Download M-Mode Echocardiography

Survey
yes no Was this document useful for you?
   Thank you for your participation!

* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project

Document related concepts

Electrocardiography wikipedia , lookup

Cardiac surgery wikipedia , lookup

Pericardial heart valves wikipedia , lookup

Quantium Medical Cardiac Output wikipedia , lookup

Artificial heart valve wikipedia , lookup

Echocardiography wikipedia , lookup

Aortic stenosis wikipedia , lookup

Atrial septal defect wikipedia , lookup

Arrhythmogenic right ventricular dysplasia wikipedia , lookup

Hypertrophic cardiomyopathy wikipedia , lookup

Lutembacher's syndrome wikipedia , lookup

Mitral insufficiency wikipedia , lookup

Transcript
9
M-Mode Echocardiography
Itzhak Kronzon, MD, Gerard P. Aurigemma, MD
Historically, M-mode (motion mode) was the first effective modality for the ultrasonic evaluation of the heart. M-mode echocardiography provides an ice pick, one-dimensional (depth only) view of
the heart.1,2 The ultrasound echoes reflected from the various cardiac interfaces are represented as dots, and their intensities by
brightness (B-mode). With the sweep of the screen (or the recording
paper), the location of each interface is represented by a line, which
provides information about its temporal location (Fig. 9.1). The
two-dimensional (2D) appearance of the tracing is the result of presenting depth (expressed as the up-down dimension of the tracing)
and width (left to right dimension, which expresses time).
An important attribute of M-mode echocardiography, compared
with 2D imaging, is its superior temporal resolution. In the current
2D-directed M-mode, data is acquired at a rate up to 1000 frames
per second, compared with 15 to 100 frames per second for 2D
echocardiography, depending on sector width and heart rate.1,2
Thus M-mode echocardiography remains important in daily clinical use, for its ability to time events during the cardiac cycle and
assess fast moving structures (e.g., valves) (see Fig. 9.1).
The limitations of M-mode are related to its one-dimensional
nature. Although the interrogating ultrasound can be tilted to visualize different structures and their anatomic relations, it may miss
other structures. Also, it may produce erroneous information about
chamber and vessel dimensions by scanning them obliquely. Therefore M-mode tracings should always be obtained with the guidance
of the two-dimensional images.
Some echocardiographers consider M-mode echocardiography
to be a mere historical relic. Many of its initial uses during the earliest decade of echocardiography have been supplanted by the
newer, more anatomically correct 2D, 3D, and Doppler modalities.
We and others feel that like history itself, older experience is still
worth studying.1 Furthermore, in selected situations, M-mode
remains a fundamental part of the routine echocardiographic exam
and provides an important supplement to the newer echocardiographic modalities. Accordingly, this chapter will demonstrate
classic M-mode images, with emphasis on its continued value in
the era of 2D and 3D Doppler echocardiography.
LEFT VENTRICLE
The most common use for echocardiography, in any of its forms,
is to assess size and function of the left ventricle (LV).3 At
present, 2D-directed M-mode echocardiography is still used to
establish cardiac chamber size and wall thickness (Fig. 9.2).
Given its superior temporal resolution, M-mode echocardiography is perfectly suited to diagnosing abnormal LV contraction
patterns, such as those seen with left bundle branch block (see
Fig. 9.2, B).4,5
It has long been appreciated that normal systolic function
includes the descent of the mitral and tricuspid annulus toward
the apex, which remains relatively stationary.5 The extent of the
descent of the base, measured in millimeters, is reflective of global
systolic function. Acronyms for this descent of the base are
TAPSE6 (tricuspid annular plane systolic excursion) and MAPSE
(mitral annular plane systolic excursion) (see Fig. 9.2, E).6
MITRAL VALVE
Normal Motion
During the rapid ventricular filling in early diastole, the anterior
mitral leaflet moves from its end-systolic closed position (D point)
