Ebook Board stiff tee - Transesophageal echocardiography (2nd edition): Part 2

CHAPTER

13

Left Ventricular Systolic
Function
Eric W. Nelson

For some reason there is a lot of focus on the left ventricle and its evaluation on TEE, both in the operating room and on the boards. This most
likely has to do with the fact that it’s pumping blood to the entire body,
thus keeping you alive. The easiest way to start your evaluation of the left
ventricle is to know what a normal left ventricle looks like.
The shape of the LV should look somewhat like a football. If you drop a
TEE probe in someone and the heart is closer to a basketball than a football, something is wrong.
So, now you know how to eyeball the heart and tell grossly if it’s normal
or not, but what about an actual measurement? LV function is typically
measured numerically by the ejection fraction (EF). That is, how much
blood that goes into the LV goes out through the aorta?

Good

Bad

EF can be calculated by measuring the fractional area of change (FAC)
of the left ventricle. A true long- or short-axis cross section is required
being careful not to foreshorten. Foreshortening is a term commonly
used by echocardiographers to describe the heart when it is compressed
because of the viewpoint taken. With modern TEE machines all you have
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to do is outline the end-diastolic area and the end-systolic area and the
machine will crunch the numbers.
FAC = (end-diastolic area – end-systolic area)/end-diastolic area
You can also estimate EF via the eyeball method, which is what most
people do. On the test you should be able to look at an image and determine the difference between an EF of 25% and 55%. Which is pretty
easy!
One thing to keep in mind whether using the eyeball method or doing an
actual measurement is don’t jump to conclusions based on one view. A
single slice may look great, but remember it’s only part of the heart and
another part may not look so good. Also, if you are foreshortening or not
getting a “true” cut of the LV your read is going to be off. Make sure you
eyeball the LV with multiple omniplane angles and also in both the transgastric and midesophageal views.

ABNORMAL LV SYSTOLIC FUNCTION
Naturally, the first thing that comes to mind is ischemia…if this wasn’t
your first thought you may want to retake your boards. There are also a
lot of other things that may cause abnormal LV function.
n

Ischemia, just can’t say it enough.

n

Ventricle—infiltrative diseases that cause restrictive physiology
such as amyloidosis cause global impairment.

n

Pericardial space—tamponade either from an effusion or
blood. TEE is great at not only making this diagnosis, but also
locating where the effusion is around the heart and whether it is
loculated.

n

Pleural space—tension pneumothorax causes decreased venous
return thus decreasing preload and ventricular function.

n

Metabolic—hypoxemia, hypoglycemia, anemia, hyperkalemia, and
a vast array of other metabolic abnormalities.

CARDIOMYOPATHIES
Hypertrophic
There are four different types of hypertrophic cardiomyopathies, although
the most famous is septal hypertrophy leading to subaortic stenosis or
“hypertrophic obstructive cardiomyopathy”, which all the cool kids just
call HOCM (pronounced hokum).
HOCM is an inherited cardiomyopathy. It is autosomal dominant with
limited penetrance, unless of course you are the patient then it is a very
penetrating diagnosis!


Chapter 13  Left Ventricular Systolic Function

With hypertrophic cardiomyopathies systolic function typically is not the
problem, rather the heart has a hard time relaxing, like that one attending
we’ve all had with the vein in his forehead that seems to keep growing
and may pop at any minute!
An important point about HOCM is the picture you see on TEE. Some
people call this the “dagger sign”. When a continuous wave Doppler
is placed across the left ventricular outflow tract, or LVOT, and the AV
the outflow pattern will resemble a dagger rather than the nice rounded
appearance of someone without this problem. This is secondary to the
ventricle being so empty at the end of systole and the septum being so
huge an obstruction actually occurs.

