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MYOCARDITIS
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evaluated by magnetic resonance imaging. Ann Rheum
Dis. 2006;65:249–252.
Friman G Fohlman J. The epidemiology of viral heart 65
disease. Scand J Infect Dis. 1993;88:7–10.
Mason JW, O’Connell JB, Herskowitz A, et al. A clini-66
cal trial of immunosuppressive therapy for myocarditis.
The Myocarditis Treatment Trial Investigators. N Engl J
Med. 1995;333(5):269–75.
Lee C, Tsai W, Hsu C, et al. Predictive factors of a 67
fulminant course in acute myocarditis. Int J Cardiol.
2006;190:142–145.
Lieberman E, Herskowitz A, Rose N, Baughman K. 68
A clinicopathologic description of myocarditis. Clin
Immunol Immunopathol. 1993;68:191–196.
Dec G, Waldman H, Southern J, et al. Viral myocarditis 69
mimicking acute myocardial infarction. J Am Coll Cardiol.
1992;20:85–89.
ACC/AHA guidelines for the clinical application of 70
echocardiography: a report of the American College
of Cardiology/American Heart Association Task
Force on Assessment of Diagnostic and Therapeutic
Cardiovascular Procedures. J Am Coll Cardiol. 1990;16:
1505–1528.
Narula J, Khaw BA, Dec GW Jr. et al. Brief report: 71
recognition of acute myocarditis masquerading as
acute myocardial infarction. N Engl J Med. 1993;328:
100–104.
Robinson J, Hartling L, Crumley E, Vandermeer B, 56
Klassen T. A systematic review of intravenous of intrave-
nous gamma globulin for therapy of acute myocarditis.
BMC Cardiovasc Disord. 2005;5:12.
Hia C, Yp W, Tai B, Quek S. Immunosuppressive therapy 57
in acute myocarditis; an 18 year systematic review. Arch
Dis Child. 2004;89:580–584.
Imazio M, Demichelis B, Parrini I, et al. Management, 58
risk factors, and outcomes in recurrent pericarditis. Am
J Cardiol. 2005;96:736–739.
Imazio M, Bobbie M, Cache E, et al. Colchicines in 59
additional to conventional therapy for acute pericarditis.
Circulation. 2005;112:2012–2016.
Chen H, Liu J, Yang M. Corticosteroids for viral myo-60
carditis. Cochrane Database Syst Rev. 2006;4:CD004471.
Baldini G, Bani E. Cardiac complications in Jennerian 61
vaccination. Clinical and echocardiographic studies.
Minerva Pediatr. 1979;31:35–39.
Matthews A, Griffi ths I. Post–vaccinal pericarditis and 62
myocarditis. Br Heart J. 1974;36:1043–1045.
Murphy J, Wright R, Bruce G, et al. Eosinophilic–63
lymphocytic myocarditis following immunization for
smallpox in a previously healthy 29–year–old man.
Lancet. 2003;363:1378–1380.
Allanore Y, Vignaux O, Arnaud L, et al. Effects of 64
corticosteroids and immunosuppressors on idio-
pathic infl ammatory myopathy related myocarditis
226
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.
Pericarditis
Theodore Chan
Medical Director, Department of Emergency Medicine, University of California,
San Diego Medical Center, Professor of Clinical Medicine, University of California,
San Diego, San Diego, California, USA
16
Section I: Case presentation
A 42-year-old man with no prior cardiac history
presented to the emergency department (ED) com-
plaining of left-sided chest pain of 2 days duration.
He described the pain as sharp and intermittent, with
radiation to his left shoulder, and worsening with
deep inspiration or upper extremity movement. The
patient stated the pain was worse when lying down to
go to sleep. He denied shortness of breath, lighthead-
edness, palpitations, nausea, or abdominal pain.
The week prior, the patient had an upper respiratory
tract infection with cough and congestion for which
he took over-the-counter medications for symptom-
atic relief. He exercised regularly, but had been unable
to do so for the last week because of his illness. The
past medical history was signifi cant for hypertension,
for which he was not taking any medication. The fam-
ily history was notable in that his father had suffered
a myocardial infarction (MI) at the age of 62.
The triage vital signs were: blood pressure 147/86
mmHg, pulse rate 98 beats/min, respiratory rate 16
breaths/min, and temperature 38.2ºC (100.7ºF). On
initial evaluation, the patient was in mild distress,
slightly diaphoretic in appearance, and sitting up on
the gurney. The physical fi ndings were notable for
clear breath sounds on lung examination, and a regu-
lar rate with no murmurs on cardiac auscultation. The
remainder of the examination was unremarkable.
