I. The five major echocardiographic views and the myocardial wall segments

  1. Parasternal short-axis view (Figures 32.132.5)
  2. Parasternal long-axis view (Figures 32.6, 32.7, 32.8)
  3. Apical four-chamber view (Figure 32.9). Beware of an apical view that does not cut through the true apex, and thus may miss apical akinesis. A true apex is usually thinner than the septal and lateral walls, and, as opposed to the other walls, moves horizontally rather than longitudinally.
  4. Apical two-chamber view (Figure 32.10).
  5. Subcostal four-chamber view. This view is particularly useful in COPD patients and patients receiving ventilator support, in whom the previous views have a poor quality (Figures 32.11, 32.12).

    Arterial distribution (Figures 32.2, 32.13). Note that LAD supplies the anterior two-thirds of the septum, while RCA supplies the inferior one-third of the septum.

II. Global echo assessment of cardiac function and structure

A. Global assessment of myocardial function

A normal wall motion is characterized by an appropriate inward endocardial movement but also appropriate myocardial thickening. A segment can be hypokinetic, akinetic, or dyskinetic. Dyskinesis is outward movement of a myocardial wall during systole, when the remaining walls have an inward movement. Dyskinesis is therefore myocardial outpouching in systole, whereas aneurysm is myocardial outpouching in both systole and diastole (see Chapter 2).

  • Views that are orthogonal to a structure allow better endocardial definition of that structure.

1. Overall assessment of LV function

  • EF:

    • Normal: > 50%
    • Mildly decreased: 40–50%
    • Moderately decreased: 30–40%
    • Severely decreased: < 30%

  • The loss of the inferior and posterior walls typically leads to an EF of 35–50%, while the loss of the anteroseptal and apical walls typically leads to an EF < 35–40%.
    Image described by caption.

    Figure 32.1(a) Frontal view showing how the parasternal short-axis views cut through the heart (cross-sectional cuts). The first structure encountered is the right ventricle, which is actually the anterior ventricle; the base of the LV and the mitral valve are encountered more posteriorly. Angling the probe more superiorly allows visualization of the aortic valve, the RA and LA, as well as the RV inflow and outflow (aortic short-axis view, dotted lines). Angling the probe more inferiorly allows visualization of the LV body and apex (dashed lines).

    (b) Parasternal long-axis cuts. The first structure encountered is the RV (more specifically, RVOT), which is actually the anterior ventricle. The LV, LA, and aortic base are encountered more posteriorly, and the interventricular septum is seen in between. Angling the probe more inferiorly (dashed lines) allows visualization of the inferior RV wall and the tricuspid valve, as well as the RA (RV inflow view). Angling the probe more superiorly allows visualization of the RVOT and pulmonic valve (RV outflow view).

    (c) Apical four-chamber cut. The first structures encountered are the apices of the LV and RV, while the atria are seen in the back. Superior angulation allows visualization of the aortic valve (five-chamber). A 90° rotation would focus on the LV–LA (two-chamber view). Further rotation opens the aortic valve (three-chamber view).

    Schematic illustration of the parasternal short-axis view and various LV segments, with their corresponding arterial supply.

    Figure 32.2 (a) Diagram of the parasternal short-axis view and various LV segments, with their corresponding arterial supply. (b) Orientation of various echo cuts.

    Image described by caption.

    Figure 32.3 (a) Parasternal short-axis view at the level of the mitral valve. Each leaflet has three cusps (A1–A3 for the anterior leaflet, and P1–P3 for the posterior leaflet). A3 and P3 are medial, towards the RV; A1 and P1 are lateral. The orientations of various echo cuts through the mitral plane are shown. (b) Echocardiogram showing the parasternal short-axis view (anterior and posterior leaflets, circles). The triangular-shaped RV is partially seen (arrow).

    Schematic illustration of the parasternal short-axis view at the level of the aortic valve.

    Figure 32.4 Diagram of the parasternal short-axis view at the level of the aortic valve (cut closer to the base than Figure 32.3, across the aortic valve, the LA/RA, and RVOT). The non-coronary or posterior cusp is always the cusp looking towards the interatrial septum. LC, left coronary cusp; NC, non-coronary cusp; RC, right coronary cusp.

    Reproduced with permission from Hanna EB, Quintal R, Jain N. Cardiology: Handbook for Clinicians. Arlington, VA: Scrub Hill Press, 2009.

    Photos depict parasternal short-axis view as described in Figure 32.4.

    Figure 32.5 Parasternal short-axis view as described in Figure 32.4. A bicuspid aortic valve may be diagnosed on this view, by assessing how the valve opens in systole: a bicuspid valve opens in an oval rather than a “Y” fashion. In diastole, a bicuspid valve may look tricuspid because a fused raphe may be seen between the fused leaflets.

    In severe AS, the aortic valve barely opens in this view; planimetry of the aortic valve area may be performed (especially by TEE). Rarely, however, the aortic valve may falsely look open if the cut is a bit below or above the valve level, masking severe AS.

    The left image shows backward (= blue) blood flow across the tricuspid valve (= TR).

    Reproduced with permission from Hanna EB, Quintal R, Jain N. Cardiology: Handbook for Clinicians. Arlington, VA: Scrub Hill Press, 2009.

    Image described by caption.

    Figure 32.6 (a) Diagram of the parasternal long-axis view. Concerning the aortic valve cusps: the lower one, close to the LA, is the non-coronary cusp (NC); the upper one, close to RVOT, is the right coronary cusp (RC). The mitral leaflet close to the aorta is the anterior mitral leaflet (A2 cusp); the mitral leaflet close to the posterior wall is the posterior leaflet (P2 cusp).

    (b) Echocardiogram showing the parasternal long-axis view. Note the coronary sinus in the AV groove (arrow), and note the descending aorta behind it (x). The coronary sinus is anterior to the bright pericardium (line), whereas the descending aorta is posterior to it and is more rigid. From top to bottom, the following structures are seen around the pericardium: coronary sinus → pericardium/pericardial effusion → aorta →  pleural effusion. The aorta separates pericardial from pleural effusion.

    The coronary sinus goes on to drain in the RA. Coronary sinus may enlarge in case of RA dilatation/pulmonary hypertension or persistent left SVC; in the latter case, coronary sinus is severely enlarged > 1 cm.

    Image described by caption.

    Figure 32.7 (a) Parasternal long-axis view. Measurements are obtained from top to bottom, between delineated points, at an oblique line crossing the mitral leaflet tips and orthogonal to the axis of the LV (line).

    (b) Aortic measurements. The annulus is a stable structure that is part of the ventricle/outflow tract and does not usually dilate. The aortic diameter at the level of the sinuses of Valsalva (i.e., the aortic dilatations that suspend the aortic cusps) is normally up to 3.7 cm, while the diameter of the proximal ascending aorta and the sinotubular junction (junction of the ascending aorta with the sinuses of Valsalva) is normally up to 3.2 cm. Aortic dilatation may occur at the level of the ascending aorta and sinotubular junction (e.g., HTN), or may involve the sinuses of Valsalva in addition to the ascending aorta (bicuspid aortic valve, Marfan disease).

    The normal diameter at the sinuses is affected by age and body surface area and should generally be < 1.9 cm/m2 (lower cutoff in younger patients).

    Reproduced with permission from Hanna EB, Quintal R, Jain N. Cardiology: Handbook for Clinicians. Arlington, VA: Scrub Hill Press, 2009.

    Image described by caption.

    Figure 32.8 (a) Parasternal RV inflow view, which is obtained by angling the probe inferiorly from the parasternal long-axis view. This view allows visualization of the RV (horizontal bar) and RA (vertical bar). The IVC entrance into the RA is seen, as well as the coronary sinus (CS) beneath it. A rigid Eustachian valve or a filamentous Chiari network separates the two (Eustachian valve is seen here). The RV walls are the anterior (a) and inferior (b) walls, and the two tricuspid leaflets are the anterior (1) and posterior leaflets (2).

    (b) The posterior leaflet is the smallest leaflet, and for that reason only one view shows it, the RV inflow view (in some patients, it is the aortic short-axis view). All other tricuspid valve views show the anterior and septal leaflets (four-chamber, subcostal, and aortic level short-axis views).

    Image described by caption.