toward the opening position, that is, anteriorly toward the interventricular septum (E point); there is a reciprocal motion of the posterior leaflet (see Fig. 9.1, A, C). The nadir of this backward motion is
called the F point. Atrial contraction reopens the leaflets (the
A point.) Near the onset of systole, the leaflets move to the closed
position (at the C point), where they remain throughout systole.
EKG
Chest wall
ARV
RS
RV
LS
AC
AV
AMV
LV
AV
PPM
PMV
PLV
A
LA
PLA
EN
EP
Lung
PER
Figure 9.1. Left ventricle. A, A schematic shows the four principal M-mode views of the heart. AMV, anterior mitral valve; ARV, anterior right ventricle;
EKG, electrocardiograph; EN, endocardial edge; EP, epicardial surface; LA, left atrial; LS, left ventricular septum; LV, left ventricle; PLA, plasminogen
activator; PLV, posterior left ventricle; PMV, posterior mitral valve; PPM, posterior papillary muscle; RS, right ventricular septum; RV, right ventricle.
30
M-Mode Echocardiography
31
9
RV
E
A
F
C
MV
D
C
B
Figure 9.1—Cont'd B, M-mode of the mitral valve. C, M-mode transducer is directed through the RV, proximal aorta, and LA. AV aortic valve leaflets and
AC aortic closure line, which, in normal individuals, is in the mid portion of the aorta. A, Anterior-most excursion of the anterior leaflet with atrial systole; C,
closure of the mitral valve and end-diastole; D, posterior-most excursions of the mitral leaflets in early diastole; E, anterior-most excursions of
the mitral leaflets in early diastole; F, closure point of the mitral valve in early diastasis; MV, mitral valve; RV, right ventricle. (A from Feigenbaum H.
Echocardiography, Philadelphia: Lea & Febiger, 5th edition, 1993; adapted and used with permission.)
A
B
SB
LVIDd
LSM
LVIDs
D
TAPSE
C
Figure 9.2. Left ventricle. A, Left ventricle of a patient with infiltrative cardiomyopathy due to amyloidosis. The walls are thick and the fractional shortening is low. B, Left bundle branch block. Compared to the normal LV echocardiogram (A), the initial downward motion of the septum (ESM) is absent,
there is a prominent downward motion of the septum in early ventricular systole (the septal "beak" [SB]) which represents unopposed RV contraction,
due to delayed activation of the posterior and lateral LV. Also, during ventricular systole, the septum moves anteriorly (arrow). Finally, there is a posterior
septal motion (PSM), which occurs after the peak upward excursion of the posterior wall (LSM), and coincides with RV filling. C, Septal motion in severe
TR. Notice the abrupt rightward motion (arrow) of the interventricular septum as the RV unloads into the RA during isovolumic systole. D, Example of
normal tricuspid annular plane systolic excursion (TAPSE), defined as 16 mm or greater.6 LVIDd, diastolic LV dimensions; LVIDs, systolic LV dimensions.
32
SECTION II Transthoracic Echocardiography
Mitral Stenosis
combination of leaflet thickening, anterior motion of the posterior
mitral leaflet, and flat EF slope is diagnostic of mitral stenosis
(Fig. 9.3, A).
The mitral leaflets open at early diastole. The leaflets are thickened
with commissural fusion. The larger anterior leaflet moves anteriorly, which also pulls the smaller posterior leaflet anteriorly.
Because of the pressure gradient across the valve throughout diastole and the lack of rapid ventricular filling phase, the leaflets do
not return toward the closure position as in normal valves.1,2 The
EF slope (see Fig. 9.1, B) is flatter than normal. The M-mode
Mitral Valve Prolapse
Unlike mitral stenosis, the valve diastolic motion is normal, and
leaflets remain closed in systole. In mitral valve prolapse the closed
mitral leaflets sag backward. This motion may occur in mid to late
RV
S
RV
LV
MV
MV
PW
A
B
AVO
Ao
LV
LA
C
D
MVC
Figure 9.3. A, Rheumatic mitral stenosis. Note the mitral valve echoes of the anterior and posterior leaflet are thickened and move in concert, because
of inflammatory valvulitis. The EF slope is diminished. B, Severe mitral valve prolapse: arrows indicate late systolic sagging or “hammocking” of the mitral
valve. C, Anterior motion of the mitral valve in a patient with hypertrophic obstructive cardiomyopathy (arrow). D, Hemodynamic tracing illustrating the
principle behind the early opening of the aortic valve in a patient with acute severe aortic regurgitation. Notice that there is pressure equilibration
