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VALVULAR HEART DISEASE
205
acute valve regurgitation or acute valve dysfunction
from endocarditis is frequently in extremis, and will
require prompt control of the airway. Rapid sequence
intubation medications that drop blood pressure
should be used with caution, as the hemodynamics of
these patients are frequently tenuous at best. Along
these lines, hemodynamic support may be necessary.
Dobutamine is a good fi rst choice, as it will help aug-
ment forward fl ow by increasing inotropy. Dopamine
can also be used; however, many patients will have
compensatory tachycardia already, and dopamine
may worsen this. Nitroprusside has also been used.
Although this appears counterintuitive, this medication
can lower afterload and facilitate forward blood fl ow,
thereby limiting retrograde fl ow via the mitral valve
and reducing pulmonary congestion.
10
Aortic balloon
counterpulsation can be very useful in the case of
mitral regurgitation, as it can help reduce preload, and
help augment forward fl ow.
11
It is contraindicated with
aortic valve pathology, as it will worsen valvular regur-
gitation. Ultimately, the patient with acute valvular
incompetence requires surgical repair (Figure 14-1).
Treatment of the patient with severe AS will depend
upon presentation. Syncope, CHF, atrial fi brillation,
or ischemic symptoms in the presence of severe AS
portend a poor long-term survival rate, usually on
the order of 2–3 years.
10
The patient may present
asymptomatically with a previously undetected sys-
tolic ejection murmur. Frequently, these patients’ fi rst
symptomatic presentation will be in the ED, such as
after their fi rst syncopal episode. Many cardiologists
and cardiac surgeons will consider valve replacement
once a patient with known stenosis becomes symp-
tomatic. Thus, it is important to communicate this
information to the patient’s cardiac team once dis-
covered by the emergency physician. If a new systolic
ejection murmur is found in a patient, even one pre-
senting for an unrelated complaint, this patient needs
echocardiography to evaluate the valve lesion and to
acquire information about a surgical replacement.
The patient with known critical aortic stenosis
who presents in acute CHF must be handled differ-
ently than the usual CHF patient. These patients are
extremely preload-dependant, as their ventricles have
to operate on a fairly rightward portion of the Frank-
Starling curve to contract with enough force to over-
come the resistance of a tightly stenoic valve. As such,
the usual treatment for heart failure (nitrates, diuret-
ics, blood pressure reduction) can be quite dangerous,
Table 14-1. Duke criteria for diagnosing endocarditis.
Major Criteria
1. Blood cultures
A. 2 blood cultures positive for IE-causing organisms
(Strep bovis, HACEK group, Staph aureus, or Viridans
streptococci, or enterococci without another source)
B. Persistently positive blood cultures: at least 2 cultures
drawn 12 hrs apart
2. Evidence of endocardial involvement
3. Echocardiographic evidence
A. Intracardiac mass on valve or associated structures
B. Abscess
C. Partial dehisance of prosthetic valve
4. New valvular regurgitation
A. Not just worsening of preexisting murmur
Minor Criteria
1. Historical factors: predisposing heart condition or intra-
venous drug abuse (IVDA)
2. Fever greater than 38°C (100.4°F)
3. Embolic phenomenon
A. Cerebrovascular accident (CVA), septic lung emboli
on chest x-ray (CXR), Janeway’s lesions
4. Immunologic evidence
A. Osler’s nodes, Roth’s spots
5. Microbiologic evidence
A. Positive blood cultures that do not meet the major
criteria
For a defi nitive diagnosis one must have 2 major criteria
OR 1 major and 3 minor criteria OR 5 minor criteria
A diagnosis of possible infective endocarditis requires
1 major criteria and 1 minor criteria OR 3 minor criteria
The diagnosis of infective endocarditis is rejected if an alterna-
tive diagnosis is much more likely OR resolution of syndrome
with < 4 days of antibiotics OR no evidence of endocarditis at
surgery or autopsy OR does not meet above criteria
Treatment of patients with acute valvular
heart disease
Due to the nature of acute valvular disease, the emergency
physician will rarely provide defi nitive care for these
patients. Nevertheless, in many cases of acute valvular
disease, the patient will have life-threatening illness, and
the emergency physician will be called upon to provide
potentially life-saving diagnosis and stabilization.
The treatment of patients with valvular heart disease
starts, as does every emergency department encoun-
ter, with assessment of the ABCs. The patient with
CHAPTER 14
206
perhaps a pulmonary artery catheter). Aortic balloon
counterpulsation can be considered as a bridge to
surgery, but is contraindicated in patients with aor-
tic insuffi ciency. Once heart failure has developed in
the patient with critical AS, aortic valve replacement
must be undertaken quickly, as the outcomes for non-
operative patients are very poor.