    Figure 32.9 (a) Diagram and (b) echocardiogram of the apical four-chamber view. Aorta and LVOT can be opened up by tilting the transducer up, creating the five-chamber view. The anterior leaflet is seen medially (1), the posterior leaflet is seen laterally (2), the anterior papillary muscle is lateral (1’), the posterior papillary muscle is medial (2’). Note that the valvular leaflets and their respective papillary muscles crisscross in this view.

    The tips of the papillary muscles define the separation between basal LV and mid-LV; the distal part of the papillary muscles separates mid-LV from apex.

    Sometimes, LV false tendon, a fibrous/fibromuscular band, is seen extending distally from the septum to the lateral LV wall. RV has coarse apical trabeculations (more coarse than LV); it has ≥3 small papillary muscles. A muscular band where the right bundle is embedded, the moderator band, may sometimes be seen spanning from the septal to the lateral RV wall, similar to the false tendon on the left.

    The tricuspid valve is more apical than the mitral valve. When both valves are at the same level, endocardial cushion defect is suspected. Advanced note: The anterior cusp (1) is A2 ± A3, the posterior cusp (2) is P1, the most lateral one; see Figure 32.3 to understand how the cusps are cut and the relation between leaflets and papillary muscles.

    (c) Apical four-chamber view in dilated cardiomyopathy: LV changes from elliptical to spherical. Note the false tendon and the moderator band, and note the descending aorta behind the LA.

    Image described by caption.

    Figure 32.10 (a) Diagram and (b) echocardiogram of the apical two-chamber view; and (c) echocardiogram of the apical three-chamber view. By opening the aorta with a counterclockwise rotation, the apical two-chamber view becomes the apical three-chamber view, where the anterior and inferior walls are replaced by the septal and posterior walls, respectively. The apical three-chamber view, also called apical long-axis view, is similar to the parasternal long-axis view, except for a different heart orientation (the beam is parallel to the aortic flow and the true apex is intercepted). Depending on the cut, three mitral cusps with two orifices may be seen on the two-chamber view (P3 next to the inferior wall, A2 in the middle, and P1 or A1 next to the anterolateral wall). Use Figure 32.3 for guidance.

    Reproduced with permission from Hanna EB, Quintal R, Jain N. Cardiology: Handbook for Clinicians. Arlington, VA: Scrub Hill Press, 2009.

    Schematic illustration of an example of the subcostal view.

    Figure 32.11(a) Diagram and (b) example of the subcostal view.

    Schematic illustration of subcostal view with a medial tilt to visualize the IVC.

    Figure 32.12 Subcostal view with a medial tilt to visualize the IVC. A large IVC (>2.1 cm), as well as its lack of 50% collapse with inspiration or sniff, signals high RA pressure. IVC is measured at a level just proximal to its junction with hepatic vein (1-2 cm proximal to the RA).

    Schematic illustration of arterial distribution of various echo segments on the short-axis view, long-axis view, and apical four-chamber view.

    Figure 32.13 Arterial distribution of various echo segments on the short-axis view, long-axis view, and apical four-chamber view. Note that the inferior septum (on the short-axis view) and the basal septum (on the four-chamber view) are supplied by the RCA. If the four-chamber cut is angled a bit posteriorly, some of the visualized mid-septum may be supplied by the RCA as well.

2. Assess for LV dilatation and RV dilatation, which are associated with LV and RV systolic dysfunction, respectively.

  1. LV dilatation is characterized by LV diameter (obtained from the short- or long-axis view) > 4 cm in systole or > 5.3 cm (women) or > 5.8 cm (men) in diastole. Measurements are obtained at the level of the mitral leaflet tips, at the base of the LV.
  2. RV dilatation (Figure 32.14) is characterized by:

    • RV size larger than LV size on the apical four-chamber view
    • RV rounded rather than wedge-shaped on the parasternal long-axis view.
    • RVOT diameter ≥ 3.0 cm on the long-axis view or the aortic short-axis view; RV maximal diameter on the four-chamber view, around the tricuspid annulus, ≥ 2.9 cm (mild dilatation) or ≥ 3.9 cm (severe). However, these measurements vary according to the way the RV is cut, particularly because the RV has a complex pyramidal shape, which limits their accuracy.
    • RV pressure overload pattern associated with severe pulmonary hypertension: the RV compresses the LV in systole and leads to a compressed D-shaped septum in systole.
    • RV volume overload pattern: the RV compresses the LV in diastole and leads to a paradoxical septal motion towards the RV in systole. In mixed RV volume and pressure overload pattern, the septum remains compressed towards the LV in both diastole and systole.
    • RA is enlarged if it is larger than LA on the four-chamber view, or if the interatrial septum bows to the left, or if the septal-lateral diameter is > 2.2 cm/m2 of BSA (4.5 cm). IVC is typically dilated in RA enlargement.

  3. A left ventricular segment that is bright and thin (<6 mm) often implies necrotic, non-viable myocardium (due to an infarct or to irreversible non-ischemic cardiomyopathy).

3. Left ventricular hypertrophy (LVH) is characterized by an increased LV mass > 115 g/m2 in men, or > 95 g/m2 in women. Increased wall thickness, which often underlies LVH, is characterized by an interventricular septal thickness or a posterior wall thickness ≥ 1.1 cm in men, or ≥ 1 cm in women. The wall thickness is severely increased if it is ≥ 1.7 cm in men, or ≥ 1.6 cm in women.

LVH is concentric when the walls are thick but the LV is not dilated. LVH is eccentric when the walls are thick and the LV is dilated. Concentric LV remodeling is characterized by thick walls without overall LVH; i.e., the LV mass is normal

LV mass is calculated using the LV wall thickness and the LV diameter on the parasternal long-axis view.

4. Left atrial size is the “hemoglobin A1c” of the left heart; if LA size is normal, it is unlikely that there are any major systolic, diastolic, or left valvular issues.

A quick way of assessing LA size is by comparing it to the aorta on the long-axis view. LA is enlarged if it is > 1.1× the aortic size. Normal LA end-systolic diameter is < 3.8 cm on the parasternal long-axis view (anteroposterior diameter) and on the apical four-chamber view (septal-lateral diameter); LA enlargement is severe if LA diameter > 5 cm. LA volume should be assessed using the planimetered LA areas on both the four- and two-chamber views (disk summation technique). This is the preferred method for LA size assessment: LA volume is normally < 34 ml/m2 of BSA; LA is severely enlarged if LA volume is > 48 ml/m2.

B. Paradoxical septal motion

Normally, the septum moves in towards the LV in systole, and relaxes towards the RV in diastole. Abnormal septal motion is characterized by a septum that moves out towards the RV in systole, or at least at one point of systole, leading to ineffective septal contraction; and moves in towards the LV in diastole, compressing the LV.

Five differential diagnoses (Figures 32.1532.18):

  1. LBBB and RV pacing. The abnormal septal motion of RV pacing is similar to LBBB, except that it involves the distal/apical septum (rather than the entirety of the septum).
  2. RV dilatation with RV volume overload.
  3. Pericardial processes (constrictive pericarditis, tamponade). Large respiratory swings (e.g., COPD) may simulate the abnormal septal motion of pericardial processes.
  4. Abnormal septal motion post-cardiac surgery.
  5. Septal akinesis in a patient with septal MI. Unlike all the other causes of septal motion abnormality, anterior and apical akinesis is also seen in this case.

As opposed to other diagnoses, pericardial processes, whether constriction or tamponade, are characterized by an abnormal septal motion that increases with inspiration and thus varies between beats, i.e., the septal collapse towards the LV in diastole varies with respiration. In other processes, the abnormal septal motion does not vary as much across beats. In addition, characteristic of constrictive pericarditis, a septal bounce may be seen during each diastole, representing an instantaneous change in the RV-to-LV push with instantaneous pressure changes.

A septal motion abnormality may also be seen in patients breathing deeply, wherein the RV pushes the septum towards the LV in deep inspiration. Like pericardial processes, this septal position varies with respiration, but septal bounce is not seen.

In a tachycardic patient, sorting out the respiratory effect may prove difficult. M-mode imaging is particularly helpful because of its high frame rate.

The abnormal postoperative septal motion is related to the fact that, after cardiac surgery, the heart is fixed anteriorly to the thorax (meaning, the RV is fixated). During systole, the whole heart moves toward that fixation site, leading to what looks like septal motion abnormality. In fact, it is an abnormal anterior motion of the whole heart, including the posterolateral wall.