between the aorta and LV, which occurs at end diastole. See text for details. Ao, Aorta; AVO, atrial valve opening; LA, left atrium; LV, left ventricle;
MV, mitral valve; MVC, mitral valve closing; PW, posterior wall; RV, right ventricle; S, septum.
M-Mode Echocardiography
33
9
E
RV
LV
MV
F
G
Figure 9.3—Cont'd E, Early closure of the mitral valve in a patient with acute severe aortic regurgitation. Note that the mitral valve (arrow) closes well
before the QRS complex, indicative of pressure equilibration between the LV and left atrium in this patient. F, Fine fluttering of the mitral valve at end
diastole in a patient with aortic regurgitation. G, E point septal separation (arrow) in a patient with idiopathic dilated cardiomyopathy. LV, Left ventricle;
MV, mitral valve; RV, right ventricle.
(Continued)
34
SECTION II Transthoracic Echocardiography
E
E
A
A
D
C
D
LV
C
LV
LA
LA
H
I
J
Figure 9.3—Cont'd H, Schematic diagram (left panel) and M-mode recording in a patient with elevated left ventricular diastolic pressure, showing the
so-called B-bump (black arrow, right panel of schematic; blue arrow in patient M-mode). I, Color M-mode in a patient with complete heart block. Left
arrow points to superimposed mitral regurgitation jet, which occurs in isovolumic systole. Right arrow points to diastolic mitral regurgitation seen in the
left atrium, following nonconducted atrial depolarization. J, Use of M-mode echocardiography to estimate size of a proximal isovelocity systolic area
(PISA). This adaptation of color M-mode allows for easy recognition of the extent of the PISA. A, Anterior-most excursion of the anterior leaflet with atrial
systole; C, closure of the mitral valve and end-diastole; D, posterior-most excursions of the mitral leaflets in early diastole; E, anterior-most excursions of
the mitral leaflets in early diastole; LA, left atrial pressure; LV, left ventricular pressure. (Schematic adapted and used with permission from Feigenbaum
H. Echocardiography. ed 5. Philadelphia: Lea & Febiger, 1993.)
M-Mode Echocardiography
35
K
9
Figure 9.3—Cont'd K, Color M-mode (see Fig. 9.5, A) Vp or flow propagation velocity in a normal individual. Ao, Aortic pressure; AVO, aortic valve
opening; LA, left atrial pressure; LV, left ventricular pressure; MVC, mitral valve closure. (H from Feigenbaum H. Echocardiography, Philadelphia: Lea &
Febiger, 5th edition, 1993; adapted and used with permission; J courtesy Dr. Roberto Lang.)
systole (see Fig. 9.3, B), and may be associated with mid-systolic
click or pansystolic (and be associated with a pansystolic mitral
regurgitation murmur).7–9
Systolic Anterior Motion of the Anterior
Mitral Leaflet
An anterior mitral leaflet that demonstrates systolic anterior motion
(SAM) is seen mainly in patients with hypertrophic cardiomyopathy; high velocity in the left ventricular outflow tract results in systolic anterior motion of the anterior mitral leaflet,10,11 due to the
Venturi effect. In these patients, the diastolic mitral valve motion
is normal. During systole, however, the anterior leaflet moves
toward the interventricular septum, and may coapt with the ventricular surface. The duration and degree of coaptation are related to
the pressure gradient (see Fig. 9.3, C).10,11
The Mitral Valve in Aortic Insufficiency
In acute aortic regurgitation the diastolic pressure in the ventricle
rises rapidly during diastole as a result of aortic runoff. In fact,
in some instances the left ventricular pressure may rise above the
LA pressure, leading to premature closure of the mitral valve
(see Fig. 9.3, D, E).12,13 When the aortic regurgitation jet strikes
the anterior mitral leaflet, a fine, fluttering. motion can be seen.
This finding suggests the presence of aortic insufficiency, but is
not a marker of its severity (see Fig. 9.3, F). None of these findings
in aortic regurgitation are reliably demonstrated by 2D echocardiography because of its inferior temporal resolution. Therefore Mmode data complements the assessment of valve regurgitation
severity in contemporary practice.
The Mitral Valve in Left Ventricular Dysfunction
Normally the mitral E point is close to the interventricular septum
(E point septal separation). In patients with left ventricular dilatation
and reduced stroke volume, the E point of the anterior leaflet is
