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…
 (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 with
irradiation 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…
 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…its
territory 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
  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 circulation
is 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…
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.
 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 coronary
arteries (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)
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.
LEFT VENTRICLE (LV) FUNCTION: EJECTION FRACTION (EF)

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

𝐸𝐷𝑉 − 𝐸𝑆𝑉
EF = 𝐸𝐷𝑉
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 formula
3) 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 the
biggest) 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.
 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:

𝐸𝐷𝑉 − 𝐸𝑆𝑉
𝐸𝐹 = 𝑥 100
𝐸𝐷𝑉

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) in
diastole as well in systole…

𝐿𝑉𝐼𝐷𝑑 − 𝐿𝑉𝐼𝐷𝑠
𝐹𝑆 = 𝑥 100
𝐿𝑉𝐼𝐷𝑑

c) When the obtained data is squared and

applied to the formula, then:

𝐿𝑉𝐼𝐷𝑑 2 − 𝐿𝑉𝐼𝐷𝑠 2
𝐸𝐹 = 𝑥 100
𝐿𝑉𝐼𝐷𝑑 2
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:

𝐿𝑉𝐼𝐷𝑑 3 − 𝐿𝑉𝐼𝐷𝑠 3
𝐸𝐹 = 𝑥 100
𝐿𝑉𝐼𝐷𝑑 3
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 the
most 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.
 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 70
to 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 (𝑲𝒂𝒑𝒆𝒙 ):
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 or
subtract 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.
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
LV WALL MOTION SCORING
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 are
evaluated, 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
 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…

𝑪𝑶 = 𝑺𝑻𝑹𝑶𝑲𝑬 𝑽𝑶𝑳𝑼𝑴𝑬 (𝒄𝒄) 𝑿 𝑯𝑹

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: 𝜋 𝑟 2 , then:

𝑪𝒓𝒐𝒔𝒔 𝑺𝒆𝒄𝒕𝒊𝒐𝒏𝒂𝒍 𝑨𝒓𝒆𝒂(𝑪𝑺𝑨) = 𝝅 𝒓𝟐

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:

𝐷 2
𝐶𝑆𝐴 = 𝜋 ( )
2
3.14
𝐶𝑆𝐴 = 𝑥 𝐷2
4

𝑪𝑺𝑨 = 𝟎. 𝟕𝟖𝟓 𝒙 𝑫𝟐

c) Now, we determine the stroke volume

(SV)…by applying the following formula:
𝑺𝑽 = 𝑳𝑽𝑶𝑻𝑪𝑺𝑨 𝒙 𝑳𝑽𝑶𝑻𝑽𝑻𝑰

𝑺𝑽 = 𝑳𝑽𝑶𝑻𝑫 𝟐 𝒙 𝟎. 𝟕𝟖𝟓 𝒙 𝑳𝑽𝑶𝑻𝑽𝑻𝑰

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):
𝑪𝑶 = 𝑺𝑽 𝒙 𝑯𝒆𝒂𝒓𝒕 𝒓𝒂𝒕𝒆
e) NORMAL SV = 70 to 100 ml NORMAL CO = 4 to 7 L/min

i) Note: 𝐶𝑂 𝑙𝑒𝑓𝑡 𝑣𝑒𝑛𝑡𝑟𝑖𝑐𝑙𝑒 = 𝐶𝑂 𝑟𝑖𝑔ℎ𝑡 𝑣𝑒𝑛𝑡𝑟𝑖𝑐𝑙𝑒

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:
2
𝑆𝑉 = 𝐿𝑉𝑂𝑇𝐷 𝑥 0.785 𝑥 𝐿𝑉𝑂𝑇𝑉𝑇𝐼

𝑆𝑉 = 2.32 𝑐𝑚 𝑥 0.785 𝑥 21 𝑐𝑚

𝑺𝑽 = 𝟖𝟕 𝒄𝒄

d) Then: 𝑪𝑶 = 𝟖𝟕 𝒄𝒄 𝒙 𝟔𝟎 = 𝟓. 𝟐 𝑳/𝒎𝒊𝒏

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

AND HEART RATE OF 62 bpm:

𝑆𝑉 = 2.12 𝑐𝑚 𝑥 0.785 𝑥 9.5 𝑐𝑚 = 33 𝑐𝑐

𝑪𝑶 = 𝟑𝟑 𝒄𝒄 𝒙 𝟔𝟐 = 𝟐. 𝟎 𝑳/𝒎𝒊𝒏

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 1.17

(0.47-1.29)
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 𝑳/𝒎𝒊𝒏𝟐
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-CH
window 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 should
be 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.
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…
 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 has
a 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 regurgitant
blood 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 (𝟒𝒗𝟐𝟐 − 𝟒𝒗𝟏𝟐 ). Thus:
If V2 = 3 m/s; and V1 = 1 m/s, we have:
𝒅𝑷
= 𝟒 𝒙 (𝟑𝟐 ) − 𝟒 𝒙 (𝟏𝟐 ) = 𝟑𝟐 𝒎𝒎𝑯𝒈
𝒅𝒕
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
𝒅𝑷
sec. Then, the dP/dt is calculated from the formula: = 𝟑𝟐 𝒎𝒎𝑯𝒈/𝒕𝒊𝒎𝒆 (𝒔𝒆𝒄𝒐𝒏𝒅𝒔)
𝒅𝒕
iv) So:
𝑑𝑃 32 𝑚𝑚𝐻𝑔
= = 800 𝑚𝑚𝐻𝑔/𝑠
𝑑𝑡 0.04
 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:

𝑑𝑃 32 𝑚𝑚𝐻𝑔
= 𝑥 1000= 711 mmHg/s
𝑑𝑡 45

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:
∆𝑷 = 𝟒 𝒙 𝟑. 𝟓𝟐 = 𝟒𝟗 𝒎𝒎𝑯𝒈
(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) in
this 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:

𝒅𝑷 𝟑𝟐 𝒎𝒎𝑯𝒈
= 𝒙 𝟏𝟎𝟎𝟎 = 𝟓𝟑𝟑 𝒎𝒎𝑯𝒈/𝒔
𝒅𝒕 𝟔𝟎 𝒎𝒔𝒆𝒄

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).
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 provided
will 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.
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 shunt
b. 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.
 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
 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, because
that 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.
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 right
heart…
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.
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 changes
b. 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.
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…
 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 annular
calcification 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) until
it opens the aortic valve and blood is
ejected from the LV…
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 almost
no 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 the
time 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:
 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 the
MV 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 blood
flow 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…
 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 is
TDI…
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 10
cm/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.
 (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…
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
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’