In the patient with endocarditis, the most important
ED treatment, after hemodynamic stabilization and
obtaining blood cultures, is starting an appropriate
antibiotic regimen. Broad-spectrum antibiotics are nec-
essary, and most empiric regimens suggest antistaphylo-
coccal and streptococcal coverage, such as oxacillin or
nafcillin 2g IV plus gentamycin 1mg/kg plus ampicillin
2g IV daily. Alternately, one gram of vancomycin can
replace the penicillin derivatives if MRSA is suspected
based on local resistance patterns. In the case of IVDA,
and can precipitously drop the blood pressure.
Frequently, these patients need inotropic support with
a drip medication such as dobutamine or dopamine.
Perhaps somewhat counterintuitively, these patients
may actually need IV fl uid if they are hypotensive,
similar to how a patient suffering a right-sided MI
may need fl uid resuscitation. In spite of traditional
thinking, Khot et al. report that in 25 patients with
severe CHF and tight AS, nitroprusside increases the
cardiac index at 6 and 24 hours with minimal side
effects.
12
However, these patients were highly selected,
and nitroprusside therapy is probably not appropri-
ate for all AS patients with CHF. Nitrate therapy can
be initiated in close consultation with the cardiologist
who will be caring for the patient, and should prefera-
bly be done in a patient who has appropriate monitor-
ing devices in place (arterial and central venous lines,
ABC’s
No
Yes
Patient with
suspected
acute valvular
regurgitation
Intubate if
necessary, CVL
should be strongly
considered
1. New murmur?
2. Evidence of CHF on exam?
3. JVD?
Cardiology
and Cardiac
surgery
consultation
Other
pressor/inotropic
agents can be
considered if still
refractory.
To OR vs. CCU
as OR/surgeon
availability dictates.
Start dobutamine and
consider nitroprusside
if pressure will allow.
Echocardiography,
TEE preferred if
patient stability
allows.
Physical
examination
Hemodynamic
instability
Figure 14.1 Flowchart for acute valvular regurgitation.
VALVULAR HEART DISEASE
207
record should also be reviewed for evidence of recent
cultures, and may provide a clue to the specifi c causative
agent; however, antibiotics should not be narrowed until
defi nitive culture data is obtained (Figure 14-2).
vancomycin should be substituted, as the rate of MRSA
in this population is very high.
13,14
Once culture results
become available, antibiotic coverage can be tailored,
but this will be after the patient is admitted. The medical
No
Yes
Patient with
Endocarditis
on Differential
Diagnosis
1. IVDA?
2. Known valve disease?
3. Indwelling vascular
catheter?
4. Other source for
bacteremia?
5. History of IE?
Oxacillin or
nafcillin 2g IV
q4 hours plus
gentamycin
1 mg/kg TID plus
ampicilin 2g IV
6x daily.
Vancomycin
1g q12hr
Plus
gentamycin
1 mg/kg TID
1. New or changed
murmur?
2. Febrile?
3. Neurologic or other
vaso-occlusive signs?
4. Pathognoic signs (Roth
spots, Janeway lesions,
Osler’s nodes?)
Obtain at least 3,
preferably 4
blood cultures.
Consider
other
diagnosis
Physical
examination
Risk Factor
assessment
IE still in the
differential?
Or, if MRS
A
suspected
Administer
empiric
antibiotics
Admit to hospital for Cardiology consult,
echocardiogram, empiric antibiotics,
pending blood culture results.
Figure 14.2 Flowchart for endocarditis management.
CHAPTER 14
208
Walsh RA O’Rourke RA. The diagnosis and manage-4
ment of acute left–sided valvular regurgitation. Curr
Probl Cardiol. 1979;4(9):1–34.
Janz TG. Valvular heart disease: clinical approach to 5
acute decompensation of left–sided lesions. Ann Emerg
Med. 1988;17:201–208.
Schoepf UJ, Yucel EK, Bettmann MA, et al. Expert Panel 6
on Cardiovascular Imaging. Suspected bacterial endocardi-
tis. [online publication]. Reston (VA): American College
of Radiology (ACR); 2006. Available at: http://www.
acr.org/SecondaryMainMenuCategories/quality_safety/
app_criteria/pdf/ExpertPanelonCardiovascularImaging/
SuspectedBacterialEndocarditisDoc17.aspx. Accessed on
July 28, 2011.
Mugge A, Daniel WG, Frank G, Lichtlen PR. 7
Echocardiography in infective endocarditis: reassess-
ment of prognostic implications of vegetation size
determined by the transthoracic and the transesopha-
geal approach. J Am Coll Cardiol. 1989;14:631–638.