The patient was placed on a cardiac monitor, and a
12-lead EKG showed a normal sinus rhythm with
slight ST elevation in the inferior and lateral leads
(Figure 16-1). There was no prior EKG available for
comparison. A complete blood count showed a mild
increase in white blood cell count (12.3k/mm
3
), but
was otherwise normal. Serum electrolytes were nor-
mal and the cardiac troponin-I level was ⬍ 0.02 ng/ml.
A chest radiograph was noted to have no signifi cant
disease.
Section II: Case discussion
Dr Peter Rosen: Is there anything in particular on this
EKG that you would fi nd diagnostic?
Dr Shamai Grossman: There is marked diffuse PR
depression that is very unusual, with the exception of
one disease entity, and that’s pericarditis. There is also
a hint of diffuse ST elevation, which is nonspecifi c,
but more consistent with pericarditis than with car-
diac ischemia.
PR: This patient has a history of hypertension that
is untreated, a family history of coronary artery dis-
ease, and a presentation that is compatible either with
an ischemic coronary syndrome or with pericarditis.
What are the clues you use to distinguish the two,
assuming that you can? Or how do you safely manage
the patient for both?
PERICARDITIS
227
on EKG. While all of these fi ndings point to pericardi-
tis, they’re not enough to exclude the diagnosis of car-
diac ischemia.
PR: This leaves me with the impression that in some of
these cases the only way that we will be able to distin-
guish between these two diseases is in the catheterization
laboratory, which may be appropriate, even though we
will probably receive a fair amount of scorn from our
cardiology colleagues once they discover that it is peri-
carditis. They will want to know why we couldn’t fi gure
it out after doing all the studies that we did. Nevertheless,
I think this case sounds more like pericarditis. I have
noticed that our colleagues in Italy are much quicker to
obtain cardiac echocardiogram (ECHO) imaging stud-
ies on patients than we seem to be. Perhaps they are just
more adept at doing them personally, or it is just their
practice style, but a cardiac echocardiogram can be a
very important study in pericarditis.
Dr Ted Chan: An echocardiogram could help pick up
any wall motion abnormality associated with an isch-
emic episode, in addition to the more common com-
plications of pericarditis, such as pericardial effusion.
An echocardiogram can also be very helpful in terms
of determining whether this patient can be treated as a
straightforward pericarditis on an outpatient basis, or
whether an admission will be necessary with concerns
for either ischemia or impending cardiac tamponade.
SG: I would make the argument that there is a time
where door-to-balloon time is a reasonable and worthy
goal. This is in a patient who has a clear cut ST eleva-
tion MI. However, in a patient whose presentation is
Dr David Brown: The clinical approach has become
more complicated in the last several years as we are
now very focused on shortening door-to-balloon time
for patients with a ST-segment elevation myocardial
infarction (STEMI). This in turn means markedly
reducing the ED time for patients who present with a
presumed STEMI. Nevertheless, this patient does not
present with the fi ndings of acute heart failure as one
might see if this were an active transmural infarction.
There are no other historical features or examination
features particularly reassuring in this case to exclude
STEMI, because the spectrum of people presenting
with ST elevation MI includes patients with positional
chest pain, pleuritic chest pain, and sharp chest pain.
The physical examination of a STEMI patient is usu-
ally unremarkable unless there is a complication of the
STEMI, such as heart failure or a valvular problem,
which doesn’t seem to be the case here. This patient
doesn’t have a rub on physical examination, which if
present might further suggest pericarditis. However,
rubs are usually absent and even when present are
very hard to hear in a busy, noisy ED. Patients with
pericarditis or suspected pericarditis often have fi nd-
ings on the EKG like this one that are consistent with
striking here, and there is PR elevation in aVR, also
striking; both fi ndings are much more consistent with
pericarditis than ST elevation MI. In addition, the
EKG has diffuse ST elevation in the precordial leads
and in II, III and aVF, and it is hard to imagine an ana-
tomic distribution of atherosclerosis in the coronary
arteries that would create these widespread fi ndings
Figure 16.1 12-lead EKG for case patient presenting with chest pain.
CHAPTER 16
228
patients. I wonder if we listen closely enough before
we conclude there is no friction rub present. I switched
to an electronic stethoscope as I started to go a little
deaf with age, and started hearing a lot more fi ndings
than I remembered hearing without it. Perhaps we
all ought to use an electronic stethoscope or at least
upgrade to a better quality stethoscope. Nevertheless,
a rub doesn’t completely rule out ischemic syndrome
as about 25% of patients with acute MIs have a rub
at some point. Do you have a feeling for when the rub
develops in pericarditis, and any particular clues for
where to listen for it besides directly over the heart?
