Download 60 - Pericarditis, Pericardial Tamponade, and Myocarditis

60 Pericarditis, Pericardial
Tamponade, and
Myocarditis
Amal Mattu and Joseph P. Martinez
KEY POINTS
• The classic symptom of acute pericarditis is sharp,
pleuritic retrosternal chest pain that radiates to one or
both trapezius ridges and changes with body position.
• The hallmark electrocardiographic findings in patients
with pericarditis include diffuse ST-segment elevation
with PR-segment depression in the same leads.
• High-dose aspirin or a nonsteroidal antiinflammatory
drug with the addition of colchicine is effective
treatment of most cases of acute pericarditis.
• Steroids should be avoided in the early treatment of
first-time pericarditis because their use may actually
increase the chance of recurrence.
• Large pericardial effusions often cause severe
tachypnea and dyspnea; however, oxygen saturation
levels are usually normal.
• Jugular venous distention is typical in patients with
pericardial tamponade, but it may be absent in those
with hypovolemia or if the tamponade developed
rapidly.
• The hallmark echocardiographic finding in patients with
pericardial tamponade is the presence of a large
effusion with diastolic collapse of the right heart
chambers.
• The classic manifestation of acute myocarditis includes
low-grade fever, tachypnea, and tachycardia out of
proportion to the fever.
EPIDEMIOLOGY
Although the greatest concern in patients with chest pain is
usually vascular causes of chest pain—acute coronary syndrome, pulmonary embolism, and aortic dissection—other
less common, but potentially deadly illnesses must be con­
sidered, including pericarditis, pericardial tamponade, and
myocarditis.
Acute pericarditis is often subclinical, so its incidence is
uncertain. However, rough estimates range from 2% to 6%,1
and this disorder may be responsible for as many as 1 in every
1000 hospital admissions.2 Although acute pericarditis is not
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usually deadly, it can be painfully disabling if not treated
appropriately.
Pericardial tamponade is a potentially deadly result of pericardial effusion. Such an effusion can develop from pericardial inflammation or cardiac trauma. Unfortunately, the early
features of tamponade can mimic those of other diseases and
lead to initial misdiagnosis.
Acute myocarditis is relatively uncommon, but it is a devastating condition that can occur and progress quickly, with
little warning. The initial findings can vary from mild, viraltype symptoms to fulminant cardiogenic shock.
PERICARDITIS
PATHOPHYSIOLOGY
The pericardium is the layer of tissue surrounding the heart. It
consists of two layers, a serous inner layer (visceral pericardium) and a fibrocollagenous outer layer (parietal pericardium). The pericardium completely encloses the ventricles and
the right atrium; a portion of the left atrium remains outside the
sac. A thin layer of plasma fluid (usually 15 to 30 mL) separates
the visceral and parietal pericardial layers and acts as a lubricant. The main function of the pericardium appears to be provision of ligamentous stability to withstand forces against the
heart. It also provides some shielding for the heart. Despite
these apparent functions, however, the majority of patients who
undergo pericardiectomy do not appear to suffer any decrease
in cardiac performance or other ill effects.
Pericarditis refers to inflammation of the layers of the pericardium. It has many possible causes (Box 60.1), but in most
cases the cause is unknown. In the majority of these idiopathic
cases the presumed cause is viral, although most attempts to
prove a viral cause have low yield. The most common viral
cause is coxsackievirus B. The most common cause of pericarditis worldwide is tuberculosis.3
PRESENTING SIGNS AND SYMPTOMS
CLASSIC
Chest pain is the typical complaint of patients with acute
pericarditis. Classically, the chest pain is sharp, retrosternal,
and pleuritic, and it radiates to one or both trapezius ridges
CHAPTER 60
Pericarditis, Pericardial Tamponade, and Myocarditis
BOX 60.1 Causes of Pericarditis
Viral infections
• Coxsackievirus B (most common)
• Coxsackievirus A
• Echovirus
• Human immunodeficiency virus
• Influenza virus
• Epstein-Barr virus
• Adenovirus
• Varicella virus
Bacterial infections
• Staphylococcus
• Pneumococcus
• Mycoplasma
• Streptococcus
• Meningococcus
• Tuberculosis
• Salmonella
• Haemophilus
• Rickettsia
Parasitic infections
• Toxoplasmosis
• Amebiasis
Fungal infections
• Histoplasma
• Aspergillus
• Blastomyces
because the phrenic nerve, which traverses the pericardium,
innervates these muscles.4 Typically, the pain also changes
with body position: it improves when the patient sits up and
leans forward and worsens when the patient lies supine.
The physical examination of patients with acute pericarditis
is usually nondiagnostic. Although some researchers report
the presence of a friction rub in up to 85% of patients at some
point in the course of the disease,5 the presence of a friction
rub at the time of initial evaluation is unreliable. When a friction rub is present, it is best heard at the left sternal border at
end-expiration with the patient leaning forward. The rub is
usually described as consisting of three components that correspond to atrial systole, ventricular systole, and rapid diastolic filling. A friction rub is thought to be caused by rubbing
of the inflamed layers of the pericardium against each other.