HOCM

AS

Keep in mind that patients with HOCM are also more prone to SAM
or systolic anterior motion of the mitral valve. Since the outflow tract
is already narrow, it’s easy for the anterior leaflet to get sucked in and
impede flow.
The definitive answer to relieving HOCM is surgical resection of the septum.
TEE plays an important role here in order to determine preop if the surgery
is necessary and postop if there was enough septum resected, not enough,
or too much. If not enough was taken the obstruction will remain, but if the
surgeon got a little greedy the patient may end up with a VSD. Also remember that there are conduction fibers running through the septum. It’s not
uncommon to have a heart block after this type of surgery.

Too Little

Too Much

Just Right

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Medical management of HOCM involves keeping the heart full; remember that the obstruction occurs when the heart is empty; and also
decreasing contractility.

Restrictive
Sometimes the only way to tell the difference between a hypertrophic
and restrictive cardiomyopathy is by looking at the posterior basal wall
of the heart. This is best appreciated in the transgastric short-axis views.
Remember, in hypertrophic cardiomyopathies the posterior basal wall is
spared, but in restrictive cardiomyopathies it is not. Oh yeah, don’t forget
that a good history and physical can also help determine the type of cardiomyopathy as well.

Restrictive

Hypertrophic

Alright, we’ve determined that we have a restrictive cardiomyopathy,
but where’d it come from? Well, the list is long and distinguished. There
are a lot of things that can “sneak” into the myocardium and cause

restriction:
namyloid
nsarcoid
n

glycogen from patients with glycogen storage disease

n

eosinophils from eosinophilic myocarditis (also known
as Loffler’s)

Like hypertrophic cardiomyopathies, restrictive cardiomyopathies
mainly present a problem in diastole that is the heart does not relax
well enough to accept blood. Remember to go over the various diastolic E/A patterns and pulmonary venous flow because these do show
up on the test!
Patients with restrictive heart disease are also prone to thrombus formation even without a wall motion abnormality. Thrombi are typically found
in the apex. Remember, the apex of the heart is best visualized in the
mid-esophageal 2-chamber view and the mid-esophageal 4-chamber
view. Thrombi may also form under the posterior mitral valve leaflet,
which may lead to a bit of mitral regurgitation.


Chapter 13  Left Ventricular Systolic Function



Dilated
Remember at the beginning of this chapter when I mentioned that the
heart shouldn’t look like a basketball? Well that’s exactly what this type

of heart looks like. It’s big, the walls are thin, and it really isn’t doing
much at all. Keep your eye out for thrombi, as there isn’t much going on
so clot formation is possible.

Clot

Like everything else there is a list of what causes dilated cardiomyopathy
nIschemic
n

Post viral

nPeripartum
nAlcohol
n

Idiopathic (a doctor’s way of saying “I just don’t know”)

n

And numerous others.

QUESTIONS
1. Which wall is spared in hypertrophic cardiomyopathy?
A.Inferiolateral
B. Posterior basal
C.Septal
D. Apical anterior
E.Anteroseptal
2. Which of the following may cause cardiomyopathy?

A.Pregnancy
B.Ischemia
C.Alcohol
D.Virus
E. All of the above
F. B and D

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3. Where is the most likely place to find thrombus in the LV?
A.Apex
B.LVOT
C.Basal septal wall
D. Lateral wall
4. Treatment for HOCM includes all of the following except:
A. Surgical resection
B.Alcohol
C.Beta blockade
D. Inotropic agents
E. Increased preload
5. What causes hemodynamic compromise in patients with HOCM?
A. Anatomic outflow tract obstruction
B. Physiologic outflow tract obstruction
C.Decreased EF
D. Restrictive myocardium

6. Which of the following causes restrictive cardiomyopathy?
A. Concentric hypertrophy
B.Alcohol
C.Ischemia
D. Iron overload
E. Celiac disease
7. Which of the following patients are prone to LV thrombus formation:
A. Atrail fibrillation
B. Hypertrophic cardiomyopathy
C.Restrictive cardiomyopathy
D. Pericardial tamponade
E. Severe MR
8. A problem in which of the following spaces may affect LV systolic
function?
A.Pericardium
B.Pleura
C.Ventricle
D.Metabolism
E. A, B, and C
F. All of the above
  9. True or false: It is possible to evaluate the ejection fraction of the
heart by one view on TEE
A.True
B.False
10.  Which view is the best to evaluate HOCM
A. Mid-esophageal 4 chamber
B. Mid-esophageal 2 chamber
C.Deep transgastric
D. Transgastric short axis
E. A and C