Cicioni C, Di Luzio V, Di Emidio L, et al. Limitations 8
and discrepancies of transthoracic and transoe-
sophageal echocardiography compared with surgical
fi ndings in patients submitted to surgery for compli-
cations of infective endocarditis. J Cardiovasc Med.
2006;7:660–666.
Reynolds HR, Jagen MA, Tunick PA, Kronzon I. 9
Sensitivity of transthoracic versus transesophageal
echocardiography for the detection of native valve
vegetations in the modern era. J Am Soc Echocardiogr.
2003;16:67–70.
Bonow RO, Carabello BA, Chatterjee K, et al. ACC/10
AHA VHD Guidelines: 2008. J Am Coll Cardiol.
2008;52:1–142
Folland ED, Kemper AJ, Khuri SF, Josa M, Parisi AF. 11
Intraaortic balloon counterpulsation as a temporary
support measure in decompensated critical aortic steno-
sis. J Am Coll Cardiol. 1985;5:711–716.
Khot UN, Novaro GM, Popovi ZB, et al. 12
Nitroprusside in critically ill patients with left ven-
tricular dysfunction and aortic stenosis. N Engl J Med.
2003;348:1756–1763.
Miro JM, Anguera I, Cabell CH, et al. Staphylococcus 13
aureus native valve infective endocarditis: report of
566 episodes from the International Collaboration
on Endocarditis Merged Database. Clin Infect Dis.
2005;41:507–514.
Millar, BC, Prendergast, BD, Moore, JE. Community–14
associated MRSA (CA–MRSA): an emerging pathogen
in infective endocarditis. J Antimicrob Chemother.
2008;61(1):1–7.
Disposition of patients with valvular disease
All patients with suspected acute valvular disease
need admission to the hospital, often to very high
levels of care. The patient with acute valvular blow-
out will frequently be brought directly to the operat-
ing room for emergent valve repair or replacement.
In the case that an operating room or cardiothoracic
surgeon is not immediately available, these patients
should be admitted to a cardiac or cardiac surgery
intensive care unit while awaiting the surgery. For the
community emergency physician, this will frequently
require transfer to a tertiary care center. Because of
the extreme instability of the blowout patient, one
should consider aeromedical transport, or at mini-
mum a ground unit with experience with vasoactive/
cardioactive drip medication, as they are frequently
required in the care of these patients. When transfer-
ring these patients via EMS services, central venous
access, arterial cannulation, and intubation should be
placed, if possible, prior to departure.
In the case of the endocarditis patient, the usual
decision-making process for level of care applies.
Patients may be admitted to a fl oor service if hemo-
dynamically stable and no deterioration in their sta-
tus is expected; otherwise ICU or step down level of
care is appropriate.
Section IV: Decision making
See Figure 14-1 and Figure 14-2.
References
Nishimura, RA, Carabello, BA, Faxon, DP, et al. ACC/1
AHA 2008 guideline update on valvular heart disease:
focused update on infective endocarditis: a report of
the American College of Cardiology/American Heart
Association Task Force on Practice Guidelines: endorsed
by the Society of Cardiovascular Anesthesiologists,
Society for Cardiovascular Angiography and Inter-
ventions, and Society of Thoracic Surgeons. Circulation.
2008;118:887–896.
Brook I. Infective endocarditis caused by anaerobic bac-2
teria. Arch Cardiovasc Dis. 2008;101(10):665–676.
DePace, NL, Nestico, PF, Morganroth J. Acute severe 3
mitral regurgitation, pathophysiology, clinical recogni-
tion, and management. Am J Med. 1985;78:293–306.
209
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.
Myocarditis
Jehangir Meer
1
& Amal Mattu
2
1
Director of Emergency Ultrasound, St Agnes Hospital Center, Baltimore, Maryland
2
Professor and Residency Director, Department of Emergency Medicine, University of
Maryland School of Medicine, Baltimore, Maryland, USA
15
Section I: Case presentation
A 36-year-old man presented to the emergency depart-
ment (ED) for evaluation of progressive chest heavi-
ness and dyspnea experienced over the prior 4 days.
The patient denied a history of the same symptoms
and any prior past medical history of cardiac or respi-
ratory problems.
He had been in good health with the exception of
“the fl u” 2 weeks earlier. At that time, he experienced
fevers, upper respiratory symptoms, myalgias, and
malaise. All of his symptoms had resolved with the
exception of malaise, which had worsened in asso-
ciation with the chest heaviness and dyspnea. He
reported progressive dyspnea on exertion to the point
now that he felt very out-of-breath walking up a fl ight
of stairs. He added that he had diffi culty laying fl at in
bed the night before because of dyspnea. He reported
mild subjective fevers throughout the day, though he
had not taken his temperature.