TYPICAL VARIATIONS
The typical findings in patients with acute pericarditis may
not always be present. Although chest pain is the most common
symptom, patients sometimes have dyspnea as the primary
complaint. When chest pain is present, it is not always
positional or pleuritic, and it may not always radiate to the
trapezius ridge. Patients may also complain of cough,
upper respiratory symptoms, nausea, or vomiting, which may
mislead the physician to an alternative diagnosis. Patients
with bacterial infections are likely to have complaints of fever,
and patients with tuberculous pericarditis are likely to report
a chronic cough, weight loss, and night sweats.
Although the presence of a triphasic friction rub is classic,
it actually occurs in only half of patients with pericarditis.6
The physical findings may also be notable for hypotension and
Connective tissue diseases
• Systemic lupus erythematosus
• Rheumatoid arthritis
• Sarcoidosis
• Amyloidosis
• Scleroderma
After myocardial infarction (MI)
• Early post-MI pericarditis
• Delayed (4 to 6 weeks) pericarditis (Dressler syndrome)
Malignancies
• Primary: mesothelioma, angiosarcoma
• Metastatic (more common): breast, lung, melanoma, lymphoma, leukemia
Radiation therapy
Thoracic aortic dissection
Medications
• Hydralazine
• Procainamide
• Methyldopa
• Penicillin
• Cromolyn sodium
• Dantrolene
• Methysergide
• Anticoagulants (heparin, warfarin)
Cardiac trauma
Cardiac surgery
jugular venous distention in the presence of pericardial tamponade (discussed later).
DIFFERENTIAL DIAGNOSIS AND MEDICAL
DECISION MAKING
A thorough differential diagnosis of a patient with chest pain
is described in Chapter 54. However, the most important
initial consideration should always be the deadly causes of
chest pain: pericarditis, acute coronary ischemia or infarction,
thoracic aortic dissection, and pulmonary embolism. Table
60.1 lists some historical and physical examination features
that are helpful in distinguishing among these conditions.
Distinction among these causes of chest pain is critical in
terms of treatment; patients with pulmonary embolism or
myocardial infarction often require treatment with anticoagulants and thrombolytics, medications that can be deadly in
patients with acute pericarditis or aortic dissection.
The diagnosis of acute pericarditis is based primarily on the
clinical findings. In many cases an electrocardiogram (ECG)
is helpful in confirming the diagnosis. Sound knowledge of
the ECG findings in patients with acute pericarditis is critical,
as well as some findings that help in diagnosing pericarditis
versus myocardial infarction (see Table 60.1). Classically,
pericarditis evolves through four ECG stages as described in
Table 60.2. The first stage of acute pericarditis, characterized
by diffuse ST-segment elevation and PR-segment depression
or downsloping (Fig. 60.1), is the most common stage encountered in the emergency department (ED). The ST segments
should be concave upward; a convex upward (“tombstone”)
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SECTION VI
CARDIAC DISORDERS
V
Table
60.1 Differential Diagnosis of Acute Pericarditis
ACUTE PERICARDITIS
ACUTE
MYOCARDIAL
ISCHEMIA OR
INFARCTION
AORTIC
DISSECTION
Chest pain
description
Sharp, pleuritic,
positional
Pressure, squeezing,
tightness
Sharp, maximal
intensity at onset
Sharp, pleuritic, abrupt onset
Chest pain radiation
Trapezius ridge
Usually to the left arm,
jaw, neck, or
shoulder; may also
radiate to the right
side
Straight to
midscapular area of the back
Not typical
Response to
nitroglycerin
Not typical
Improves
Not typical
Not typical
Vital signs
Tachycardia and fever
common
Fever not typical; blood
pressure and heart
rate are variable
Hypertension
common
Occasionally low-grade fever,
tachycardia and hypoxia
common
Other physical
examination
findings
Friction rub common
during course, though
less common on initial
evaluation
Fourth heart sound is
“classic” in cases of
cardiac ischemia;
third heart sound if
heart failure present
Occasional pulse
deficits
Occasional leg swelling or
tenderness if embolus
originated in the legs
Electrocardiographic
findings
(See Table 60.2) Early:
diffuse ST-segment
elevation and
PR-segment
depression
Absence of reciprocal
ST-segment
depression
Sinus tachycardia
common; bradycardia
and atrioventricular
(AV) blocks uncommon
ST-segment elevation
or depression typically in an anatomic distribution
corresponding to the involved coronary vessel
Tachycardia or
bradycardia and AV
blocks not
uncommon
Left ventricular
hypertrophy if
chronic
hypertension
present
Variable ST-segment
or T-wave changes
Sinus tachycardia
common
Sinus tachycardia common;
bradycardia and AV blocks
uncommon
Large emboli often associated
with T-wave inversions, most
commonly in right precordial
leads and less commonly in
inferior leads
ST-segment elevation possible
but uncommon
Chest radiography
findings
Usually normal;
cardiomegaly if large
pericardial effusion
present
Cardiomegaly if chronic
left ventricular