Schematic illustration of an example of RV enlargement and RV volume overload on the parasternal short-axis view and apical four-chamber view.

Figure 32.14(a) Example of RV enlargement and RV volume overload on the parasternal short-axis view and apical four-chamber view. The interventricular septum is flattened and pushed toward the LV in diastole (lines). The interatrial septum is also bowing towards the LA (cross). (b) M mode across the lateral tricuspid annulus in 4-chamber view. The longitudinal excursion of this annulus over time is shown, and is called tricuspid annular plane systolic excursion (TAPSE). TAPSE reflects RV shortening/contraction, and is measured by any of the blue lines. It is reduced here (12 mm, normal ≥17 mm). The distance is the same whether the oblique or vertical blue line is used, as distances are only measured vertically on M mode (horizontal plane represents time).

Image described by caption.

Figure 32.15 During systole, in LBBB: (1) the septum moves in towards the LV; (2) then the septum relaxes while the posterior wall moves in; (3) the septum moves in again at the end, not because it is contracting but because the RV is relaxing and pushing it. Thus, the septum moves in twice (1 and 3), while the posterior wall moves in between (2), when the septum is relaxed. The distance between the peak of (1) and the peak of (2) is the septal-to-lateral M-mode delay, an index of dyssynchrony (>130 ms → significant).

Schematic illustration of m-mode imaging shows paradoxical septal motion of RV volume overload (outward in systole, inward in diastole).

Figure 32.16 M-mode imaging shows paradoxical septal motion of RV volume overload (outward in systole, inward in diastole). This paradoxical motion is seen in both inspiration and expiration; it may be a bit more prominent in inspiration, but unlike constrictive pericarditis or tamponade, it is not much more prominent. M-mode allows a fine analysis of how various structures move during the cardiac cycle. QRS is used to time events.

Schematic illustration of constrictive pericarditis.

Figure 32.17 Constrictive pericarditis. Two septal abnormalities and one posterior wall abnormality are seen on M-mode (D corresponds to the septal position in diastole):

  • Septum is pushed toward the LV in inspiration (arrow) and toward the RV in expiration (=respirophasic septal shift).
  • The RV-to-LV diastolic push varies with instantaneous pressures (= septal bounce, circle).
  • The posterior wall is stiff/horizontal in diastole after the initial brisk expansion (= plateau, line).

In RV volume overload, the RV pushes the septum towards the LV in all diastolic cycles with no marked respiratory variation: the abnormal motion is systolo-diastolic, not respiratory. Moreover, only one sharp septal motion towards the LV is seen in diastole.

Schematic illustration of pericardial processes are characterized by septal compression towards the LV in inspiration, and towards the RV in expiration.

Figure 32.18 Pericardial processes are characterized by septal compression towards the LV in inspiration, and towards the RV in expiration.

C. Valvular structure assessment

1. Mitral valve (Figures 32.1932.21)

  • Degenerative valve: leaflet(s) are thick, elongated, ± prolapsed into the LA. If, in addition to the prolapse of the leaflet body, the free edge is overriding the other leaflet and turned towards the LA rather than the LV, the leaflet is called flail leaflet; this is usually secondary to chordal rupture (a piece of chorda is usually seen flopping in the LA).
  • Rheumatic valve: thick, calcified valve with a stiff posterior leaflet and a stiff anterior leaflet tip. The anterior leaflet body is, however, mobile. The combination of a stiff anterior leaflet tip and a flexible body gives the anterior leaflet a hockeystick shape on the parasternal long-axis view. On the short-axis view, the commissures are fused and the valve only opens in its center (“fish mouth” mitral valve).
  • Mitral annular calcifications involve the mitral annulus rather than the leaflets (in contrast to a rheumatic process). The annulus is calcified, but the leaflets’ tips are free. Calcifications are mainly seen at the posterior aspect of the annulus and increase in incidence with age, high LV pressure (HTN, AS), and renal disease. Only the posterior annulus, which is a muscular structure, calcifies; the anterior annulus is a fibrous structure that only calcifies in radiation heart disease. Calcifications may, however, extend to the base of both the posterior and anterior leaflets on the four-chamber view (not the leaflet tips, and not the anterior annulus on the long-axis view).

2. Aortic valve

III. Doppler and assessment of valvular regurgitation and stenosis

A. Types

  1. Color Doppler: color Doppler assigns color to blood flow velocity and direction. The maximal Doppler velocity that can be sampled unambiguously and attributed a blue or red color is called the Nyquist or aliasing limit. Beyond this limit, the color becomes mosaic.
  2. Continuous-wave (CW) spectral Doppler: CW Doppler traces the highest flow velocity along one line swept by the Doppler probe. Therefore, it captures the velocity across the narrowest point or obstruction. It continuously captures waves and is not dependent on the Nyquist limit.
  3. Pulsed-wave (PW) spectral Doppler: PW Doppler traces the velocity at one point along the line swept by the cursor, rather than the whole line swept. It samples waves intermittently, at a specified sampling rate. Therefore, the maximal velocity that can be detected across this one point cannot exceed a certain limit, called the Nyquist limit.

B. Routine Doppler interrogations

1. Color Doppler is performed at the level of each valve to assess regurgitation (see Figures 32.2332.33)

By “eyeballing” the view, regurgitation appears as a color going backward between chambers, opposite to the normal flow (e.g., any flow from LV to LA, RV to RA, or aorta to LV). It is blue (backward) for the mitral and tricuspid valves on TTE. It usually has a higher velocity than the Nyquist limit, which leads to color aliasing (= mixed, mosaic color). Also, when severe, it is usually turbulent, with high variance of velocities (turbulent flow, coded as green color).

2. CW Doppler is performed at the level of each valve to assess forward-flow velocity, and, consequently, valvular stenosis (see Figures 32.34, 32.35, 32.36)

Normally, the forward peak velocity across each valve is 1 m/s. An increase in flow velocity corresponds to valvular stenosis.

The peak pressure gradient across a valve can be estimated using this equation (modified Bernoulli equation):

upper P e a k g r a d i e n t equals 4 times normal upper V Subscript v a l v e Baseline squared

This is how gradient is estimated across the aortic valve and the severity of a stenosis is assessed. For spectral Doppler assessment, it is important to obtain a view parallel to the flow.

3. PW Doppler is used to see the velocity at one particular point, such as the mitral inflow (E/A), tricuspid inflow, pulmonary vein inflow (systolic, diastolic, atrial waves), and LVOT flow (Figures 32.37, 32.38)

PW has a limited capacity to measure high velocities that exceed twice the Nyquist limit (>2 m/s), particularly at greater depths.

Two types of velocities are analyzed on CW or PW Doppler: peak velocity and velocity–time integral (VTI).VTI corresponds to the area enclosed by the CW or PW Doppler velocity profile. It is measured in cm (velocity × time) and corresponds to the distance traveled by blood across the interrogated point during one cardiac cycle.

4. Tissue Doppler assesses the movement of cardiac structures rather than blood flow (Figures 32.39, 32.40)

Tissue Doppler is useful to assess:

  1. Mitral annular velocities during diastole (E’ and A’). E’ is the annular recoil toward the base during early diastolic filling; A’ is the annular recoil during atrial systole. Lateral E’ is normally ≥ 10 cm/s, medial E’ is ≥ 7 cm/s. The reduction of E’ indicates diastolic dysfunction or high left-sided filling pressures.
  2. Dyssynchrony of various myocardial segments, manifested as different times from QRS onset to peak systolic velocity (or peak strain) between different walls. The assessment of mechanical dyssynchrony is particularly useful in patients with low EF and QRS 130–150 ms, as it may help identify the responders to biventricular pacing. In patients with HF and QRS < 130 ms, the use of echocardiographic dyssynchrony for identifying potential responders to biventricular pacing has not shown any value.
  3. Occult or manifest myocardial dysfunction. The radial myocardial displacement, velocity, and strain can be determined on the short-axis view; the longitudinal displacement, velocity and strain can be determined on the apical views. A dysfunctional segment may get pulled and displaced by a normal adjacent segment; therefore, a normal displacement or velocity of one myocardial segment does not necessarily imply normal function. Myocardial strain, on the other hand, assesses the percent change in distance between 2 points, i.e., myocardial deformation, and the strain rate assesses the change in velocity between 2 points. Myocardial strain allows an accurate determination of segmental function and may be determined using tissue Doppler or better yet today, automated ultrasound tissue imaging called speckle tracking (Appendix).