He had no abdominal or back pain, lower extremity
edema, nausea, diarrhea, anorexia, or headaches. The
patient took no medications except for multivitamins,
and had no family history of early cardiac disease.
He did not smoke cigarettes or use illicit drugs. He
customarily jogged 4 miles per day 3 times per week,
and had never had any of these symptoms during his
workouts. Notably, he had been too fatigued to exer-
cise over the past 2 to 3 weeks.
The vital signs were: temperature 38ºC (100.4ºF),
pulse 145 beats/min, respirations 28 breaths/min,
blood pressure 87/40 mmHg, pulse oximetry 96%. A
fi nger-stick glucose level was 100 mg/dl.
The physical examination revealed basilar rales in
both lung fi elds, and mild jugular venous distension.
The cardiac, abdomen, back, and extremity exami-
nations were normal, and the pulses were symmetric
bilaterally, though slightly weak. The skin was cool
and slightly moist.
The patient was placed on a cardiac monitor and
supplemental oxygen was provided. An EKG demon-
strated sinus tachycardia, an intraventricular conduc-
tion delay (QRS 100 ms), and nonspecifi c ST-segment
abnormalities. The patient reported that he had never
had an EKG before. A chest X-ray study demonstrated
cardiomegaly and pulmonary vascular prominence
in the upper lung fi elds, consistent with mild heart
failure. Laboratory studies were normal with the
exception of a troponin-I level of 3.5 mcg/L (normal
⬍1.0 mcg/L).
Section II: Case discussion
Dr Peter Rosen: This patient sounds like he was well-
conditioned; he ran frequently, and has now under-
gone a change in his ability to perform exercise that
CHAPTER 15
210
for pericarditis, but can help if you hear it. As for PR
depression, I don’t think that I’ve seen that in any
other condition except pericarditis. Usually there are
also clues in the history favoring pericarditis, such as
a positional component with chest pain, and classic
relief with sitting up and leaning forward; however, I
haven’t found these very helpful. I have noticed that
most patients with pericarditis get relief with changing
positions, some sitting up and leaning forward, some
by lying down, some by lying on their side. Fever alone
doesn’t distinguish coronary artery disease from myo-
carditis or pericarditis, because, up to 30% of acute
MI patients can run a low-grade fever as they necrose
heart muscle. Higher fevers would be more suggestive
of a viral infection, but this is a picture that could also
be compatible with acute endocarditis even without
a drug abuse history. I’ve seen a number of patients
who were not IV drug abusers and without underly-
ing valvular disease, yet who had acute endocarditis.
Would you get blood cultures on this patient or an
echocardiogram?
AM: I would obtain blood cultures on this patient
to evaluate him for possible endocarditis, and an
echocardiogram to look for evidence of this diagnosis.
We always think about using echocardiograms to look
for vegetations on the valves, but with myocarditis it
would be useful to demonstrate diffuse wall motion
abnormalities or a pericardial effusion, which may be
found in either pericarditis or myocarditis. For these
reasons, I would obtain an echocardiogram urgently,
if not emergently.
PR: This patient has already declared himself as need-
ing admission, given that whatever his underlying
problem is, he’s presenting with acute heart failure
and a large heart. An echocardiogram could help us
sort out whether there was a pericardial effusion, a
regional wall abnormality, or a cardiomyopathy. What
if the patient appeared to be less ill? What about the
patient who presents more with positional chest pain,
a pericardial friction rub, or perhaps an EKG sug-
gestive of pericarditis? What should you use as your
indications for admission, as not all patients with
pericarditis need admission, and some patients who
have myocarditis initially look more like pericarditis?
SG: If I have a patient who has a history of posi-
tional chest discomfort without a history of coronary
artery disease; without a history of similar symptoms
he was conditioned to do. This prior conditioning may
not protect him from having coronary artery disease.
I think that it’s rare to see patients suddenly change
their exercise pattern without having underlying cor-
onary artery disease. He’s in the right age group, and
certainly it’s prudent to do the kind of work up that
was done here. Are there any clues in the history or in
the physical examination that could help trigger the
thought of myocarditis, and to help you distinguish it
from coronary artery disease?