hypertrophy present;
evidence of heart
failure may be
present
Cardiomegaly
common if chronic
left ventricular
hypertrophy
present; wide
mediastinum
common
Usually normal; most common
abnormalities are elevated
hemidiaphragm, atelectasis,
small pleural effusion
Cardiac biomarkers
Levels usually normal;
mild elevations not
uncommon
Elevations typical in
myocardial infarction
Levels normal
Large emboli occasionally
associated with mild
elevations in troponin or brain
natriuretic peptide
Table 60.2 Electrocardiographic Stages of Acute
Pericarditis
Stage I
Diffuse ST-segment elevation and PR-segment
depression (except in leads V1 and aVR)
Stage II
Resolution of the ST-segment and PR-segment
changes
T-wave flattening in the same leads
Stage III
T-wave inversions in the same leads
Stage IV
Normalization of electrographic abnormalities
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PULMONARY EMBOLISM
morphology virtually excludes the diagnosis of pericarditis
and rules in acute myocardial infarction. ST-segment depression may be present in leads aVR and V1 in a patient with
pericarditis but is unlikely to be present in any of the other 10
leads. In fact, the presence of ST-segment depression in any
of the other 10 leads should be considered the “reciprocal”
changes of acute myocardial infarction.
These four stages generally progress over the course of days
to weeks. The ECG changes in the second and third stages
usually occur in the same leads in which abnormalities in the
initial stage occurred.
Although the abnormalities noted on an ECG are typically
described as “classic” for acute pericarditis, physicians should
CHAPTER 60
Pericarditis, Pericardial Tamponade, and Myocarditis
I
II
V1
V2
III
V3
aVR
V4
aVL
V5
aVF
V6
Fig. 60.1 Acute pericarditis. The electrocardiogram demonstrates diffuse ST-segment elevation with PR-segment depression in multiple
leads.
be aware that these findings are typical only for acute viral
pericarditis. Other forms of pericarditis less commonly cause
PR-segment depression and occasionally cause less pronounced ST-segment elevation. In these cases, the diagnosis
must be based purely on the clinical rather than the ECG
findings.
Laboratory studies are rarely helpful in the diagnosis of
acute pericarditis. Patients may have an elevated white blood
cell count because of pain or infection (or both). Other serum
markers of inflammation, including the erythrocyte sedimentation rate and C-reactive protein value, are often elevated, but
such elevations are nonspecific. Cardiac biomarkers may be
minimally elevated but should not demonstrate the rise and
fall typical of myocardial infarction. Chest radiography is also
rarely helpful in the diagnosis of acute pericarditis; it is used
mainly to evaluate for alternative causes of chest pain (e.g.,
pneumonia, aortic dissection).
Echocardiography can be useful in distinguishing between
acute pericarditis and acute myocardial infarction. Echocardiograms in patients with pericarditis lack the focal wall
motion abnormalities that are typical of echocardiograms in
those with myocardial infarction. Echocardiography is also
useful to look for evidence of pericardial effusion, a potential
complication of acute pericarditis (see later). If a large pericardial effusion is present, pericardiocentesis (ultrasonographically guided in a stable patient) can be performed to
obtain fluid for testing for infections and cytologic analysis.
are effectively treated with high-dose aspirin (2 to 4 g daily)
or nonsteroidal antiinflammatory drugs (NSAIDs). Ibuprofen
is effective in most cases and has fewer side effects than other
NSAIDs; the pain usually improves significantly within days
with ibuprofen therapy. If the patient’s symptoms persist, an
alternative NSAID is indicated. Indomethacin is often used
for severe cases because of its stronger antiinflammatory
effect, although it should be avoided in patients with a history
of ischemic heart disease because it may decrease coronary
blood flow.4,7 Evidence now suggests that addition of colchicine (1.0 to 2.0 mg for the first day and then 0.5 to 1.0 mg/
day for 3 months) to the standard regimen is effective in hastening the resolution of acute symptoms and also preventing
recurrence rates, regardless of the cause of the pericarditis.8
Colchicine is also effective in cases of recurrent pericarditis.9,10 The use of corticosteroids is generally reserved for
recurrent cases of pericarditis that are unresponsive to aspirin
or NSAIDs plus colchicine. Initiation of steroids early in the
course of first-time pericarditis may actually be an independent risk factor for recurrence.8
Patients with bacterial or other nonviral infectious causes
of pericarditis should be treated aggressively with antimicrobial therapy. Large infected pericardial effusions require
drainage as well. Management of neoplastic causes of pericarditis should be targeted at treating the underlying malignancy. Patients with uremic pericarditis require urgent
hemodialysis.