Chapter 13  Left Ventricular Systolic Function



ANSWERS
1.B
2.E
3.A
4.D
5.B
6.D
7.C
8.F
9.B
10.E

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CHAPTER

14

Segmental Left Ventricular
Systolic Function

John C. Sciarra and Christopher J. Gallagher

MYOCARDIAL SEGMENT IDENTIFICATION
Hear ye, hear ye. The Office of Homeland Security is not going to shoot
me for revealing any state secrets here. You will need to know these segments and you will need to know which coronaries feed which walls and
which segments.
I kid thee not.
I speak not with forked tongue.
This is a for sure on the test.
The first time you see it you’ll quasi freak, because it looks so complex,
but when you think of all the other stuff you memorized to get this far, it’s
not so bad. Plus there’s a logic to it, so don’t go off the deep end.
First, the whole thing, then we’ll back up and break it down.
A

SEGMENTS—DON’T FREAK

B

DONUT AT EACH SLICE
I

Basal 6
Mid

6
S

Apical 4
Not in

apical

C

Not in
apical

P

WHICH LEVEL IS DONUT?
Basal?
(see MV)

D

L
AS

A

WHICH WALL IS WHICH?
Septal

ME 4-Chamber

Mid?
(see Paps)
Apical
(nothing)

Lateral
Inferior

ME 2-Chamber
Anterior

ME LAX

Posterior

Anteroseptal

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I found it easiest to start with the cross sections. That way you can at
least always know what’s “directly across” from you. Then you can take
the long views and start to put it together.
So, think of three of these lying on top of each other, starting at the top
of the ventricle, right next to the mitral valve. Three layers of six:
The basal 6 segments are next to the mitral valve.
The middle 6 segments are next down, at the level of the papillary
muscles.
The lower, or apical, 6 segments come next.
BUT WAIT!
Though it would make sense to do 6/6/6, the SCA (perhaps fretting

about the demonic number 666 from The Omen), only recognizes four
segments in the ever-narrowing apex.
Lose the posterior and the anteroseptal segments there. In the apical,
you just have inferior, anterior (across from each other, remember), and
septal and lateral (across from each other too).
Now, put it back together, piece by piece, until it makes sense. If you are
still confused, stay tuned for the 17 segment chapter.

CORONARY ARTERY DISTRIBUTION
AND FLOW
REAL WORLD NOTE  Major, major importance that you know this. This ties in
with the extremely practical dilemma that you face on a daily basis: “Is the new
graft working?” If a wall fed by, say, the right coronary graft was working, and now
is not working, hey, look at the graft for kinks, disconnects, clots, dissections. It’s
a hell of a lot easier to recognize the problem and fix it now than to find out later
and lose a chunk of myocardium.

TEST NOTE  Vintage testable material here, folks. A little brutal memorization
(come on, there are only three vessels, it’s not that bad) and you should nail these
questions.


Chapter 14  Segmental Left Ventricular Systolic Function



Pictures tell it all:


A

CORONARY DISTRIBUTION

B

Right

RV and Inferior Wall

Circumflex

Posterior and Lateral

LAD

Septal, AS, Anterior

CORONARY DISTRIBUTION
LAD

4-Chamber

Right
Circumflex
Right

2-Chamber

Know
these cold!

