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UNUSUAL CAUSES OF MYOCARDIAL ISCHEMIA
65
Takotsubo cardiomyopathy, also known as •
apical ballooning syndrome, classically presents
in postmenopausal women complaining of chest
pain or dyspnea after a stressful exchange, with
electrocardiographic changes suggestive of acute
myocardial infarction with ST-segment elevation.
Consider coronary artery dissection and pulmonary •
embolism in pregnant women or women in the
early postpartum period with chest pain and
dyspnea.
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Variants of the disease present similarly to TC,
including nonapical ballooning syndrome, where
hypokinesis or akinesis is seen at the mid-ventricular
segments on ventriculogram, but the apex and base
are spared (compared to basal sparing with classic
TC).
38,42
Patients with this variant have been reported
to be younger and less likely to have cardiogenic
shock or pulmonary edema than their TC counter-
parts.
42
An inverted Tako-tsubo syndrome also exists,
where hypokinesis occurs at the cardiac base with
apical sparing.
38
T wave inversion is less common in
both these variants than it is in TC.
42
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mined. Reasonable initial management includes aspi-
rin, nitrates (blood pressure allowing), and heparin,
managing as one would a patient with acute coronary
syndrome. Beta-adrenergic blockade is helpful when
a hyperkinetic base leads to outfl ow tract obstruc-
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cian at the bedside. The most common complication
is congestive heart failure (20–30%), where ejection
fraction is reduced and diuretics are usually helpful.
Inotropic support and even intra-aortic balloon coun-
terpulsation can be employed for cardiogenic shock if
it occurs.
38,46
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ventricular free wall rupture, left ventricular throm-
bus, outfl ow obstruction, mitral valve dysfunction, and
rarely, dysrhythmia or death.
38,46
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the rule, with infrequent recurrence. Ejection fraction
improves in days to weeks, and complete resolution of
cardiac dysfunction is expected at 4–8 weeks. The role
of pharmacologic management to prevent recurrence
is unclear at this time.
37–39,46
Section IV: Decision making
Electrocardiographic manifestations (e.g., ST- •
segment elevation), as well as serum marker
evidence (e.g., elevated cardiac troponins), of acute
myocardial infarction are not absolute evidence of
acute coronary occlusion; other disease processes
may be the culprit but are diagnosed by exclusion
of obstructive coronary disease.
Traumatic and spontaneous coronary artery •
dissections are most likely to affect the left anterior
descending artery; aortic dissection, if it involves a
coronary artery ostium, most likely affects the right
coronary artery.
CHAPTER 4
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UNUSUAL CAUSES OF MYOCARDIAL ISCHEMIA
67
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SECTION TWO
Cardiac Dysrhythmias
5
71
Cardiovascular Problems in Emergency Medicine: A discussion-based review, First Edition.
Edited by Shamai A. Grossman and Peter Rosen.
© 2011 John Wiley & Sons, Ltd. Published 2011 by John Wiley & Sons, Ltd.
Bradyarrhythmias
Colleen Birmingham
1
& Edward Ullman
2
1
Fellow in Medical Toxicology, New York University Medical Center/ New York City
Poison Center, New York, New York, USA
2
Assistant Professor of Medicine, Harvard Medical School, Director of Medical Student
Education, Division of Emergency Medicine, Beth Israel Deaconess Medical Center,
Boston, Massachusetts, USA
Section I: Case presentation
A 75-year-old man presented to the emergency depart-
ment (ED) with a chief complaint of weakness. The
patient reported feeling unwell for several days. He
complained of some shortness of breath on ambulation
and felt very lightheaded after walking, but there had
been no loss of consciousness. He denied any cough,
fever, chills, or chest pain. Prior to this episode, he
could perform all of his activities of daily living with-
out issue. The paramedics reported that the patient
was found in a seated position in no apparent distress.
His symptoms somewhat improved with oxygen.
The past medical history included a myocardial
infarction 5 years prior with a preserved ejection frac-
tion, hypertension, and hyperlipdemia. Medications
included: aspirin, Lipitor, metoprolol, and Lasix.