TREATMENT
FOLLOW-UP AND NEXT STEPS IN CARE
Treatment of patients with acute pericarditis should be targeted at the underlying cause. The majority of patients with
viral, rheumatologic, posttraumatic, or idiopathic pericarditis
The majority of patients with acute pericarditis can be treated
as outpatients, with the symptoms generally resolving within
2 weeks. Outpatient management is suitable for patients with
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SECTION VI
CARDIAC DISORDERS
mild symptoms, hemodynamic stability, and ability to tolerate
oral medications. Reasonable indications for admission
include fever or suspicion of a bacterial cause of the pericarditis, immunosuppression, pericarditis associated with trauma,
presence of a moderate to large pericardial effusion, and
hemodynamic instability. A history of active anticoagulant
use is generally considered a poor prognostic factor and warrants hospital admission as well.4
PERICARDIAL TAMPONADE
PATHOPHYSIOLOGY
Trauma or inflammation of the pericardium can cause fluid to
accumulate within the intrapericardial space. Normally, the
pericardium is capable of stretching and accommodating 2 L
of fluid or more when the fluid accumulates very slowly.11
However, if the fluid accumulates more rapidly than can be
accommodated by the distensibility of the pericardium, especially in the case of trauma, in the presence of fibrotic pericardium, or if the volume of pericardial fluid is excessive,
significant intrapericardial pressure results and can produce
pericardial tamponade.
Pericardial tamponade develops when intrapericardial fluid
produces sufficient pressure to compress the cardiac chambers. Compression of the chambers impairs ventricular
diastolic filling and stroke volume. Initial compensatory
mechanisms, especially tachycardia, may temporarily sustain
cardiac output. However, as pericardial fluid continues to
increase, the compensatory mechanisms begin to fail, and
diminished cardiac output, hypotension, and full cardiovascular collapse ensue.
The typical causes of pericardial tamponade include any
disorder that results in acute or chronic pericardial inflammation, as well as conditions in which a patient sustains penetrating trauma to the heart or cardiac surgery. The conditions
previously noted to cause pericarditis are common precipitants of pericardial tamponade. The composition of the intrapericardial effusion varies according to the precipitating
cause; in bacterial pericarditis, for example, the effusion is
often pus, and in cardiac trauma or cardiac surgery, it is often
blood and clots. Regardless of the composition of the effusion,
the physiology that leads to pericardial tamponade and the
immediate treatment are similar.
PRESENTING SIGNS AND SYMPTOMS
CLASSIC
The typical symptoms associated with a large pericardial effusion are nonspecific. Malaise, generalized weakness, ascites,
and edema are common in patients with subacute or chronic
effusions as a result of poor cardiac function.12 Many other
symptoms are related to compression of adjacent mediastinal
structures by the effusion. Dyspnea and cough are common
and may be due to displacement or compression of bronchial
structures or lung tissue by the effusion. Dyspnea on exertion
is common as well and results from impairment of venous
return and cardiac output. Patients often report a sense of
dysphagia, which is due to esophageal compression. Hiccups
518
may occur as a result of esophageal compression and involvement of the phrenic and vagus nerves. Hoarseness may result
from compression of the recurrent laryngeal nerve.12
Physical findings are also often nonspecific. Tachycardia
and tachypnea are common. Despite the presence of tachypnea and dyspnea, however, oxygen saturation levels are
usually normal because the effusion itself does not impair
alveolar air exchange. Lung sounds are generally normal as
well. Findings of hypoxia or focal abnormalities on lung
examination should suggest a superimposed pulmonary condition or an alternative diagnosis. Fever is common if the
underlying cause is infectious. Pericardial friction rubs are
reportedly common if the underlying cause is inflammatory,13
although diminished heart sounds are also frequent because
of reduced cardiac function and attenuation of their transmission by the effusion.
When a pericardial effusion produces pericardial tamponade, additional findings are notable. Decreased cardiac function produces hypotension and shock. Jugular venous
distention is typically present because of impaired venous
return. Pulsus paradoxus (drop in systolic blood pressure of
greater than 10 mm Hg during normal inspiration) is also
typical, although its presence has limited specificity for pericardial tamponade. Several other conditions that are associated with hypotension or dyspnea (or both) can also produce
pulsus paradoxus, including massive pulmonary embolism,
hemorrhagic shock, and obstructive lung disease.12 Death is
usually preceded by pulseless electrical activity.14
TYPICAL VARIATIONS
Although the symptoms and physical findings already noted
are common, certain conditions may produce unexpected
findings in the presence of pericardial tamponade. Patients
who have severe hypothyroidism or uremia or who take atrioventricular nodal blocking agents (e.g., calcium channel
blockers, beta-blockers, digoxin) may have a relative bradycardia. Jugular venous distention is typical in pericardial tamponade as well, but it is often absent in patients who are
hypovolemic or in whom the pericardial tamponade developed
very quickly (e.g., after cardiac trauma). Overt hypotension
may be absent as well in patients with a history of severe
antecedent hypertension.12,15
DIFFERENTIAL DIAGNOSIS AND MEDICAL
DECISION MAKING
A complete differential diagnosis of hypotension and shock
is beyond the scope of this chapter. However, the emergency
physician (EP) should always consider other typical causes of
hypotension, especially those that similarly produce jugular
venous distension: massive pulmonary embolism, large left
ventricular myocardial infarction with cardiogenic shock,
right ventricular myocardial infarction, acute aortic or mitral
valve insufficiency, and superior vena cava syndrome.
