2.

CONTACT HOURS

Recognizing
and managing
different types of carditis
Get a beat on endocarditis, myocarditis, and pericarditis.
By Susan Simmons-Holcomb, RN-CS, ARNP, MN

ENDOCARDITIS
Find out how to identify and intervene if
your patient has this potentially fatal heart
inflammation.

tion include valvular damage (whether congenital or

acquired), presence of a prosthetic valve, and damage to
cardiac structures. Damage to the walls of the endocardium
is particularly attractive to many organisms: Although
Streptococcus viridans adheres directly to an intact endothelium, the other organisms that cause endocarditis
adhere to thrombi that form after injury. Enmeshed in the
platelet-fibrin thrombus, the organisms proliferate and do
their damage. The thrombi can also embolize, causing
infection and infarction elsewhere in the body.

A 12-year-old boy, recently adopted from a foreign country, comes into your clinic for a general physical examination and vaccinations. Hes never had routine health care,
and previous infectious illnesses were treated conservatively. While examining him, you notice a pansystolic murmur
best heard at the apex.
Endocarditis, also known as infective endocarditis,
involves inflammation of the innermost layer of the heart.
(For a refresher on the hearts layers, see Like an onion.)
Structures involved in endocarditis can include the valves,
chordae tendineae, cardiac septum, or the lining of the
chambers. Typically, endocarditis is caused by bacterial
infection with Streptococcus viridans or Staphylococcus
aureus. Other possible infective organisms include Gramnegative bacteria, Enterococcus faecalis, Staphylococcus epidermidis, Streptococcus pneumoniae, Pseudomonas
aeruginosa, Candida albicans, Aspergillus, and viruses such
as coxsackievirus and adenoviruses. Rheumatic fever, a
streptococcal infection, was once a common cause of endocarditis. Thanks to the availability of antibiotics, rheumatic
fever now accounts for only about 30% of cases.
Mortality associated with endocarditis is highabout
25% in the United States. The rate is even higher when the
infection involves a prosthetic heart valve or is complicated
by heart failure, abscess formation, or stroke.
Conditions that make the endocardium ripe for infecCardiac Insider

Recognizing danger
Symptoms of endocarditis, which are nonspecific, include
fever, chills, night sweats, fatigue, anorexia, weight loss,
and pain in the muscles, joints, and back. Be suspicious if
you see petechiae when you examine the palpebral conjunctivae (insides of the eyelids), neck, anterior chest, abdomen, or oral mucosa. Also look for Janeway lesions
(nontender maculae) on the patients palms and soles,
Oslers nodes (tender, erythematous, raised nodules) on the
fingers and toe pads, and splinter hemorrhages under the
fingernails. Fundoscopic examination may reveal oval,
retinal hemorrhages with pale centers known as Roths
spots. Microemboli, vasculitis, and embolism are responsible for all of these findings, which carry the potential for
such serious complications as vision loss, stroke, renal infarction, and splenic infarction. Another ominous sign is
the development of a new cardiac murmur. Further diagnostic testing for endocarditis is indicated for all cases of
new murmur associated with fever.
Diagnosis of endocarditis is based on the Duke criteria,
4

