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ONLINE EXCLUSIVE • CONTINUING EDUCATION
Cardiovascular Emergencies:
Pericardial Effusion and Cardiac Tamponade
Jo Ann Flounders, MSN, CRNP, OCN®, CHPN
ardiac tamponade is a life-threatening emergency that
occurs when excessive fluid in the pericardial space,
called a pericardial effusion, creates increased pressure
in the pericardial sac that compromises the heart’s ability to
fill and pump. Consequently, cardiac output decreases and
systemic perfusion is impaired (Dietz & Flaherty, 1993;
Hunter, 1998). The distinction between pericardial effusion
and cardiac tamponade is important. Pericardial effusion is an
anatomic diagnosis of abnormal pericardial fluid accumulation that has no hemodynamic consequences, whereas cardiac
tamponade is a physiologic diagnosis of varying amounts of
pericardial fluid that causes increased pressure and resultant
hemodynamic consequences (Harken, Hammond, & Edmunds, 1997).
C
diac tamponade (Harken et al., 1997; Knoop & Willenberg;
Smeltzer & Bare, 1996). Anthracyclines, such as doxorubicin
or daunomycin, can be responsible for the development of
pericardial effusions (Chabner & Myers, 1993).
People with cancer may experience pericardial effusions
and cardiac tamponade caused by nonmalignant conditions,
although the incidence is less compared to malignant causes.
Diseases such as rheumatoid arthritis, systemic lupus erythematosis, hypoalbuminemia, renal failure, or hypothyroidism
may cause increased serous fluid in the pericardial sac or serous effusion (Bullock, 2000; Lawler, 1999). Infectious pericarditis caused by bacteria, fungus, virus, or tuberculosis can
cause cardiac tamponade as a result of accumulation of large
volumes of infected fluid. Other cardiovascular conditions,
such as chest trauma, aneurysm, improper insertion of a cen-
Etiology
Although cardiac tamponade can be caused by malignant or
nonmalignant conditions, malignant disease resulting in pericardial effusion is a major cause of cardiac tamponade in many
patients (Keefe, 2000; Knoop & Willenberg, 1999; Markiewicz, Borovik, & Ecker, 1986; Pass, 1997). Malignant invasion of the pericardium or myocardium may be the result of
metastatic tumors or direct extension of a primary tumor (DeMichele & Glick, 2001). Whereas primary tumors of the heart,
such as mesotheliomas and sarcomas, occur rarely, malignant
invasion of the heart by metastases or direct extension occurs
more frequently (Knoop & Willenberg; McAllister, Hall, &
Cooley, 1999). Malignancies that cause secondary tumor involvement, either by metastasis or local extension, include lung,
breast, and esophageal cancers. Hodgkin’s and non-Hodgkin’s
lymphomas frequently involve the mediastinum and pericardium. Leukemias can infiltrate the myocardium and cause small
effusions (Keefe; Knoop & Willenberg). Sarcomas, melanomas, and liver, gastric, and pancreatic malignancies also can
metastasize to the heart.
Cancer treatment also may cause pericardial effusion with
resultant cardiac tamponade (Knoop & Willenberg, 1999).
Radiation therapy of more than 4000 cGy to the mediastinal
area can cause pericarditis, leading to the development of car-
Goal for CE Enrollees:
To further enhance nurses’ knowledge of cardiovascular
emergencies of patients with cancer.
Objectives for CE Enrollees:
On completion of this CE, the participant will be able to
1. Describe two cardiovascular emergencies for patients with
cancer.
2. Describe medical management of the cardiovascular emergencies.
3. Discuss nurses’ role in the care of patients with cardiovascular emergencies.
Jo Ann Flounders, MSN, CRNP, OCN ®, CHPN, is a nurse practitioner at Consultants in Medical Oncology and Hematology in Drexel
Hill, PA.
Digital Object Identifier: 10.1188/03.ONF.E48-E55
ONF – VOL 30, NO 2, 2003
E48
tral venous catheter, or complications secondary to angiography, can cause serosanguinous pericardial effusion and subsequent tamonade (Bullock; Schafer, 1997).
Physiology
The heart and segments of the great vessels are surrounded by the pericardium, a thin, tough fibrous sac with
two layers (Knoop & Willenberg, 1999; Maxwell, 1997;
Schafer, 1997). The inner layer, called the visceral pericardium, is a serous membrane connected to the surface of the
heart. The outer fibrous membrane of the pericardium is the
parietal layer, which provides strength and protection and is
in direct contact with the chest wall at the left sternal position (Schafer). Between the visceral membrane and the parietal membrane is the pericardial cavity that cushions the
myocardium.