    The global ventricular function may also be simply and routinely assessed using annular tissue Doppler. On the annular Doppler, S’ is the forward systolic movement of the annulus in systole (longitudinal fibers). S’ ≤ 7 cm/s correlates with LV systolic dysfunction. At the tricuspid annulus, S’ < 10 cm/s correlates with RV systolic dysfunction.

C. Routine Doppler calculations

1. Volume and flow calculations

Volume and flow can be derived from velocity using the continuity equation, which states that blood volume that crosses a cardiac area during one cardiac cycle = area × VTI. Thus:

upper B l o o d v o l u m e equals pi normal r squared times upper V upper T upper I equals 0.785 times normal d squared times upper V upper T upper I left-parenthesis normal r i s r a d i u s comma normal d i s d i a m e t e r right-parenthesis

upper P e r s e c o n d f l o w a c r o s s a p o i n t equals b l o o d v o l u m e d i v i d e d b y upper V upper T upper I d u r a t i o n comma i period e period comma e j e c t i o n d u r a t i o n

Stroke volume is, thus, equal to: 0.785 × LVOT d2 × LVOT VTI

Cardiac output is equal to: stroke volume × heart rate

2. Aortic valve area (AVA) calculation using the continuity equation

StartLayout 1st Row upper A upper V upper A times a o r t i c v e l o c i t y left-parenthesis a o r t i c p e a k v e l o c i t y o r a o r t i c upper V upper T upper I o n upper C upper W upper D o p p l e r right-parenthesis 2nd Row equals upper L upper V upper O upper T a r e a times upper L upper V upper O upper T v e l o c i t y left-parenthesis upper L upper V upper O upper T p e a k v e l o c i t y o r upper L upper V upper O upper T upper V upper T upper I o n upper P upper W upper D o p p l e r right-parenthesis EndLayout

LVOT diameter should be measured at the insertion of the aortic valve leaflets (i.e., at the annulus, not below it), parallel to the leaflets’ plane, in early systole (largest diameter). A falsely low LVOT measurement is a common cause of a falsely low AVA.

3. Calculation of the systolic PA pressure using the TR jet

Capture of TR jet by CW Doppler is necessary for the calculation of PA pressure. While many normal individuals have mild TR that allows this calculation, over 50% of patients, including some patients with severe pulmonary hypertension, do not have an adequate TR jet envelope.

According to the Bernoulli equation, the pressure difference between RV and RA in systole equals 4 × VTR 2.

Thus, RV systolic pressure = 4 × VTR 2 + RA pressure. In the absence of pulmonic stenosis, RV systolic pressure is equal to PA systolic pressure.

4. Assessment of RA pressure

RA pressure is assessed on the basis of IVC diameter and inspiratory collapse:

  1. IVC ≤ 2.1 cm with > 50% inspiratory collapse → RA pressure = 0–5 mmHg
  2. IVC ≤ 2.1 cm but < 50% inspiratory collapse,

    or IVC > 2.1 cm with > 50% inspiratory collapse → RA pressure = 5–10 mmHg

  3. IVC > 2.1 cm with < 50% collapse → RA pressure ≥ 15 mmHg, or ≥ 20 mmHg if 0% collapse. Also, even in the intermediate category (ii), if the collapse is ~0% or if the systolic flow of the hepatic veins is blunted, RA pressure is severely elevated.
    Image described by caption.

    Figure 32.23 MR, four-chamber view. The blue, backward flow between the LV and the LA is MR. The regurgitation can be graded by measuring the regurgitant (blue) area (arrow) and comparing it to the LA area. If the regurgitant area is > 40% LA area → severe MR (this also applies for TR: jet area > 30% of RA area → severe TR). This provides a quick idea of the severity of MR, but is not very reliable. Increasing the color gain or lowering the Nyquist limit of the backward flow on the color scale (horizontal arrow) increases the regurgitant/turbulent area and makes the MR look more severe. The best Nyquist limit for regurgitation assessment is 50–60 cm/s. To obtain the best color gain, increase the gain until noise is seen in cardiac tissues, then slightly reduce it just until the noise disappears.

    Reproduced with permission from Hanna EB, Quintal R, Jain N. Cardiology: Handbook for Clinicians. Arlington, VA: Scrub Hill Press, 2009.

    Photo depicts severe MR on four-chamber TEE view.

    Figure 32.24 Severe MR on four-chamber TEE view. Severity criteria of MR:

    1. Look at the small spherical portion of the regurgitant jet that is on the side of the ventricle rather than the atrium. As the blood is flowing back from the LV to the LA, it goes through a narrow neck that corresponds to the vena contracta (VC) of the mitral orifice. The flow converging towards the mitral orifice forms hemispheres of increasing velocities, the areas of which are called proximal isovelocity surface areas (PISA). The hemisphere of interest is the one where aliasing occurs (double arrow). Thus, the radius of the PISA corresponds to the distance between the narrowest neck of flow and the outer aliasing line (double arrow). The larger this hemisphere (>0.9–1.0 cm), the more severe the MR. PISA allows calculation of the effective regurgitant orifice (ERO). If the backward aliasing limit is set at 40 cm/s on the regurgitant color bar (arrow), ERO is estimated as:

      (PISA radius)2/2

      If PISA radius is 0.9 cm, ERO is ~0.4 cm2. MR is severe if ERO ≥ 0.4 cm2. ERO can be used to calculate the regurgitant volume (= ERO × VTI of the regurgitant flow) and the regurgitant fraction. Regurgitant volume > 60 ml or regurgitant fraction > 50% signifies severe MR. PISA is affected by eccentricity of the jet, but less than MR jet area; another limitation is that the PISA should be a 180° hemisphere. A flattened, squashed PISA has a wider base but a shorter diameter (shorter double arrow); the short diameter underestimates the PISA area as the calculation assumes PISA is round.

    2. The diameter of the MR flow at its vena contracta neck, i.e., the narrowest part (mitral valve level), can be estimated. The larger the diameter, the more severe the MR (≥7 mm → severe MR).
    3. A severe regurgitation should lead to enlargement of the backward chamber (LA in MR, RA in TR, LV in AI). In addition, the forward chamber often enlarges because of the volume overload. Except in acute cases, a normal-size backward chamber rules out severe regurgitation.
    4. Other severity criteria of MR:

      • Increased forward flow and velocity across the mitral valve in diastole: E velocity > 1.2 m/s
      • Reversal of the systolic S flow of one or more pulmonary vein(s): specific for severe MR, but not sensitive, as LA compliance may prevent this flow reversal (compensated chronic MR). Moreover, if the jet is eccentric, reversal of flow may be seen in some but not all of the veins. Blunting of S flow, rather than reversal, is also consistent with severe MR but is not specific.

    When MR seems severe but LA is not enlarged, make sure that MR is present throughout systole. What seems like severe MR by color or PISA is moderate if it only encompasses 50% of systole or end-systole (this may occur with mitral valve prolapse and with functional MR). The duration of MR is evaluated by CW Doppler or by color M-mode across the mitral valve.

    Photo depicts MR, long-axis view.

    Figure 32.25 MR, long-axis view. The blue flow between LV and LA is MR (arrow). It is eccentric, posteriorly directed, and at least moderate in severity. When MR is eccentric, consider it more severe than it appears (MR that appears mild is likely moderate). An eccentric jet that turns around the left atrial wall in a circular way is severe MR (Coanda effect). A well-visualized PISA hemisphere (arrowhead) despite a Nyquist limit of 69 cm/s is concerning for severe MR. A posteriorly directed MR usually implies either anterior leaflet prolapse or posterior leaflet tethering from inferior akinesis.

    Photo depicts systolic flow reversal of pulmonary venous flow in a patient with severe MREnd.

    Figure 32.26 Systolic flow reversal of pulmonary venous flow in a patient with severe MR. Normally, S flow has the same direction as D flow.

    Photo depicts CW Doppler across the mitral valve on an apical four-chamber view.