separated from the septum by a distance of at least 8 mm. Interestingly, this expression of unfavorable LV remodeling was the first
echocardiographic finding that appeared directly related to prognosis (see Fig. 9.3, G).14–16 A second M-mode sign of LV dysfunction
is a disturbance in the A-C line, which is usually rapid and
straight. In patients with noncompliant LVs, atrial systole results
in a significant elevation in LV diastolic pressures. The M-mode
reflection of this phenomenon is an interruption in the normal
A-C closure line, which is known as the A-C shoulder or B bump
(see Fig. 9.3, H).17,18
Color M-Mode
This multiparametric display features flow events superimposed on
the M-mode display and is perhaps the best method available to
time regurgitant events. As is shown in Figure 9.3, I, color M-mode
graphically demonstrates both systolic and diastolic mitral regurgitation in the same patient. Doppler color M-mode can be used for
the measurement of the hemisphere maximum radius in the calculation of the proximal isovelocity area (PISA)19 (see Fig. 9.3, J).
This technique can be used when the MV leaflets are not well
visualized, making it difficult to decide where to place the measurement of the PISA radius. We have also found this technique useful
in cases of atrial fibrillation where the average of several PISA radii
must be determined.
AORTIC VALVE
Normal Motion
The aortic valve can be seen in the middle of the aortic root. The right
and the noncoronary cusps move in systole to the opened position,
and they move in diastole toward the closed position, creating the
impression of rectangles connected by strings (see Fig. 9.1, A, C).
The ejection time, a descriptor of forward stroke volume, can be
timed from the aortic valve opening to its closure. Fine fluttering
of the opened leaflets is not uncommon. In patients with aortic
stenosis, the leaflets appear thickened and calcified and have diminished excursion. A bicuspid aortic valve may have eccentric closure
line (Fig. 9.4, A).
36
SECTION II Transthoracic Echocardiography
Ao
LA
A
B
D
C
Figure 9.4. Aortic valve. A, M-mode echocardiogram in a patient with a bicuspid aortic valve. Arrow indicates eccentric closure line. B, In hypertrophic
cardiomyopathy (HCM), there is midsystolic closure (arrows) indicating left ventricular outflow tract obstruction with diminution in forward flow. As the LV
pressure rises and then overcomes the dynamic obstruction, the aortic valve opens a second time. Opening of the aortic valve is associated with
reduced forward stroke volume. C, In subaortic membrane. The aortic valve envelope shows a rapid upward swing followed by restoration to a midaortic position without secondary opening (white arrow). This is in contrast to the M-shaped envelope in patients with hypertrophic obstructive cardiomyopathy. D, Early aortic valve opening (black arrow) in a patient with acute severe aortic regurgitation. In the first and third beats following a longer
cycle, there is more opportunity for pressure equilibration between the LV and the aorta because the filling of the left ventricle is augmented. This leads to
premature opening of the aortic valve. Ao, Aorta; LA, left atrium. (Image courtesy Dr. Theo E. Meyer.)
The Aortic Valve in Hypertrophic Obstructive
Cardiomyopathy
PULMONIC VALVE
Normal Motion
In hypertrophic obstructive cardiomyopathy the systolic anterior
motion may result in left ventricular outflow obstruction, and
therefore flow across the aortic valve will be decreased in
midsystole. The M-mode will show a midsystolic closure of the
aortic valve (see Fig. 9.4, B). In discrete subaortic stenosis to a subaortic membrane, by contrast, the valve opens well in early systole,
and then suddenly returns to near closure position, where it stays for
the rest of systole (see Fig. 9.4, C).
In most cases where motion is normal, only the anterior leaflet of
the pulmonic valve can be depicted on M-mode. This leaflet
moves posteriorly and remains opened during systole. At end
diastole, with right atrial contraction, the right ventricular pressure approaches the pulmonary arterial end-diastolic pressure,
resulting in posterior motion of the pulmonic valve (A-wave)
(Fig. 9.5, A).2,20,21
Premature Aortic Valve Opening