Dr Shamai Grossman: In this particular patient, there
are some very specifi c clues that may be applicable
to any patient in which you might consider the diag-
nosis of myocarditis. First, this is a young man, and
although young men can have coronary artery dis-
ease, it is less likely. He has never had disease before,
of cardiac or any other etiology. He presents with a
fever, and in particular, he presents with a fever and
symptoms that sound like he’s having congestive heart
failure (CHF) or left ventricle (LV) dysfunction. All of
those things are very suggestive, almost classic, for a
patient who has myocarditis. Patients who just have
coronary artery disease usually do not present febrile,
they will often have some symptoms suggestive of
ischemia aside from dyspnea, although dyspnea itself
can be a manifestation of angina, and they generally
are older.
PR: Is it rare to see myocarditis without an element
of pericarditis?
Dr Amal Mattu: It seems that many of the patients
diagnosed with myocarditis have both myocarditis and
pericarditis, and often times it is referred to as “myo-
pericarditis.” There may be some selection bias in my
statement because pericarditis tends to be a little bit
easier to diagnose based on the classic EKG changes
with diffuse ST elevation and PR depression, whereas
myocarditis by itself may be more frequently missed
because there’s no specifi c EKG fi nding associated with
pure myocarditis.
PR: Pericarditis can be very hard to diagnose before
it develops specifi c changes and classical fi ndings may
not be present early on. A pericardial friction rub is
a useful clue for pericarditis, although it shouldn’t be
relied on for that diagnosis. I recall that a pericardial
friction rub can be heard in up to 40% of patients with
acute myocardial infarction (MI), depending on how
often and where you listen, so clearly it isn’t diagnostic
MYOCARDITIS
211
the history that you presented, I would also call it trau-
matic pericarditis. Slipping and falling does not sound
like a severe enough event to be a cardiac contusion.
However, it’s often very diffi cult, when patients pres-
ent to an ED with chest pain and an elevated troponin,
to distinguish between myopericarditis and a true
acute coronary syndrome. Often we have to assume
the worst, admit them to the hospital, and perhaps
even require a cardiac catheterization. If you’re lucky,
you see classic pericarditis fi ndings with ST elevations
and PR depressions, but without a diagnostic EKG,
the only other way to be certain about the diagnosis is
to follow the progression of cardiac enzymes.
In an acute coronary syndrome, the patient’s tro-
ponin levels should follow the classic rise and fall:
with a rise within 24 hours and elevations for typically
about a week. In pericarditis and myocarditis, the rise
does not go very high; usually it’s a relatively small ele-
vation in troponin, which usually falls to normal levels
within 24–48 hours. I am unaware of studies that dif-
ferentiate myopericarditis from an acute coronary syn-
drome based purely on troponins. As a result, a lot of
these patients end up in the catheterization laboratory
and are diagnosed with myopericarditis only after the
angiogram is clean for coronary artery disease.
PR: My patient did respond very well to steroids.
Within 48 hours she was pain-free, but in follow-up,
her physician, worried about the troponin rise, sent
her off for a cardiac catheterization, which was nega-
tive. Subsequently, as the symptoms subsided, she’s
done quite well.
SG: To complicate matters, growing data suggest that
elevated troponins can be found in patients with sep-
sis, in patients with pulmonary emboli, or in other
patients who truly are very sick, but are not having
an acute coronary syndrome. This is contrary to what
is generally thought about troponin, namely that tro-
ponin is myocardial specifi c, or is specifi c for an acute
coronary syndrome.
AM: There are a large number of diseases that are
now known to produce some elevation in troponin;
not necessarily huge increases in troponin, but it’s
really thrown a huge monkey wrench into the con-
cept that we can simply diagnose acute MI based on
an elevated troponin. Importantly, we’re also learning
now that when somebody has a non-ACS cause of a
troponin rise, in most cases you need to still worry
associated with coronary artery disease; a friction rub
on physical examination; an EKG not concerning for
ischemia, but consistent with pericarditis; and I’ve
convinced myself that this is pericarditis, then I would
do a bedside ultrasound to feel comfortable with send-
ing the patient home. I think most emergency medi-
cine physicians should be able to determine whether
there is a pericardial effusion. If there is no pericardial
effusion in a patient who very clearly has pericardi-
tis, and who is hemodynamically stable, then that
patient should be able to be discharged home with
follow-up within 48 hours. These patients mostly do
very well. Myocarditis, isolated from pericarditis, is a
somewhat different entity, and without a classic his-
tory it can be very diffi cult to make this particular
diagnosis in the fi rst place. These patients often end
up admitted to the hospital simply because it’s hard to
fi gure out what’s going on, or what is the etiology of
their presentation.
PR: The patient who looks predominantly like peri-
carditis, perhaps with a concomitant viral syndrome,
in the absence of an effusion, is safe to manage as an
outpatient. I would not start such a patient on steroids,
but I usually do start nonsteroidal antiinfl ammatory
medication, and I’m quick to add steroids.