Initial vital signs were: blood pressure 80/48 mmHg,
heart rate 45 beats/min, respiratory rate 16 breaths/
min, and temperature 36.7°C (98°F). The patient was
in no apparent distress. The pulmonary examination
was clear to auscultation. The cardiac examination
showed a bradycardic rhythm with a 1/6 systolic
murmur heard loudest at the apex. The extremities
showed a trace pedal edema. The rectal examination
was hemocult negative. The rest of the physical exam-
ination was unremarkable.
An EKG was performed (Figure 5-1).
Dr Peter Rosen: We often worry about tachycardias,
but this case illustrates bradycardia, which is another
mal defi nition of bradycardia? Does it include rate as
well as symptoms, or is it rate alone?
Dr Richard Harrigan: I would split bradycardia into
symptomatic and asymptomatic, with the gener-
ally accepted cutoff being 60 beats per minute as the
threshold below which we defi ne as bradycardia.
PR: What if you have a well-conditioned runner or
bicyclist whose resting pulse is about 40 beats? Is that
ever a concern, or can you just assume that it is the
conditioning?
RH: This demonstrates the need for taking a more
detailed history, such as asking “Have you ever been
told that you run a slow pulse?” The conditioning
history needs to be included when obtaining a medi-
cal history of a bradycardic patient. Further, we must
remember that we are talking about a normal distribu-
tion, and although 59 beats per minute is termed bra-
dycardia and 61 beats per minute is not, in truth it is
relative and heart rate is a spectrum of fi ndings. Also,
bradycardia is relative to the person’s conditioning. I’ve
even seen people whose resting heart rate is in the high
thirties, and they tolerate this well. Rather than treating
a number, we have to look at the whole picture.
PR: One of the things that makes us a little anx-
ious about asymptomatic bradycardia is that some
CHAPTER 5
72
stressed. For this reason, it’s important to ask an older
person with a bradycardia not only about how he or
she presently feels, but also how he or she feels when
climbing stairs, running for a bus, or even doing daily
activities around the house.
SG: This bradycardia may refl ect simple senile degen-
eration of the conduction system. So, in truth, the bra-
dycardia does represent heart disease, but very often
disease that is well-tolerated and sustainable over
many years.
PR: I remember fi rst learning about drop attacks as
a medical student, but I can’t say I have ever seen a
patient present with a history of “I’m feeling well but
every once in a while I just fall over unconscious.” I
think that the more common symptoms of bradycar-
dia are what our patient today experienced: lighthead-
edness, mild dyspnea on exertion, and weakness. It’s
interesting that this man had this condition develop
rather rapidly. Does that suggest to you that this prob-
ably relates less to an acute heart attack that involves
his conduction system and more to a medication?
SG: I would offer a third possibility: this can be related
simply to the slow senile deterioration of his conduc-
tion system, and not related to any acute process. All
three of these are possibilities. Generally, in something
that is more abrupt, you would think that it would be
related to either an acute myocardial infarction or a
well-conditioned athletes have cardiomegaly. This
probably represents the enlargement of exercise
rather than the enlargement of disease. I’m not
sure that there’s an easy way to distinguish between
the two beyond the onset of symptoms.
PR: We know that well-conditioned athletes can have
a normal bradycardia at rest. Do they also sustain
that bradycardia through mild exercise, or do they
just accelerate as they need to? Will you see someone
well-conditioned who fails to develop a tachycardia
with exercise?
Dr Shamai Grossman: It will take more exertion for
a well-conditioned athlete to reach a maximum heart
rate. An unconditioned athlete may run 10 minutes, and
reach a maximum heart rate, and a well-conditioned
athlete may take 10 hours to reach that same maximum
heart rate. The better the conditioning, the more reserve
your heart has.
PR: Are there elderly patients who have bradycardia
that is not symptomatic, or not representative of heart
disease?
RH: Although there are elderly patients who have
asymptomatic or benign bradycardia, medications
may also be contributing to this. In this case the bra-
dycardia may be inappropriate, yet the patient is still
not symptomatic. They also may not be symptomatic
because they lead a sedentary lifestyle, and are not
Figure 5.1 Case presentation EKG.