DB: I fi nd that if a rub is present, it is very helpful
in supporting the diagnosis of pericarditis, but when
absent it is not useful to exclude the diagnosis of peri-
carditis. The rub can be fl eeting, can be intermittent,
and therefore examining the patient more than once
and in a quiet room away from all the noises and
monitor beeps can be very helpful. The easiest way
to hear a friction rub is to sit the patient up, and have
them lean forward. Occasionally I have only heard
the rub in the back. Doing a more complete cardiac
examination than you would routinely do on a patient
with chest pain is useful and may increase the likeli-
hood that one will hear a rub.
SG: If you can hear a three-component rub you are
almost certainly dealing with pericarditis.
PR: I know classically we fi nd positional change help-
ful in differentiating pericarditis from an ischemic
syndrome, but this is probably like any other physical
fi nding—if it’s there it may be helpful, but if it’s not
there it doesn’t exclude anything.
What are your indications for admission in a patient
with pericarditis?
DB: If I’m convinced the diagnosis is pericarditis, and
I’m able to establish clinically either by a formal or
bedside echocardiogram that there is no signifi cant
pericardial effusion, then I would feel comfortable
discharging such a patient to be treated with non-
steroidal antinfl ammatory agents (NSAIDS) and to
have close follow-up. Having said that, this assumes
that I was satisfi ed with my history, physical exami-
nation, and EKG in excluding myocardial infarction,
and didn’t feel that the patient needed to be evaluated
any further for cardiac ischemia. It also assumes that
I could obtain at least a bedside ECHO in a timely
fashion in the ED or as an outpatient. In the absence
less clear, and which may be suggestive of pericarditis,
I think it behooves us to be as thorough as possible
and investigate all other causes. If you can obtain an
echocardiogram in a relatively expeditious fashion in
the ED, then I think you should. One ethically must
say, “My priority here is to take the best care of the
patient.” There is morbidity associated with cardiac
catheterization, and if I can avoid this, then I should.
PR: I think that is fair. Nevertheless, there will be cases
that we rush to the catheterization laboratory because
we can’t sort it out easily in the ED, and if we err on
the side of caution and go to the catheterization labo-
ratory too quickly, that is preferable to getting there
too late. On the other hand, an inadvertent trip to the
catheterization laboratory is also expensive, time con-
suming, and may deprive a deserving ischemic patient
of a procedure needed expeditiously.
DB: I am not advocating that strategy, as from a public
health standpoint I think it makes no sense. The prob-
lem is that we are being held to a sensitivity marker
without a specifi city marker. We can take every single
patient that comes through the ED to the catheteriza-
tion laboratory, and have a door-to-balloon time of
60 minutes or less on every patient without being crit-
icized. Yet, if we take our time and do an echocardio-
gram on these patients, 1 in 50 might have a STEMI
and we are going to get penalized for these cases.
SG: Our real job is giving appropriate care to a
patient, and sending a patient to the catheterization
laboratory who doesn’t belong there is not good care.
Every time we take a patient to the catheterization
laboratory, there is morbidity and mortality.
PR: The pragmatic reality is that we do things ide-
ally that don’t happen in the real world, and I think
it is much more probable that the emergency physi-
cian is going to abdicate responsibility for making the
distinction in consultation with the cardiologist. This
is not because he should do so, but is because he is
more likely to do so, as the personal benefi t/reward
relationship is better with shared responsibility. I still
think we should be teaching responsibility, and trying
to imbue a sense of empowerment in our trainees that
they have the right to do what’s best for the patient.
We also appear to have no trust in our physical
diagnosis examinations, probably because we become
reluctant to use them, but I think that auscultating a
pericardial friction rub can be very helpful in these
PERICARDITIS
229
would ever use them unless my consultant strongly
desired them. There is some recent literature in Europe
that talks about combining NSAIDs with colchicine,
and I think that some of those studies also looked at
steroids, but did not fi nd them much more helpful.
PR: I think steroids are more likely to be useful in
traumatic pericarditis, where I haven’t found much
benefi t from NSAIDs. Most of the patients I see with
fresh pericarditis in the ED I never see again, so I don’t
know if they have benefi ted from NSAIDs. But, I have
seen a number of patients who came back to the ED
with traumatic pericarditis who had been started on
NSAIDs, and they did seem to benefi t from adding
steroids.
Is there a difference between pericarditis that devel-
ops from a viral infection, such as from coxsackie
virus, which is the most common viral agent, and a
traumatic pericarditis from striking your chest wall?
TC: Traumatic pericarditis is more likely to need
admission for observation and concern for an under-
lying myocardial contusion or other injuries.
PR: What are the complications of pericarditis, other
than tamponade from the effusion?
DB: Tamponade is clearly the most concerning com-
plication. The development of tamponade can be
insidious, or it can be more rapid if there is hemor-
rhagic conversion and the patients bleed into their
pericardium. Unless there is an associated myocardi-
tis, there is not much risk of dysrhythmia or of other
complications of heart muscle disease.
SG: Although rare, constrictive pericarditis should be
in the back of your mind as a complication. This is
only seen in patients who have recurrent pericardi-
tis where ultimately there is an encasement of the
heart with fi brous tissue from the pericarditis. With
constrictive pericarditis, one would see patients who
have the clinical presentation or an EKG suggestive
of pericarditis, but might have concomitant signs of
congestive heart failure. Calcifi cations on the chest
X-ray study or pericardial thickening on echocardio-
gram are also suggestive of constrictive pericarditis.
Management will be somewhat different, as these
patients will need to have the pericardium resected or
a pericardial window created.
PR: Do you have a sense for how quickly the effusion
can develop? In other words, if we are using effusion
of those two conditions, it would be reasonable to
admit a patient like this to an observation unit for
serial cardiac markers and EKGs, and to obtain an
ECHO study in the morning, assuming this is the
middle of the night.
PR: Most of us agree that the presence of an effusion
is worrisome and would warrant putting the patient
into the hospital. How accurate are chest X-ray and
ultrasound studies in revealing an effusion?
TC: An echocardiogram is much better than a chest
radiograph. I believe the cutoff for detecting a signifi -
cant effusion on X-ray study would be somewhere
between 200 and 250 cc of fl uid, but an ultrasound
study should be able to pick up 50 cc of fl uid.
Therefore, you cannot rely on a chest X-ray study
to detect a pericardial effusion; you would have to
obtain an echocardiogram.
SG: I might add that we may not need a formal echocar-
diogram on all these patients, as we have become very
adept at bedside ultrasound in the ED. I think most of
us would put a probe on a patient, and if we see an
effusion, then we arrange a formal echocardiogram. If
we don’t see an effusion, we would likely be satisfi ed
that the patient didn’t have any of the complications
of pericarditis.
PR: The conventional wisdom is to start therapy with
NSAIDs, but I am underwhelmed by their effective-
ness in pericarditis. Would you ever keep a patient
in the ED to see if he or she is going to respond to
NSAIDs before discharge?
SG: I usually start these patients on ketorolac in the ED
because it is a rapid-acting antiinfl ammatory agent,
and I’ve had good success with it. Using ketorolac
offers me an opportunity to look at the patient after
they have had time to respond. Assuming the patient
improves, I’m convinced that the patient indeed has
pericarditis, and I am no longer concerned with myo-
cardial ischemia or other etiologies of the symptoms,
then I would be comfortable sending that patient
home on an oral antiinfl ammatory such as ibuprofen
or naproxen. I cannot recall a pericarditis patient who
did not respond to ketorolac in the ED.
PR: What are your indications for steroids and when
would you start them?
TC: The literature on the benefi t of steroids in peri-
carditis is equivocal, to be honest, and I’m not sure I
CHAPTER 16
230
effusion, but was otherwise normal. During hospital-
ization, repeat cardiac examinations revealed a faint
three-phase friction rub with the patient in the left lat-
eral position. With a presumptive diagnosis of acute
pericarditis, the patient was subsequently treated
with antiinfl ammatory medications and discharged.
He recovered uneventfully with full resolution of
symptoms. Six months later, a repeat EKG revealed
resolution of the ST-segment fi ndings seen on the ED
presentation.
Section III: Concepts
Background/Epidemiology
The normal pericardium is a double-layered fi brose-
rous sac that envelops the heart and base of the great
vessels within the middle mediastinum. The inner vis-
ceral pericardium and outer parietal pericardium are
each approximately 1–2 mm thick, and are separated
by the pericardial cavity, which contains 15–50 ml of
serous pericardial fl uid in a healthy individual. The
pericardium protects the heart, as well as constrains
the motion of the heart, and is an important determi-
nant of cardiac fi lling.
1
Acute pericarditis, or infl ammation of the pericar-
dium, can present in many clinical settings including
the ED, and has a wide range of causes (Table 16-1).
The disease is often accompanied by some degree of
underlying myocarditis, or infl ammation of the super-
fi cial myocardium adjacent to the infl amed pericar-
dium.
2
The term “myopericarditis” has been used to
describe a primary pericarditis with lesser degree of
related myocardial infl ammation, whereas the term
“perimyocarditis” indicates a primary myocarditis
with accompanying overlying pericarditis, though the
terms are used interchangeably.
3
The true incidence and prevalence of percarditis are
unknown. Autopsy studies, however, indicate a prev-
alence of approximately 1%, suggesting the potential
for subclinical cases.