The mesothelial cells of the visceral pericardium produce
10–50 ml of clear serous lubricating fluid that prevents friction between the membranes during contraction and relaxation of the heart (Mangan, 1992). This pericardial fluid arises
from the lymphatic channels surrounding the heart (Schafer,
1997) and normally is reabsorbed and drained by the lymphatic system into the mediastinum and right heart cavities
(Uaje, Kahsen, & Parish, 1996).
Pathophysiology
Excessive fluid can accumulate in the pericardial sac for a
variety of reasons (Beauchamp, 1998). As malignant invasion
of the pericardium occurs, the invasive malignancy or the
pericardial tissue itself may produce excess fluid in response
to the malignant process (Smeltzer & Bare, 1996). Pericardial
fluid can collect when lymphatic and venous flow is obstructed by tumor, therefore preventing reabsorption of fluid
(Mangan, 1992). Invasive tumors also can bleed, and because
blood accumulates more rapidly than transudates or exudates,
these pericardial effusions tend to progress to cardiac tamponade more rapidly (Keefe, 2000).
Cardiac tamponade results when cardiac function is impaired by pressure exerted by pericardial effusion. As pericardial fluid increases, the increased pressure in the pericardium
compresses all four chambers of the heart (Beauchamp, 1998;
Bullock, 2000; Knoop & Willenberg, 1999; Mangan, 1992).
The right atrium and right ventricle initially are compressed,
leading to decreased right atrial filling during diastole. As less
venous blood returns to the right atrium, increased venous
pressure results, which is evidenced by jugular vein distention, edema, hepatomegaly, and increased diastolic pressure.
Continued compression of the heart leads to decreased diastolic filling of the ventricles as well, causing decreased stroke
volumes, decreased cardiac output, and poor tissue perfusion.
The body attempts to compensate with cardiac stimulation by
the adrenergic nervous system, resulting in tachycardia and
peripheral vasoconstriction. Decreased tissue perfusion causes
activation of the renin-angiotensin-aldosterone system as the
body attempts to increase blood volume and improve stoke
volume (Bullock). As a result, workload on the failing heart
is greatly increased. As these compensatory mechanisms are
exhausted, a cycle of increased fluid, with decreased cardiac
output and decreased venous return, will cause circulatory
collapse and lead to shock, cardiac arrest, and death if not
corrected (Schafer, 1997).
The severity of cardiac tamponade depends on the amount
of pericardial effusion, the rate of accumulation, and the degree of pericardial compromise (Schafer, 1997). Onset may be
gradual or rapid. If fluid accumulates slowly, the parietal pericardium is able to stretch to compensate for the increased
pressure and large amounts of fluid may be tolerated without
symptoms. However, when fluid accumulates rapidly, the
pericardial pressure rises quickly, compensatory mechanisms
cannot adapt, and severe cardiac tamponade results (Bullock,
2000; Knoop & Willenberg, 1999; Schafer; Smeltzer & Bare,
1996).
The risk of cardiac tamponade for patients with cancer corresponds to the etiologic factors that cause cardiac tamponade.
Figure 1 presents a summary of patients with cancer who are
at risk for cardiac tamponade.
Assessment
Signs and symptoms of cardiac tamponade are related to
the amount and rapidity of onset of pericardial fluid accumulation and require a careful and thorough history and review
of symptoms. Clinical manifestations increase in severity if
pericardial fluid rapidly accumulates or if a small pericardial
effusion progresses into a large effusion (Knoop & Willenberg, 1999; Mangan, 1992; Schafer, 1997). Therefore,
patients may be initially asymptomatic when pericardial effusions are small or develop slowly.
Early symptoms of pericardial effusion with tamponade
include
1. Dyspnea, which is usually the most common presenting
symptom (Shepherd, 1997)
2. Retrosternal chest pain that increases when patients are
supine and decreases when leaning forward because of
compression of the heart
3. Cough, dysphagia, hoarseness, or hiccups caused by mechanical compression of nerves of the esophagus, bronchi,
and trachea (Uaje et al., 1996)
4. Dizziness, lightheadedness, or agitation caused by hypoxia
5. Weakness, fatigue, and malaise resulting from decreased
cardiac output
6. Palpitations
7. Vague gastrointestinal complaints, including anorexia,
nausea, and vomiting because of visceral congestion and
venous stasis (Mangan, 1992; Pass, 1993).