With severe aortic regurgitation, there is a rapid rise of left ventricular diastolic pressure and a rapid decline in the aortic diastolic
pressure. With left atrial contraction, the left atrial (and left ventricular) diastolic pressure may rise above the aortic diastolic pressure,
resulting in premature (end-diastolic) aortic valve opening (see
Fig. 9.4, D).
Severe Pulmonary Hypertension
In severe pulmonary hypertension, the pulmonary artery diastolic
pressure is much higher than the right ventricular diastolic pressure.
In this hypertension situation, the right atrial contraction will have
no effect on the pulmonic valve end-diastolic position. No A-wave
is seen, in spite of normal sinus rhythm (see Fig. 9.5, B). Another
finding seen in pulmonary hypertension is the “flying W” sign seen
during pulmonic valve systolic opening. This unusual motion, with
M-Mode Echocardiography
Pulmonary
hypertension
Normal
37
Pulmonic
stenosis
9
Pulmonic
valve
PA
PA
PA
RV and PA
pressures
RV
A
RV
RV
d
B
C
Figure 9.5. Pulmonary valve. A, Schematic of the pulmonary valve in a normal individual, a patient with pulmonary hypertension, and a patient with
pulmonic stenosis. Lower part of the diagram demonstrates right ventricular and pulmonary artery pressures in the three scenarios. B, The "flying W"
sign in a patient with severe pulmonary hypertension. C, Taken from a study of a patient with severe valvular pulmonic stenosis; note the exaggerated
atrial contraction motion, as shown in the schematic. Red overlay has been placed to simulate schematic shown in A. (A from Feigenbaum H. Echocardiography, Philadelphia: Lea & Febiger, 5th edition, 1993.)
midsystolic closure and late systolic opening, may be the result of
increased pulmonary vascular resistance.20,21 The abnormal
absence of the pulmonic valve A-wave, together with the presence
of flying W sign, are highly suggestive of severe pulmonary hypertension. They can be used when Doppler estimation of pulmonary
artery pressure is not possible because of the lack of tricuspid or
pulmonic regurgitation.
PERICARDIAL DISEASE
Pericardial effusion is better demonstrated by 2D echocardiography
than by M-mode echocardiography. However, the timing of the
abnormalities seen in cardiac tamponade and constrictive pericarditis can contribute to the understanding of the pathophysiology of
these conditions; this issue is reviewed in Figure 9.6.
CARDIAC TAMPONADE
M-mode can demonstrate pericardial effusion as well as the respiratory variations in ventricular size and valve excursion. Because of
ventricular interdependence, inspiration results in less pulmonary
venous return and transmitral flow, which leads to a phasic decline
in left ventricular volume. This process is reversed during
inspiration. The M-mode echocardiogram (recorded simultaneously with respiratory tracing) shows the septal inspiratory shift
toward the LV. This is the echocardiographic equivalent of the paradoxical pulse.22–24
The exact timing of diastolic right ventricular collapse can also
be demonstrated by M-mode echocardiography (see Fig. 9.6, A, B).
In some cases of pulmonary hypertension or chronic right-sided
pressure overload with RV hypertrophy, LA or even LV collapse
may occur before RV or RA collapse is seen. This may also be seen
in instances of low filling pressure. The elevation of right atrial
pressure seen in most cases of tamponade can be confirmed by
M-mode tracing of the inferior vena cava (IVC) near its communication with the right atrium. An IVC diameter of more than 20 mm,
with reduced (less than 50%) decrease during inspiration or “sniff”
indicates elevated right atrial pressure, usually greater than 15 mm
Hg (IVC plethora) (see Fig. 9.6, C).
CONSTRICTIVE PERICARDITIS
This difficult clinical diagnosis can still be supported by an array of
M-mode echocardiographic findings.25,26 These findings include
(1) pericardial thickening; (2) IVC plethora (see earlier discussion);
(3) inspiratory septal shift toward the LV (The right ventricular
38
SECTION II Transthoracic Echocardiography
B
A
RV
10mm
LV
a
a
b
b
A
D
C
EKG
ARV
RS
LS
DM
ASM
PPM
E
Figure 9.6. Pericardial disease. A, Cardiac tamponade: Large pericardial effusion and diastolic collapse of the right ventricular free wall, indicated by