The primary means of diagnosing pericardial tamponade
is via two-dimensional echocardiography. A pericardial
effusion is easily seen in most patients on subcostal or
parasternal views (Fig. 60.2). An echo-free space should be
visible throughout the cardiac cycle when the pericardial
effusion is at least 25 mL.3 The presence of a pericardial effusion in combination with hypotension and echocardiographic
CHAPTER 60
Pericarditis, Pericardial Tamponade, and Myocarditis
Fig. 60.2 Large pericardial effusion. The ultrasonogram is a
subcostal four-chamber view of the heart that demonstrates a large
pericardial effusion (arrow). The patient also had dynamic changes
consistent with pericardial tamponade—right atrial and right
ventricular diastolic collapse. (Courtesy Dr. Brian Euerle, Director of
Emergency Ultrasound, Emergency Medicine Residency, University
of Maryland School of Medicine.)
evidence of early diastolic right ventricular collapse and
late diastolic right atrial collapse is diagnostic of pericardial
tamponade. In approximately 25% of cases, the left atrium
also demonstrates collapse, a very specific sign of tamponade.
The left ventricle rarely demonstrates collapse except in
specific conditions such as localized postoperative tamponade.12 Other echocardiographic findings that may be found
in patients with pericardial tamponade are a dilated inferior
vena cava without inspiratory collapse and beat-to-beat swinging of the heart within the pericardial fluid (when the effusion
is large).3
Other imaging studies can be helpful in evaluating these
patients as well. Computed tomography (CT) and magnetic
resonance imaging are very accurate in detecting pericardial
effusions, in addition to diagnosing alternative conditions.
However, they should not be used in patients with borderline
or overt hemodynamic instability because of the need to
remove such patients from the ED for the procedures. Chest
radiography is primarily used to evaluate the patient for alternative diagnoses as well, such as pneumonia or pulmonary
edema. In patients with a large pericardial effusion, cardiomegaly is a nearly universal finding (Fig. 60.3). The chest
radiograph is particularly helpful in this setting if previous
radiographs are available that demonstrate a normal-sized
heart. Previous radiographs that show the massive cardiomegaly to be new are highly suggestive of a large pericardial
effusion.
The ECG can be helpful in the diagnosis of large pericardial
effusions. The most common abnormality is tachycardia,
especially in the presence of tamponade. Low voltage is
common as well and is caused by attenuation of the electrical
impulse as it passes through the effusion before reaching
the ECG electrodes. Although low voltage is nonspecific, the
presence of new low voltage (in comparison with previous
ECGs) is much more specific for large pericardial effusions.
Fig. 60.3 Large pericardial effusion. The chest radiograph
demonstrates massive cardiomegaly, a nearly universal finding in
patients with large pericardial effusions.
The third “classic” ECG abnormality is electrical alternans.
Electrical alternans refers to beat-to-beat variation in amplitudes of the ECG complexes (Fig. 60.4) and is attributed to
“swinging” of the heart back and forth within the pericardial
fluid. Electrical alternans is present in less than one third of
cases of pericardial tamponade. Although none of these three
findings individually is completely diagnostic of large pericardial effusions, the combination of all three is very highly
specific.
TREATMENT
Initial management of patients with pericardial tamponade
should focus on the typical ABCs of resuscitation (airway,
breathing, circulation). Certain caveats should be made,
however. Although the primary pathophysiologic abnormality
underlying hemodynamic compromise in patients with pericardial tamponade is ventricular filling, the benefit of volume
infusion to improve filling is controversial. Animal studies
have shown variable results with respect to the hemodynamic
benefit of volume infusion,12,16 which may improve systemic
perfusion only in patients with hypovolemia. Strong supporting data in humans are lacking, however. In patients with
traumatic pericardial tamponade, large-volume infusions may
actually precipitate further deterioration.17 Strong evidence
supporting specific inotropic agents is lacking as well,
although theoretically agents that reduce the elevated vascular
resistance,12 such as dobutamine and milrinone, would seem
ideal. Mechanical ventilation should generally be avoided
except in patients with respiratory failure; the positive airway
pressure associated with mechanical ventilation decreases
venous return and cardiac output.