Spring 2006

developed at Duke University in

Like an onion...
1994. These criteria add echocardio. . . the heart has more than one layer.
graphic changes to the previous Beth
Israel criteria: persistent bacteremia
(positive blood cultures, found in
91% of patients), new regurgitant
murmurs, and vascular complicaFibrous
pericardium
tions.
Echocardiographic findings inSerous pericardium
clude definitive evidence of vegeta(Parietal layer)
tion or thrombus on valves or other
endocardiac structures, abscesses, or
Pericardial cavity
disruption of a prosthetic valve.
Serous pericardium
Transthoracic echocardiography
(Visceral layer or epicardium)
(TTE) is highly accurate for identifyMyocardium
ing vegetations, but the accuracy can
be reduced in up to 20% of adults
Endocardium
because of obesity, chronic obstructive pulmonary disease, or chest-wall
deformities. Transesophageal echocar The outer layer, or pericardium, is a fibrous sac that surrounds the heart
diography, if available, may be more
and the roots of the great vessels, the venae cavae, and aorta. The pericardiaccurate than TTE because it excludes
um itself can be divided into two layers: the outer fibrous layer and the inner
the variables previously mentioned
serous layer. The pericardial cavity between the parietal and visceral layers
contains about 50 ml of fluid to minimize friction between the two layers.
and allows closer visualization of
The middle layer of the heart, the myocardium, is the muscle that drives
common sites for vegetations and
cardiac contraction.
other abnormalities. Transesophageal
The endocardium, the innermost layer, is a smooth, thin surface that lines
echocardiography also affords better
the cardiac chambers, valves, and other endocardiac structures.
visualization of prosthetic heart
valves.
Other, less specific criteria include increased erythrocyte
anticoagulant therapy before developing endocarditis,
sedimentation rate, anemia, leukocytosis, and microscopic
however, hell continue on anticoagulation while being
hematuria. Hyperglobulinemia is common. A positive
treated for endocarditis and undergo frequent neurologic
rheumatoid factor and proteinuria may also occur.
monitoring.
Additional lab or diagnostic changes depend upon compliHeart failure related to valvular problems is more comcations affecting other parts of the body, such as the central
mon with aortic valve infections than with infections of the
nervous system, kidneys, and lungs.
mitral or tricuspid valve. Valvular dysfunction can progress
in spite of antibiotic therapy, and the patient may need
Treating endocarditis
valve replacement surgery to prevent decompensated heart
Priorities include supporting cardiac function, eradicating
failure from jeopardizing his life. Valve reinfection, a possithe infection, and preventing complications, such as sysble surgical complication, carries a far lower mortality rate
temic embolization and heart failure. Embolization occurs
than does delaying surgery.
in up to 50% of patients, with emboli traveling to the brain,
Patients at high risk for endocarditis (such as those with
lungs, coronary arteries, spleen, bowel, and extremities. Emprosthetic heart valves) require antibiotic prophylaxis
boli that travel to the brain usually lodge in the middle
before certain invasive procedures, including dental extraccerebral artery and are often fatal. Embolic events are most
tions. Penicillin is the usual prophylactic antibiotic of
common in the first 2 weeks; the risk drops dramatically as
choice; a macrolide antibiotic is an alternative for patients
time goes on, but predicting which patients will develop
sensitive to penicillin. Teach the patient to tell all his health
catastrophic embolic events is nearly impossible.
care providers, including his dentist, about his condition
Despite the risk of embolization, anticoagulation isnt
and the need for prophylactic antibiotics.
recommended for patients with endocarditis because of
Returning to our 12-year-old patient, an echocardiothe risk of intracerebral hemorrhage. If the patient was on
gram shows mitral valve regurgitation, but its not severe
Spring 2006

Cardiac Insider

Inflammation and fibrosis

Myocarditis is triggered by a virus or another underlying
cause (see What can trigger myocarditis?). Leukocytes,
lymphocytes, and macrophages infiltrate the myocardium, leading to inflammation and interstitial fibrosis
in the myocardium. Because inflammation and fibrosis
reduce blood flow, areas of the myocardium may become necrotic. This necrosis may be patchy or global.
Cardiac contractility decreases, leading to a reduction
in cardiac output (CO). If CO falls significantly, the
patient may experience overt left ventricular failure and
die. In less serious cases, the patient is still at risk for
complications or death from dilated cardiomyopathy.
In the United States, most clinically significant cases of
acute myocarditis are caused by the coxsackievirus type B.
The patient may have upper respiratory symptoms such
as fever, chills, and sore throat. Other possible signs and
symptoms include abdominal pain and nausea, vomiting,
diarrhea, arthralgia, and myalgia. These generally occur
up to 6 weeks before the patient has signs and symptoms
of myocarditis, such as chest pain and overt heart failure
with dyspnea. Specific signs and symptoms of myocarditis
depend on the type of infection and the degree of myocardial damage. In children, symptoms of myocarditis are
nonspecific and include fever, respiratory distress, poor
feeding, and cyanosis.