• Patients with malignancies that metastasize to the pericardium, such as
breast, lung, esophagus, gastrointestinal, and hepatic malignancies; sarcoma; and melanoma
• Patients with hematologic malignancies, such as leukemia and lymphoma
• Patients with primary tumors of the heart, such as mesothelioma and sarcoma
• Patients who have been treated with radiation therapy of 4000 cGy or
greater to the mediastinal area
Figure 1. Patients With Cancer at Risk for Development of
Cardiac Tamponade
Note. Based on information from Hunter, 1998; Knoop & Willenberg, 1999.
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Late symptoms of cardiac tamponade include
1. Increasing retrosternal chest pain, causing patients to assume a forward-leaning position
2. Progressive dyspnea at rest and orthopnea caused by decreased cardiac output and hypoxia, as well as decreased
lung expansion caused by the enlarged mediastinum
3. Peripheral edema resulting from venous congestion
4. Confusion, restlessness, or apprehension caused by hypoxia and decreased cerebral perfusion (Beauchamp, 1998;
Hunter, 1998; Knoop & Willenberg; Mangan; Schafer
1997; Shepherd).
Physical Examination
Pericardial effusions frequently are not suspected until the
late signs and symptoms of cardiac tamponade occur. This is
primarily a result of the fact that early symptoms may be nonspecific or falsely attributed to tumor progression. In addition,
symptoms of increased pericardial effusion and cardiac tamponade resemble symptoms of pulmonary complications and
often are mistaken for pulmonary or pleural metastasis. Many
patients with malignant pericardial tamponade also have pleural effusions (i.e., accumulation of fluid in the pleural space
between the lung and chest wall), as well as malignant parenchymal pulmonary involvement (Beauchamp, 1998; Shepherd, 1997). Consequently, diagnosis of pericardial effusion
and tamponade is challenging, although imperative, because
if not recognized and treated aggressively, the outcome potentially is fatal.
After consideration of risk factors and review of symptoms
indicative of cardiac tamponade, a physical examination must
be completed. Possible early signs of cardiac tamponade include
1. Muffled heart sounds, undetectable or weak apical pulse,
or positional pericardial friction rub caused by increased
pericardial fluid
2. Mild tachycardia of 100 beats per minute caused by compensatory adrenergic stimulation
3. Mild peripheral edema and abdominal distention as a result
of venous and visceral congestion
4. Fever caused by an inflammatory process in the pericardium (Beauchamp, 1998; Bickley, 1999; Hunter, 1998;
Mangan, 1992).
As cardiac tamponade progresses, patients will appear critically ill. Physical examination may reveal pulsus paradoxus
or hepatojugular reflux, which are possible features of cardiac
tamponade (Schafer, 1997). Pulsus paradoxus is a decrease or
absence of the amplitude of the pulse on inspiration (Beauchamp, 1998). Normally, a decrease in systolic blood pressure
occurs with inspiration because breathing causes cyclic
cardiocirculatory changes (Knoop & Willenberg, 1999).
However, this mechanism is exaggerated during cardiac tamponade because the myocardium is constricted and inspiration
causes the diaphragm to exert additional pressure on the pericardial sac. The left ventricle receives less blood, causing decreased stroke volume, decreased cardiac output, and, therefore, decreased blood pressure during inspiration (Beauchamp; Mangan, 1992; Schafer).
Pulsus paradoxus often is a late sign of cardiac tamponade
that can be detected by assessing blood pressure with a sphygmomanometer. Inflate the cuff to 20 mmHg above the normal
systolic pressure. While slowly deflating the cuff, observe the
patient’s respiratory rate and note the mmHg when Kortokoff
sounds (i.e., the tapping sounds heard during auscultation of
a blood pressure) are heard only during expiration. Note the
mmHg when sounds are heard during both inspiration and
expiration. Pulsus paradoxus is a difference greater than 10
mmHg between the first Kortokoff sound during expiration
and the mmHg when sounds are heard during both inspiration
and expiration. In patients with cardiac tamponade, sounds are
heard during expiration alone for a prolonged period of time
(Beauchamp, 1998; Mangan, 1992).