Treatment of pericardial tamponade is drainage of the
intrapericardial fluid (pericardiocentesis). Drainage is best
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SECTION VI
CARDIAC DISORDERS
I
aVR
II
aVL
III
aVF
V1
V2
V3
V4
V5
V6
II
Fig. 60.4 Large pericardial effusion. The electrocardiogram demonstrates the three classic findings in a patient with a large pericardial
effusion: sinus tachycardia, low voltage, and electrical alternans.
performed via needle aspiration under echocardiographic, CT,
or fluoroscopic guidance. In patients who exhibit rapid cardiac
decompensation or are in cardiac arrest, the EP should perform
emergency pericardiocentesis without waiting for imaging
guidance. The procedure is performed with a 16- or 18-gauge
needle, most commonly inserted into the left paraxiphoid area
of the chest. The needle is pointed downward at an approximately 30-degree angle to the chest to bypass the left costal
margin and is aimed toward the left shoulder. The needle
should be inserted and advanced slowly until the pericardium
is penetrated and fluid is aspirated. Use of a sheathed needle
can facilitate the process—once the pericardium has been
penetrated, the core of the needle can be removed with the
sheath left in the pericardial space to assist in further removal
of fluid.12 Some researchers have advocated attaching ECG
leads to the hub of the needle so that when the pericardium is
penetrated, an injury pattern (i.e., ST-segment elevation) will
be noted.18 However, a recent review recommends against this
practice because of the likelihood of misleading results.12
In patients with acute cardiac decompensation, aspiration
of even 10 to 20 mL of blood should be sufficient to produce
some hemodynamic improvement. However, once full cardiac
arrest has occurred, pericardiocentesis has a limited success
rate. Potential complications of pericardiocentesis include
puncture or laceration of the cardiac chambers, injury to coronary vessels, pneumothorax, ventricular dysrhythmias, pneumopericardium, and delayed infection.19 These complications
are more common in the setting of emergency pericardio­
centesis, which is sometimes performed without imaging
guidance.
Because pericardiocentesis is less likely to be successful in
patients with clotted hemopericardium, surgical drainage will
be necessary. Surgical drainage is also required in patients in
whom intrapericardial bleeding is present (e.g., postoperative
pericardial tamponade, traumatic pericardial tamponade, pericardial tamponade with aortic dissection). In these patients,
pericardiocentesis is temporizing at best; in conjunction with
520
surgical drainage, definitive repair of the bleeding sites is
essential. Additional therapy should focus on treating the
underlying cause of the pericardial inflammation that led to
pericardial tamponade.
FOLLOW-UP AND NEXT STEPS IN CARE
Patients with pericardial tamponade should be admitted to an
intensive care setting for definitive therapy and close hemodynamic monitoring. If surgical therapy is indicated, emergency surgical consultation is mandatory. When surgical
therapy is not planned, cardiology consultation is most
appropriate for the performance of pericardiocentesis under
echocardiographic guidance. Nephrology consultation is also
appropriate for urgent hemodialysis in patients with uremia.
MYOCARDITIS
PATHOPHYSIOLOGY
Myocarditis is an inflammatory condition that causes myocardial damage, usually because of infectious, immunologic,
or toxin-mediated conditions (Box 60.2). Myocarditis can
be manifested as mild constitutional symptoms, moderate
cardiopulmonary symptoms, or fulminant cardiopulmonary
decompensation leading to death. In the majority of adult
cases, the myocardial damage is believed to be caused by
autoimmune processes that are often triggered by viral or
other infections,20 whereas in neonates and infants, injury to
myocytes is believed to occur more often because of direct
injury by the pathogen itself.21
Approximately 10% of postmortem examinations demonstrate some degree of histologic evidence of myocarditis.
However, most of the patients were not clinically symptomatic
CHAPTER 60
Pericarditis, Pericardial Tamponade, and Myocarditis
BOX 60.2 Causes of Myocarditis
Viral infections (most common)
• Coxsackievirus (most common virus)
• Echovirus
• Human immunodeficiency virus
• Influenza virus
• Parainfluenza virus
• Epstein-Barr virus
• Adenovirus
• Varicella virus
• Cytomegalovirus
• Herpesvirus
• Rabies virus
• Poliovirus
• Hepatitis A, B, C, or D virus
• Rubella virus
• Mumps virus
• Rubeola virus
Bacterial infections
• Staphylococcus
• Borrelia (Lyme disease)
• Legionella
• Corynebacterium diphtheriae
• Tuberculosis
• Mycoplasma
• Streptococcus
• Meningococcus
• Chlamydia (pneumoniae and psittaci)
• Enterococcus
Parasitic infections
• Toxoplasmosis
• Trypanosomiasis
before death.22 Conversely, in patients in whom myocarditis
is diagnosed clinically, only one third have histologic findings
consistent with the disease. Even in cases that progress to
dilated cardiomyopathy, only 40% of patients have microscopic evidence of myocarditis. Consequently, the actual incidence of myocarditis is unknown.23
PRESENTING SIGNS AND SYMPTOMS
CLASSIC
The clinical manifestations of myocarditis usually begin days
to weeks after the acute infection, especially when viruses are
implicated as the cause. However, only 50% of patients report
a recent upper respiratory or gastrointestinal viral type of
infection.23 The initial symptoms are nonspecific and constitutional in nature: low fever, fatigue, malaise, myalgia, and
arthralgia. These mild symptoms are often the reason for
initial misdiagnosis or delays in proper diagnosis of this condition. Cardiopulmonary symptoms, especially mild dyspnea
and chest pain, are common as well. The chest pain can be
pleuritic, sharp, and positional, much like pericarditis, or substernal and squeezing, much like typical ischemic pain.