enough to warrant surgery. The health care provider gives

him a medical-alert bracelet to wear identifying the need
for prophylactic antibiotics for various procedures, and his
adoptive family is educated about the need for prophylactic
antibiotics. Hes referred to a pediatric cardiologist, wholl
monitor his condition as he grows up.

MYOCARDITIS
Although usually mild, this inflammation of the
heart muscle can be fatal. Heres how to intervene.
Dave Mannheim, 37, arrives at your emergency department (ED) complaining of shortness of breath and chest
pain. He recently had symptoms of an upper respiratory
infection, including fever and chills. A chest X-ray shows
cardiac enlargement.
An electrocardiogram (ECG) shows nonspecific
ST-segment and T-wave abnormalities and left axis deviation. Your assessment reveals jugular vein distension,
bibasilar crackles, and peripheral edema. The ED physician suspects myocarditis.
A relatively rare disorder, acute myocarditis is an
inflammation of the myocardium, the hearts muscular
layer. If not treated, it can lead to coronary artery
thrombus, coronary ischemia, dilated cardiomyopathy,
cardiac arrhythmias, and sudden death. Difficult to
diagnose, myocarditis should be considered if myocardial infarction (MI) has been ruled out in a patient with
dyspnea and chest discomfort, especially if he has a history of recent viral illness.

Finding clues
The following diagnostic tests can help you determine if a
patient has myocarditis or another condition.
A chest X-ray may show an enlarged heart with evidence
of heart failure, such as prominent blood vessels or fluid
within the lungs.
An ECG may show arrhythmias, as well as ST-segment
and T-wave abnormalities. Decreased QRS amplitude and
transitory Q-wave development suggest myocarditis. You
also may notice a heart block. The ECG usually returns to
normal within 2 months.
Echocardiography is less likely to be as definitive as it is
for diagnosing pericardial effusion. Changes noted on
echocardiography include diffuse hypocontractility and
cardiac chamber hypertrophy. In some cases, echocardiography reveals valvular dysfunction and pericardial effusions.
Endomyocardial biopsy through cardiac catheterization
may be performed to confirm the diagnosis of myocarditis. However, because of the patchy nature of myocarditis,
results are accurate only about 65% of the time.
Lab studies may show an increase in creatine kinase
(CK), an increased erythrocyte sedimentation rate, and an
increase in white blood cells (leukocytosis).

What can trigger myocarditis?

Myocarditis can be idiopathic or triggered by:
viruses, most commonly coxsackievirus type B
and adenoviruses. Other viruses that can cause myocarditis include coxsackievirus type A, echovirus,
influenza, hepatitis, HIV, rubella, mumps, and
cytomegalovirus.
tropical diseases such as Chagas disease, which is
caused by the parasite Trypanosoma cruzi
bacterial infections including Rickettsia, Salmonella typhi, Coxiella burnetii, diphtheria, tuberculosis, streptococci, meningococci, staphylococci, and
Lyme disease
fungal infections
chemicals and drugs, including chemotherapy and
occasionally antibiotics used to treat another infection
autoimmune diseases, such as lupus, rheumatoid
arthritis, ulcerative colitis, and scleroderma.

