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.
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
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%.
2. Assess for LV dilatation and RV dilatation, which are associated with LV and RV systolic dysfunction, respectively.
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.
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.
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) ischaracterized 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 sizeis 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.
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).
RV dilatation with RV volume overload.
Pericardial processes (constrictive pericarditis, tamponade). Large respiratory swings (e.g., COPD) may simulate the abnormal septal motion of pericardial processes.
Abnormal septal motion post-cardiac surgery.
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.
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
Aortic valve thickening (sclerosis) and calcification are precursors of AS. Also, aortic sclerosis and calcification are associated with coronary atherosclerosis
A bicuspid aortic valve is characterized by fusion of two cusps, most commonly the right and left cusps (85%); a raphe is frequently seen between the two fused cusps, and this may create the false impression of a tricuspid valve. Therefore, on the aortic short-axis view, instead of analyzing how many cusps are seen when the valve is closed, it is best to analyze how the aortic valve opens. An elliptical rather than a triangular opening is a hint to a bicuspid valve (Figure 32.22).
III. Doppler and assessment of valvular regurgitation and stenosis
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.
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.
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 32.23–32.33)
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):
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:
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.
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.
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:
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
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 × VTR2.
Thus, RV systolic pressure = 4 × VTR2 + 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:
IVC ≤ 2.1 cm with > 50% inspiratory collapse → RA pressure = 0–5 mmHg
IVC ≤ 2.1 cm but < 50% inspiratory collapse,
or IVC > 2.1 cm with > 50% inspiratory collapse → RA pressure = 5–10 mmHg
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.
IV. Summary of features characterizing severe valvular regurgitation and stenosis (see Tables 32.1, 32.2)
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.
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.
PISA radius ≥ 0.9 cm (regurgitant Nyquist limit set at 40 cm/s)
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.
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.
Pulmonary venous flow: Blunted S is consistent with severe MR, reversed S is specific for severe MR Cons:
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)
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
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)
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
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.
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
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.
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)
Large jet area (Nyquist limit of 50–60 cm/s)
Vena contracta > 7 mm (Nyquist limit 50–60 cm/s)
PISA radius > 0.9 cm (at a Nyquist limit of 28 cm/s ≠ MR)
TR jet dense ± triangular with early peaking (V-wave cutoff)
Hepatic venous S blunting, or, worse, reversal (reversal is specific for severe TR)
RA/IVC size is always increased in severe chronic TR
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 equationa 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.
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.
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.
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).
VII. Echocardiographic determination of LV filling pressure and diastolic function
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: