ASE LV Function

8/15/2019 ASE LV Function

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TO BE CONTINUED WITH SECTION 4: PRINCIPLES OF CARDIAC HEMODYNAMICS AND CARDIAC CYCLE.

(FROM NEC-PART-III-ABDOMEN-CARDIAC IN DESKTOP, ECHO!

1) The Left Side: Systole, Stress and Diastolic Function…

2) CORONARY ARTERY DISEASE

a)

ISCHEMIC HEART DISEASE: is left sided heart disease… 1. Is manifested by abnormalities in cardiac function and structural changes due to myocardial

ischemia

a. Most common cause of myocardial ischemia is atherosclerotic CAD…

1) Which causes coronary artery narrowing or occlusion with reduced blood supply to a

particular area of the myocardium where oxygen demand can exceed supply resulting in

ischemia with regional wall motion abnormalities (RWMA)…

(i) The identification of RWMA by echo can therefore reveal a great deal about the

status of the coronary circulation.

(ii)

MI involves extreme ischemia with myocyte necrosis.

2) The great majority of the testing in echo is done to assess the LV function and the

assessment especially of ischemia with stress echo.

b) ATHEROSCLEROSIS…

1) Is the primary cause for

ischemia, is a plaque that

builds up over time.

Atherosclerosis is a

generalized disease, not

only affecting the coronary

arteries but all the vessels,

like aorta, renal arteries,

femoral arteries, etc.

(i) As plaque builds up, it

can start to ulcerate or

break off…once it

breaks off or ulcerate, then thrombus formation occurs around it and underneath,

with vessel narrowing…

(ii) As plaque builds up and thrombus formation occurs, an embolic event may occur…

1. An embolic event occurs not only from the plaque, but also from vegetations or a

tumor.

c) Coronary spasm: may be another cause for ischemia. Here, the coronary artery closes down with

spasms, preventing blow flow from getting to the myocardium, causing chest pain and symptoms

compatible with a MI…


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(i) By the time the patient gets to the cath lab,

the spasm has gone away. It looks like the

patient has a totally normal coronary

arteries, even though it looks like the

patient has had an ischemic event.

d) SIGNS AND SYMPTOMS OF CORONARY EVENTS…

(i)

Angina pectoris: typical chest pain withirradiation to the left arm accompanied

with chest pressure…

1. Note: this is not always the typical and

most common sign of an MI. Severe MI

can present without chest pain or

whatsoever…just the patient may feel

stomach discomfort, with nausea

sensation and “not feeling good”…and

still the patient may have a 100%occlusion LAD with 99% of the circ and

even 80% of the RCA!. Patients can

never have the symptoms of chest

pain, no SOB.

2. Also difficult can sometimes be

women because often they do not

have the typical signs or symptoms…

a. Maybe they may present with

palpitations, dyspnea, diaphoresis and nausea and pressure/heaviness in

the chest with or without left arm pain.

3. In diabetics, the diagnosis of an MI is difficult because these patients have often

atypical signs and symptoms or may occur silently.

4. Then, of course, there is sudden cardiac death (SCD) as the primary

manifestation of sever CAD. Is therefore important to identify people who are

more at risk for this and provide interventions to avoid SCD.

a. The diagram is a demonstration of the ischemic cascade outlining the

sequence of events as the

magnitude of ischemia or coronary

flow reduction progresses from

none-to-severe.

e) CORONARY ARTERY ANATOMY:

The coronary arteries supply blood to the heart and

originate from the two initial branches of the aorta: the

left coronary artery (LCA) and the right coronary artery

(RCA), which originate from the left and right sinus of

Valsalva, respectively…


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The initial portion of the LCA constitutes the left main CA

or LMCA: it branches into the left anterior descending

artery (LAD) and the left circumflex artery (LCx)…

o Note: anatomically there are only two CAs, the LCA

and RCA. But, in clinical parlance it is often said

that there are three CAs: the RCA, LCA and LCx.

The LAD supplies the largest portion of the LV…itsterritory encompassing about 50% of the LV. It gives: a)

septal branches that penetrate into the anterior 2/3 of

the IVS…b) diagonal branches which supply large areas of

the anterior wall of the LV and smaller areas of the

anterior wall of the RV,

o (Fig. A) LAD artery and its major branches in RAO

(right anterior oblique) view.

o The other half of the LV is supplied by both the RCA

and the LCx. The RCA course within the right atrioventricular groove, it

is the principal supply source to the RV. During this initial

course, the RCA gives off the acute marginal (AM)

branches to supply the margin of the heart made up by the

RV…

o (Fig. B) Dominant RCA and its major branches (PDA

& PLBs) in LAO (left anterior oblique) view.

In a roughly mirror-image pattern, the LCx runs in the left

atrioventricular groove and gives off obtuse marginal

(OM) branches. They run parallel to the long axis of the

heart and supply the obtuse margin of the heart made up

by the lateral wall of the LV…

o (Fig. C) Nondominant LCx artery and its major

branches visualized in a caudally and rightward

RAO (right anterior oblique) view.

The inferoposterior aspects of the IVS and the LV are

supplied by the posterior descending artery (PDA) and

one or more posterolateral branches (PLBs)…

The PDA runs initially along the posterior interventricular

groove and its course is parallel to that of the LAD in the

anterior interventricular groove …

Along its interventricular course, the PDA gives off septal

branches to the inferior aspect of the IVS and then meets

the LAD in the apical portion of the posterior IVS…

PLBs are arterial branches that run along the long axis of

the LV and roughly parallel to the PDA and Oms.o PLBs supply the inferior and posterior walls of the

LV


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Coronary Dominance: dominance refers to whether the RCA or the LCX supply a larger section

of the LV: in about 70% of cases, the RCA subtends a larger section of the LV than the LCx (the

so-called right-dominant circulation); in about 20% of cases, the contribution of the two

arteries is equal (co-dominant or balanced circulation); in the remaining 10%, the LCx is larger

than the RCA (left-dominant circulation).

o NOTE: remember, 50% or more of the LV is supplied by the LAD artery.

o

It is the origin of the PDA and the PLBs that determines whether the coronary circulationis right-dominant, left-dominant, or codominant…

Right dominant circulation: the PDA and PLBs are branches of the RCA;

Left dominant circulation: the PDA and PLBs are terminal branches of the LCx;

Codominant circulation: both the RCA and LCx supply the PDA and/or PLBs.

PERFUSION TERRITORIES

NAME FOR CARDIAC PLANES: the

ASE nomenclature

recommendation of short, vertical

long, and horizontal long axes has

been used for the cardiac planes

generated by SPEC, PET, cardiac

CT, and CMR…

As shown in the diagram,

these planes are oriented

at 90˚ relative to each

other.

For TTE 2D echo, a similar system

is recommended and it is widely

used…

In echo, the PSAX plane approximated the short-axis views in the other modalities…

The apical 2-chamber echo view approximates the vertical long-axis view…

The apical 4-chamber echo view approximates the horizontal long-axis view of other modalities.

NUMBER OF SEGMENTS: the muscle and cavity of the LV can be divided into segments. The heart is divided

into apical, mid-cavity and basal thirds perpendicular to the LV long axis…


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1. The number of myocardial segments for echo

had originally been 20, but was subsequently

reduced to 16 segments. Thus, the LV is divided

into equal thirds perpendicular to the long axis

of the LV… this will generate 3 circular basal,

mid-cavity, and apical short-axis slices of the

LV… o The segment system were developed

mainly for analysis of regional LV wall

motion and did not include the true

apex, devoid of cavity.

o With the introduction of contrast

studies for the assessment of perfusion,

the apex segment or apical cap beyond

the LV cavity becomes pertinent and a

17-segment model is more appropriate for assessment of LV WMAs and

myocardial perfusion with echo.

2. As shown in the diagram, the basal third

corresponds to the area extending form the mitral annulus to the tips of the papillary muscles at end

diastole.

3. The mid-cavity slice is a region that includes the entire length of the papillary muscles.

4. The apical slice is selected from the area beyond the papillary muscles to just before the cavity ends.

5. The true apex (segment 17) or apical cap is the area of myocardium beyond the end of the LV cavity.

NAMING AND LOCATING THE SEGMENTS: the segments should be named and localized with reference to

the long axis of the LV and the 360˚ (bull’s eye) view on the short axis.

Using the denominations of “basal”, “mid -cavity”

(or simply “mid”) and “apical” as part of the

name defines the location along the long axis of

the LV from the apex to the base.

With regard to the bull’s eye segmental location,

the “basal” and “mid” view is divided into 6

segments of 60˚ each…

The attachment of the RV wall to the LV is used to

identify and separate the septum from the LV

anterior and inferior free walls…

o The circumferential locations in the basal

and mid-cavity are: anterior (1, 7),

anteroseptal (2, 8), inferoseptal (3, 9),

inferior (4, 10); Inferolateral (5, 11) (AKA as “posterior wall”); and anterolateral (6, 12 ) (aka

“lateral wall”). o As an example, using this system, segments 1 and 7 identify the locations of the anterior wall

at the base and mid-cavity…the appropriate names are “basal anterior” and “mid anterior’

segments.


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o The septum: delineated by the attachment of the RV, is divided into anterior and inferior

segments…segments 2 and 3 are called “basal anteroseptal” and “basal inferoseptal”

respectively.

As the LV tapers while approaching the true apex, it became appropriate to use only 4 segments,

represented by 13, 14, 15, and 16 segments.

o The names are: “apical anterior” (13); “apical septal” (14); “apical inferior” (15); and “apical

lateral” (16). The apical cap: represents the true muscle at the extreme tip of the LV where there is no longer

cavity present , and this is defined as segment 17, called the apex .

ASSIGNMENT OF SEGMENTS TO

CORONARY ARTERIAL TERRITORIES:

6. The assignment of the 17 segments

to one of the 3 major coronaryarteries (CAs) I shown in the diagram.

7. There is a huge variability in the CAs

blood supply to the wall segments…

8. The greatest variability occurs at the

level of segment 17, which can be

supplied by any of the three CAs.

9. Segments 1, 2, 7, 8, 13, 14 and 17 are

assigned to the LCA distribution…

10.

Segments 3, 4, 9, 10, and 15 are assigned to the RCA when it is dominant… 11. Segments 5, 6, 11, 12, and 16 generally are assigned to the LCx artery.

12. (NOTE: the 17-segment is more useful for perfusion applications)


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13. Examples of variability: in the 2-CH view we have the anterior and inferior wall, the anterior is supplied

by the red section, which is the LAD…

14. If there is an inferior wall motion abnormality, that would correlate with the RCA.

15. In the short axis, the anterior wall is supplied by the LAD, the lateral wall is supplied by the circumflex

and the inferior wall is supplied by the RCA

LEFT VENTRICLE (LV) FUNCTION: QUANTITATIVE EVALUATION

1) There are other ways than echo to evaluate EF…that would

be by nuclear imaging or cardiac cath, but echo is the

easiest and readily available method.

a) EF is a predictor for mortality. A poor EF correlates with

a higher mortality

b) Echo helps in the decision making of device

implantation…a patient with an EF of 25% may get a

device as opposed to a patient with 35% that would not

get a device.

2) There are different ways of assessing LV function: the EF is

the most utilized. The fractional area change (FAC) by

which instead of measuring motion we measure an area.

Another way is by using the wall motion scoring index and

evaluating the motion of the different segments. From the

Doppler methods, the most frequently utilized is the

measurement of the CO; other ways are measuring the

Dp/Dt index, the Tei index (also called the myocardial performance index), tissue Doppler imaging (TDI)

3) The last one is by utilizing M-mode.


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LEFT VENTRICLE (LV) FUNCTION: EJECTION FRACTION (EF)

1) The EF formula is one you need to know for the boards:

EF = −

2) This formula will reoccur: if using the FAC method, instead

of plotting volume whether measured by Simpson’s or by

M-mode, you will utilize areas with the same basic formula3) If EF is between 50 and 55%, some people consider that as

a “low normal”, but if the value is below 50%, that is

considered mildly hypokinetic…

a) As we increase above 65%, that would be a

hyperdynamic or hyperkinetic EF.

4) SIMPSON’S CALCULATION

a) Also called the “method of disks” is an accurate way

of assessing the EF… b) The biplane method (using the 4-CH and 2-CH views)

is the most accurate.

1. It assumes that the LV is cone-shaped (bullet)

structure.

c) We look at and then

trace the inside

volume of the heart

during diastole

(when volume is thebiggest) at and end-

systole (when the

volume is the

smallest). There are

two different ways

of measuring those

volumes:

1. It can be done by

looking at the

EKG for timing,

but we also got

to make sure

that we have the

largest and the

smallest

dimensions,

measured as the

inside area

2. Or it can be done

by looking at the volume.


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a. The guidelines tell us that we should combine both methods

d) The Simpson’s method takes the 4-CH and 2-CH views at end-diastole and end-systole and creates a

structure of “staked discs” at each one of the planes. There are 20 disks. Each “disc” has a volume

that, when summation occurs, we obtain a cavity volume, which is applied to the formula:

=

100

5) EF CALCULATION VIA M-MODE

a) In pediatrics, the method more commonly

used to calculate EF is the FRACTIONAL

SHORTENING method vs the EF method. Both

can be derived by M-mode linear dimension

trace at the papillary muscle level …

b) Fractional shortening (FS): it measures the

IVS, the LV internal dimension (LVID) indiastole as well in systole…

=

100

c) When the obtained data is squared and

applied to the formula, then:

=

100

a. By squaring the linear dimensions, we obtain an AREA!

b. Inherently limited.

d) When the data is cubed and applied to the formula, we obtain the EF:

= −

100

a. By cubing the linear dimensions, we obtain a VOLUME!

b. More reliable that the previous methods.

c. Utilized in large-scale/epidemiologic studies.

e) The bigger problem here is that we are ONLY assessing two segments of a total of 17 segments…the

result of this disadvantage is that we end up either underestimating or overestimating the true EF…

1. That’s why M-mode is NOT a good way to report EF…

2. Make sure that on your report, the numbers for EF come from the Simpson’s biplane method.

3. In pediatrics, reporting the values for M-mode based FS is acceptable because children do not

have wall motion abnormalities (WMAs) and therefore, children do not need volumes…for themost part, in children the wall motion is very symmetric. Children do not have MI’s. In children,

the WMA’s are more the type of global abnormalities, rather than regional WMA’s as it occurs

in adult patients with MI’s.


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f) EF and APICAL CORRECTION:

1. Application: when you have a LV with an akinetic apex and a

very active motion present in the basal segments. When

tracing an M-mode through the compensatory e hyperactive

basal segments in the PLAX view, while the apical sections

are not moving at all, you will obtain an EF in the range of 70to 80% even though the apical segments are not moving. It is

obvious that the resulting EF is very inaccurate…

a. Here the need for a correction. According to Quinones

et.al., we use an apical correction factor ():

1) If apical contraction is normal, add 15% of the

calculated EF…

2) If the apex is hypokinetic, add 5% of the calculated

EF…

3)

If the apex is akinetic, either do not add anything orsubtract 5% of the calculated EF…

4) Finally, if the apex is dyskinetic or aneurysmal, subtract 10% of the calculated EF.

A more practical way of “correcting” the EF is as follows:

NOTE: all in all, the best way for determining EF is the SIMPSON’S BIPLANE METHOD that uses 12 segments

(6 from the 4-CH view and 6 segments from the 2-CH view) instead of only two segments, for calculating an

accurate, more global EF.

SEMI-QUANTITATIVE WALL MOTION SCORING:

The next thing we may want to do regarding LV function evaluation is to look at the endocardial wall

motion patterns and try to obtain a score out of it…this is the semi-quantitative wall motion scoring.


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When we perform an echo evaluation, we make assessments not only of

the movement of the muscle (the “excursion”), but also of the thickening

of the segments (% thickening)…

1) Special attention is put to the actual endocardial thickening…

a) NORMAL: If the wall moves more than 5 mm and thickens

b) HYPOKINETIC: if the wall moves less than 5 mm (but still moves)…

and thickens less than 25%.

c) AKINESIS: if the wall does not move and does not thicken

d) DYSKINESIS: it the wall moves in the wrong direction, outwards in systole rather than in.

2) REGIONAL WALL MOTION SCORING INDEX

(WMSI): is another, traditional method that

has been used in the past and not frequently

now-a-days. Seen more in stress echo rather

than in clinical echo. It is a quantification

method of scoring. Basically, what we’ll do is

look at each of those segments and then

give that segment a score/numeric value to

the degree of contractile dysfunction in each

segment…

a) The theoretical maximum score value for a WMSI

is 5 in the scoring system depicted in the

table…such a score would assume that all LV

segments are aneurysmal! b) Once all segments are given individual scores, a

total score is calculated as a sum of the individual

scores…

c) A wall motion score index (WMSI) is then

calculated as a ratio between the total score and

the number of evaluated segments.

d) The WMSI is a dimensionless number. For a 17-

segment LV, the total score is 17 (all segments

have normal contractility). Since all segments areevaluated, the WMSI of a normal heart is 17/17 = 1

i) For abnormal ventricles, the higher the WMSI,

the more severe the contractile dysfunction.

(1) For example, in a patient with an MI

secondary to proximal LAD occlusion,

akinesis was observed in the entire apical

region (segments 13, 14, 15, and 16), while

hypokinesis was observed in the remaining LAD territory (segments 1, 2, 7, and 8).

Segments in the territories of other coronaries were normal… (a) This patient’s global WSMI was calculated:

[4 (3) + 4 (2) + 8(1)]16⁄ = 1.75

LV WALL MOTION SCORING


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e) Why use this scoring when we have Simpson’s?

i) This scoring system is useful when, for example, a patient has great PLAX and SAX windows but

a terrible 4-chamber view where it is impossible to evaluate any wall motion…here, since the

PLAX and SAX views are great, we can still get a

good WMSI.

(1) So, this method would be an alternative

when it is impossible to obtain Simpson’s.

DOPPLER METHODS: THE CARDIAC OUTPUT (C0)

Besides the 2D methods, there are Doppler methods

available to evaluate LV function. The most commonly used

Doppler method is the determination of the CO…

= () 1) CO is an easy way to evaluate the LV function, done by measuring the cross sectional area (CSA) of the

LVOT and flow volume through the same LVOT… a) Flow Volume: is determined by multiplying the LVOT area

times the PW Doppler determined Volume Time Integral (VTI)

in the LVOT…

Note: VTI = distance in cm that blood travels with each stroke

b) It is assumed that the LVOT geometric form is a circle with a

radius r . Since the area of the circle is equal to: , then:

() =

Given that in echo we don’t use the “radius r” but instead we use the “diameter D”, and since the “r”

is equal to half the diameter “D” or… r = D/2, then:

= (

2 )

=.

= .

c) Now, we determine the stroke volume

(SV)…by applying the following formula:

=

= .

d) Once the SV has been calculated, we can now determine the CO, which is defined as the effective

volume of blood expelled per unit time (L/min):

= e) NORMAL SV = 70 to 100 ml NORMAL CO = 4 to 7 L/min

i) Note: = ℎ


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2) SV & CO CALCULATION EXAMPLE: (heart rate: 60 bpm)

a) Calculation of SV involves careful measurement of the LVOT

diameter in systole at the level of the aortic annulus from the PLAX

view. The aortic annulus is the most accurate location for SV

calculations. An inner-edge to inner-edge method is employed. In

this case, the LVOT diameter was measured at 2.3 cm…

b)

Next, we measure the LVOTvti with the PW Doppler sample volume placed in the LVOT of an apical view: 3-CH or 5-CH. The sample

volume is placed at the same location as where the diameter was

measured. Then, the VTI has been traced around the LVOT curve. In

this case, the LVOTvti was measured at 21 cm…

c) Next, we apply the SV formula:

=

0.785

= 2.3 0.785 21

=

d) Then: = = . /

3) SV & CA CALCULATION EXAMPLE IN A PATIENT WITH DILATED CMP

AND HEART RATE OF 62 bpm:

= 2.1 0.785 9.5 = 33

= = . /

a) In this patient, the LVOTd was measured in the PLAX window and

the LVOTvti was measured from an apical window. Here, both

forward SV and CO are reduced, as evidence of heart failure.

NORMAL REFERENCE VALUES FOR VELOCITIES & VTI

LVOT Aorta Mitral

Vmax (m/s) 0.88

(0.47-1.29)

1.17

TVI (cm) 20-24 18-25 10-13

4) CARDIAC INDEX (CI): is the CO corrected for the individual BSA…

a) CO is the volume of blood pumped from the LV each minute…

b) BSA (body surface area) is the calculated surface area of the human body…

c)

BSA is calculated with the Mosteller formula.d) The normal average BSA is 1.9 m² for men and 1.6 m² for women…

i) It depends, however, on gender and age

e) The normal CI is 3 to 4 /


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5) DIFFERENT AREAS EVALUATED FOR SV

CALCULATION :

a) Typically, the areas evaluated for

determination of SV and CO have been

the LVOT, with the Doppler

interrogation taking place from the

apex of the heart…either from a 5-CHwindow of from an apical 3-CH

window, as depicted in the top

illustration (A)…

i) This is the most accurate and the

most commonly utilized method.

b) The illustration in the middle (B) shows

the SV calculated from the diameter

measured at the mitral annulus level.

Consequently, a MV inflow VTI shouldbe utilized for the calculation.

c) The bottom illustration (C) shows the

SV calculated from the PSAX view, with

measurement of the PA diameter and

the pulmonary artery waveform VTI.


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6) USING LVOT PEAK VELOCITIES INSTEAD OF VTI FOR THE SV CALCULATION :

a) In a normal patient with a normal EF, the typical velocities at the LVOT level are around 1 m/s…

i) If you have a LVOT velocity of, maybe, 0.6 m/s then you should think strongly about the patient

having a low CO, with an EF probably in the 10 – 15 % range!

ii) Now, in the other direction. Let’s say we have a LVOT velocity in the range of 1. 5…this most

probably will be caused by a hyperdynamic LV, obstruction to the LVOT, in volume depleted

patients with hyperdynamic pattern, or hyperthyroidism, etc.

iii) So, by looking at your LVOT velocities, you can obtain some more information regarding the

hemodynamic status of the patient.

iv) It is important to note that in echo “everything” should make sense. So, if you have an LVOT

velocity of 0.6 m/s and you have also measured an EF of 60%...these data obviously doesn’t

make sense, does not match up. Some measurement is wrong. May be useful to go back and

take a look at the area where the LVOT velocity was measured, maybe it is too far back into the

LV…(the PW measurement got to be within 1 cm of the aortic valve in the LVOT)

7) SV PITFALLS: Any inaccuracy measuring the LVOT may create a substantial error in flow calculation,

taking into account the square of the radius…

8) SV as well as EF are afterload-dependent parameters…


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a) A preload decrease (severe anemia) or afterload increase (Aortic stenosis, hypertension) negatively

affects the LV systolic function and may cause underestimation of it.

b) Conversely, decreased afterload (e.g. mitral regurgitation, or IVS defect) can cause a false

impression of preserved LV function even in the presence of a serious myocardial compromise.

DOPPLER EVALUATION OF LV FUNCTION: THE dP/dt

This parameter, dP/dt is the maximum rate of LV pressure

development during systole and has been measured

invasively in the cath lab…but, a MR spectral envelope can be

used in echocardiography to perform a similar calculation. It

is a parameter indicating how well the myocardium contracts

1) Someone with a normal EF, will present with a vigorous

systolic contraction, with blood ejected rapidly and

strongly in systole…if it happens that this patient also hasa MR, the regurgitant jet will, of course, be consequently stronger.

a) As a contrast, a patient with an EF of 10% will present

with a considerable slower and weaker blood ejection

during systole. As anticipated, this patient’s MR will

certainly be sluggish!

2) So it happens that, by looking at any patient’s MR we can

tell if the patient’s heart is contracting strongly and fast or if

that heart’s contractility is poor, as an evidence of a bad

heart that is taking a long time to squeeze that regurgitantblood back into the LA.

3) DEFINITION : Is the rate of LV pressure change (rise) during

the isovolumic contraction period…

a) DP/dt is another index of LV contractility, it is estimated

from the time interval (dt) required for the CW Doppler

MR jet velocity to increase from 1 to 3 m/s…

i) Then, the LV pressure rise is derived from the

Bernoulli equation (

). Thus:

If V 2 = 3 m/ s ; and V 1 = 1 m/s , we have:

=

()

() =

ii) According to this equation, the time required for the LV to increase the MR velocity from 1 m/s

to 3 m/s, is the time required to increase the LV pressure by 32 mm Hg.

iii) Now that we have the dP value, we got to find the denominator, which is the dt value…this value

is found by the machine after placing the cursors…In the above example, the dt is equal to 0.04

sec. Then, the dP/dt is calculated from the formula:

= / ()

iv)

So:

=

. = 800 /


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b) When the time is expressed in milliseconds, a

multiplication by a conversion factor of 1000 is

necessary. Example:

i) Here dt is 0.045 sec, which is equivalent to 45 ms.

Then:

=

1000= 711 mmHg/s

c) Another example: CW Doppler of MR in a patient

with severe LV systolic dysfunction…

i) Note that the peak velocity of the MR jet is 3.5

m/s, which according to Bernoulli, corresponds to

only a 49 mmHg gradient across the MV during

systole:

∆ = . = (Normally the pressures in the LV are 120/10 and

the normal gradient in systole is usually much

larger)

ii)

Pulmonary capillary wedge pressure (PCWP) inthis patient was 50 mm Hg (Normal = 12 mmHg)

iii) And systolic blood pressure was low at 96 mmHg…

iv) Calculating the dP/dt we get:

=

= /

v) The patient’s depressed systolic function is also reflected in a decreased dP/dt.

NORMAL REFERENCE VALUES FOR dP/dt:

4) Visual Clues: if a MR jet is sharp, straight up and down (it goes straight down and straight back up), you

can think of this as a strong heart.

a) But when you look at a sluggish, rounded, more parabolic-shaped MR jet…this heart is taking longer

to eject the blood out because the muscle pump is failing…(a bad heart has dP/dt less than 1000).


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3D VOLUME CALCULATION

Is the most accurate calculation but it has many limitations…

a) Expensive and thus, everybody does not have it

b) Those who have it, may not be using it because it

requires some practice

c)

And, if the images are not good, the volumes providedwill not be accurate…

i) Thus, today, EF by Simpson’s biplane is the most

useful. (maybe in 5-10 years 3D methods would

become the gold standard)

LEFT VENTRICLE (LV) FUNCTION: QUALITATIVE EVALUATION

“EYEBALL” assessment is a non-quantitative, much more subjective

way of evaluating LV function, and therefore, not as accurate as

the quantitative methods…

1) Its accuracy is influenced by the interpreter’s

experience, because there is a learning curve to

look at the walls, assess their motion and

“eyeball” its EF…

2) Reason enough for the ASE not to recommend this

method for assessing LV function

3) QUALITATIVE REGIONAL WALL MOTION

ANALYSIS:

a) Very important to evaluate not only the

motion of the endocardium but also its

thickening and try to correlate it with a

coronary territory…especially in stress echo.

b) Normal wall motion: it squeezes well and it

thickens well.

c) Hypokinetic : it doesn’t contract as strongly as

it should and thickens less than 40%.

d) Akinetic : characterized by a segment that

does not contract and does not thicken either.

e) Dyskinetic : instead of an inward motion, a

segment/s exhibit outward systolic motion

and without wall thickening

The best way to evaluate for motion is to go by

segments: evaluate first the basal segment, then the

mid-cavity segment and then the apical

segment…then go around the apex and evaluate the same way, this time by looking at the opposing wall.


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You can leave you cursor in diastole and use it as a “beacon” to see how much the segment moves. That is

the segment’s excursion in systole that will allow you to see how well it thickens: we see motion as well as

thickening…

4) What is measured is the endocardial border, the one that has an inward excursion and thickens.

5) Another useful “technic” to help in the evaluation is to put a marker (i.e. a pencil) in the center of the

LV and look at each segment and evaluate how it squeezes toward that pencil…

6)

Stop trying to get a “good view” instead of looking at wall motion details. Experience interpreters do

not worry much about getting a good picture as compared to getting a good view at any wall motion

abnormality that may be present.

7) Video Link 1

8) VIDEO LINK 2

9) Video Link 3

LEFT VENTRICLE (LV) FUNCTION: EVALUATION with CONTRAST

1. Currently there are two FDA approved for LV opacification: Definity® and Optison®. The latter is not

being manufactured and Definity has become the primary opacification method.

a. It is composed of tiny microbubbles that are less than the size of a RBC, in the 2 to 7 micron

range, containing a perfluoropropane gas with a shell/covering. Definity has a lipid covering.

b. The contrast agent in injected via IV, travel with the RBCs to the heart and then the U/S beam

bounces off of those microbubbles, providing a bright reflection that clearly delineates the

endocardial border.

2. Apical Hypertrophy vs. WMA: Video link

3. CONTRAST EF ASSESSMENT:

a. If you can’t see more than two segments or two

continuous segments, that’s when contrast is indicated

b. Contrast is also indicated in a bad heart where we

cannot see the apex, where an apical thrombus is

suspected, because if a thrombus is identified, that will

change the treatment.

4. CONTRAST CONTRAINDICATIONS:

a.

In patients who have a known left-to-right shuntb. Known allergies to the agent: there can be an allergic

reaction in 1: 3,000 to 5,000 patients…(2-3 reactions a year)

i. Typical allergic reaction presents with back pain, SOB.

http://localhost/var/www/apps/conversion/tmp/scratch_6/Windows%20Media%20Player%5b2%5d.wmvhttp://localhost/var/www/apps/conversion/tmp/scratch_6/Windows%20Media%20Player%5b2%5d.wmvhttp://localhost/var/www/apps/conversion/tmp/scratch_6/Video%20Link%202.wmvhttp://localhost/var/www/apps/conversion/tmp/scratch_6/Video%20Link%202.wmvhttp://localhost/var/www/apps/conversion/tmp/scratch_6/Video%20Link%203.wmvhttp://localhost/var/www/apps/conversion/tmp/scratch_6/Video%20Link%203.wmvhttp://localhost/var/www/apps/conversion/tmp/scratch_6/Apical%20Hypertrophy%5d.wmvhttp://localhost/var/www/apps/conversion/tmp/scratch_6/Apical%20Hypertrophy%5d.wmvhttp://localhost/var/www/apps/conversion/tmp/scratch_6/Apical%20Hypertrophy%5d.wmvhttp://localhost/var/www/apps/conversion/tmp/scratch_6/Video%20Link%203.wmvhttp://localhost/var/www/apps/conversion/tmp/scratch_6/Video%20Link%202.wmvhttp://localhost/var/www/apps/conversion/tmp/scratch_6/Windows%20Media%20Player%5b2%5d.wmv


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c. Many discussions about what kind of patient should be

given contrast or not…

i. Care should be especial in patients requiring long

monitoring because of instability

ii. The ASE has a website: “Contrast Zone” dedicated to

the use of contrast and different policies,

implementation, protocols and procedures

CAD/ ISCHEMIC HEART DISEASE (IHD) COMPLICATIONS:

1. Ischemic Cardiomyopathy: the patient will present with a poor LV

function. VIDEO LINK: Aneurysm vs. Pseudoaneurysm

d. Segmental WMAs will be present

e. Post-infarct remodeling occurs

2. True Aneurism: it may have a thin wall, not full thickness. Localized

dilatation with wall thinning that may move outward in systole that

has a brighter appearance. They occur in areas where the infarcted

myocardium has become weakened and thinned.

a. It is called aneurysm because it will no longer be possible to retain

the true bullet shape of the LV. In contrast with pseudoaneurysm,

“true” aneurysms have a wide neck (at least half the D of the

aneurysm itself) and are lined by myocardium rather than

pericardium (scar)

b. A chronic ventricular rupture is called a pseudoaneurysm: the

distinction between this and a true aneurysm is that the wall of

the true aneurysm is composed of myocardium, but with a

pseudoaneurysm the myocardium has been breached and the

pseudoaneurysm is lined with pericardium. The neck is typically

smaller.

c. Rupture of the ventricular free wall is usually a

devastating complication, causing rapid hemorrhage

into the pericardium and fatal cardiac tamponade in

about 75% of the cases.

i. Sometimes the ventricular rupture can be

contained by adhesions of thrombosis, causing

a more stable (but still very dangerous)

situation which can be repaired.

3. Valve Dysfunction: Functional MR may occur (VIDEO LINK),

as seen in the picture where the MR jet is posteriorly

directed.

a. With an off-axis view, a small area of aneurysm can be detected and can also be seen that the

papillary muscle is not moving and is brighter… i. This is called “papillary muscle dysfunction” secondary to an MI in the area of the

papillary muscle resulting in a lack of relaxation of the papillary muscle which pull open

http://localhost/var/www/apps/conversion/tmp/scratch_6/aneurysm.wmvhttp://localhost/var/www/apps/conversion/tmp/scratch_6/aneurysm.wmvhttp://localhost/var/www/apps/conversion/tmp/scratch_6/aneurysm.wmvhttp://localhost/var/www/apps/conversion/tmp/scratch_6/Valve%20Dysfunction.wmvhttp://localhost/var/www/apps/conversion/tmp/scratch_6/Valve%20Dysfunction.wmvhttp://localhost/var/www/apps/conversion/tmp/scratch_6/Valve%20Dysfunction.wmvhttp://localhost/var/www/apps/conversion/tmp/scratch_6/Valve%20Dysfunction.wmvhttp://localhost/var/www/apps/conversion/tmp/scratch_6/aneurysm.wmv


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the MV posterior leaflet, causing non-coaptation between the anterior and posterior MV

leaflet.

4. Thrombus: typically a thrombus is associated with an area

that is hypokinetic or akinetic, where the blood flow

becomes more stagnant with “spontaneous echo contrast”

formation, characteristic of a low flow state, which gives

origin to a thrombus… a. First presentation may be in the form of a stroke

secondary to a part of the thrombus that has

embolized.

b. Differential with mass: it helps by putting all the

pieces together…a thrombus more typically occur in a

patient who is post-MI and that has an akinetic

apex.

i. Location: This case would be unlikely to

be a mass, maybe a myxoma, becausethat location in the apex, is an unusual

location for a myxoma

5. Papillary Muscle Rupture (Video Link): acute, large

MR can occur as a result of pap muscle rupture or pap

muscle dysfunction and most commonly occurs in

inferior myocardial infarction…

a. Usually the leaflets are coming together and

pointing towards the LV. In the picture we see the anterior MV leaflet going upwards into the

left atrium: important DD with MV prolapse, where the tips point towards the LV cavity

b. When rupture occurs, it is usually due to rupture of the posteromedial pap muscle, which has a

single blood supply usually from the RCA or LCx artery, whereas the anterolateral papillary

muscle has a dual blood supply.

c. Patients may present with acute pulmonary

edema, cardiogenic shock and a new systolic

murmur. Urgent surgical intervention is required.

d. Another cause of papillary rupture is trauma

6. Septal Rupture: rupture of the IVS, due to focal area of

myocardial necrosis, causes an acquired VSD…

a. There is a sudden deterioration of the patient’s

condition along with a harsh systolic murmur…the

acute left-to-right shunt overloads the RV which

cannot take that excess volume

b. It is associated with a high mortality and requires

urgent surgical intervention…

c. It can be imaged with 2D and its flow is detected with

color Doppler.

d. Note: when rupture occurs in the free wall, the result

is a pseudoaneurysm.

http://localhost/var/www/apps/conversion/tmp/scratch_6/PapMuscleRupture.wmvhttp://localhost/var/www/apps/conversion/tmp/scratch_6/PapMuscleRupture.wmvhttp://localhost/var/www/apps/conversion/tmp/scratch_6/PapMuscleRupture.wmvhttp://localhost/var/www/apps/conversion/tmp/scratch_6/PapMuscleRupture.wmv


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7. Pericardial Effusion: this can occur following an MI. PE occurring 2-10 weeks after an MI is likely to be

due to Dressler’s syndrome, a form of pericarditis aka post myocardial infarction syndrome…

a. Dressler’s syndrome is thought to be an autoimmune response, caused by the release of

myocardial antigens. It may also be seen after cardiac surgery

b. Patients present with pleuritic chest pain, fiber and a pericardial friction rub.

8. Right Ventricular Involvement: If we see a patient with an inferior wall motion abnormality, we know

that wall is supplied by the RCA, so we need to look at the thickening and wall motion of the rightheart…

a. The RV is hypokinetic, may be dilated…

b. The IVC is dilated

9. LV Obstruction with Hyperdynamic Base in LAD Occlusion: on a

rare occasion, a hyperdynamic LV is observed where the

hyperdynamic motion occurs at the base, while the apex is

akinetic…this may be the cause of a “hyperdynamic” obstruction of

the LVOT showing a dynamic late-peaking gradient. (Video Link)

CARDIAC TESTING AND PROCEDURES:

1. Exercise Indications:

a. Diagnosis of myocardial ischemia

b. Chest pain/angina

c. Baseline EKG changes

d. Follow up interventions (PTCA, CABG)

e. Risk stratification post MI

f.

Valvular exercise tolerance (MS, MR)

g. Pro-operative clearance

h. PHR is 220 – age

2. Exercise Contraindications:

a. MI in the last 48 hours

b. Unstable angina or current chest pain

c. Uncontrolled hypertension

d. Uncontrolled arrhythmias

e. Unable to walk

f. Severe AS

g. Decompensated CHF

h. Mobile LV thrombus

3. Exercise Protocol:

a. Typically get vitals and baseline imaging

b. Get the patient on the treadmill as long and as fast

as it can go

c. Then, patient back to the bed and try to get the

pictures in less than a minute (usually 45 seconds)d. Stop the test when the patient can’t go anymore or if

significant EKG changes are present.

http://localhost/var/www/apps/conversion/tmp/scratch_6/Outflow%20Obstruction.wmvhttp://localhost/var/www/apps/conversion/tmp/scratch_6/Outflow%20Obstruction.wmvhttp://localhost/var/www/apps/conversion/tmp/scratch_6/Outflow%20Obstruction.wmvhttp://localhost/var/www/apps/conversion/tmp/scratch_6/Outflow%20Obstruction.wmv


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4. Dobutamine Indications:

a. Similar indications as exercise testing, with

the only exeption is that the patient is not

able to exercise…that’s when the patient

will have a Dobutamine exercise test.

5. Dobutamine Contraindications:

a.

Active chest pain with EKG changesb. Uncontrolled hypertension

c. Uncontrolled afib or tachyarrhythmias

d. Aortic dissection or aneurysm

e. High grade heart block

f. Decompensated CHF

g. Mobile LV thrombus

h. Electrolyte imbalance (Low K)

6. Dobutamine Protocol:

a.

You still acquire baseline images at rest,10 mcg, peak Dobutamine dose, and then

at recovery…

b. The pictures are displayed in a quad

format.


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SYSTEMIC HYPERTENSIVE DISEASE (SHD):

1. Defined as hypertension, greater than 140/90

a. The abnormalities seen are initiated with a diastolic

dysfunction with impaired relaxation

b. Then, we start to see systolic dysfunction and overtime, the LV

will dilate…

c.

Most Common Echo Findings with SHD are:

i. LVH

ii. Aortic root dilatation

iii. Aortic valve sclerosis

iv. Mitral annular calcification

v. LA enlargement

vi. Afib

2. LVH:

a. LVH is the most commonly seen change associated with SHD

and is accompanied by diastolic dysfunction with impaired

relaxation…

i. The difference between LVH and HOCM is more often

the location of the thickening…

ii. In LVH the hypertrophy is more uniform, concentric

around the LV versus a case of HOCM where the

thickening is irregular, more regional than concentric…

iii. Both of them have a normal sized chamber. (VIDEO)

3.

Aortic Root Dilatation: (VIDEO LINK) a. Typically, the aortic annulus measures 13 mm ± 1 mm/m² or

20 to 31 mm…

b. The normal aorta dilates at the level of the sinuses by

approximately 6mm/m² (29-45 mm) and then tapers to within

2-3 mm of annular size at the sinotubular junction.

c. We usually see at the sinus of Valsalva: it is what is called

“ecstatic aorta” where the aorta normally gets a bit bigger in

systole and then comes back down in diastole…when it does

not come back down, we get an aortic root dilatation… d. Aortic root dilatation can cause reduced coaptation of the

aortic valve cusps: look for any distortion of the valve and

Doppler for assessment of regurgitation.

4. Aortic Valve Sclerosis: (VIDEO LINK)

a. Characterized by progressive fibrosis and calcification and

thickening of the aortic valve, beginning at the cusp bases…

b. The early stage of this process is often referred as “aortic

sclerosis”, which is often a prelude to the development of

significant stenosis later on.5. Mitral Annular Calcification: it is manifested by shadowing posterior to the calcification, as occurs in

the picture right…

http://localhost/var/www/apps/conversion/tmp/scratch_6/LVH.wmvhttp://localhost/var/www/apps/conversion/tmp/scratch_6/LVH.wmvhttp://localhost/var/www/apps/conversion/tmp/scratch_6/LVH.wmvhttp://localhost/var/www/apps/conversion/tmp/scratch_6/AoRootDilat.wmvhttp://localhost/var/www/apps/conversion/tmp/scratch_6/AoRootDilat.wmvhttp://localhost/var/www/apps/conversion/tmp/scratch_6/AoRootDilat.wmvhttp://localhost/var/www/apps/conversion/tmp/scratch_6/AoSclerosis.wmvhttp://localhost/var/www/apps/conversion/tmp/scratch_6/AoSclerosis.wmvhttp://localhost/var/www/apps/conversion/tmp/scratch_6/AoSclerosis.wmvhttp://localhost/var/www/apps/conversion/tmp/scratch_6/AoSclerosis.wmvhttp://localhost/var/www/apps/conversion/tmp/scratch_6/AoRootDilat.wmvhttp://localhost/var/www/apps/conversion/tmp/scratch_6/LVH.wmv


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a. Relatively common in the elderly and in renal failure, most

commonly occurs in the posterior part of the annulus. In

severe cases, it can extend right around the annulus.

b. It is thought to be a marker of CAD and indicator of

cardiovascular risk…

c. If massive, it can extend into the leaflets and cause mitral

stenosis. Unlike rheumatic stenosis, mitral annularcalcification does not affect the leaflet tips or cause fusion

of the commissures.

6. Left Atrial Enlargement:

a. LA enlargement is evaluated both in the apical 4-CH where

we evaluate for volume, or form a parasternal view,

measuring the size of the LA by M-mode from the trailing

edge to the leading edge at end systole…

i. A dimension greater than 3.8 cm in women and 4 cm

in men is considered as LA enlargement… ii. In this patient, the LA dimension is 4.5 cm…thus, it is

enlarged

iii. It leads to atrial fibrillation.

DIASTOLIC FUNCTION

1. Heart failure not only occurs secondary to decreased

contractility of the LV… in up to 50% of the cases, heart failure

occurs also due to the LV being incapable to relax…

a. Relaxation is an active process and occurs during

diastole…thus, diastolic heart failure. Echo is the best

method to evaluate for diastolic function.

2. The etiology of diastolic dysfunction is varied: it could be

secondary to CAD with scarred walls, to chronic hypertension

with hypertrophy where the LV compliance is diminished and

does not relaxes as well, in CRF, HCMP, and RCMP…

3. And many other reasons… if the patient is coming with SOB or

lower extremity edema, those are the typical signs of diastolic

heart failure….

a. Among other symptoms are

arrhythmias, SOB not related to

coronary disease… and dyspnea on

exertion may be present.

4. Hemodynamics and Stages of Diastole:

a. During systole, after MV closure, the

LV pressures rises steadily (IVCT) untilit opens the aortic valve and blood is

ejected from the LV…


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b. At certain point, the LV pressure descends…when it is below the aortic pressure, that’s

when the aortic valve closes, starting the diastole first stage: the IVRT, which is the time

after aortic valve closure, but before MV opening. Here the LV pressure decreases while

both valves are closed. At certain point, the LV pressure goes below the LA pressure and the

MV opens, initiating the diastolic rapid filling face represented by the E wave of the mitral

inflow…

c.

After the E wave, a stage where pressures in the LV and LA are equalized ensues and almostno flow occurs…this is diastasis.

d. Diastasis is followed by atrial “p” contraction

(the “atrial kick”), or atrial systole, where

pressures in the LA are again higher than in the

LV…this stage is represented by the A wave of

the mitral inflow waveform.

e. Diastole: Isovolumic Relaxation Time (IVRT):

i. It occurs after the systolic ejection and

the closure of the aortic valve. Then thetime between the aortic valves closure

and the mitral valve opening is the

IVRT…

ii. During this time, the LV is relaxing

without a change in volume. This is an

energy requiring process, active LV

relaxation…then, the pressure in the LV

falls below the pressure in the LA and

the MV opens, starting the passive or

“rapid filling” period…

f. Diastole: Passive/Rapid Filling:

i. With passive and rapid flow of blood

from the LA into the LV…

1. This is the E wave upward

deflection of the MV inflow

profile, where in the normal

patient, the majority of blood

flows into the LV…

2. Then, the MV starts to close

again (the “applause”

movement of the MV seen with

echo) because there is no

pressure difference between the

LA and LV since the LA’s blood has flowed into the LV and pressures are

equalized. No more flow and we have the diastasis period…

3. Diastasis lasts until the LA contracts during late diastole and ejects the rest of

the remaining blood into the LV: the A wave of the MV inflow pattern.

g. Diastole: Atrial Contraction:


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i. Atrial systole is consistent with the A wave

which occurs right after the P wave and

before the QRS complex in the EKG…

ii. The atrial contraction contributes with 1/3 of

the filling volume of the LV.

iii. In the case of afib, there is no atrial

contraction and thus, no A wave seen on theMV inflow.

DIASTOLIC FUNCTION ECHO EVALUATION

In deciding about the status of diastolic function, mitral inflow still

is the most important evaluation, but lately, tissue Doppler is one

of the most important factors in the evaluation of the function,

especially when compared with the mitral inflow.