Hepatojugular reflux is defined as an elevation in jugular
venous pressure by 1 cm or more (Schafer, 1997). Elevate the
head of the bed to a position at which jugular venous pulsations are visible, usually 30°–45°. Exert pressure continuously
over the right upper quadrant of the abdomen for 30–60 seconds while observing the jugular pressure. Increased venous
congestion causes an increase in jugular pressure with abdominal pressure resulting in positive hepatojugular reflux
(Dietz & Flaherty, 1993; Schafer).
In addition to pulsus paradoxus and hepatojugular reflux,
other late signs of cardiac tamponade include
1. Resting tachycardia greater than 100 beats per minute
caused by adrenergic stimulation to compensate for reduced cardiac output
2. Tachypnea caused by decreased cardiac output, hypoxia,
and limited expansion of the lung resulting from the enlarged mediastinum
3. Hypotension from reduced cardiac output
4. Narrow pulse pressure caused by compression of the heart
that, in turn, causes decreased systolic and increased diastolic blood pressure
5. Pale, ashen, and diaphoretic skin with cool, clammy extremities and peripheral cyanosis from reduced cardiac
output, hypoxia, and peripheral vasoconstriction
6. Increased central venous pressure, marked jugular venous
pressure, ascites, hepatomegaly, and peripheral edema,
caused by venous congestion
7. Oliguria progressing to anuria as a result of decreased renal blood flow
8. Impaired consciousness, progressing to obtundation,
caused by decreased cerebral perfusion (Beauchamp,
1998; Hunter, 1998; Knoop & Willenberg, 1999; Mangan,
1992; Schafer, 1997; Shepherd, 1997).
Diagnostic Studies
Although not diagnostic for cardiac tamponade, a routine
chest x-ray and electrocardiogram (ECG) may be the initial
tests that identify abnormalities and reveal the need for more
diagnostic testing (Mangan, 1992). An anterior-posterior chest
x-ray may demonstrate an enlarged cardiac silhouette resulting from the increased amount of fluid in the pericardial sac
(Lawler, 1999). Chest x-rays in more than half of patients with
pericardial effusions demonstrate cardiac enlargement, mediastinal widening, or hilar adenopathy (DeMichele & Glick,
2001). The heart may develop a water-bottle appearance on
chest x-ray, with loss of the normal contours of the pericardial
reflection (Pass, 1993). However, the chest x-ray cannot differentiate between possible causes of an enlarged heart shadow, and, because of this lack of specificity, the chest x-ray
does not provide conclusive evidence to support a pericardial
effusion (Mangan; Schafer, 1997).
The ECG changes often are nonspecific, but may show tachycardia, premature contractions, and electrical alternans
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(i.e., an ECG pattern of alternating amplitude of the P wave
and the QRS complex with every other beat, caused by excessive heart movement in the increased fluid of the pericardium)
(DeMichele & Glick, 2001; Knoop & Willenberg, 1999;
Mangan, 1992). Diffused low voltage (less than 5 mm) in the
limb leads and precordial leads of an ECG can be an indication of significant pericardial effusion.
The most specific and sensitive noninvasive test for pericardial effusion or cardiac tamponade is the two-dimensional
echocardiogram (2-D echo), which has become the imaging
technique of choice when malignant pericardial effusion is
suspected (DeMichele & Glick, 2000; Shepherd, 1997). A 2D echo uses painless ultrasound waves to create a picture of
the heart, including the function of the heart. The classic
echocardiographic finding suggestive of cardiac tamponade is
collapse of the right atrium and ventricle because of the pressure of the increased pericardial fluid (Beauchamp, 1998).
One benefit of the 2-D echo is that it can be completed at bedside if patients are too ill to be transported. Other imaging
techniques used to detect cardiac tamponade may be magnetic
resonance imaging and computerized tomography scans, both
of which can detect small and large effusions, pericardial
thickening, and pericardial masses (Lawler, 1999; Shepherd).
Medical Management of Cardiac Tamponade
Cardiac tamponade is a life-threatening emergency. The
immediate goal of treatment for cardiac tamponade is the removal of the pericardial fluid to restore hemodynamic stability. The degree of decrease in cardiac output and hemodynamic instability must be considered because emergency
intervention may be needed to prevent a fatal outcome.