    Figure 32.27 CW Doppler across the mitral valve on an apical four-chamber view. The flow is directed backward (arrow) from the LV to the LA, and projects below the baseline on CW Doppler. (a) The flow is dense (white) but not as white as the forward flow, and thus is probably moderate MR. (b) Acute or decompensated severe MR may lead to a late indentation of the CW signal, related to a large V wave and decreased LV–LA pressure gradient at end-systole. This is called the V-wave cutoff sign, and leads to an early-peaking, triangular MR shape.

    On the apical views, because of similarities in direction of AS and MR jets and because of beam width artifact, AS Doppler interrogation may capture MR jet, creating the false impression of severe AS velocity. Unlike AS, MR jet starts immediately at MV closure, immediately after the mitral inflow A wave, at the peak of R wave on the ECG (white line). The timing of the two jets and a back-and-forth sweeping of the transducer help differentiate the two.

    Photo depicts severe TR seen from the short-axis view (aortic valve level) (arrow).

    Figure 32.28 Severe TR seen from the short-axis view (aortic valve level) (arrow). The same criteria described under Figure 32.24 can be used for TR to assess severity. To estimate ERO, set the backward flow aliasing limit at 28 cm/s (instead of 40). Also, annular dilatation ≥ 3.5 cm correlates with severe functional TR. Use the same vena contracta and ERO values as in MR, use jet area > 30% RA area, and look for hepatic vein flow reversal and RA enlargement.

    Reproduced with permission from Hanna EB, Quintal R, Jain N. Cardiology: Handbook for Clinicians. Arlington, VA: Scrub Hill Press, 2009.

    Image described by caption.

    Figure 32.29 TR. CW Doppler across the tricuspid valve on a four-chamber view (see that the line swept is on the right side, arrow). TR looks very dense (white) on CW Doppler, which often means large-volume moderate or severe regurgitation. Unlike the density of the regurgitation, the peak velocity does not correlate with the severity of the regurgitation. This peak velocity correlates with the pressure gradient between the two chambers (here: RV to RA), and hence PA pressure. Severe pulmonary hypertension may occur with mild, non-dense TR, yet the velocity would be high (>4 m/s); conversely, severe, dense TR may be seen with a low TR velocity when PA pressure is not elevated (e.g., primary TR).

    Photo depicts aortic insufficiency (AI).

    Figure 32.30 Aortic insufficiency (AI). Long-axis view shows blue–backward flow from the aorta to the LV, i.e., AI. Assess AI severity by looking at:

    1. Vena contracta, which is the narrowest portion of the jet (between the two dots, at the valve orifice). Vena contracta > 6 mm implies severe AI.
    2. Width of the AI jet just below the aortic valve, on the long-axis view (between the two arrows). This is the AI size as the jet starts to expand, just below the vena contracta (within 1 cm of the aortic valve). If AI jet > 60% of the LVOT diameter (which is the diameter between the two walls at the aortic valve insertion) → severe AI. AI jet width is better evaluated on the parasternal views than the apical views, which tend to falsely “widen” the AI jet.
    3. Pressure half-time (on CW Doppler, Figure 32.33)
    4. PISA in the aorta (semi-circle)
    5. Holodiastolic reversal of flow in the thoracic aorta (suprasternal view) or abdominal aorta (subcostal view), which is highly sensitive for severe AI (except acute AI where LV and aortic pressures equalize in end-diastole, and where, conversely, PHT becomes highly sensitive).

    In (a), AI is moderate; in (b), AI is mild.

    Image described by caption.

    Figure 32.31 AI. The width of the AI jet may also be assessed on the aortic short-axis view. Here, look for a central blue or mixed-color “flame” in diastole (arrow), which corresponds to AI jet. AI jet area that is > 60% of the whole aortic circle area implies severe AI. AI jet may look falsely enlarged if the cut is well below the regurgitant orifice, or falsely reduced if AI is eccentric. In order to obtain the accurate AI width, the transducer may be angled up until the AI flow is lost; the AI that is seen just before the flow is lost corresponds to the jet width. The latter maneuver is best performed on the TEE’s aortic short-axis view.

    Reproduced with permission from Hanna EB, Quintal R, Jain N. Cardiology: Handbook for Clinicians. Arlington, VA: Scrub Hill Press, 2009.

    Photo depicts aI on three-chamber apical view.

    Figure 32.32 AI on three-chamber apical view. This view is not accurate for measurement of the jet width area and vena contracta. Being parallel to the flow, it is excellent for recording of Doppler flow and measurement of AS gradient or AI pressure half-time, but it is not accurate for width measurement. When assessing thickness of a structure or flow, it is best to be orthogonal to the structure or flow. Note AI’s PISA, which is the spherical jet on the side of the aorta.

    Photo depicts aI spectral Doppler assessment on an apical five-chamber view.

    Figure 32.33 AI spectral Doppler assessment on an apical five-chamber view. The flow between the aorta and the LV is directed upward (along the direction of the arrow). The slope of this regurgitant flow depends on how closely the LV and aortic pressures approximate during diastole, and thus how severe and acute AI is. The steeper the slope, the more severe and quick is the rise of LV diastolic pressure.

    This is called pressure half-time (PHT), which is the time needed for the pressure gradient to decrease in half. If PHT < 250 ms → steep slope → severe AI. Note, however, that a chronic severe but compensated AI with compensated LV may have PHT > 250 ms. PHT correlates more with acuity and decompensation of AI than its severity.

    PHT of AI is different from PHT of MS, where a steeper slope implies less severe MS.

    Also, the density of this regurgitant flow correlates with severity (the whiter it is in comparison to the forward flow, the larger the AI volume and the more severe the regurgitation).

    In this case, note that the patient has AI with PHT < 250 ms but also significant AS, with a peak forward velocity of 4 m/s. AI exaggerates the AS velocity (increased stroke volume), while AS may exaggerate AI severity by the PHT method, as it impairs LV compliance.

    Image described by caption.

    Figure 32.34 AS. CW Doppler across the aortic valve on the apical five-chamber view. The flow directed down is the aortic flow in systole (along the direction of the arrow). The normal peak velocity is 1 m/s. Velocity > 2 m/s signals AS; velocity ≥ 4 m/s implies severe AS, which is the case here.

    The peak pressure gradient may be calculated from peak velocity using the modified Bernoulli equation (= 4 V2). The mean pressure gradient integrates all the gradients underneath the velocity envelope. Echo may underestimate the pressure gradient if the interrogation angle is not parallel to the flow, or if the jet envelope is incomplete (may need to increase the gain settings). Search for the best envelope and the highest gradient in multiple views (apical five-chamber, apical three-chamber, right parasternal, and suprasternal views).

    Caution: increased CW velocity is not necessarily AS, because CW samples the highest velocity along the whole line swept and not only the aortic valve. It may be LVOT obstruction, where the velocity is increased across the LVOT rather than the aortic valve. In this case, the PW velocity is increased across the LVOT, whereas the localized aortic PW velocity is not increased (PW localizes the site of obstruction, even though it may not be able to record the exact velocity). Also, in LVOT obstruction, the gradient peaks late and the CW velocity has a late-peaking dagger shape.

    In low-output states, the gradient may be low despite severe AS. Severe AS is diagnosed by using the dimensionless index (LVOT PW velocity divided by aortic valve CW velocity). Either VTI or peak velocity may be used. The index is normally ~1, and an index < 0.25 implies severe AS with AVA<25% of normal. If the index is >0.25, AS is likely non-severe, even if AVA measures <1 cm2 (–>false LVOT diameter measurement).

    In AF, the velocity and the gradient decrease after the short R–R cycles (as opposed to MS). For AVA calculation, use LVOT VTI and aortic valve VTI obtained after the same R–R cycle lengths. For peak/mean gradient estimation, control the rate and average the gradients from several beats; however, since AF reduces cardiac output, AS severity is better gauged by the highest gradient (long R-R) than by averaging down gradients.

    AS gradient is often underestimated, not overestimated. AS gradient may rarely be overestimated when AS and MR jets are confused on the apical five-chamber or three-chamber view. MR jet starts exactly at the peak of R wave, whereas AS jet starts a bit later.

    Photo depicts severely increased velocity on aortic Doppler.