I had a patient a couple of summers ago who was
a middle-aged woman who, while picking up her son
from hockey practice, slipped on the walkway in the
ice rink and fell against a post. She presented a few
days later with severe, ischemic sounding pain, chest
wall tenderness, a very audible pericardial friction
rub, and an EKG with nonspecifi c ST-T wave changes
without the PR depressions typical of pericarditis. She
was referred to our hospital for admission for isch-
emic heart disease because the troponin was slightly
elevated, but I chose not to admit her because I
thought she had traumatic pericarditis. How can you
differentiate between traumatic and ischemic peri-
carditis? What can the physician expect to happen
to the troponin and other cardiac enzymes with both
pericarditis and myocarditis, and how do you distin-
guish them from ischemic changes?
AM: Based on the history you provided, it doesn’t
sound like ischemia was the etiology. I am unaware
of a case of acute coronary syndrome (ACS) being
precipitated by acute trauma. I would make sure the
trauma was not just a red herring, and that she wasn’t
having these symptoms before the trauma. Based on
CHAPTER 15
212
precipitant, which may take you out of the myocardi-
tis category. An echocardiogram may demonstrate an
atrial myxoma, lymphoma, or other tumors that may
be a precipitant of acute LV dysfunction. A patient
who presents without any evidence of an infectious
process, without any other signs suggesting ischemia
as its etiology, or some of the other more atypical
causes of myocarditis, such as cocaine abuse, but with
sudden onset of LV dysfunction, may need a biopsy.
To review, the elements that would help me discern
an etiology would be a careful history, an echocardio-
gram, and occasionally, when you have exhausted all
else, some patients may require a myocardial biopsy
to make a defi nitive diagnosis.
PR: Are there any metabolic causes of patients pre-
senting like this? For example, we know older patients
don’t always present with all of the signs of acute thy-
rotoxicosis, but instead, present with cardiac disease.
AM: I’m not aware of thyroid disorders causing
myocarditis. From a metabolic standpoint, there are
some rheumatologic disorders that can produce myo-
carditis, as well as medications and hypersensitivity
reactions, but by far the majority of patients have
infectious causes.
SG: Sarcoidosis and lupus are associated with myo-
carditis, but I am also not aware of any thyroid
etiologies.
PR: To switch directions, I fi nd that patients with high
resistance pulmonary edema often don’t need intu-
bation, and usually respond to lowering peripheral
resistance and unloading the heart, and can recover
pretty quickly, whereas the patients who have pump
failure from coronary artery disease fare better if you
intubate them early because the work of breathing is
more than their failing heart can sustain. Would we
be prudent to go ahead and intubate this patient with
myocarditis? This is another form of pump failure.
This patient is relatively stable now, but it seems likely
that he’s going to get worse before he gets better.
AM: We can probably expect that he will get worse,
and he’s already working hard to breathe. He’s a
36-year-old healthy man, and so that might be why
he appears to be somewhat “stable.” He has a heart
rate of 145 beats per minute, a classic tachycardia out
of proportion to fever. He’s tachypnic to 28 breaths
per minute, already slightly hypotensive, and he’s
about that elevation in troponin because even if it’s
not ACS, the elevation in troponin in most cases is
still a good predictor of short-term and long-term
adverse events. That applies for pulmonary emboli,
sepsis, neurologic abnormalities, CHF, and likely for
myopericarditis as well.
PR: I suspect that it does represent some damage to the
myocardial cell, which is causing it to leak enzymes.
Returning to our case, we have a patient with myo-
carditis deteriorating into heart failure. He does not
appear to be failing because of peripheral resistance,
but appears to be failing due to pump failure, with the
disease affecting his ability to produce a normal car-
diac output. What sort of therapeutic considerations
should the emergency physician undertake as he pre-
pares to get this patient admitted?
AM: The emergency physician needs to keep one word
in his mind as he approaches this patient and that is,
“supportive.” One must be supportive in every possi-
ble way, because there’s no other effective therapy for
myopericarditis except supportive therapy. In regards
to pump failure, probably dobutamine would be the
best choice of medication if the patient continues to be
hypotensive and has worsening heart failure. Diuretics
might be useful as well. I would not use preload or
afterload reducing medications, given that the patient
is already hypotensive. I would consult cardiology as
quickly as possible. There are some studies indicat-
ing that with very aggressive supportive therapy with
pressors, or with an intraaortic balloon pump, these
patients can survive with reasonable outcomes. If all
else fails, some of these patients may benefi t from car-
diac transplantation, but there is no simple drug or
combination of drugs that fi xes these people. One can
only try very aggressive supportive therapy, support-
ing the pump and supporting the oxygenation, and
getting cardiology involved early.