the arrow. B, Large circumferential pericardial effusion (upper pair of downward arrows) and left atrial collapse (lower pair of downward arrows), indicating increased intrapericardial pressure leading to ventricular diastolic and left atrial systolic collapse. When filling pressures are low, this constellation
of findings is called low pressure cardiac tamponade. C, In patient with tamponade, the vena cava is dilated and does not collapse. D, Constrictive
pericarditis. E, Schematic of normal septal motion (left) and recording from a patient with constrictive pericarditis. Note the diastolic posterior motion of
the septum (DM), as well as the second reverberation in the septum (ASM), which corresponds to atrial systole.
cavity dimension increases during inspiration and decreases during
expiration, and there are reciprocal changes in the LV. During
expiration, the mitral valve opening duration is longer than that during inspiration) (see Fig. 9.6, D); (4) diastolic septal “bounce”
(characteristic early diastolic notch) as well as a late diastolic
reverberation in the septum, around the time of atrial contraction
(see Fig. 9.6, D, E); and (5) premature opening of the pulmonic
valve due to elevation of the right ventricular end-diastolic pressure
without pulmonary hypertension, and relatively low pulmonary
artery diastolic pressure.
Doppler Echocardiography: Normal Antegrade Flow Patterns
REFERENCES
1. Feigenbaum H: Role of M-mode technique in today’s echocardiography, J Am Soc
Echocardiogr 23:240–257, 2010.
2. Feigenbaum H: Echocardiography, ed 5, Malvern, Pa, 1993, Lea & Febiger.
3. Lang RM, Bierig M, Devereux RB, et al: Recommendations for chamber quantification, J Am Soc Echocardiogr 18:1440–1463, 2005.
4. Grines CL, Bashore TM, Boudoulas H, et al: Functional abnormalities in isolated
left bundle branch block. The effect of interventricular asynchrony, Circulation
79:845–853, 1989.
5. Jones CJ, Raposo L, Gibson DG: Functional importance of the long axis dynamics
of the human left ventricle, Br Heart J 634:215–220, 1990.
6. Rudski LG, Lai WW, Afilalo J, et al: Guidelines for the echocardiographic assessment of the right heart in adults: a report from the American Society of Echocardiography, J Am Soc Echocardiogr 23:685–713, 2010, quiz 786–688.
7. Dillon JC, Haisse CL, Chang S, et al: Use of echocardiography in patients with
prolapsed mitral valve, Circulation 43:503–507, 1971.
8. Kerber RE, Isaeff DM, Hancock EW: Echocardiographic patterns in patients with
the syndrome of systolic click and late systolic murmur, N Engl J Med
284:691–693, 1971.
9. Popp RE, Brown OR, Silverman JF, et al: Echocardiographic abnormalities in the
mitral valve prolapsed syndrome, Circulation 49:428–433, 1974.
10. Henry WL, Clark CE, Griffith JM, et al: Mechanism of left ventricular outflow
obstruction in patients with obstructive asymmetric septal hypertrophy (idiopathic
hypertrophic subaortic stenosis), Am J Cardiol 35:337–345, 1975.
11. Pollick C, Rakowski H, Wigle ED: Muscular subaortic stenosis: the quantitative
relationship between systolic anterior motion and the pressure gradient, Circulation 69:43–49, 1984.
12. Botvinick EH, Schiller NB, Wickramasekaran R, et al: Echocardiographic demonstration of early mitral valve closure in severe aortic insufficiency. Its clinical
implications, Circulation 51:836–847, 1975.
13. Perez JE, Cordova F, Cintron G: Diastolic opening of the aortic valve (AV) in a
case of aortic insufficiency due to AV fenestration, Cardiovasc Dis 5:254–257,
1978.
10
39
14. Ahmadpour H, Shah AA, Allen JW, et al: Mitral E point septal separation: a reliable index of left ventricular performance in coronary artery disease, Am Heart J
106:21–28, 1983.
15. Child JS, Krivokapick J, Perloff JK: Effect of left ventricular size on mitral E point
to ventricular septal separation in assessment of cardiac performance, Am Heart J
101:797–805, 1981.
16. Massie BM, Schiller NB, Ratshin RA, et al: Mitral-septal separation: new echocardiographic index of left ventricular function, Am J Cardiol 39:1008–1016, 1977.
17. Konecke LL, Feigenbaum H, Chang S, et al: Abnormal mitral valve motion in
patients with elevated left ventricular diastolic pressures, Circulation
47:989–996, 1973.
18. Ambrose JA, Teichholz LE, Meller J, et al: The influence of left ventricular late