Supportive care of patients with cardiac tamponade includes
ongoing pharmacologic therapy to maintain blood pressure and
cardiac functioning during all treatment modalities (Uaje et al.,
1996). Mild cardiac tamponade initially may be treated cautiously with diuretics, such as furosemide or spironolactone, as
well as with corticosteroids, such as prednisone. Administration
of blood products, plasma, and saline will expand circulatory
volume and delay circulatory collapse. Oxygen therapy may
be initiated. Vasoactive drugs may be used to maintain perfusion. Isoproterenol can increase heart rate and low-dose
dopamine can improve cardiac contractility (Beauchamp,
1998; Braunwald, 1997; Schafer, 1997).
Several options for treatment of cardiac tamponade exist.
Percutaneous pericardiocentesis, a drainage technique frequently used as the initial treatment for cardiac tamponade,
also is useful as a diagnostic tool (Beauchamp, 1998; Harkin
et al., 1997; Knoop & Willenberg, 1999; Lawler, 1999; Mangan, 1992; Pass, 1993). Under guidance by either cardiac
catheterization or 2-D echo, a needle is inserted percutaneously into the pericardial sac to aspirate the fluid and decompress the tamponade. Echocardiographically guided pericardiocentesis can be performed at bedside. Unguided
aspiration only should be used in extreme emergency situations. The benefit of pericardiocentesis is that the tamponade
is relieved quickly, but complications of the procedure include
puncture of the cardiac muscle, abscess, dysrhythmia, and
infection.
Pericardiocentesis also is useful as tool for cytologic diagnosis. The aspirated pericardial fluid is classified as either a
transudate or an exudate. A transudate, which has low protein
levels, is a fluid that has leaked from blood vessels as a result
of mechanical factors, such as cirrhosis. An exudate, which is
rich in protein, is a fluid that has leaked from blood vessels
with increased permeability. Malignant effusions often are
exudates that contain cellular debris resulting from irritation
of the serous membrane by sloughed cancer cells (Maxwell,
1997). Malignant effusions usually are serosanguinous, as
compared to the clear straw color of normal pericardial fluid
(Schafer, 1997). Cytologic examination of the fluid is necessary to determine the etiology of the effusion and determine
appropriate medical management.
Pericardial fluid may reaccumulate, therefore a definitive
medical or surgical treatment usually follows pericardiocentesis to prevent recurrence of cardiac tamponade.
Pericardial sclerosis involves instillation of chemicals into
the pericardial sac through a pericardial catheter after the pericardial space has been drained. The purpose is to create an
inflammatory response with resultant fibrosis and sclerosis to
prevent reaccumulation of fluid in the pericardial space. Some
of the chemicals used are doxycycline, bleomycin, cisplatin,
or vinblastine (Hunter, 1998; Pass, 1993).
Surgical procedures also can provide effective palliative
treatment for recurrent malignant cardiac tamponade. A partial pericardiectomy, or pericardial window, creates a surgical
opening in the pericardium to drain fluid into the pleural or
peritoneal compartments. However, pericardial drainage will
be less than optimal if a pleural effusion or peritoneal effusion
(i.e., ascites) already exists (Harken et al., 1997). A total pericardiectomy (i.e., removal of the visceral pericardium) is used
to treat radiation-induced constrictive pericarditis (Hunter,
1998). These procedures are performed in the operating room
under general anesthesia (Beauchamp, 1998). Another surgical procedure is percutaneous balloon pericardiotomy, which
uses a balloon-tipped catheter to tear the pericardium and create a window for drainage. This procedure usually is performed in a cardiac catheterization lab.
After the patient has been stabilized, long-term goals can be
addressed, including treatment of any underlying malignancy
(Schafer, 1997). Treatment choices will depend on patients’
primary diagnosis, performance status, and stage and aggressiveness of the disease (Lawler, 1999; Mangan, 1992). Radiation therapy can be used when tumors of the pericardium are
radiosensitive. Radiation therapy is contraindicated when the
area involved has been irradiated previously. Systemic antineoplastic therapy may be administered if the malignancy is
chemotherapy sensitive (DeMichele & Glick, 2001).
Nursing Care
Recognition of early signs and symptoms of pericardial effusion and cardiac tamponade can allow for treatment before
life-threatening circulatory collapse occurs. Nurses frequently
are able to perceive subtle changes in patient status. Accurate
and thorough ongoing assessment of cardiopulmonary and hemodynamic status is necessary to identify early abnormal
changes. Nursing assessment includes strict monitoring of vital signs, including assessment for pulsus paradoxus, as well as
assessment of level of consciousness, ECG tracings, respiratory
status, and skin and temperature changes (Smeltzer & Bare,
1996). Accurate monitoring of intake and output is necessary,
including assessment for edema or oliguria and anuria. Regular assessment also includes examination for positive
hepatojugular reflux as well as measurement of abdominal girth
to detect ascites (Schafer, 1997).