1
Clinically, approximately 5% of
all chest pain patients who are not diagnosed with
an acute myocardial infarction may have pericarditis
as the etiology for their presentation.
4
However, the
underlying causes of acute pericarditis are changing.
For example, the rising incidences of HIV infection,
invasive cardiac procedures, and radiation therapy
have all resulted in an increase in acute pericarditis
associated with these underlying etiologies. Acute
as one of the criteria for admission, and we don’t see
one on a patient, how rapidly is the patient likely to
develop one at home that would make us concerned
about follow up?
SG: This would depend on the etiology of the peri-
carditis. A viral pericarditis would be more likely
to have a rapid onset; pericarditis from tubercu-
losis or the many noninfectious etiologies, such as
malignancy, uremia, or post-radiation, would be
more likely to develop an effusion slowly, as you
gradually develop the effects of the primary disease
process.
PR: Would you look for other causes of pericarditis,
perhaps new renal failure as the etiology of the peri-
carditis, or are you comfortable with trying to distin-
guish between viral and bacterial etiologies?
TC: In this particular case, the patient has a clear
precipitating infectious history. He had congestion
and a cough in the 2 weeks preceding the onset of
his chest pain, and he’s otherwise healthy. Although
hypertension will put him at risk for renal failure
and uremia, I would expect to see other signs and
symptoms consistent with uremia before I tried to
attribute his pericarditis to renal failure. On the
other hand, there is probably some additional his-
tory that we should obtain from this patient. Is he
in the military, for example? Did he get a smallpox
vaccination, as there is an association between acute
pericarditis and that vaccination? By obtaining more
history, we might be better able to focus or limit
our considerations to a viral etiology, which is most
likely in this case.
PR: Is there any benefi t to giving an antiviral agent?
TC: I am unaware of a literature suggesting antivirals
to be effective in viral pericarditis.
PR: I think pericarditis is a lot more common than we
sometimes expect, and given our propensity to worry
about ischemic coronary syndromes, we often fail to
think of the diagnosis, and so fail to look for and rec-
ognize the EKG changes.
Case resolutions
The patient was admitted with a preliminary diagnosis
of new onset angina. Serial cardiac markers were nor-
mal. An echocardiogram revealed a small pericardial
PERICARDITIS
231
Initial workup history and physical examination
The classic presentation for acute pericarditis is chest
pain, central or retrosternal in location, sharp and
pleuritic in nature, and often sudden in onset and
severe. The pain is worse with recumbency or in the
supine position, and accordingly the patient is often
sitting up and leaning forward in an effort to relieve
the symptoms. The pain can radiate to the neck,
arms, or shoulders, making it diffi cult to differentiate
pericarditis from mycobacterium tuberculosis is now
less common in developed countries, but remains an
important infectious etiology of the disease in devel-
oping parts of the world.
Most cases of acute pericarditis resolve without
major long-term sequelae. However, depending on
the underlying etiology, certain patients may be at
risk for signifi cant complications, including recurrent
pericarditis, chronic or constrictive pericarditis, peri-
cardial effusions, and cardiac tamponade.
Table 16-1. Causes of Acute Pericarditis
Infectious
Viral Coxsackie A and B, hepatitis viruses, HIV, EBV, CMV, varicella, rubella,
mumps, rubeola, poliomyelitis, rhinoviruses, vaccinia, parvovirus B19, others
Bacterial Streptococcus (pneumococcus, meningococcus, gonococcus), hemophilus,
treponema pallidum, borreliosis, chlamydia, listeria, rickettsial, M. tuberculosis,
others
Fungal Candida, histoplasma, blastomyces, others
Parasitic Entamoeba histolytica, echinococcus, toxoplasma, others
Autoimmune
Disorders
Lupus, rheumatoid arthritis, sarcoidosis, scleroderma, Sjogren’s syndrome,
Reiter’s syndrome, ankylosing spondylitis, Wegener’s granulomatosis, giant-cell
arteritis, polymyositis, dermatomyositis, familial Mediterranean fever, Churg-
Strauss syndrome, Periarteritis nodosa, acute rheumatic fever, Stevens-Johnson
syndrome, TTP, leukoclastic vasculitis, others
Metabolic and
Endocrine
Renal failure/uremia, dialysis-related
Addison’s disease, DKA, hypothyroidism,
gout, scurvy, cholesterol pericarditis, pregnancy
Malignancy-
related
Primary or
metastatic
Mesothelioma, sarcoma, melanoma
Breast and lung cancers
Lymphoma, leukemia
GI cancers, carcinoid, others
Secondary Postradiation therapy
Adjacent
structures
and other
organ system
Cardiac and
vascular
Myocarditis
Acute myocardial infarction
Postmyocardial infarction, Dressler’s syndrome,
aortic dissection, aortic aneurysm
Postcardiac or tho-
racic procedure
Postpericardiotomy, cardiac surgery
Postcatheterization, pacemaker placement, ablation
Pulmonary Pneumonia, pulmonary embolism, empyema,
pulmonary infarction
GI Pancreatitis, infl ammatory bowel disease, esophageal diseases
Perforation (esophageal or gastric)
Trauma
Penetrating injury
Blunt chest/cardiac trauma
Medications
and drugs
Hydralazine, penicillin, phenytoin, procainamide,
INH, rifampin, dantrolene, doxorubicin, methyldopa, methysergide, sulfona-
mides, cocaine, others
Idiopathic
CHAPTER 16
232
is present, the radial pulse may disappear with inspi-
ration, but this is a late fi nding. The pathophysiologic
response to tamponade is a tachycardia, but for poorly
understood reasons, immediately prior to the patient
arresting, a bradycardia will suddenly develop. The
removal of even a small volume of fl uid can restore
life-sustaining cardiac function. Acute tamponade will
often develop with 200–300 cc of fl uid, but chronic
effusions that have developed more slowly can some-
times contain up to a liter or more of serosanguinous
fl uid. Viral-induced effusions are easy to aspirate;
however, those associated with bacterial pericarditis
can be very viscous, and may require surgical removal
as they cannot easily be aspirated through a needle.