Patients with congestive heart failure may report more
• Trichinosis
• Echinococcosis
• Chagas disease
Medications/toxins
• Methyldopa
• Penicillin
• Hydrochlorothiazide
• Sulfamethoxazole
• Lithium
• Doxorubicin
• Cyclophosphamides
• Zidovudine
• Acetaminophen
• Lead
• Arsenic
• Carbon monoxide
• Cocaine
• Ethanol
• Interleukin-2
• Anabolic steroids
• Radiation therapy
Connective tissue diseases
• Systemic lupus erythematosus
• Rheumatoid arthritis
• Dermatomyositis
• Sarcoidosis
Miscellaneous
• Giant cell arteritis
• Kawasaki disease
• Cardiac transplant rejection
• Peripartum state
significant dyspnea, as well as cough, orthopnea, paroxysmal
nocturnal dyspnea, and edema. Less commonly, patients may
initially be seen after a syncopal episode, usually the result of
a bradydysrhythmia.
The physical findings are often notable for low-grade fever,
tachypnea, and tachycardia. Classically, the patient has “tachycardia out of proportion to the fever”—extreme tachycardia
without obvious hypovolemia or high fever (Fig. 60.5).
Patients may also experience bradycardia if a high-grade
atrioventricular block develops (Fig. 60.6). Evidence of congestive heart failure is frequently present as well: jugular
venous distention, bibasilar rales on lung examination, a third
heart sound (S3) on cardiac examination, and peripheral
edema. Patients with advanced or fulminant myocarditis may
arrive at the ED in full cardiogenic shock.
TYPICAL VARIATIONS
Pediatric patients tend to have early, nonspecific symptoms,
including fever, viral upper respiratory symptoms, and poor
feeding. In more severe cases, the infant or neonate may
exhibit severe tachycardia, tachypnea, sweating while feeding,
respiratory distress, and cyanosis or other signs of poor perfusion. Tachydysrhythmias and bradydysrhythmias, especially
those involving a high-grade atrioventricular block, are
521
SECTION VI
CARDIAC DISORDERS
I
II
III
aVR
V1
V4
aVL
V2
V5
aVF
V3
V6
II
Fig. 60.5 Sinus tachycardia (rate of 150 beats/min) in a patient with myocarditis.
aVR
V1
V4
aVL
V2
V5
aVF
V3
V6
Fig. 60.6 Sinus rhythm with atrioventricular (AV) dissociation and a high-grade AV block in a patient with myocarditis.
common as well. Severe myocarditis in the very young is often
also manifested as pulmonary edema, cardiogenic shock, and
multiorgan hypoperfusion.
DIFFERENTIAL DIAGNOSIS AND MEDICAL
DECISION MAKING
The differential diagnosis of myocarditis is extremely broad
because of the nonspecific nature of the initial findings.
522
Patients who are initially seen with cardiopulmonary symptoms have a slightly more limited differential diagnosis, but
initial consideration should as always be focused on the most
deadly diseases that produce chest pain or dyspnea: acute
coronary syndrome, aortic dissection, pulmonary embolism,
acute pericarditis or pericardial tamponade, esophageal
rupture, cardiogenic pulmonary edema, and pneumonia.
The initial diagnostic evaluation should be prompted by
clinical suspicion. The finding of cardiopulmonary complaints, unexplained tachycardia, or evidence of congestive
CHAPTER 60
Pericarditis, Pericardial Tamponade, and Myocarditis
heart failure on examination in young patients should prompt
consideration of myocarditis. An ECG and chest radiograph
are appropriate initial tests in these patients. Despite the
absence of a specific or single diagnostic ECG abnormality,
the majority of patients with myocarditis have at least some
abnormality noted on the ECG. The most common abnormalities are sinus tachycardia (see Fig. 60.5) and nonspecific
ST-segment or T-wave changes. Other abnormalities that
may occur in patients with myocarditis are conduction abnormalities (new fascicular blocks, new bundle branch blocks,
and atrioventricular blocks), atrial or ventricular tachydysrhythmias and bradydysrhythmias, overt ischemic changes
(T-wave inversions, ST-segment changes), and Q-wave formation. The ischemic changes are often indistinguishable
from those seen with true cardiac ischemia or myocardial
infarction. If the pericardium is also involved (myopericarditis), PR-segment depression with concurrent ST-segment
elevation may be found. If a pericardial effusion develops, low
voltage may occur. The ECG findings are rarely completely
normal.