Cardiac Insider

Spring 2006

Treating myocarditis
Fortunately, most cases of viral myocarditis are mild and
self-limiting. Treatment is supportive, aimed at promptly
recognizing and treating cardiac arrhythmias, preserving
myocardial function, and preventing heart failure and
other complications, such as dilated cardiomyopathy. If
the underlying cause of myocarditis is Lyme disease or another bacterial infection, the patient will receive antibiotics
as indicated. Monitor for arrhythmias, especially in the
acute phase.
Mainstays of treatment include providing supplemental
oxygen, limiting myocardial oxygen demand, and enhancing circulatory support and CO if needed. Patients who
develop heart failure may be treated with angiotensinconverting enzyme (ACE) inhibitors, diuretics, and sodium
restriction. Anticoagulation may be indicated to reduce the
risk of thrombosis and pulmonary embolism. In more
severe cases of myocarditis, the patient may need inotropic
support with such intravenous drugs as dobutamine.
Myocarditis appears to make patients sensitive to digoxin. If your patient is taking it, monitor him for toxicity.
Intravenous immunoglobulin may be given to enhance
the immune system and limit the disease. In severe cases,
the patient may need heart transplantation.
During the acute phase of myocarditis, keep the patient
on bed rest because activity increases myocardial oxygen
demand. Teach him about his medications and when he
can resume activities and exercise.
Mr. Mannheim, who had severe myocarditis with dilated cardiomyopathy, has an ejection fraction below 35%.
Hes put on sodium restriction, furosemide, and an ACE
inhibitor and will be evaluated to determine if his heart
failure can be managed medically or if hell need a heart
transplant.

A closer look at pericarditis

ST segment
elevated and concave
T wave
elevated

QT
QT interval
normal for heart rate

What is pericarditis?
The pericardium is a double-walled fibroserous sac that
surrounds and supports the heart. Normally, 15 to 50 ml
of fluid separates the two layers. In pericarditis, the pericardium becomes inflamed. Excess fluid may accumulate
in this space, resulting in a pericardial effusion.
Many cases of pericarditis are mild and self-limiting.
But others, if not treated, can progress to chronic constrictive pericarditis or to cardiac tamponade, in which
accumulated fluid compresses the heart and obstructs
blood flow into the ventricles.
The rate of fluid accumulation is critical. Rapid accumulation of a small amount of fluid can produce severe
signs and symptoms. Its more likely to lead to cardiac
tamponade or cardiovascular collapse than a slow accumulation, even if the amounts of fluid accumulating
slowly are larger. When the accumulation is slow, the
body has time to compensate for the change and the
patient may experience few or no symptoms. (For some
of the causes of pericarditis, see Triggers of trouble.)

PERICARDITIS
Learn how to distinguish this disorder from other
causes of chest pain and intervene.
A 42-year-old female runner recovering from an upper
respiratory infection comes to your ED complaining of
chest pain thats sharp, constant, worse when shes lying
down, and alleviated with sitting up and leaning forward.
Serum CK-MB, myoglobin, and troponin I levels rule
out acute MI. The ECG shows widespread ST segments
that are elevated and concave (see A closer look at pericarditis), and you auscultate a pericardial friction rub.
The ED physician, suspecting pericarditis, orders a
stat bedside echocardiogram to assess for pericardial
effusion.
Spring 2006

Signs of trouble
Chest pain, the most common symptom, is the reason most
patients seek help. Its usually described as sharp and constant and located in the midchest (retrosternal). Because
leaning forward while sitting may alleviate the pain, this is
considered a hallmark sign of pericarditis. Lying down or
inhaling can worsen the pain. Pain from pericarditis may
radiate to the neck, shoulders, and back; radiation to the
ridge of the left trapezius muscle is specific for pericarditis.
Depending on the cause of the pericarditis, the patient also
may have fever, malaise, tachypnea, and tachycardia.
7

Cardiac Insider

The most important physical sign of acute pericarditis is

a pericardial friction rub, although this is present in only
about 50% of cases. A high-pitched scratching and grating
sound, its heard best with the diaphragm of the stethoscope.
Listen for a pericardial friction rub at the left lower
sternal border. Pericardial friction rubs may be intermittent or so soft that theyre hard to hear. To enhance your
ability to hear a pericardial friction rub, auscultate the
heart at the left lower sternal border with the patient sitting up, leaning forward, and holding her breathor listen after exhalation.
In cardiac tamponade, which can be fatal if not recognized and treated promptly, the patient commonly has
pulsus paradoxus (during inspiration, systolic blood pressure is at least 10 mm Hg lower than during expiration).
Pericarditis is one of the three most common causes of
cardiac tamponade (along with cancer and uremia).
Cardiac tamponade is characterized by limited ventricular
filling, elevated intracardiac pressures, and reduced CO.
Classic clinical signs of cardiac tamponade include falling
arterial pressure, rising venous pressure, and faint heart
sounds.