LAD
LAX
Circumflex

LAD

Let’s put it into words, just in case you’re less of a visual learner.
The right coronary feeds the inferior wall and right ventricle.
The left anterior descending feeds the anterior and septal walls. (No wonder an LAD infarct is so problematic.)
The circumflex feeds the posterior and lateral wall.
Everyone studies the hell out of this issue, drawing the pictures over and
over again, flashcards, you name it. Get this stuff down but down.
Here is a little memory helper I made up, I call it the “coronary artery
memory helper”:
LM → LAD → Diags (the “D” in lad leads into the “D” in diagonals).
Circ → OMs (circumferential looks like the circumference of the “O” in
Obtuse Marginal).
RC → PDA (the right hand [RCA] writes on the palm pilot pda).

NORMAL AND ABNORMAL SEGMENTAL
DYSFUNCTION
Assessment and Methods
Keep your eyes open, that’s the method. The wall motion abnormalities you see will not be subtle. Every test-taker since the dawn of time
emphasized that to me.

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“You’ll see it moving, then BOOM, it ain’t moving.”
And in real life, that’s what you see too. As soon as a wall gets ischemic,
the motion disappears. Keep in mind, the normal movement of a wall is
thickening and an inward movement.
At the meeting, they get a little more scientific than this, saying “Normal
contractility results in 30% thickening of the wall, hypokinetic is 15%,
akinetic is, well, 0%, and dyskinetic means it bulges outward”.
Others gets a little more Gestalty:
n

Normal is normal-looking.

n

Hypokinetic is hypokinetic-looking.

n

Akinetic is akinetic.

n

Dyskinetic is dyskinetic-looking.

Golly.
All of this high-tech ranking is groovy, but you just have to look at a
bunch of echos and try to peg, “Which wall is not happening?”. This can

be harder than it seems, so be systematic about it. Look at one section
and (this according to the great Cahalan himself) say, “Systole, systole,
systole” and see if that particular section moves.
In the OR, I’ll put my finger in the center of the ventricle on the monitor
and see if different wall segments move in toward my finger.
One trick I stumbled upon is the value of fast forward. Tape a bit, then
rewind and look at the walls in fast motion. Believe it or not, when the
ventricle’s going super fast, the dyskinetic or akinetic wall stands out
better than at regular speed.
In your studying, look at either the tapes or the CDs. This is a total “moving picture experience”, for there is no other way than to drill these.
On the tapes from the 2002 meeting, they recorded the “Regional Wall
Motion Unknown” session. That is the best way I found to practice picking out the “mystery wall motion abnormality.” (Quit laughing as I mention “tapes”, go online and look up a few examples of regional wall
motion abnormalities on the Internet.)

DIFFERENTIAL DIAGNOSIS
Well, gee whiz, what else could it be?
Wise counsel says, “Believe bad news and act accordingly”. Other than
a graft not working or a native vessel being occluded, there aren’t too
many other things it could be. The main aspect of the differential should
center on which catastrophe afflicted your graft:
n

Air embolus (particularly after an open procedure).


Chapter 14  Segmental Left Ventricular Systolic Function


n

Spasm of the internal mammary (a surgeon at the meeting and in
the tapes points out that spasm of the internal mammary graft is an
oft-cited excuse. In reality, the graft was poorly placed, kinked, or
clotted off, and the all-encompassing excuse of “Oh, it must have
been spasm” is pulled out for public consumption.).

n

Too long of a graft, leading to a kink.

n

Too short of a graft, leading to a squinking shut of the graft as it’s
stretched flat as a pancake.

n

Clot from, perhaps, hypotension and stasis (Eeek! That can be a
result of “Anesthetica Imperfecta”!).

nDissection.

Whatever it may have been, when you see a new wall motion abnormality
that you thought you should have fixed, take a look-see.

CONFOUNDING FACTORS
Tethering can throw you off the hunt when examining regional wall
motion abnormalities.


TETHERING
Can’t move as well.
Infarcted./Dead and gone.
Can’t move as well.

A hypo-, dys-, or akinetic area can “hold back” a normal area. (You may
be able to run around pretty energetically, but if I jump on your shoulders
and say, “Yeehaa! Giddyap!”, your motion may slow down considerably.
You have been tethered by my bulk.)
The angle of your examination may throw you off too. If you get a really
foreshortened view of the ventricle, for example, you may not get a clean
look at one segment; rather, you’ll see a lot of segments at once and
won’t be able to make a clean diagnosis.