    Figure 32.35 Severely increased velocity on aortic Doppler. Several features suggest LVOT obstruction rather than AS: (1) the velocity has a late-peaking dagger shape (tilted line), and is “skinnier” than the aortic velocity seen in Figure 32.34; (2) on color Doppler, the aliasing (arrow) occurs below the aortic valve level (double arrow). To confirm LVOT obstruction, PW Doppler may be swept throughout the LVOT and the aortic valve. PW Doppler cannot record velocities over 1.5–2 m/s, but will indicate that the velocity is increased across the LVOT rather than the aortic valve. Exact assessment of the velocity with CW ensues.

    Photo depicts MS assessment.

    Figure 32.36 MS assessment.

    (a) CW Doppler across the mitral valve (MV) on the apical four-chamber view. The flow is directed from the LA (which is down on this view) to the LV (up) along the direction of the arrow. A mean gradient > 5 mmHg at rest, or 10–15 mmHg with exercise, corresponds to severe MS. Passive leg raising should be performed to assess stress gradient. CW, not PW, should be used to capture the gradient.

    The downslope of the rapid diastolic filling (E wave, first wave) may be used to estimate MV area: a slow downslope means that LA pressure does not equalize with LV pressure even in late diastole (no diastasis), which corresponds to severe MS. The pressure half-time is the time it takes the pressure gradient to decrease in half [i.e., time it takes E velocity to decrease by 30%], and is long in severe MS. MV area = 220 divided by pressure half-time. However, for the same valve area, LA and LV pressures more readily equalize in case of increased LV diastolic pressure (AI, severe LVH), which makes the downslope look steeper → MV area will be seemingly larger and MS will be seemingly less severe.

    High E wave may merely result from MR or HF and when MAC coincides, this high E may be falsely considered high gradient and MS. Unlike MS, E wave of the latter cases has a sharp downslope.

    (b) If E wave has a “ski slope” shape, (i.e., initially steep then slow downslope), use the slow downslope portion to calculate the pressure half-time. An associated MR or high output state increases the early E-wave velocity and the overall gradient, but the later E slope remains unchanged.

    In AF, the pressure gradient varies between different beats (↑ with short R–R cycles, as LA emptying decreases), but the shape and slope of the CW envelope remain unchanged. Mean gradient increases as in any tachycardia (or exercise), but pressure half-time and MV area remain unchanged. PHT = pressure half-time.

    Schematic illustration of PW Doppler at the level of the mitral valve.

    Figure 32.37 PW Doppler at the level of the mitral valve. During diastole, forward flow is recorded across the MV: E is the rapid diastolic filling, A is the filling related to atrial contraction. E occurs after T wave, while A occurs after P wave and almost coincides with QRS.

    Schematic illustration of PW Doppler across the pulmonary veins on a four-chamber view, pulmonary veins being behind the LA (cursor).

    Figure 32.38 PW Doppler across the pulmonary veins on a four-chamber view, pulmonary veins being behind the LA (cursor). S and D represent, as it is seen, forward systolic and diastolic flow toward the LA. A wave corresponds to atrial systole, when LA pressure increases and prevents forward blood flow: A is a reversed flow wave. Normally, S is slightly > D or slightly < D. A severely reduced S wave implies elevated LA pressure.

    The hepatic venous flow on the subcostal view looks similar to the pulmonary venous flow (S, D, A), except that S and D waves are below the baseline, whereas A wave is above the baseline.

    Schematic illustration of myocardial tissue Doppler at the level of the mitral annulus.

    Figure 32.39 Myocardial tissue Doppler at the level of the mitral annulus. The cursor is placed on the myocardial lateral or medial annulus. E’ and A’ waves occur in diastole, on the downward negative side (diastolic recoil). In systole, a forward positive motion S’ occurs. Lateral E’ annular velocity is usually higher than medial E’. Measure both lateral and medial E’, and calculate E/E’ for each E’, and for the average E’.

    The cursor should be positioned within 0.5 cm of the leaflet insertion site and should be parallel to the plane of cardiac motion.

    In myocardial dysfunction (systolic or diastolic), IVCT and IVRT increase, leading to an increase of the following ratio: (IVCT + IVRT)/ejection time (ejection time corresponds to S’ time). This ratio, called myocardial performance index or Tei index, may be calculated using myocardial annular Doppler and is normally < 0.4.

    Reproduced with permission from Hanna EB, Quintal R, Jain N. Cardiology: Handbook for Clinicians. Arlington, VA: Scrub Hill Press, 2009.

    Schematic illustration of 2D tissue strain imaging of the LV on a two-chamber view.

    Figure 32.40 2D tissue strain imaging of the LV on a two-chamber view. Strain between two myocardial points = % change in distance between the two points = (distancebetween these points in systole – distancein diastole)/distancein diastole. Normal regional strain values are –20 to –12; abnormal values are –8 to +20. The red color corresponds to normal strain, while the blue/purple corresponds to abnormal strain. In this figure, the antero-apex is blue and therefore dysfunctional.

    The time display (right image) shows the peak systolic strain of each segment and the strain curve throughout systole then diastole; the segment moving in the opposite direction to the baseline is a dyskinetic segment (apex). Courtesy of Carmen Ilie and Fred Helmcke, who provided this image.

IV. Summary of features characterizing severe valvular regurgitation and stenosis (see Tables 32.1, 32.2)

Table 32.1 Severe valvular regurgitation.

Mitral regurgitation

  1. Jet area > 40% of LA area or eccentric jet swirling around the LA wall (Coanda effect), at a Nyquist limit of 50–60 cm/s and a proper color gain.
    Pros: area <20% makes severe MR very unlikely
    Cons: eccentricity reduces jet area; low color gain and high Nyquist falsely reduce the jet area. Conversely, inappropriately high color gain and low Nyquist limit falsely increase the jet area.

  2. Vena contracta ≥7 mm at a Nyquist limit of 50–60 cm/s. Vena contracta is the narrowest part of the regurgitant flow, i.e., the neck at the origin of MR.
    Pros: accurate, even in eccentric MR. Vena contracta < 3 mm makes severe MR unlikely.
    Cons: does not reliably distinguish moderate from severe MR. Also, should be measured in a view orthogonal to the regurgitation (parasternal long-axis), not an apical view, which tends to falsely widen the vena contracta. It is not accurate if multiple jets are present.

  3. Flow convergence

    • PISA radius ≥ 0.9 cm (regurgitant Nyquist limit set at 40 cm/s)
    • ERO ≥ 0.4 cm2
    • Regurgitant volume ≥ 60 ml/beat (regurgitant volume = ERO × MR VTI)
    • Regurgitant fraction = regurgitant volume/(regurgitant volume + stroke volume at the LVOT) > 50%
      Cons: may underestimate MR if jet is eccentric (but better than jet area in this case), if multiple jets are present, or if PISA convergence is squashed rather than round (crescentic PISA), as in functional MR with dilated LV; thus, 0.3 cm2 is a better ERO cutoff in functional MR. It may overestimate MR if convergence is not a full hemisphere.

  4. Mitral E-wave velocity > 1.2 m/s
    Pros: very sensitive, regardless of eccentricity. A lower E velocity or E/A reversal ~ excludes severe MR.
    Cons: not specific. E velocity increases with high LA pressure and AF.

  5. Pulmonary venous flow: Blunted S is consistent with severe MR, reversed S is specific for severe MR

    • Blunted or reversed S may not be seen in compensated severe MR, where LA compliance absorbs the regurgitant flow and prevents pulmonary venous abnormalities
    • Blunted S may be seen with high LA pressure or AF, and is not specific for severe MR
    • All four pulmonary veins must be sampled on TEE (eccentric MR flow may enter and reverse the flow of one pulmonary vein only)

  6. CW MR Doppler as dense as the forward mitral flow; or dense and triangular with early peaking (V wave cutoff), indicative of decompensation.

    This supports severe MR, but dense flow may also be seen with moderate MR

  7. A flail leaflet is highly specific for severe MR, regardless of color Doppler findings (only feature that does not rely on Doppler).