Findings on plain chest radiographs are often frequently in
mild or early cases of myocarditis. However, most patients
with cardiopulmonary complaints have some radiographic
signs of congestive heart failure: cardiomegaly, pulmonary
vascular redistribution, interstitial edema, and frank pulmonary edema. Pleural effusions may be present as well.
Laboratory studies typically ordered in the ED include
evaluation of markers of inflammation and cardiac biomarkers. Inflammatory markers, such as the white blood cell count,
erythrocyte sedimentation rate, and C-reactive protein value,
are expected to be elevated, but unfortunately, such elevations
are nonspecific. Measurements of markers are sometimes
used to monitor the course of the disease after the diagnosis
is made. Cardiac biomarkers, including troponin and creatinine phosphokinase values, are also sometimes elevated. The
initial elevations in cardiac biomarkers are frequently indistinguishable from those expected with acute myocardial
infarction. Serial measurements of cardiac biomarkers can
be helpful, however, because the levels do not tend to rise
and fall as quickly with myocarditis as with myocardial
infarction.
Echocardiography may also be helpful in the ED, especially
when there is confusion in distinguishing between myocarditis
and acute coronary syndrome. Echocardiography in patients
with acute coronary syndrome (with active ischemia) usually
demonstrates focal wall hypokinesis. Patients with myocarditis can also have focal hypokinesis, but they are more likely
to have diffuse hypokinesis and multichamber dilation as
well.23 In addition, the echocardiogram can demonstrate
evidence of complications, such as pericardial effusion or
intracardiac thrombus.
Endomyocardial biopsy is usually considered the “gold
standard” for the diagnosis of myocarditis. Evidence of microscopic myocardial inflammation with various levels of necrosis is generally used to diagnose and categorize stages of
myocarditis.23,24 However, biopsy is not feasible in the ED.
Additionally, recent reports have questioned the sensitivity
and specificity of the test.23,25
Other tests that can be ordered by the EP are viral cultures,
blood cultures, and other immunologic studies. These tests are
rarely helpful in the acute setting but may of use to inpatient
physicians during the hospital course.
TREATMENT
Close attention should be paid to the ABCs of resuscitation
because patients with fulminant myocarditis can decompensate rapidly. The mainstay of treatment of myocarditis is primarily supportive with a focus on hemodynamic support and
management of complications. Congestive heart failure and
hypoxia should be treated as usual, with high-flow oxygen,
preload and afterload reduction, and diuretics. The patient’s
fluid status must also be monitored closely because of the risk
for congestive heart failure. Bradydysrhythmias should be
managed as usual. Patients with high-degree atrioventri­cular
blocks often require pacemaker placement. Tachydysrhythmias should generally be managed as usual, although preference should be given to titratable medications because drugs
with negative inotropic effects can precipitate unpredictable
hemodynamic collapse in these patients with myocarditis,
whose status is tenuous. Intramural thrombi noted on echocardiography should be treated with anticoagulation. The
benefit of prophylactic anticoagulation is uncertain, especially
given the risk that these patients have for hemopericardium.
Additional myocardial workload reduction can be accomplished through fever reduction and correction of anemia.23
Patients in shock should be treated aggressively. Adequate
perfusion should be achieved in hypotensive patients through
the use of vasopressors (e.g., dopamine, norepinephrine) and
positive inotropic agents (e.g., dobutamine). Ventricular assist
devices, intraaortic balloon counterpulsation, and cardiopulmonary bypass have been used successfully in some patients
during the wait for clinical improvement or cardiac
transplantation.23
Antiviral therapy may be helpful during the patient’s hospital course if a viral cause of the myocarditis has been determined. Other therapies should be focused on the determined
underlying condition (e.g., Lyme carditis, toxin-induced myocarditis). Immunosuppressive medications have been used
successfully in some patients in the later stages of illness, but
this experience appears to be anecdotal only.26 The use of
corticosteroids lacks good evidence of benefit as well. Highdose intravenous gamma globulin has been used successfully
in some pediatric patients, with improvement in ventricular
function at 1 year.23
FOLLOW-UP AND NEXT STEPS IN CARE
Patients in whom myocarditis is suspected should be admitted
to the hospital. Cardiac monitoring should be started to assess
for the development of dysrhythmias, and close hemodynamic
monitoring is indicated as well. Critical care, infectious
disease, and cardiology consultants should be involved in the
care plans for these patients. Because patients with severely
decompensated cardiac conditions may require cardiac transplantation, appropriate surgical consultants should also be
involved in the care of patients with severe myocarditis.
REFERENCES
References can be found
www.expertconsult.com.
on
Expert
Consult
@
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CHAPTER 60
Pericarditis, Pericardial Tamponade, and Myocarditis
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