LEFT VENTRICULAR ANEURYSM
An aneurysm is a thinning of the entire wall of a structure. So, on echo,
a ventricular aneurysm is seen as a dyskinetic region (bulges outward in
systole) that has a diastolic contour abnormality (keeps bulging outward
even after systole is over). In other words, the damned thing is always
bulging out. Kind of the “love handles” of the heart.
Of specific diagnostic interest, an aneurysm has a smooth transition from
normal myocardium to thinned aneurysm. There is no sharp angle or neck
(as we’ll see with pseudoaneurysms or ventricular ruptures in just a minute).

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The love handle analogy helps again. Love handles (however much they
may plague us, uh, more mature gentlemen) at least have an aesthetically pleasing smoothness as they transition from the torso to the love
handle proper.
Aneurysms are most often found in the apex, though they can occur
elsewhere. And aneurysms, with their underlying stasis, can give rise to
thrombi.

LEFT VENTRICULAR RUPTURE
For a big-time ventricular rupture, skip the TEE. Grab a pathology text
and head for the refrigerated surgical suite in your hospital’s basement.
A survivable rupture through the myocardium but contained within a
“skin” of pericardium is called a “pseudoaneurysm”. On echo, you don’t
see the smooth transition of the true aneurysm; rather, you see a narrowed neck at the site of the breakthrough.


PSEUDOANEURYSM

Narrow
neck

Ruptured
ventricle “held”
by pericardium
Abrupt

If you want to get all quantitative and anal about it, the ratio of the neck to
the maximum diameter of the pseudoaneurysm should be less than 0.5.
But give me a break; if you know what happened, the difference between
an aneurysm and a pseudoaneurysm should jump out at you.

QUESTIONS
1. Regarding myocardial stunning:
A. Ischemia tends to produce more severe wall motion abnormalities
B. Stunned myocardium shows a gradual improvement and function
in the first minutes to hours following separation from bypass
C. Stunned myocardium may be recruited to contract with inotropic
stimulation
D. Inotropic stimulation may worsen function in an ischemic segment
E. All of the above
2. Concentric LV hypertophy is:
A. A really big heart
B. Commonly called “cow heart”
C. Wall thickness increased in proportion to the increase in
chamber size
D. Wall thickness increased out of proportion to chamber size
E. Wall thickness inversely porportional to chamber size




Chapter 14  Segmental Left Ventricular Systolic Function

3. Eccentric LV hypertophy is:
A. A really big heart
B. Commonly called “cow heart”
C. Wall thickness increased in proportion to the increase in
chamber size
D. Wall thickness increased out of proportion to chamber size
E. Wall thickness inversely porportional to chamber size

ANSWERS
1.E.
2.D.
3.C.

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CHAPTER

15

The 17 Segment Model
John C. Sciarra

(Update note: In the ancient history of the first edition, there were 16 segments. Apparently we have evolved a 17th segment!)
This chapter requires some artist skill. When I say some, I mean very little. If you can draw a line and a circle you are, for the purposes of this
chapter, an artist.
The 17 segment model is the way we as doctors communicate which
sections of the heart we are talking about. It is also a great tool for
designing test questions. For example, the patient is a gunshot wound
victim, and he has a hole in segment 8. What coronary artery is spurting
blood? What leads on the ECG do you expect to see abnormalities? See
what I mean? Well, I am not going to tell you the answer; you just have to
read on—and draw. And draw you will. You will draw what I call:
“The 17 Segment Star”.

First off, draw a line. Just a straight line. As seen below this is a straight line.


A line

Wow, that was not so bad. Now comes the tricky part. You have to add
two more lines in a cross pattern as seen below. It kind of reminds me of
an asterisk, or star. That’s you–an echo star!


Grip your pencil tightly because I am going to ask you to do something
completely different. Draw a circle on top of your star.