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Nursing interventions include pain management, care of
pericardial catheters, position changes to minimize shortness
of breath, postoperative care, and administration of oxygen
(Hunter, 1998; Schafer, 1997). Instructions regarding appropriate and timely physician notification of complications that
occur after discharge can help to initiate early interventions.
Assessment and intervention for the side effects of radiation
therapy, such as fatigue and skin alterations, as well as the side
effects of chemotherapy, such as nausea, vomiting, stomatitis, or pancytopenia, can aid in minimizing symptoms. Nurses
should assess for possible ineffective coping and depression.
Referral for home nursing services or hospice care should be
considered as needed.
Additional Cardiac Complications of Cancer Therapy
In addition to pericardial effusion and cardiac tamponade,
people with cancer may develop any cardiovascular disease
(Keefe, 2000). Oncology nurses should be aware that acute
heart failure might be a complication experienced by patients with cancer and that heart failure occasionally is
caused by the cancer treatment itself. Anthracyclines, such
as doxorubicin, and the anthracenedione mitoxantrone can
cause signs and symptoms of heart failure as a result of treatment-induced cardiomyopathy caused by myocyte damage
and myocardial cell loss (Keefe; Steinherz & Yahalom,
1993). ECG changes that have been detected after administration of anthracyclines include supraventricular dysrhythmias, heart block, and ventricular tachycardia. In addition, ECG-gated pool scans can be completed to assess
global left ventricular function and ejection fraction. The
ECG-gated pool scan is a procedure in which the measured
amount of radioactive tracer in the chambers of the heart is
proportional to the volume of blood in the chambers (Bullock & Henze, 2000). ECG-gated pool scans have shown
major decreases in ejection fraction that reach a nadir within
24–48 hours after anthracycline administration. As a result,
congestive heart failure can occur in certain patients (Chabner & Myers, 1993).
Tachycardia is the initial sign that an anthracycline is causing cardiomyopathy, followed by decreased exercise tolerance. However, these signs sometimes are overlooked and attributed to other causes, such as anemia, pain, or fever
(Keefe). Fluid overload occurs next. The response of a normal
heart to increased blood volume usually is dilatation of the
chambers of the heart and hypertrophy of the ventricles (Bullock, 2000). However, anthracycline-induced cardiomyopathy
is associated with little increase in left ventricular size, and,
therefore, patients may experience severe symptoms of heart
failure (Keefe). Avoidance of anthracycline-induced cardiomyopathy includes measurement of the ejection fraction and
ongoing evaluation of patients for symptoms, including referral to a cardiologist for high-risk patients, monitoring cumulative dose, and dose adjustment or discontinuation when necessary. Treatment includes diuretics, digitalis, and angiotensin-converting enzyme inhibitors.
Cardiac complications can occur as a side effect of other
cancer treatments. Trastuzumab (Herceptin® [Genentech, Inc.,
South San Francisco, CA]) is a recently developed monoclonal antibody to the HER2 receptor (Cooper & Cooper,
2001; Keefe, 2000). The incidence of heart failure increases
when trastuzumab is administered in conjunction with an
anthracycline such as doxorubicin or epirubicin. Therefore, a
baseline ejection fraction always should be obtained before
administration of trastuzumab to detect underlying asymptomatic left ventricular dysfunction (Keefe). Patients must be
monitored closely during therapy with trastuzumab.
Cardiotoxicity also can be caused by administration of 5fluorouracil, which can cause coronary artery spasm with resultant angina, dysrhythmias, myocardial infarction, cardiac
arrest, or sudden death (Keefe, 2000; Steinherz & Yahalom,
1993). Cardiac toxicity occurs very rarely with initial doses
and is more common with subsequent doses toward the end of
a five-day infusion. Deaths have been reported to occur in
symptomatic patients who continued therapy despite warning
signs and symptoms (Keefe).
Conclusion
Nurses must be aware that cardiac complications can occur
as a complication of cancer treatment. Oncology nurses commonly administer chemotherapy and have frequent and prolonged encounters with patients. Ongoing, accurate, and thorough cardiovascular assessment is necessary to detect dysrhythmias or changes in functional status, such as increased
weakness, decreased endurance, or exercise intolerance. Early
detection of subtle changes and signs and symptoms of cardiac complications can prevent increased cardiotoxicity.