The classic fi nding on examination that indicates
an acute pericarditis is the pericardial friction rub,
typically described as a high-pitched “scratchy,”
“raspy,” “creaky,” or “squeaky” sound best heard
along the left sternal border at end expiration with
the patient leaning forward. This rub was previously
thought to be caused by infl amed visceral and pari-
etal pericardial surfaces rubbing against one another,
but it is also present when there are large effusions
separating these surfaces. The rub is described as hav-
ing three components, corresponding to atrial systole,
ventricular systole, and early rapid ventricular fi ll-
ing. However, the rub is often heard as a biphasic or
monophasic, as well as a triphasic, sound. Unlike a
pleural rub from pleuritis, the pericardial friction rub
is audible and does not vary throughout the respira-
tory cycle. The presence of a pericardial friction rub
is virtually pathognomonic with near 100% specifi c-
ity for pericarditis, but has low sensitivity because it
tends to be transient, and intermittently comes and
goes over hours.
5,8
Accordingly, repeated and frequent
auscultations over time will increase the sensitivity
and likelihood of detecting this fi nding.
The remainder of the physical examination should
focus on assessing overall cardiac function, and detect-
ing the underlying etiology of the acute pericarditis.
Etiologies/Differential diagnosis
A wide variety of etiologic conditions can cause acute
infl ammation of the pericardium, producing serous,
purulent, or dense fi brinous material within the
pericardial sac. These conditions include infectious
etiologies, most commonly of viral origin; systemic
autoimmune, metabolic, or endocrinologic disorders;
from acute cardiac ischemia, particularly given the
likelihood of some degree of associated myocardi-
tis. However, pain radiation to the trapezius muscle
ridge, which is innervated by the phrenic nerve and
stimulated by pericardial infl ammation, makes acute
pericarditis more likely.
5
Clinical presentation of the disease, however, can
be quite variable, likely refl ecting the underlying eti-
ology, degree of myocardial involvement, and pres-
ence of complications. Many cases may be subtle or
subclinical, with little evidence of cardiac or systemic
signs or symptoms. On the other hand, the clinical
presentation may refl ect the underlying cause of the
acute pericarditis. A history of febrile illness has been
reported in half of all cases of myopericarditis of sus-
pected viral etiology.
6
Similarly, patients may present
with other symptoms consistent with a viral infection,
including myalgias, malaise, and respiratory and gas-
trointestinal complaints. A history of recent cardiac
surgery or intervention should raise the possibility of
a postprocedure pericarditis.
With signifi cant myocardial involvement, patients
may complain of fatigue, decreased exercise capacity,
shortness of breath, and palpitations in addition to
chest pain. These presenting complaints should raise
concern for diminished cardiac function potentially
resulting from a large pericardial effusion or cardiac
tamponade.
The initial physical examination should fi rst focus
on vital signs and an assessment of cardiac function.
Hypotension and tachycardia may be the result of
decreased cardiac output from accumulated pericar-
dial fl uid and increased pressure, reducing fi lling of
the right heart chambers. The neck veins should be
examined for any distension indicating decreased
cardiac fi lling. The presence of a pulsus paradoxus,
a decrease in systolic arterial pressure greater than
10 mmHg with inspiration, may herald cardiac tam-
ponade physiology; this is more common with certain
etiologies, including acute pericarditis from neoplas-
tic, tuberculosis, and purulent (bacterial) causes.