diastolic filling on the A wave of the left ventricular pressure trace, Circulation
60:510–519, 1979.
19. Zoghbi WA, Enriquez-Sarano M, Foster E, et al: Recommendations for evaluation
of the severity of native valvular regurgitation with two-dimensional and Doppler
echocardiography, J Am Soc Echocardiogr 16:777–802, 2003.
20. Weyman AE, Dillon JC, Feigenbaum H, et al: Echocardiographic patterns of
pulmonic valve motion with pulmonary hypertension, Circulation 50:905–910, 1974.
21. Nanda NC, Gramiak R, Robinson TI, et al: Echocardiographic evaluation of
pulmonary hypertension, Circulation 50:575–581, 1974.
22. Armstrong WF, Schilt BF, Helper DJ, et al: Diastolic collapse of the right ventricle
with cardiac tamponade: an echocardiographic study, Circulation 65:1491–1496,
1982.
23. Feigenbaum H, Zaky A, Grabhorn LL: Cardiac motion in patients with pericardial
effusion. A study using reflected ultrasound, Circulation 34:611–619, 1966.
24. Leimgruber PP, Klopfenstein HS, Wann LS, et al: The hemodynamic derangement associated with right ventricular diastolic collapse in cardiac tamponade:
an experimental echocardiographic study, Circulation 68(3):612–620, 1983.
25. Pool P, Seagren C, Abbasi A, et al: Echocardiographic manifestations of constrictive pericarditis: abnormal septal motion, Chest 68:684–688, 1975.
26. Candell-Rivera J, Garcia del Castillo H, Permanyer-Miralda G, et al: Echocardiographic features of the interventricular septum in chronic constrictive pericarditis,
Circulation 57:1154–1158, 1978.
Doppler Echocardiography: Normal Antegrade
Flow Patterns
Mohamed Ahmed, MD, Gerard P. Aurigemma, MD
Four modalities of Doppler echocardiography are currently available for use with a wide variety of applications: pulsed wave
(PW) Doppler, continuous wave (CW) Doppler, color flow imaging, and tissue Doppler imaging. Each modality plays an important
role in the overall assessment of the patient with heart disease.
Whereas M-mode and two-dimensional echocardiography provide
structural and functional data, tissue Doppler imaging supplements
the assessment of myocardial function, including diastolic function. Doppler echocardiography is the modality on which noninvasive assessment of cardiac hemodynamics depends. The purpose of
this chapter is to review the normal antegrade intracardiac flow
using PW and CW.
BASIC CONCEPTS
Doppler echocardiography is based on the important concept that
backscattering of the ultrasound from moving blood cells will
appear higher or lower in frequency than the transmitted frequency
depending on the speed and direction of blood flow. Velocities are
calculated using the formula:
V ! 2Fo ! cos θ
C
where ΔF represents Doppler shift (the difference between the
transmitted frequency and the backscattered frequency), V is the
velocity of the moving blood cells, F0 is the transducer frequency,
ΔF ¼
cos θ is the cosine of the angle of the incidence, and C is the velocity
of propagation in the soft tissues, including the myocardium. For
cardiac applications, the velocity of propagation in the myocardium
is 1540 M/sec and cos θ is 1 (because the angle of the incidence is
0 or 180 degrees). To calculate Doppler velocities, the formula can
be rearranged:
V¼
ΔF ! C
2Fo ! cosθ
All commercially available ultrasound machines provide flow
velocities data.
Quantification of flow velocity is obtained with either PW or
CW Doppler. PW Doppler records flow velocities at one specific
location, whereas CW Doppler records flow velocity along the
entire pathway of the ultrasound beam (Fig. 10.1). The former is
used to quantitate flow in a given locus, but can only measure
velocity over a limited range. The latter permits the measurement
of high velocity flows, but does not determine the location of the
signal because signals from the entire length of the ultrasound beam
are included in the spectral CW Doppler tracing. By convention,
flow toward the transducer is displayed, spectrally, above the zero
baseline and flow away, below the zero baseline. By convention in
echocardiography, the y-axis is the velocity (in m/sec) and the
x-axis represents time (in seconds).
PW Doppler is used to assess velocities across normal valves or
vessels to calculate flow and assess cardiac function. Common
applications include measurements of stroke volume (SV), cardiac
10