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Good job Picasso, you have drawn the basic foundation for the 17 segment model. Next we have to number the segments. Start in the lower
left, inside the circle, and do 1 thru 6, as seen below.

5
6

4

1

3

Always
start here

2

Now start again outside the circle at the same lower left and do 7
thru 12. It should look like this. If you are not drawing at this point and
just reading you are missing the point. Get out your pen and do it.


11

5

12

10

6

4

1

3
9

7
2

8


Chapter 15  The 17 Segment Model



13 thru 17 start close to your original starting point, which is the bottom. Circle around and finish at the bottom with 17. 17 is the apex or
bottom of the heart, so that is where the number should be. It should
look like this:


15
11

5

12

10

6

4
14

16
1

3
9

7
2

8
13
17

That’s it. Now you have to practice this without looking. Go ahead. Find
a piece of paper and start with the line, and finish with 17. You should be
able to do this in 5 seconds. I am waiting…. Do it.
Now that you are an artist, you may feel like painting your living room.
Hold on, since we now need to go over how your master work relates
to the heart. Your 17 segment model is a segmental version of the cross
section of the heart as seen below, which you may recognize from other
sections in this book. Or a dozen other inferior books on TEE.


“WALL PAIRS” IN CROSS SECTION

Inferior
Septal

Anterior

I

Lateral
S

Posterior
P
L

AS
A

Schematic of LV in Cross Section

Anteroseptal

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We start at the top of the heart and work our way to the bottom, numbering as we go. “Wait” you say. The number one is in the wrong place. This
is due to the fact that in TEE things are backwards from trans-thoracic
scanning. I just put these images here to show you how the numbers
relate to the levels: basal, mid, apical, and apex.


Apical

Mid

Basal
1

7
13

14

8

12

9

11

2

6

3

5

16

15

10
4
LAD

RCA

LCX

This is the image you might see in most cardiology textbooks—if you
ever dared to crack one open.


1
7
2

13

8
14

3

9

17
15

12

6

16
11
5

10
4
1. Basal anterior
2. Basal anteroseptal
3. Basal inferoseptal
4. Basal inferior
5. Basal inferolateral
6. Basal anterolateral

7. Mid-anterior
8. Mid-anteroseptal
9. Mid-inferoseptal
10. Mid-inferior
11. Mid-inferolateral
12. Mid-anterolateral

13. Apical anterior
14. Apical septal
15. Apical inferior
16. Lateral
17. Apex

Alright, let’s get back to the world of anesthesia. This next image is the

one that has the positional planes lined up as the heart sits in the chest
and as the probe is at the back of the heart. Our orientation is the top
of the page is the back of the heart—the inferior portion—and the front
of the heart is at the bottom of the page or TEE image—anterior. This
should all be crystal clear in the cool exploded 3-D image I made below,
which I drew from an actual exploded heart.


Chapter 15  The 17 Segment Model





Inferior
SEGMENTS
Septal

Posterior

1–6

Lateral

Anterior
septal

7–12
RV

13–16

17

Anterior

To review the coronary anatomy. Which really shouldn’t be necessary—but what the heck:
LM → LAD → Diags (the “D” in LAD leads into the “D” in diagonals).
Circ → OMs (circumferential looks like the circumference of the “O” in
Obtuse Marginal).
RC → PDA (the right hand writes on the palm pilot pda).
(I hope those little memory hints help.)
This appears in another portion of the book. Learning thru repetition is
a time-honored teaching tool they say. And they say it over and over for
some reason.


A

CORONARY DISTRIBUTION

B

Right

RV and Inferior Wall

Circumflex

Posterior and Lateral

LAD

Septal, AS, Anterior

CORONARY DISTRIBUTION
LAD

4-Chamber

Right
Circumflex
Right

2-Chamber
LAD
LAX
Circumflex

LAD

Know
these cold!