7
The
best way to determine a pulsus paradoxus is to infl ate
the sphynomanometer above systolic pressure. While
auscultating over the brachial artery, determine the
difference between the onset of the fi rst Korotkoff
sound and when it becomes steady. If this difference is
greater than 12 mmHg, a pulsus paradoxus is present.
It is very diffi cult to try to measure this difference in
conjunction with a patient inspiration. If tamponade
PERICARDITIS
233
such as doxorubicin, may also cause acute pericarditis.
Cancer-related pericarditis has a high rate of complica-
tions, including the development of large pleural and
pericardial effusions.
A wide variety of other noninfectious diseases,
including endocrinologic, metabolic, and autoim-
mune diseases, can all result in acute pericarditis or
myopericarditis. Common causes in these categories
include systemic lupus erythematosus, end-stage renal
failure and uremia, and a variety of connective tissue
and rheumatologic disorders.
Testing
The 12-lead electrocardiogram can provide useful
information in the diagnosis of acute pericarditis.
Typical electrocardiographic abnormalities result
from the degree of subepicardial infl ammation and
myocardial involvement. Classically, the EKG in
acute pericarditis evolves through 4 stages, occur-
ring over a period of several weeks. Stage I, occurring
in the fi rst hours or days, is characterized by dif-
fuse ST elevations, concave upward in morphology,
most prominent in the anterior and inferior leads.
12
Reciprocal ST depressions may be seen in leads aVR
and V1. There are also PR segment deviations from
the normal P wave polarity with depressions dif-
fusely, most prominent in leads V5 and V6, as well
as elevation in lead aVR and possible. The PR seg-
ment changes may precede the ST-segment fi ndings.
In stage II, which occurs over several days to 3 weeks,
the PR- and ST-segment changes resolve. There may
also be T wave fl attening with decreased amplitude. In
stage III, diffuse T wave inversions are seen. Finally,
in stage IV, the T waves normalize and the EKG
returns to baseline after several weeks.
This typical evolution on EKG, particularly the rapid
early stage I fi ndings, may be missed or not recorded
electrocardiographically. In addition, atypical fi ndings
are common depending on the underlying myocardial
tissue involvement and infl ammation. In the setting of
myopericarditis, ST-segment changes, particularly of
a local or regional nature, earlier T wave inversions,
and various cardiac dysrhythmias are more common
than with simple acute pericarditis.
6
Accordingly, fi ndings associated with acute peri-
carditis can be diffi cult to differentiate from acute isch-
emia electrocardiographically. Morphologically, the
ST-segment elevation in ischemia is more commonly
traumatic injury such as esophageal perforation or
invasive cardiac procedures; extension of other local
infl ammatory processes; malignancy and neoplasm
spread; medications and drugs; and, most commonly,
idiopathic causes (see Table 16-1).
Advances in pericardial fl uid collection and analysis,
as well as immunohistochemistry and PCR techniques,
have allowed more comprehensive determination of
the etiologies of acute pericarditis; even with this,
however, the cause of pericarditis still cannot be
determined in up to 30% of patients.
1
Of those where
a cause can be determined, infection remains the most
common. Viral agents account for the large majority
of cases, particularly enteroviruses such as coxsackie,
adenoviruses, and infl uenza. HIV-related pericardial
disease is common, and immunosuppressed patients
are at risk for a variety of opportunistic pathogens
such as cytomegalovirus.
9
An unusual viral-mediated
pericarditis has been reported following smallpox
vaccination with vaccinia virus.
10
Though less common than viral pathogens, bacte-
rial pericarditis typically causes a purulent pericarditis
that has greater risk of complications. Bacterial infec-
tion can spread to the pericardium hematogenously,
or by direct extension from nearby organs, particu-
larly the lungs. Mycobacterium tuberculosis remains
an important cause of the disease in developing coun-
tries, as well as in immunosuppressed patients. Risk
of rapid pericardial fl uid formation and tamponade is
high in with these infections.
Acute pericarditis and myopericarditis have been
associated with both early and late acute myocardial
infarction. Dressler’s syndrome is an acute pericarditis
that develops late, more than one week after an acute
infarction. Acute infl ammation of the pericardium is
common after cardiac surgery as part of the postperi-
cardiotomy syndrome. While less common, patients
undergoing percutaneous cardiac procedures, includ-
ing pacemaker placement, ablation or angioplasty,
and coronary artery stenting, are also at risk for acute
pericarditis.
11
Neoplastic-related pericarditis can arise from a num-
ber of pathophysiologic mechanisms, including primary
malignancy (rare), direct tumor invasion, lymphatic or
hematogenous spread, or as a complication of therapy.