Important supportive features

  • LA enlargement is universal in all severe MR, except, occasionally, acute MR. A normal LA size ~ excludes severe MR except in the acute setting
  • LV enlargement, particularly with normal EF, strongly supports severe MR (not as sensitive as LA enlargement, which occurs earlier)
  • If MR appears severe yet LA is not enlarged, it is possible that MR is not holosystolic. A large MR jet with a large PISA is not severe if it is brief, as seen sometimes with mitral valve prolapse (end-systolic)
Aortic insufficiency

  1. Vena contracta width (narrowest neck at the origin of AI on the long-axis view) ≥ 7 mm
    AI jet width ≥ 60% of LVOT diameter (long-axis view)
    AI jet cross-sectional area ≥ 60% of LVOT area (short-axis view) at a Nyquist limit of 50–60 cm/s
    Note: AI jet size is different from vena contracta. AI jet size is the AI size just below the vena contracta, as the jet starts to expand (within 1 cm of the aortic valve)
    Cons: eccentric AI, such as bicuspid AI, may be underestimated, because the jet abuts the mitral valve or the septum and shrinks in velocity (color). Color doppler correlates with velocity more than volume; the regurgitant volume may be high, yet color may abate quickly. This is even more so when assessed in a 2D plane where it is narrowest (in the long-axis view). Conversely, AI may be overestimated when the measurement is performed too low below the vena contracta, or in the apical views

  2. Flow convergence (PISA): ERO ≥ 0.3 cm2
    Cons: the rounded flow convergence is more difficult to measure in AI than in MR, as it is shadowed by the thick +/- calcified aortic leaflets.
  3. CW Doppler pressure half-time (PHT) < 250 ms
    Cons: depends on LV compliance and LVEDP. PHT may be > 250 ms in chronic, compensated severe AI. PHT may be < 250 ms in moderate AI with decompensated LV dysfunction and high LVEDP (e.g., severe HTN). Also, vasodilators may reduce diastolic aortic pressure and thus, PHT.
    PHT > 500 ms ~ excludes severe AI

  4. Holodiastolic flow reversal in the descending aorta (suprasternal view) or, worse, in the abdominal aorta (subcostal view). This is assessed by PW Doppler. Early to mid-diastolic reversal suggests moderate AI. Cons: may not be holodiastolic in acute severe AI; non-compliant aortas may exaggerate it.
  5. Other features

    • CW Doppler signal as dense as the forward flow. Cons: significant overlap between moderate and severe AI
    • M-mode of the mitral valve shows leaflet fluttering or early closure. This not only indicates severe AI but decompensated AI

Important supportive feature

  • LV enlargement is universal in chronic severe AI. A normal LV size ~ excludes severe AI, except in the acute setting. LA enlargement is very common in severe AI
Tricuspid regurgitation (same type of features and limitations as MR)

  1. Large jet area (Nyquist limit of 50–60 cm/s)
  2. Vena contracta > 7 mm (Nyquist limit 50–60 cm/s)
  3. PISA radius > 0.9 cm (at a Nyquist limit of 28 cm/s ≠ MR)
  4. TR jet dense ± triangular with early peaking (V-wave cutoff)
  5. Hepatic venous S blunting, or, worse, reversal (reversal is specific for severe TR)

RA/IVC size is always increased in severe chronic TR

Pulmonic regurgitation

  • As opposed to AI, where the jet width below the neck determines severity, in PR, the jet length and the total jet area in the RV correlate with severity. In severe PR, the color jet goes deep into the RV, beyond the RVOT (use a large Doppler sector to visualize). In mild PR, the jet length is < 1 cm
  • CW Doppler: dense PR signal with steep deceleration and termination of PR flow in mid-diastole (severe PR leads to equalization of PA and RV diastolic pressures in mid-diastole). This early termination of PR flow may, however, be seen when milder PR is associated with severe RV failure and elevated RVEDP

RV is always enlarged in chronic severe PR. In a patient with significant PR, RV enlargement without any other cause suggests severe PR

Table 32.2 Severe valvular stenosis: severe AS, including low-gradient AS, and severe MS.

Aortic stenosis
Peak velocity ≥ 4 m/s, mean gradient ≥ 40 mmHg, and AVA ≤ 1 cm2 by continuity equation a
Typically, in severe AS:

  • Peak LVOT velocity is < 1 m/s
  • LVOT velocity/aortic valve velocity ≤ 0.25 (dimensionless index [DI]). DI is, in fact, a component of AVA calculation (AVA = LVOT area × DI). As opposed to AVA calculation, the dimensionless index is not subject to the bias of LVOT diameter measurement: DI ≤0.25 implies AVA ≤25% of normal

LVOT velocity may be > 1 m/s when severe AS is associated with moderate AI or high-output states (anemia, fever), cases in which DI remains < 0.25; or when severe AS is associated with significant septal bulge and subaortic obstruction. It may be falsely elevated if the LVOT cursor is placed too close to the aortic valve or the septal bulge, in the aliasing

Differential of paradoxical low-gradient AS with normal EF (AVA ≤ 1 cm2 with low gradient < 40 mmHg):

  • Echo mismeasurements (50%), particularly under-measurement of LVOT diameter or aortic velocity. A high DI (>0.3) generally rules out truly severe AS.
  • Low-flow, low-gradient truly severe AS: hypertension and concentric LV hypertrophy explain the low output
  • Normal-flow, low-gradient truly severe AS: low gradient is related to misalignment of AVA and gradient cut-points in the guidelines (AVA of 1 cm2 corresponds to a gradient of ~30 mmHg if CO=5.5 L/min)

AS is likely severe if AVA≤ 0.8 cm2 with mean gradient >30 mmHg; or if DI ≤0.25.

Mitral stenosis (see Section VIII.C)

  • Mild and moderate MS: MVA > 1.5 cm2, gradient usually < 5 mmHg at a normal heart rate (60–85 bpm)
  • Severe MS: MVA 1.0–1.5 cm2, gradient usually ≥ 5 mmHg at a normal heart rate
  • Very severe MS: MVA < 1.0 cm2, gradient usually > 10 mmHg

Doppler assesses the transmitral gradient very accurately, as it is easy to align the cursor with the transmitral flow. Caveats:

  • High E wave may merely result from MR or HF and be falsely interpreted as high gradient, and when MAC coincides, be falsely considered MS. The E wave of the latter cases has a sharp downslope.
  • (ii) A high gradient does not necessarily imply severe MS: mild anatomic MS (MVA > 1.5 cm2) may have a severe gradient in the presence of tachycardia or high-output state. Thus, MVA characterizes the anatomic severity of MS better than the gradient.

The estimation of MVA using one of 4 methods (mitral inflow pressure half-time, continuity equation, PISA method, and planimetry) is subject to measurement errors. Pressure half-time may falsely ↓ and MVA may falsely ↑ in patients with LV dysfunction (HTN, elderly)

a AVA = (0.785 × LVOT diameter2) × LVOT velocity/aortic valve velocity.

LVOT is assumed to be circular, but it is in fact elliptical and underestimated. LVOT diameter should be measured at the insertion of the aortic valve leaflets (= annulus), rather than 5-10 mm below it (LVOT is largest and most circular at the annulus). LVOT is measured in the long-axis view, in early systole (largest diameter, inner edge to inner edge). In the presence of protruding annular calcification, LVOT measurement is extended beyond the outer edge of the calcification.

LVOT velocity is obtained by positioning the pulsed Doppler ~5 mm proximal to the stenotic valve (not too close to the valve). Avoid catching the high-velocity convergence proximal to the aortic valve. In case of septal bulge, place the cursor further down, away from the bulge. Either VTI or peak velocity may be used.

V. M-mode echocardiography

M-mode echocardiography is derived from 2D echo (see Figures 32.41, 32.42, 32.43; also Figures 32.1532.18).

M-mode graphically displays the movement of cardiac structures along one line swept by the probe. It can assess valvular opening, chamber size, and subtle abnormalities of cardiac motion (such as RV compression by pericardial effusion). It has a very high temporal resolution and rapid sampling rate (1000 frames/s vs 30/s for 2D) that allows recording of subtle motion and timing of cardiac events.

VI. Pericardial effusion

A. Size (see Figures 32.44, 32.45)

A pericardial effusion is small if < 1 cm, moderate if 1–2 cm, and large if > 2 cm. The effusion is measured as the summation of the anterior and posterior dimensions at end-diastole, i.e., when it appears smallest. A small effusion is usually localized posteriorly, while a large effusion is usually circumferential. A swinging heart, i.e., a heart that changes position in a phasic manner, may be seen with large effusions. An echo-free space that is present only anteriorly suggests an epicardial fat pad rather than a pericardial effusion; unless loculated, a pericardial effusion usually gravitates and predominates posteriorly in the supine position, or is circumferential.