PR: Is there any way of distinguishing infectious myo-
carditis from patients with a different etiology of myo-
carditis? The etiology appears to be infectious in this
patient, probably viral, but what about the patients
who have amyloidosis, or patients who present this
way who have malignancies in their heart?
SG: The echocardiogram in this patient is potentially
very useful in differentiating the etiology of the myo-
carditis. An echocardiogram may be useful for look-
ing for valvular disease, or endocarditis as perhaps the
MYOCARDITIS
213
management, but it is important to keep in mind that
although viruses are the most common causes, there
are some other diseases that may be associated with
myocarditis. Thus, you may need to take respiratory
or contact precautions.
Case resolutions
The patient was admitted to the coronary care unit
and underwent urgent echocardiography, which dem-
onstrated diffuse myocardial hypokinesis. An urgent
cardiac catheterization was performed to rule out an
acute coronary syndrome, given the positive troponin
level. The catheterization demonstrated no coro-
nary lesions, and so the patient continued supportive
therapy for a presumed diagnosis of myocarditis. The
patient’s congestive heart failure and hemodynamic
status worsened, requiring mechanical ventilation
and the use of vasopressors on hospital day two, but
he made a gradual recovery and was discharged from
the hospital after 10 days.
Section III: Concepts
Background
Myocarditis is generally defi ned as an infl ammation
of the myocardium from a nonischemic cause. It is an
acute infectious or immunological emergency that is
uncommon, but which can have devastating or fatal
consequences if untreated or misdiagnosed. Its initial
presentation can be variable, and some patients pres-
ent in severe distress and cardiogenic shock. Their
initial presentation may be with acute chest pain, dys-
pnea or profound weakness. On the other hand, other
patients may have milder symptoms and variable car-
diac dysfunction. Yet another group of patients have
predominately infectious symptoms (gastrointestinal
or respiratory), and the clinician may ignore or over-
look subtle cardiac symptoms, to the patients’ peril.
Long-term cardiac dysfunction and cardiomyopathy
are not uncommon. Many patients exhibit a full recov-
ery, while some go on to develop chronic cardiomyo-
pathy; a small minority, however, progress to death or
require cardiac transplantation. Histopathologically,
myocarditis is characterized by diffuse or focal myo-
cardial infl ammation. In the industrialized world, it
need for cardiac transplantation.
1
early in the time course of his disease. Taking some
of the stress off the heart would probably be a good
idea in this patient, and again, that would be a form
of aggressive supportive therapy. Thus, it would be
reasonable to intubate him. However, one, must
be careful that when you intubate this hypotensive
patient and increase intrathoracic pressure, you may
drop the preload, dropping the blood pressure more.
Hopefully that would be offset by giving concomitant
inotropes.
SG: Once you determine this is more likely to be myo-
carditis in etiology rather than ischemic in etiology,
then your likelihood of turning the patient around
rapidly in the ED diminishes signifi cantly, so even non-
invasive ventilation, which is usually very effective for
heart failure patients, is not going to be an appropri-
ate solution in this patient; this makes intubation in a
more emergent fashion particularly appropriate.
PR: Are there any precautions that we need to be con-
cerned about for this patient’s caregivers, as we would
if he had, let’s say, meningitis? He has a viral disease.
What precautions, if any, are there?
SG: I’m not sure that he has a viral disease. I think
that he has an infectious disease, but the infectious
causes of myocarditis are myriad. There are bacte-
rial etiologies, there are viral etiologies, and there are
tapeworms that cause it. Chagas disease is one of the
well-known etiologies of myocarditis. I think that
you fi rst have to get a better idea of what’s the most
likely infectious etiology. Does this patient come from
a place where tuberculosis (TB) is endemic? Does this
patient have a history of a positive purifi ed protein
derivative (PPD) test? If yes, you must worry that this
may be the etiology of the myocarditis, and if that’s
the case, then the patient needs isolation, and very
careful care on the part of the healthcare workers. If
the patient describes having been exposed to people
who are having similar, but benign viral syndrome
symptoms, you might be able to be less cautions, and
putting the patient in isolation may not be necessary.
AM: I would emphasize TB; immigrants from Africa
and HIV-positive patients are at higher risk of having
tuberculosis as the cause of myopericarditis. Within
the past month, we’ve had a patient with methicillin-
resistant Staphylococcus aureus (MRSA) myoperi-
carditis with a large MRSA pericardial effusion and
tamponade. I’m not sure it should change our ED
CHAPTER 15
214
found, of which the enteroviruses (Coxsackie A and B)
are the most frequently encountered. Coxsackie B virus
is ubiquitous, with at least half of the general population
thought to be seropositive.