1)

Mitral Inflow:a) The E wave is seen going upwards during the early diastolic

rapid filling period…

b) It is followed by the diastasis period with a tiny blood flow

c) Then atrial contraction occurs during the late systolic

phase and the A wave appears…

(1) The normal E/A ratio is 1.5 to2

ii) In afib, where the A wave is absent, and the patient is

deprived from the atrial kick, that’s when the patient

becomes really symptomatic since 1/3 of the bloodflow into the LV is missing…the patient really depends

on that 30% of volume coming into the LV, whose

absence decreases the CO with SOB

d) We see that the differences in pressure correlate very well

with how the LV fills

e) First Stage of Diastolic Dysfunction: Impaired Relaxation:

f) Initially we see increases in LV end-diastolic pressure

which results in a diminished pressure difference with the

LA… i) Because there is less pressure difference, there is less

filling as well…and the E wave becomes smaller during

the early diastolic phase…small E, large A.

(1) Resulting also in more blood being retained in the

LA, which, upon each atrial contraction, the

resultant A wave becomes higher than the E wave:

we see a small E wave and a large A wave with

inversion of the E/A ratio to less than 1, which characterizes impaired relaxation.

g)

Last Stage of Diastolic Dysfunction: Restrictive Filling:

h) Restrictive filling profile is not only characterized by increased pressure in the LV, but also inside

the LA as well. Identifying this restrictive filling pattern is important to risk stratify those patients

since this pattern increases in mortality…


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i) Increases in LA pressure correlates with increases in mortality. An E/A ratio greater than 2, typical

of a restrictive filling pattern, also correlates with an

increase in mortality…

i) Finding a restrictive filling pattern and treating the

condition, helps in reducing the mortality.

2) Tissue Doppler (TDI or Tissue Doppler Imaging):

a)

The next important evaluation of diastolic dysfunction isTDI…

b) TDI is performed with PW in the medial or lateral mitral

annulus: the typical protocol will include both, the

medial and lateral annulus evaluation…

i) The lateral annulus velocity is a little bit higher than

the mitral annulus velocity…

(1) The typical waveform contains an S (systolic) upstroke, then an E’ (or Em) downstroke,

followed by a second downstroke, the A’ (or Em) wave…

(2)

Normally, the E’ wave is greater than 10 cm/sec…When the E’ velocity is between 8 to 10cm/sec, it is when diastolic dysfunction is most likely…

(a) If E’ velocity is less than 8 cm/sec , the patient has diastolic dysfunction…which could be

impaired, pseudonormal, restrictive or else.

3) Combining Mitral Inflow and

Tissue Doppler :

a) This combination takes the

form of the E/E’ ratio, which

will be helpful in the

characterization of the different

forms of diastolic dysfunction…

b) After Impaired Relaxation

diastolic dysfunction (above)

the next stage is:

4) Pseudonormal Diastolic

Dysfunction: here, the mitral inflow

waveform looks like a normal

waveform with an E/A ratio

between 1 and 2, making a

characterization difficult…

a) What allows a differentiation between a “normal” mitral inflow from an abnormal “pseudonormal”

pattern is to look at the TDI waveform…

b) A normal appearing E mitral inflow combined with a DTI E’ annulus wave lower than 8 cm/sec will

yield an E/E’ ratio greater than 12…

i) An E/E’ ratio greater than 12 and 15 will define a “pseudonormal” diastolic dysfunction…

(1) A Valsalva maneuver here, to unmask the pseudonormal, will be useless here because the

diagnosis of a pseudonormal diastolic dysfunction has been confirmed by a high E/E’ ratio.

However, it could help for documentation. Besides, performing a Valsalva is not always a

clear cut parameter.


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(a) The best next

parameter to

characterize

diastolic

dysfunction is

Pulmonary Veins

Doppler. c) Example: What is the stage

of diastolic dysfunction in

the above? We have the

following data:

E = 53.3 cm/s A= 84.9 cm/s E/A= 0.6 DT= 285 ms

PV S= 48.9 cm/s PV D= 38.5 PV a Reverse Vel. = 20.2 cm/s

S’ = 7.60 cm/s Lat. E’ Vel. = 4.87 cm/s Lat. A’ Vel. = 9.94 cm/s E/E’ = 10.9

d) The mitral inflow is small E and big A, compatible with impaired relaxation…E/A ratio less than 1

i) Just by looking at the

mitral inflow, we know

this is an impaired

relaxation case.

e) Now, what’s the stage of the

next example?

E = 128 cm/s A= 32.6 cm/s E/A= 3.9 DT= 236 ms

PV S= 000 cm/s PV D= 43.3 cm/s PV a Reverse Vel. = 25.5 cm/s

S’ = 4.48 cm/s Med. E’ Vel. = 4.19 cm/s Med. A’ Vel. = 4.00 cm/s E/E’ = 34.1

(1) Now, the mitral inflow shows a restrictive pattern with a huge E wave, tiny A wave, an E/A

of 3.9… (i) The E’ wave less than 8 cm/s (here at 4 cm/s) points to severe diastolic dysfunction

(b) Combined with a large E, a small E’ and a huge E/E’ ratio of 34.1…it defines a restrictive

diastolic dysfunction…


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f) Yet another

example:

E = 143 cm/s A= 101 cm/s E/A= 3.9 DT= 183 ms

PV S= 40.3 cm/s PV D= 56.3 cm/s PV a Reverse Vel. = 20.8 cm/s

S’ = 0.05 m/s Med. E’ Vel. = 0.05 m/s Med. A’ Vel. = 0.06 m/s E/E’ = 24.9

i) Note the TDI units are now in meters/s, for which the E’ is only 5 cm/s, lower than the A’ wave

which is 6 cm/s…

(a) The normal appearing mitral E to A waves with a ratio greater than 2 is in fact a

“pseudonormal pattern”, unmasked by a decreased E’ and a huge E/E’ ratio, which is

compatible with a restrictive filling pattern…associated with increased LA pressure.

(b) Looking at the PV waveform, with a diastolic predominance which is compatible with

increased LA pressure.

(i)

Note: normal PV pattern is “systolic predominance”. (2) In cases of impaired relaxation, there is increased LV filling pressures. The next stage in

diastolic dysfunction is bounded to increased LA pressures as well…

(a) Thus, a pseudonormal and restrictive diastolic dysfunction is compatible with increased

LV filling pressures AND increased LA pressures, which is associated with increased

mortality


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5) Yet another

example:

E = 180 cm/s A= 83.8 cm/s E/A= 2 DT= 130 ms

PV S= 52.6 cm/s PV D= 44.1 cm/s PV a Reverse Vel. = 33.2 cm/s

S’ = 4.89 m/s Med. E’ Vel. = 10.3 cm/s Med. A’ Vel. = 0.00 m/s E/E’ = 18

a) Normal E/A ratio

b)

Normal PV pattern with systolic predominance

c) Normal DTI pattern with E’ greater than A’

Documents

ASE LV Function