BRADYARRHYTHMIAS
73
beats are a compensatory measure of your heart for not
being able to do what it’s supposed to do from the sinus
node. It’s not a ventricular dysrhythmia. We don’t want
to make escape beats go away. It’s very important not
to eradicate them before you can fi x what is making the
heart beat so slowly.
PR: We have a patient who is bradycardic, with a blood
pressure that undoubtedly represents an abnormally
low pressure for him given his age and his history of
hypertension. Since one of his medications is a beta-
blocker, would you simply withdraw the beta-blocker
and watch him, or would you administer some gluca-
gon while you withdraw the beta-blocker?
SG: I don’t think it’s a good idea to leave this elderly
patient with a history of coronary disease in a rela-
tively hypotensive state. Presumably the hypotension
is secondary to the bradycardia; therefore, I would
like to increase the heart rate. The simplest thing to
do with probably the fewest side effects is to try to
reverse the beta-blockade with glucagon and calcium,
and see if that helps.
PR: I am constantly surprised at how often people get
into trouble with medications that they have been tak-
ing for a long period of time. Beta-blockers are a fre-
quent culprit. I have seen numerous patients who claim
they haven’t altered the dose in years, yet suddenly they
are symptomatic. Is there something associated with
beta-blockade that suddenly precipitates symptoms,
just as hypokalemia precipitates dig-toxicity? Is there
anything that makes beta-blockade suddenly likely to
have an overdose effect?
RH: Concomitant medications that also slow the
atrioventricular (AV) node could be a culprit. In addi-
tion to taking extra beta-blocker, other medications
like a calcium channel blocker, digoxin, or clonidine
may have been co-administered to this patient. You
can also have bradycardia and various degrees of
heart block in hyperkalemia. In this case we are not
seeing other signs of hyperkalemia, making this diag-
nosis unlikely.
PR: He has been treated with furosemide, which
would make him more likely to be hypokalemic.
SG: I would not hastily rule out a metabolic abnor-
mality. Hypokalemia and, less frequently, hypocal-
cemia and hypomagnesemia, can cause a variety of
dysrhythmias including premature atrial contractions
perhaps medication overdosage. It is, however, also
conceivable that a patient reaches a certain threshold
and this is when the symptoms commence.
PR: The abruptness may also refl ect a change in physi-
cal activity. If it is the fall season, and the patient went
out to rake leaves, which he hasn’t done since a year
ago, this might not really represent an acute change
in exercise tolerance. With tachycardia, we are quick
to slow it down, while with bradycardia, we are also
quick to think of ways to speed it up. In the past, it
seemed like everybody reached for atropine the minute
they got a pulse count less than 60. Is that still an itch
we scratch, or have we become a little more disciplined
about who we try to pharmacologically speed up?
RH: I hope we have become more disciplined. What
we should do when we have a heart rate like this, with
45 beats per minute reported to us by the nursing
staff, is ask the time honored question of “How does
the patient look?” followed by “What is the blood
pressure?” If the blood pressure is adequate, and the
patient looks well, I would not drop everything and
run into the room to administer a medication. In cases
where the patient has been symptomatic but is in no
apparent distress, yet the blood pressure is low with
a slow heart rate, I think you still should take some
time to re-evaluate the situation, in order to repeat the
vital signs before you cause more problems with your
treatment than had you left the bradycardia alone.
PR: I wouldn’t fault anyone urgently placing an intra-
venous line in this patient, but I would be very cau-
tious in immediately attempting to speed up his rate.
PR: We have an electrocardiogram (EKG) in which
there appears to be some nonconducting P waves; lead
2 looks like the second beat is different from the fi rst
beat, there is a P wave, and then there is another one
subsequently, so it almost looks like there is a two-to-
one block. I also see some extra beats. So it wouldn’t
be stretching too far to read this as some degree of
high grade heart block with ventricular escape beats.
PR: Historically, whenever we found anything that
looked like a premature ventricular contraction
(PVC), we would try to eradicate it with lidocaine.
Why isn’t it a good idea to try to eradicate an escape
ventricular beat?
