = RV

QTOT

× 100

356 N.S. Anavekar, J.K. Oh

Figure 11 Concept of hemispheric shells of identical flowvelocities used in proximal isovelocity surface area determina-tO

P

Ivr

R

cbfloavttf(

rc

Figure 12 Color flow imaging of mitral regurgitation (MR)without shift in aliasing velocity (a). In (b) the baseline of thecolor scale is shifted and radius of color aliasing from the mitralvalve is measured. This information is used along with the max-imal mitral regurgitant velocity and time velocity integral todsw

C

Thheoqgvr2ti

R

ion of regurgitant volumes. (Reproduced with permission fromh et al. [44].)

roximal isovelocity surface area

f the regurgitant orifice area is known, the regurgitantolume can be estimated as the product of the effectiveegurgitant orifice (ERO) area and regurgitant velocity TVI.

V = ERO × TVIREGURG

The regurgitant orifice area can be estimated using theoncept of proximal isovelocity surface area [40—42]. Aslood flow converges toward the regurgitant orifice, bloodow velocity increases with the formation of multiple shellsf isovelocity of hemispheric shape (Fig. 11). The flow ratet the surface of a hemispheric shell with the same flowelocity (isovelocity), should be equal to the flow rate acrosshe regurgitant orifice. By adjusting the Nyquist limit ofhe color flow map, the flow velocity at a hemispheric sur-ace, proximal to the regurgitant orifice can be determinedFig. 12a and b).

QAt Hemispheric Shell = 2�r2 × vN

∴ QAt Hemispheric Shell = 6.28r2 × vN

QERO = ERO × vREGURG

QHemispheric Shell = QERO

∴ 6.28r2 × vN = ERO × vREGURG

∴ ERO = 6.28r2vN

vREGURG

RV = ERO × TVIREGURG

∴ RV =[

6.28r2vN

vREGURG

][TVIREGURG]

The concept of PISA, as discussed above for determiningegurgitant orifice area and volume, can also be applied toalculate the area of a stenotic valve [43].

etermine the regurgitant volume by the proximal isovelocityurface area method. Ao, aorta; LV, left ventricle. (Reproducedith permission from Oh et al. [44].)

onclusions

he 2-dimensional echocardiographic examination of theeart provides insight into structure and function, and thisas been greatly complemented by the advances in Dopplerchocardiography, which provides hemodynamic evaluationf the heart. Both systolic and diastolic function can beuantitated by blood pool and tissue Doppler. Pressureradients, intracardiac pressures, valve areas, regurgitantolume, and shunt volume can be noninvasively determinedeliably. Based on Doppler hemodynamics as well as on-dimensional echocardiography, most hemodynamic condi-ions can be managed surgically as well as medically withoutnvasive hemodynamic measurements.

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lossary

f: frequency shift (Hz)t: transmitted frequency (Hz)

r: received frequency (Hz)RF: pulse repetition frequency (Hz): velocity (m/s)TR: tricuspid valve regurgitant velocity (m/s)PR: pulmonary valve regurgitant velocity (m/s)

CPRE

N.S. Anavekar, J.K. Oh

MR: mitral valve regurgitant velocity (m/s)AR: aortic valve regurgitant velocity (m/s)PEAK : velocity at peak pressure (m/s)REGURG: maximum regurgitant velocity (m/s)PHT : velocity at pressure half time (m/s)N: aliasing velocity (m/s): speed of sound in blood (1540 m/s)P: pressure gradient (mmHg)VSP: right ventricular systolic pressure (mmHg)AP: right atrial pressure (mmHg)AEDP: pulmonary artery diastolic pressure (mmHg)BP: systolic blood pressure (mmHg)ASP: left atrial systolic pressure (mmHg)BP: diastolic blood pressure (mmHg)VEDP: left ventricular end-diastolic blood pressure (mmHg)PEAK: peak pressure (mmHg): flow rate (mL/s): area (cm2)VI: time velocity integral (cm)VIMV: time velocity integral through mitral valve (cm)VILVOT: time velocity integral through LVOT (cm)V: stroke volume (mL): radius (cm): diameter (cm)MV: mitral valve annular diameter (cm)LVOT: left ventricular outflow tract diameter (cm)R: heart rate (beats/min)O: cardiac output (L/min)SA: body surface area (m2)

I: cardiac Index (L/min/m2)HT: pressure half time (ms)V: regurgitant volume (mL)RO: effective regurgitant orifice (cm2)