Lung tumors, breast cancer, and lymphomas are the
most common cancers that may metastasize to the peri-
cardium.
12
Radiation therapy, particularly for breast
cancer, as well as certain chemotherapeutic agents
CHAPTER 16
234
infl ammation and complications, but the exact clinical
role for each has yet to be determined.
1,3
Pericardiocentesis and fl uid drainage may be diag-
nostically or therapeutically indicated in patients
with large pericardial effusions, and for those with
suspected or confi rmed purulent or neoplastic peri-
carditis. Depending on the clinical presentation and
etiologies considered, fl uid may require analysis with
a variety of studies, including cell count, Gram’s stain,
culture, PCR assays (for suspected viral causes),
adenosine deaminase activity (which may indicate
M. tuberculosis), triglycerides (for chylous effusions),
cytology studies, and pH, LDH, protein and glucose
levels (to determine the nature of the fl uid collection),
as well as other more advanced tests. Pericardial
biopsy may be indicated for recurrent pericarditis or
pericardial fl uid collections of unknown etiology.
Disposition
Most cases of acute pericarditis have a benign course
and are self-limited, with management that is largely
supportive and focused on pain relief, and on poten-
tial complications. In uncomplicated cases, primarily
viral and idiopathic, the mainstay of initial therapy is
treatment with the NSAIDs. Therapy may be required
for weeks to relieve symptoms. Indomethacin should
be avoided in patients with coronary artery disease
because of an association with diminished coronary
blood fl ow.
17
Aspirin can be used as alternative, and
may be preferable for patients who have suffered a
recent myocardial infarction. Colchicine has been
shown to be a useful adjuvant to conventional therapy,
signifi cantly reducing the recurrence rate for patients
with fi rst-time acute pericarditis.
18
Corticosteroid treat-
ment is controversial because of evidence suggesting the
potential for increased risk of recurrence.
3,19
Steroids
have been recommended for use only after patients fail
conventional therapies, and also may have some utility
in tuberculosis pericarditis.
1
Therapy should otherwise
focus on the specifi c etiology of the acute pericarditis,
if identifi ed and treatable.
Hospitalization is not always necessary, and
patients may potentially be managed as outpatients
in unequivocal and uncomplicated cases. Follow-up
care should be assured in these cases to monitor reso-
lution, and to check for the development of complica-
tions. Recurrence of the disease is common, and may
occur in up to 30% of patients.
convex (dome-shaped) than concave, localized rather
than diffuse, and T wave inversions may occur at
nearly the same time, unlike those associated with
acute pericarditis. PR-segment depression is also not
seen with ischemia. In addition, the evolution of elec-
trocardiographic fi ndings occurs over a much shorter
time frame with an ischemic infarction (hours to days),
than with acute pericarditis (days to weeks). Studies
also suggest that an ST-segment elevation-to-T wave
apex (ST/T ratio) of greater than 0.25, particularly in
lead V6, is more suggestive of acute pericarditis.
2,6,13
On laboratory testing, the cardiac enzymes, includ-
ing troponin and CK-MB, are often elevated in acute
pericarditis, and are thought to result from epicardial
infl ammation rather than myocyte necrosis.
7
The level
of troponin elevation correlates with the magnitude
of ST-segment elevation and usually resolves after 1–2
weeks, but prolonged elevations may indicate a sig-
nifi cant myocarditis. Troponin elevations seen with
acute pericarditis do not necessarily portend a poor
outcome from the disease.
14,15
Other serologic tests including markers of acute
infl ammation, such as CBC, CRP, and ESR, are often
elevated in the setting of acute pericarditis, but the
clinical utility of these fi ndings remains unclear.
7
In
general, additional laboratory tests should be guided
by clinical presentation and possible etiologies, and
may include other, more specifi c, tests, such as HIV
serologies and various autoimmune disease markers.
Imaging should begin with a chest radiograph.
While frequently normal, the radiograph may reveal
an enlarged cardiac silhouette as a result of a large
pericardial effusion, with greater than 250 mL of
accumulated fl uid in the sac.
Transthoracic echocardiography has been recom-
mended in the evaluation of patients with pericardial
disease, and in particular, to fi nd the complications
associated with acute pericarditis.
16
Echocardiography
is useful for detecting the presence of a pericardial effu-
sion, including small fl uid collections, and also provides
information on cardiac function, which may aid in the
diagnosis of constrictive pericarditis. Newer modalities,
including doppler imaging and intracardiac echo, may
increase its use in the future. However, in straightfor-
ward unequivocal cases of acute pericarditis with no
evidence of complications and no poor prognostic indi-
cators, emergent echocardiography may be unnecessary.
7
MRI, CT and radionuclide scanning have been shown
to provide excellent visualization of the pericardial sac,