RH: In this case, that may be what’s maintaining your
patient’s blood pressure and cerebral perfusion. Escape
CHAPTER 5
74
our cardiology service than we used to have, but also
I can remember that it was very hard to get capture
in the ED without concomitant echo or fl uoroscopy
to help you guide the wire. Do you think that we just
don’t do it frequently enough to get good at it, and
that’s why we have so much trouble?
SG: The truth is that I’ve fl oated transvenous wires
a number of times with success and good capture,
but that happens less and less frequently because
I work at institutions where cardiology is readily
available. They strongly prefer to place wires under
fl uoroscopy control, which makes it a far easier and
safer procedure. I think in an ideal world you would
always fl oat a wire under fl uoroscopy, but in the real
world, where sometimes we have to do things in less-
than-ideal conditions (especially in the ED), it can
still be accomplished. Unfortunately for emergency
physicians, I don’t think we get much opportunity,
and therefore I don’t think we have a lot of expertise.
This may be why there isn’t as much success as we
would like to see.
PR: If you were at an institution where you didn’t have
a cardiologist readily available, but you did have access
to an emergency ultrasound, would you use that to
help you fl oat the wire? Would you use external pacing
while you were trying to place the internal wire?
RH: If the patient has a reasonable blood pressure
and mental status, I would avoid external pacing as
it may make it technically more diffi cult to place an
internal wire. Ultrasound would be useful for two
reasons. One, it makes placing an IJ line less risky
because you can place it under ultrasound visualiza-
tion; although this is not a procedure that we fear, it
has complications, and in a sick, elderly patient, we
don’t need more complications. With ultrasound you
feel better about placing that line, and placing it early.
Two, ultrasound would also be useful to look for the
appearance of the wire in the right ventricle. Given
this patient’s body habitus, you probably have a good
chance of visualization. However, it’s going to be hard
to man the ultrasound probe and the pacing wire at
the same time, so you are going to need another per-
son with you. Rather than rely on looking up at the
cardiac monitor to see when we have capture, this
may be a useful adjunct.
PR: It’s going to be the rural emergency physician
who’s stuck with this patient without much support.
(PACs) and PVCs, sinus bradycardia, and AV block,
as well as ventricular tachycardia and ventricular
fi brillation.
PR: It would be worthwhile to look at a basic met-
abolic panel while you straighten everything out.
Regardless, this is a patient who is declaring himself
as unsafe to send home. Historically, we used to try
to treat these patients pharmacologically with brady-
cardia before reaching for a pacing wire. If atropine
in suffi cient doses didn’t speed up the heart (and it
almost never did), then we would try isoproterenol.
RH: The main concern with atropine in the face of
ongoing cardiac ischemia is that it may increase myo-
cardial oxygen demand with the resultant tachycardia,
yet we still use it if we must. I can’t think of the last time
I used isoproterenol. I believe this is the case because of
the lack of good data that it’s helpful more than harm-
ful, particularly with concerns again about increased
myocardial oxygen demand, potentially worsening
cardiac ischemia.
PR: If the patient hasn’t responded to either calcium
or glucagon, at what point would you consider reach-
ing for a pacer?
SG: I would place external pacing pads on this patient
the minute I realized he was bradycardic. Although
right now he is bradycardic and is maintaining some
blood pressure, I don’t know what will happen in
the very near future. Should the blood pressure drop
further, or should he develop further bradycardia, for
example, if the heart rate drops from 35 to 25 beats
per minute, I would either administer atropine and see
if there is a response, or pace him. At the same time, I
would have someone on the phone with the cardiolo-
gist or, depending on the institution, I would have my
nurses set up for me to fl oat a transvenous wire. Most
patients don’t tolerate external pacing for prolonged
periods of time. To review, I would fi rst set up exter-
nal pacing pads, have atropine at the bedside, and then
watch the patient. I might then try glucagon or calcium
to see if I can reverse the beta-blockade. Should he
deteriorate, I would probably try atropine, and if that
doesn’t succeed, try external pacing with the plan to
place a transvenous pacer either by cardiology, or if
need be, by myself in the ED.
PR: I haven’t fl oated a pacer wire in probably
20 years, likely because we have better support from