Triggers of trouble
In up to half the cases of pericarditis, the cause isnt
known (idiopathic pericarditis). Some of the other
causes of pericarditis are listed below.
Infection
viruses (most common known cause of pericarditis), including adenoviruses, echoviruses, and
coxsackieviruses
tuberculosis
bacteria, such as pneumococcus and streptococcus
fungi, including Candida
Cardiac complications
acute myocardial infarction
postpericardiotomy syndrome
Autoimmune or hypersensitivity reactions
rheumatic fever
rheumatoid arthritis
systemic lupus erythematosus
Drugs
hydralazine
procainamide
minoxidil
isoniazid
Other causes
neoplasms
trauma

Diagnostic testing
In 90% of patients with acute pericarditis without massive pericardial effusion, ECGs will be abnormal. Besides widespread ST-segment elevation, youll notice
reciprocal depression in lead aVR and sometimes lead
V1. After several days, the ST segments return to normal
and T waves invert.
If the patient has a large pericardial effusion, you may
see premature atrial beats and atrial fibrillation on ECG.
If cardiac tamponade is present, youll see low-voltage
QRS complexes and electrical alternans (periodic alternation in the size of the QRS complexes between normal
and small, coincident with respiration). The ECG
changes associated with pericarditis may take months
to resolve, with T-wave changes returning to normal
last.
An echocardiogram is the preferred imaging method
for diagnosing pericardial effusion or tamponade.
However, a chest X-ray may be ordered to rule out pulmonary pathology. This may show an enlarged cardiac
silhouette (often described as a water bottle shape) if
more than 250 ml of pericardial fluid is present. If the
effusion is large or cardiac tamponade is present, the
health care provider may order a pericardiocentesis and
lab analysis of the fluid to determine the source of the
effusion.
Other lab tests that may be ordered include cardiac
Cardiac Insider

enzyme levels (including troponin) to rule out MI, a

complete blood cell count, blood culture, and inflammatory markers such as C-reactive protein and erythrocyte
sedimentation rate. The tests ordered will depend on the
patients clinical status and the suspected cause of pericarditis; for example, renal studies if the patient is uremic, testing for human immunodeficiency virus (HIV),
or tuberculosis testing.

Easing the squeeze

A patient can be treated as an outpatient if shes clinically
or hemodynamically stable, the effusion is small, myocardial ischemia or infarction has been ruled out, and oral
medications control her pain. The usual treatment includes nonsteroidal anti-inflammatory drugs (NSAIDs)
such as aspirin or indomethacin to manage pain and reduce inflammation. Therapy continues for up to 2 weeks.
If an NSAID doesnt control pain adequately, the health
care provider may order an oral opioid such as codeine,
hydrocodone, or tramadol.
Someone with a large effusion should be hospitalized
and monitored for cardiac tamponade. In the hospital,
8