9
Seroepidemiologic studies
suggest the majority of cases of Coxsackie B virus infec-
tion are subclinical; have a benign, self-limited course;
and have seasonal peaks in the summer and fall.
Bacterial causes of myocarditis include Lyme dis-
ease, legionella, mycoplasma, diphtheriae, tubercu-
losis, chlamydia, and streptococcus. In Lyme disease,
a tick-borne infection transmitting the spirochete
Borrelia burgdorferi, patients commonly present with
an erythema chronicum migrans rash and rheumato-
logic symptoms; fewer than 10% of patients develop
myocarditis, which can be manifested with atrio-
ventricular blocks and other conduction abnormali-
ties. Diphtheria myocarditis occurs in two thirds of
patients infected with Corynebacterium diphtheria,
but is clinically signifi cant in only 10% of patients.
Immunocompromized patients, whether second-
ary to HIV, cancer, or postcardiac transplant, show a
higher rate of clinical and subclinical myocarditis; the
infectious agents most often seen include Toxoplasma
gondii and cytomegalovirus. Travelers returning from
overseas can develop myocarditis secondary to para-
sites causing Chagas disease, trichinosis, and echi-
nococcosis. Worldwide, Chagas disease is the leading
cause of myocarditis and dilatated cardiomyopathy.
Trichinosis can occur after ingestion of the nematode
Trichinella spiralis, found in undercooked meat, espe-
cially pork. Echinococcosis develops after ingestion of
the tapeworm Echinococcus granulosus.
Noninfectious etiologies or secondary causes of
myocarditis, such as cardiotoxins and collagen vas-
cular disorders, usually occur in older patients taking
multiple medications. Immunologic etiologies can be
subdivided into postviral and postmyocardial injury
syndromes, connective tissue diseases, and infl am-
matory bowel disease. Connective tissue diseases
implicated in myocarditis include systemic lupus ery-
thematosis, rheumatoid arthritis, sarcoidosis, churg-
strauss syndrome, acute rheumatic fever, sjogren’s
syndrome, and kawasaki disease in children.
Several medications and chemicals have also been
associated with development of myocarditis. Cocaine,
an illicit cardiotoxin, can cause myocyte damage by
different mechanisms. The chemotherapeutic drug
doxorubicin has been implicated in left ventricular
dysfunction and myocarditis.
Epidemiology
Histological evidence of myocarditis has been found
in up to 10% of general autopsies, but clinical myo-
carditis was not suspected in the majority of these
patients.
2
The overall incidence of disease in the gen-
eral population is unknown, in part due to the wide
spectrum of clinical presentations, which ranges from
asymptomatic patients to patients exhibiting severe
hemodynamic instability and death. In the group of
patients diagnosed clinically with myocarditis, and
having had an endomyocardial biopsy, one-third have
histologic evidence consistent with myocarditis. Of
those patients who go on to develop dilatated cardio-
myopathy, 40% have microscopic confi rmation.
The natural history of myocarditis in large popu-
lations is unknown, because there is no established
noninvasive diagnostic test for confi rmation, clinical
manifestations are variable, the diagnosis can be chal-
lenging, and invasive endomyocardial biopsy is uti-
lized in a minority of patients.
3
Men are slightly more
predisposed to the development of myocarditis than
women, and a fulminant presentation is seen more
often in infants and children. Additionally, up to 20%
of young patients with sudden cardiac death have been
found to have histologic evidence of myocarditis.
4
Etiologies of myocarditis
Acute myocarditis can be categorized into two broad
categories (Table 15-1): infectious and noninfectious.
5,6
The infectious category is further broken down into
viral, bacterial, fungal, and parasitic agents, while the
non-infectious group can be subdivided into immuno-
logic, post-irradiation, medication/chemical, and idio-
pathic. One study fi nds half the patients admitted to
a European hospital have an infectious etiology, while
the other half is idiopathic.
7
Of the infectious agents,
viruses are the most common (Coxsackie’s, adenovi-
rus, Epstein-Barr, infl uenza A and B, parainfl uenza,
mumps). Additionally, bacteria (mycoplasma, chla-
mydia and streptococcus), postvaccination status, and
medications are implicated as causative factors. Other
infectious agents include other viruses (cytomegalo-
virus; rubella; rubeola; hepatitis A, B, and C; human
immunodefi ciency virus; varicella zoster; echovirus;
and poliovirus)
8
In the industrialized world, viruses are the most
common cause of myocarditis when an etiology can be