B. IVC plethora

IVC plethora has a sensitivity of 97% for tamponade, but a specificity of only 40%, as it may occur with any right heart failure. On hepatic vein Doppler, a flat D wave (Y descent) corresponds to impeded right-sided diastolic filling and thus tamponade.

C. Pre-tamponade echocardiographic signs (see Figure 32.46)

  • RV compression in early diastole. On M-mode, the RV continues to collapse after systole (inward indentation), while the LV is expanding. This is the most specific and latest tamponade sign. RVOT gets compressed earlier than the remaining RV walls.
  • RA compression during ventricular systole. RA collapses excessively during atrial systole, then stays inward after atrial systole. RA collapse that persists for > 1/3 of cardiac cycle is specific for tamponade.
  • > 25% inspiratory decrease of mitral inflow E velocity and aortic velocity (variation of 25% in reference to the highest E velocity, not the lowest). This is due to the LV compression by the RV. This Doppler finding is the corollary of pulsus paradoxus. Make sure to track E wave, not A.
  • 40% expiratory decrease of tricuspid inflow E velocity.

Respiratory E variations are the earliest and least specific pre-tamponade findings. They are followed by progressive RA/RV collapse.

Tamponade is a clinical diagnosis. The echocardiographic signs appear earlier than clinical tamponade and pulsus paradoxus; they suggest hemodynamic abnormalities that are the substrate for tamponade, but on their own they do not establish the diagnosis of tamponade.

Tamponade may occur as a result of a localized effusion compressing one particular chamber, such as RV, LV, LA, RA, or pulmonary veins, as after cardiac surgery. This is more difficult to diagnose, and only some of the tamponade echocardiographic signs are seen. TEE may be more helpful in showing the localized effusion and cardiac chamber compression (e.g., isolated pulmonary venous compression).

Schematic illustration of m-mode across the mitral valve on the parasternal long-axis view.

Figure 32.41 M-mode across the mitral valve on the parasternal long-axis view. The first structure intercepted, at the top, is the RVOT wall (white line); the second structure is the RV cavity (dark); the third structure is the septum; the fourth structure is the anterior leaflet of the MV (closes in systole and opens in diastole), and the fifth structure is the posterior mitral leaflet.

The anterior mitral leaflet has two waves in diastole: E (rapid filling) and A, similar to the mitral inflow Doppler. Examples of disease states:

  • In MS, the E-wave downslope becomes flat horizontal (flat EF slope), and the posterior leaflet is drawn to the anterior leaflet.
  • In high LVEDP, there will be a small extra wave (B bump) interrupting A emptying in the LV (at the location of the dot). B bump is shown on the right images.
  • In SAM, the anterior leaflet will be drawn to the septum in end-systole or, worse, all systole (in the direction of the arrow).
  • In severe AI, one may have early closure of the mitral valve or diastolic mitral fluttering.
  • In tamponade, early diastolic inward indentation of the RVOT is seen.

By moving the interrogation line towards the mid LV, the systolic movement of the septum and the LV posterior wall can be assessed (see Figures 32.1532.18).

Schematic illustration of m-mode across the aortic valve on the long-axis view.

Figure 32.42 M-mode across the aortic valve on the long-axis view. The first structures encountered are the RVOT wall and cavity. Then the aortic walls (rather than LV walls) are encountered and, inside them, the aortic valve. The aortic valve opens well here (open box in systole [arrow]). Disease states:

  • In severe AS, the box becomes flat. In bicuspid aortic valve, the line of closure in diastole is eccentric
  • In HOCM, there is mid-systolic notching (partial closure) of the box.
  • In low cardiac output, there is early gradual closure of the aortic valve (the box becomes a triangle: >).
  • In severe AI, the aortic valve may start opening in end-diastole, as LVEDP rises and equalizes with aortic diastolic pressure.

Reproduced with permission from Hanna EB, Quintal R, Jain N. Cardiology: Handbook for Clinicians. Arlington, VA: Scrub Hill Press, 2009.

Schematic illustration of examples of M-mode across the mitral valve.

Figure 32.43 Examples of M-mode across the mitral valve.(a) Posterior mitral leaflet prolapse. See how the posterior leaflet moves posteriorly in mid-to-late systole, creating a “gap” in the mitral closure, and thus MR (arrows). (b) SAM of the anterior leaflet in HOCM, with the anterior leaflet touching the septum in systole, creating a gap away from the posterior leaflet. (c) Flat EF slope in diastole suggests MS (mitral valve is steadily open throughout diastole, with no diastasis). Also, the posterior leaflet is pulled towards the anterior leaflet (commissural fusion) (arrow). Ant, anterior mitral leaflet; Post, posterior mitral leaflet.

Schematic illustration of diffuse pericardial effusion on long-axis view, identified as a black band above the RV (upper arrow) and a black band posterior to the LV.

Figure 32.44 Diffuse pericardial effusion on long-axis view, identified as a black band above the RV (upper arrow) and a black band posterior to the LV. In this case, posterior to the LV, there are two black bands separated by the pericardium: pericardial effusion and pleural effusion (lower arrows). Differentiate pleural from pericardial effusion: the pericardial effusion is anterior to the descending aorta (X), whereas the pleural effusion extends behind the aorta. The coronary sinus is in the AV groove, anterior to the pericardium (dot).

Reproduced with permission from Hanna EB, Quintal R, Jain N. Cardiology: Handbook for Clinicians. Arlington, VA: Scrub Hill Press, 2009.

Schematic illustration of pericardial effusion on multiple views.

Figure 32.45 Pericardial effusion on multiple views. In a supine position, a free-flowing effusion gravitates and predominates over the posterior aspect of the LV. The posterior aspect is the one seen on the long-axis view (posterolateral aspect) and the four-chamber view. This has to be distinguished from the effusion at the inferior/diaphragmatic aspect of the LV, which is more anterior and is the one seen on the subcostal view (used for subcostal pericardiocentesis).

Image described by caption.

Figure 32.46 (a) Pericardial effusion (stars) and pleural effusion (bar). The latter is behind the level of the descending aorta. RVOT is compressed in diastole, at a time when the mitral valve is open (RVOT diastolic indentation is marked by arrow).

(b) RVOT collapse in early diastole on M-mode. Always time events to the ECG; systole starts at the peak of R wave and occupies the ST–T segment, whereas diastole starts beyond the T wave. Events may also be timed to the mitral opening on M-mode. After the systolic dip, the RVOT should be expanding outward in diastole (as in the solid line), rather than pushed inward (dashed line). The presence of two dips, a systolic dip and a diastolic dip soon after the RV starts to expand out, is characteristic of tamponade. For the diastolic dip to be diagnostic, the M-mode has to cut the RVOT in an orthogonal fashion. D, diastole; S, systole.

VII. Echocardiographic determination of LV filling pressure and diastolic function

A. Main parameters

(see Chapter 5, Figure 5.2)

Diastolic E flow and E/A ratio-Diastolic E flow is affected by: (1) LA pressure, (2) LV relaxation, which is impaired in both diastolic dysfunction and systolic dysfunction, and (3) heart rate and PR interval. Impaired LV relaxation reduces E velocity; however, severe hypovolemia with low left-sided filling pressure may reduce E and E/A ratio even in the absence of a relaxation problem. Prolonged PR interval and sinus tachycardia reduce E and E/A ratio and may be associated with E–A fusion without any relaxation problem. On the other hand, high left-sided filling pressures but also high elastic recoil in normal young patients may elevate E velocity.

One echocardiographic parameter correlates solely with LV relaxation and is thus reduced in any LV dysfunction, systolic or diastolic, regardless of filling pressure: mitral annular recoil velocity (E’). Therefore:

normal upper E slash normal upper E prime equals left-parenthesis upper L upper A f i l l i n g p r e s s u r e times upper L upper V r e l a x a t i o n right-parenthesis slash upper L upper V r e l a x a t i o n equals upper L upper A f i l l i n g p r e s s u r e

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Nov 27, 2022 | Posted by in CARDIOLOGY | Comments Off on Echocardiography

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