The author would like to thank John Sprandio, MD, of Consultants in Medical Oncology and Hematology, Drexel Hill, PA, for reviewing this manuscript.
Author Contact: Jo Ann Flounders, MSN, CRNP, OCN®, CHPN,
can be reached at [email protected], with copy to editor at
[email protected].
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S. Smeltzer & B. Bare (Eds.), Brunner and Suddarth’s textbook of medicalsurgical nursing (8th ed., pp. 309–316). Philadelphia: Lippincott-Raven.
Steinherz, L., & Yahalom, J. (1993). In V. DeVita, S. Hellman, & S. Rosenberg (Eds.), Cancer principles and practice of oncology (pp. 2370–2385).
Philadelphia: Lippincott-Raven.
Uaje, C., Kahsen, K., & Parish, L. (1996). Oncology emergencies. Critical
Care Nursing Quarterly, 18(4), 26–34.
FLOUNDERS – VOL 30, NO 2, 2003
E53
ONF Continuing Education Examination
Cardiovascular Emergencies: Pericardial Effusion and Cardiac Tamponade
Contact Hours: 1.1
Passing Score: 80%
Test ID #: 03-30/2-01
Test Processing Fee: $15
The Oncology Nursing Society is accredited as a provider
of continuing education (CE) in nursing by the
• American Nurses Credentialing Center’s Commission on
Accreditation.
• California Board of Nursing, Provider #2850.
8.
CE Test Questions
1. A client is seen in the emergency room with a diagnosis
of early pericardial effusion with tamponade. The nurse
could expect the patient to describe
a. Peripheral edema, confusion, and dyspnea.
b. Coughing, weakness, palpitations, and dyspnea.
c. Restlessness, constant chest pain, and progressive dyspnea.
d. Dyspnea, apprehension, and increasing chest pain
without relief.
2. The diagnostic procedure with the highest sensitivity of
detecting a pericardial effusion or cardiac tamponade is
a. Routine chest x-ray film.
b. Electrocardiogram.
c. Positron emission tomography.
d. Two-dimensional echocardiogram.
3. Cardiac tamponade is best defined as excessive fluid in
the
a. Pericardium that leads to increased ventricular filling
and decreased cardiac output.
b. Pericardial space that leads to increased pericardial
pressure and increased cardiac output.
c. Pericardial sac that leads to increased pericardial effusion and increased pressure on the heart.
d. Pericardial space that leads to increased pericardial
pressure and decreased systemic perfusion.
4. A patient with a stage III breast cancer of her left breast
is considered at risk for developing cardiac tamponade
primarily because of her
a. Treatment with paclitaxel.
b. Breast cancer diagnosis.
c. History of congestive heart failure.
d. Treatment with radiation therapy of 3000 cGy.
5. Which nursing diagnosis should the nurse plan to address
first for a patient with pericardial effusion?
a. Risk for pain
b. Risk for infection
c. Risk for ineffective coping
d. Risk for alteration in cardiac output
6. What physical examination findings would be consistent
with early signs of cardiac tamponade?
a. Pulsus paradoxus
b. Muffled heart sounds
c. Narrowing pulse pressure
d. Tachycardia of 125 beats per minute
7. Ms. Jones has a cardiac tamponade and will require medi-
9.
10.
11.
12.
13.
cal treatment. The medical intervention that would first
be used is
a. Administering diuretics and corticosteroids.
b. Removing the fluid from the pericardial space.
c. Administering saline to expand circulatory volume.
d. Administering vasoactive drugs to maintain perfusion.
Mr. Smith underwent a pericardiocentesis. The aspirated
pericardial fluid was sent for cytology. What characteristic of this fluid would indicate it is a malignant effusion?
a. Low protein levels
b. Clear straw color
c. Low specific gravity
d. Contained cellular debris
Ms. Broad is receiving her fourth cycle of doxorubicin.
Which assessment finding may first indicate that Ms.
Broad is developing cardiomyopathy?
a. Dyspnea
b. Tachycardia
c. Hemoglobin of 9.5 g/dL
d. Decreased exercise tolerance
Mr. Brown has a pericardial effusion with tamponade. He
is most likely to describe chest pain that
a. Decreases when lying on his back.
b. Is worse in the morning than evening.
c. Is constant despite position or activity.
d. Decreases when he is leaning forward.