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So let’s answer our question from the beginning. Remember gunshot to

segment 8? Look at your drawing. Segment 8 is right in the middle of the
anterior portion of the heart. Kind of a bulls-eye if you will. The anterior
wall is the distribution of the LAD. See how easy that was. So he as a
hole in his LAD! Quick, get a doctor!
At this point I should be able to shout out a segment, and you shout out
a coronary artery—and vice versa. If not, go back to the beginning and
start reading again. And this time draw it out. Lastly, I want to explain
how some of the TEE planes relate to my 17 segment star. If you draw
some dashed lines in between the lines of the star, these represent the
planes of the TEE probe in certain views. The four-chamber view slices
thru segments 3 and 6, for example. Next is the two-chamber view with
the plane going anterior to inferior. Last is the ME long-axis cutting segments 7 and 4 among others.


I

S

P

AS

L

LAD

LCX

al
t. s

ept
An

Posterior

Ante

rior

Inferior

l
era
Lat

tal

A

Sep

144

RCA

So there you have it. The star makes it all come together. I recommend
trying to draw the 17 segment star in a few days to see if you remembered it. Then in the future, during say, some exam, you see a question
involving the coronary arteries, wall segments, or ECG changes, just
draw the star and figure it out. Nothing will stop your star power!

Chapter 15  The 17 Segment Model



QUESTIONS
1. Ischemia in the RCA would give wall motion abnormalities in
segment 2 or 5?
2. Segment 14 is hyperkinetic. You tell the surgeon which graft is
down?
3. The patient from the beginning of the chapter gets better, gets a
gun and goes all gangster on his shooter for revenge. He aims for
the LAD. Does he hit segment 2 or 12?

ANSWERS
1. Quick draw your 17 segment model, and look at the back wall.
Hmmm… must be 5.
2. Quick draw your 17 segment model... and it looks like 14 is lateral,
so it must be the circumflex.
3. Quick draw your 17 segment model, and guess he is accurate and
hits 2 which is anterior.

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CHAPTER

16

Assessment of Perioperative
Events and Problems
Ricardo Martinez-Ruiz and Christopher J. Gallagher

HYPOTENSION AND CAUSES OF
CARDIOVASCULAR INSTABILITY
REAL WORLD NOTE Let’s face it, cowboys and cowgirls, this is the real crux of
the whole deal with echo. All the cool physics and gradients and Doppler stuff are
necessary for the test. And if you’re going to do cardiac echo, you need to know all
the neato-frito valve details. But as TEE gets more and more common, the day will
come when every single anesthesiologist or ICUologist will need to know at least
the basics of TEE to figure out what’s going on when a patient gets unstable.

The TEE is the anticrash weapon of choice.
When badness happens (and we’ve all seen it happen), you might not
have a Swan or CVP. And even if you do, you’re still wrestling with numbers that tell you something, but not the whole picture. You are left with a
set of numbers from which you infer, or hope, you have the picture.
The TEE gives you the real picture, right now, no need for a leap of faith.
Cahalan points out in the tapes and at the meetings that, even with only a little TEE experience, most people can diagnose the most common problems
in mere minutes. After all, when most patients go to caca, you want to know:
n

Heart, full or empty?

n

Ventricle, good or bad?

n

Tamponade, yes or no?

For most problems, then, Cahalan gives us a nice, neat, easy-to-understand
and inherently obvious breakdown of the main causes of hypotension:
1. End-diastolic area decreased, ventricle contracting OK—You’re low
on volume. The heart is empty, so fill it.
2. End-diastolic area increased, ventricle contracting poorly—
You have a bad and already overfilled ventricle. Fix whatever’s
causing the global hypokinesis (Get a blood gas! Don’t forget the
basic stuff!), and once you’ve fixed what you can fix, it’s time for
inotropes or ventricular support of some kind.
3. End-diastolic volume normal or low, ventricle contracting well or
hyperdynamic—You have a problem with the volume not “going
where it’s supposed to go”. Either the volume is all going out into
a vastly dilated circulatory tree (anaphylaxis with low systemic

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