Spring 2006

more severe pain usually can be managed with patientcontrolled morphine. If pain continues to be severe, the
health care provider may order more aggressive therapy
with additional medications such as prednisone, a glucocorticoid.
When the cause of pericarditis is infective, administer
antibiotics or antifungal drugs as indicated, depending
on the microorganisms isolated from pericardiocentesis.
A patient with uremic pericarditis may require dialysis.
If pericarditis recurs frequently, is disabling, or continues for more than 2 years, the patient may need pericardiectomy.
Our case patient, the runner, is diagnosed with acute
viral pericarditis secondary to a viral infection and a
small pericardial effusion. Shes prescribed antiinflammatory therapy with aspirin and bed rest.
Reassure your patient that her chest pain doesnt mean
shes having a heart attack, and tell her that the pain
from pericarditis may take several months to resolve.
Until the pain and fever subside, she should restrict her
activities and avoid vigorous exercise. Teach her about
her medications, encourage her to keep all follow-up
appointments, and tell her to notify her health care

provider immediately if any changes in symptoms occur,

such as a return or worsening of chest pain.
Whether your patient has endocarditis, myocarditis,
or pericarditis, if you learn how to assess the condition
and intervene effectively, you can help her recover quickly without complications.
SELECTED REFERENCES
Braunwald E, et al. (eds). Harrisons Principles of Internal
Medicine, 16th edition. New York, N.Y., McGraw-Hill, 2005.
Ferrieri P, et al. Unique features of infective endocarditis in childhood. Circulation. 105(17):2115-2125, April 30, 2002.
Le T, Bayer A. Combination antibiotic therapy for infective endocarditis. Clinical Infectious Diseases. 36(5):615-621, March 1, 2003.
Tedeschi A, et al. High-dose intravenous immunoglobulin in the
treatment of acute myocarditis. A case report and review of the literature. Journal of Internal Medicine. 251(2):169-173, February 2002.
Susan Simmons-Holcomb is a nurse practitioner at the Walk-In
Health Care of Olathe in Olathe, Kan.; a nurse practitioner and
nutrition consultant at Sastun Center of Integrative Health Care in
Mission, Kan.; and a consultant in continuing nursing education at
Kansas City (Kan.) Community College.
The author has disclosed that she has no significant relationship
with or financial interest in any commercial companies that pertain to this educational activity.
Source: Reprinted from Recognizing and managing different types of carditis,
TravelNursing2005, S Simmons-Holcomb, June 2005.

Earn CE credit online:

Go to http://www.nursingcenter.com/CE/nursing
and receive a certificate within minutes.
INSTRUCTIONS

Recognizing and managing different types of carditis

We also offer CE accounts for hospitals and other health
care facilities on nursingcenter.com. Call 1-800-787-8985 for
details.

TEST INSTRUCTIONS
To take the test online, go to our secure Web site at
http://www.nursingcenter.com/ce/nursing.
On the print form, record your answers in the test answer section of the CE enrollment form on page 10. Each question has
only one correct answer. You may make copies of these forms.
Complete the registration information and course evaluation.
Mail the completed form and registration fee of $19.95 to:
Lippincott Williams & Wilkins, CE Group, 2710 Yorktowne Blvd.,
Brick, NJ 08723. We will mail your certificate in 4 to 6 weeks. For
faster service, include a fax number and we will fax your certificate within 2 business days of receiving your enrollment form.
You will receive your CE certificate of earned contact hours
and an answer key to review your results. There is no minimum
passing grade.
Registration deadline is February 29, 2008.

PROVIDER ACCREDITATION
Lippincott Williams & Wilkins (LWW), the publisher of Cardiac
Insider, will award 2.5 contact hours for this continuing nursing
education activity. Lippincott Williams & Wilkins is accredited
as a provider of continuing nursing education by the American
Nurses Credentialing Centers Commission on Accreditation.
This activity is also provider approved by the California Board
of Registered Nursing, Provider Number CEP 11749 for 2.5 contact hours. LWW is also an approved provider by the American
Association of Critical-Care Nurses (AACN 00012278, CERP
Category A), Alabama #ABNP0114, Florida #FBN2454, and Iowa
#75. LWW home study activities are classified for Texas nursing
continuing education requirements as Type 1. Your certificate is
valid in all states.

DISCOUNTS and CUSTOMER SERVICE

Send two or more tests in any nursing journal published by
LWW together and deduct $0.95 from the price of each test.

Spring 2006

Cardiac Insider