Ms. Cord has Her2-neu-positive breast cancer and has
been ordered to receive trastuzumab and doxirubicin.
What assessment study should be performed prior to beginning this regimen?
a. Chest x-ray
b. Ejection fraction
c. Echocardiogram
d. Electrocardiogram
A client is receiving the last day of chemotherapy of her
third cycle. She begins to complain of steady and severe
pain in her chest that is radiating down her left arm.
Which chemotherapy agent is she receiving that may
cause these symptoms?
a. 5-fluoruracil
b. Epirubicin
c. Doxorubicin
d. Trastuzumab
A patient is to undergo a partial pericardiectomy. This
procedure is best described as
a. A surgical procedure where the visceral pericardium
is removed.
b. A surgical procedure that will create a window in the
pericardium to drain fluid into the pleural compartments.
c. A procedure performed in the radiology department
where a needle will be inserted into the pericardial sac
to aspirate the pericardial fluid.
d. A procedure performed in the cardiac catherization lab
that uses a balloon-tipped catheter to tear the pericardium to create a window for drainage.
ONF – VOL 30, NO 2, 2003
E54
14. A patient is to have chemicals installed into the pericardial sac after the space has been drained. What is the rationale for this procedure?
a. Pericardial washings to prevent collapse of the pericardial sac
b. Pericardial sclerosis to remove any malignant effusion
that remained
c. Pericardial scraping to deliver cytotoxic agents to the
site of metastasis
d. Pericardial sclerosis to create an inflammatory response with resultant fibrosis and sclerosis
15. What nursing interventions are essential for early detection of cardiac tamponade in high-risk patients?
a. Evaluation of daily electrocardiogram tracings
b. Frequent monitoring of vital signs
c. Daily evaluation of input and output
d. Evaluation of daily electrolyte lab results
16. A patient with which type of cancer is at the least risk for
developing pericardial tamponade?
a. Leukemia
b. Lung cancer
c. Spinal cord tumor
d. Esophageal cancer
17. Which is the most appropriate statement regarding the
difference between pericardial effusion and cardiac tamponade?
a. Cardiac tamponade is an anatomic diagnosis with no
hemodynamic consequences.
b. Pericardial effusion is a physiologic diagnosis with no
hemodynamic consequences.
c. Cardiac tamponade is a physiologic diagnosis with resultant hemodynamic consequences.
d. Pericardial effusion is an anatomic diagnosis that has
resultant hemodynamic consequences.
Oncology Nursing Forum Answer/Enrollment Form
Cardiovascular Emergencies: Pericardial Effusion and Cardiac Tamponade (Test ID #03-30/2-01)
4. The deadline for submitting the answer/enrollment form is
two years from the date of this issue.
5. Contact hours will be awarded to RNs who successfully complete the program. Successful completion is defined as an
80% correct score on the examination and a completed evaluation program. Verification of your CE credit will be sent to
you. Certificates will be mailed within six weeks following
receipt of your Answer/Enrollment Form. For more information, call 866-257-4667, ext. 6296.
To receive continuing education (CE) credit for this issue, simply
1. Read the article.
2. Print this page and indicate your answers on the form. Also,
complete the program evaluation.
3. Mail the completed answer/enrollment form along with a
check or money order for $15 per test payable to the Oncology Nursing Society. Payment must be included for your examination to be processed.
Instructions: Mark
your answers clearly by
placing an “x” in the
box next to the correct
answer. This is a standard form; use only the
number of spaces required for the test you
are taking.
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Program Evaluation
1. How relevant were the objectives to the CE activity’s goal?
2. How well did you meet the CE activity’s objectives (see page E48)?
• Objective #1
• Objective #2
• Objective #3
3. To what degree were the teaching/learning resources helpful?
4. Based on your previous knowledge and experience, do you think
that the level of the information presented in the CE activity was
minutes
5. How long did it take you to complete the CE activity?
Not at all
Low
Medium
High
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❑ My check or money order payable to the Oncology Nursing Society is enclosed. U.S. currency only. (Do not send cash.)
After completing this form, mail it to: Oncology Nursing Society, P.O. Box 3510, Pittsburgh, PA 15230-3510.
For more information or information on the status of CE certificates, call 866-257-4667, ext. 6296.
FLOUNDERS
– VOL
30, 2,
NO
2, 2003
ONF – VOL
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