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Volume 10, Part 3
May 2004
CARDIOLOGY
Board Review Manual
Cardiac Tamponade:
Diagnosis and Treatment
Endorsed by the Association for Hospital Medical Education
®
CARDIOLOGY
BOARD REVIEW MANUAL
Sponsored by
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CARDIOLOGY BOARD REVIEW MANUAL
STATEMENT OF
EDITORIAL PURPOSE
The Hospital Physician Cardiology Board Review
Manual is a peer-reviewed study guide for fellows and practicing physicians preparing for
board examinations in cardiology. Each
bimonthly manual reviews a topic essential to
the current practice of cardiology.
PUBLISHING STAFF
PRESIDENT, GROUP PUBLISHER
Cardiac Tamopnade:
Diagnosis and Treatment
Series Editor: A. Maziar Zafari, MD, PhD, FACC
Assistant Professor of Medicine, Division of Cardiology, Department of
Medicine, Emory University School of Medicine, Atlanta, GA
Director, Critical Care Unit, Atlanta Veterans Affairs Medical Center,
Decatur, GA
Bruce M. White
EDITORIAL DIRECTOR
Debra Dreger
EDITOR
Robert Litchkofski
ASSISTANT EDITOR
Rita E. Gould
EXECUTIVE VICE PRESIDENT
Barbara T. White
EXECUTIVE DIRECTOR
OF OPERATIONS
Contributors:
Fadi M.F. Alameddine, MD
Cardiology Fellow, Division of Cardiology, Department of Medicine,
Emory University School of Medicine, Atlanta, GA; Cardiology Fellow,
Atlanta Veterans Affairs Medical Center, Decatur, GA
Andro G. Kacharava, MD, PhD
Assistant Professor of Medicine, Division of Cardiology, Department of
Medicine, Emory University School of Medicine, Atlanta, GA; Staff
Cardiologist, Atlanta Veterans Affairs Medical Center, Decatur, GA
Jean M. Gaul
PRODUCTION DIRECTOR
Suzanne S. Banish
ADVERTISING/PROJECT MANAGER
Patricia Payne Castle
SALES & MARKETING MANAGER
Deborah D. Chavis
Table of Contents
Introduction. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2
Patient Presentation. . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2
Physiology and Pathology . . . . . . . . . . . . . . . . . . . . . . . . 2
NOTE FROM THE PUBLISHER:
This publication has been developed without involvement of or review by the
American Board of Internal Medicine.
Approach to Diagnosis. . . . . . . . . . . . . . . . . . . . . . . . . . . 3
Treatment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6
Summary Points . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8
References. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9
Endorsed by the
Association for Hospital
Medical Education
Cover Illustration by mb cunney
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Communications, Inc., will not be liable for any errors of omission or inaccuracies in this publication. Opinions expressed are those of the
authors and do not necessarily reflect those of Turner White Communications, Inc.
Cardiology Volume 10, Part 3 1
CARDIOLOGY BOARD REVIEW MANUAL
Cardiac Tamponade:
Diagnosis and Treatment
Fadi M.F. Alameddine, MD, and Andro G. Kacharava, MD, PhD
INTRODUCTION
Cardiac tamponade is a compression of the heart
caused by an excessive accumulation of contents in the
pericardium. These contents can include fluid, blood,
pus, or gas resulting from inflammation, trauma, or
rupture of the heart. The 3 principal features of cardiac
tamponade are elevation of intracardiac pressures, limitation of ventricular filling, and reduction of cardiac
output. Severe cardiac tamponade can lead to hemodynamic deterioration and shock. The quantity of fluid
necessary to produce this critical condition may be as
small as 150 mL if the effusion develops rapidly, or
more than 2000 mL if the effusion develops slowly and
the pericardium has time to stretch and adjust to the
increasing volume.1
Multiple medical conditions can lead to cardiac tamponade. The 4 most common causes of accumulation
of fluid in the pericardium in an amount sufficient to
cause serious obstruction to the cardiac inflow of blood
are neoplastic and infectious diseases, idiopathic pericarditis, and uremia. Cardiac surgery and percutaneous
coronary interventions are frequent iatrogenic causes
of cardiac tamponade.
PATIENT PRESENTATION
A 57-year-old man with a 3-hour history of worsening
shortness of breath is brought by ambulance to the emergency department. The patient reports a 1-month history of chest discomfort and mild shortness of breath that
has become progressively worse within the past several
days. His last general medical examination was performed 3 months earlier. At that time, he was in good
health, and his primary care physician reemphasized the
need for him to comply with his diabetes, hypertension,
and hyperlipidemia medications.
On initial physical examination in the emergency
department, the patient is in respiratory distress, tachy-
2 Hospital Physician Board Review Manual
cardic, and hypotensive with peripheral cyanosis. Cardiovascular examination is remarkable for attenuated
heart sounds and extreme elevation of venous pressures.
Breathing sounds are normal. An electrocardiogram
(ECG) shows decreased amplitude of QRS complexes
but otherwise is unremarkable. Echocardiography is
performed and confirms the diagnosis of cardiac tamponade. Emergent needle pericardiocentesis is performed, and 1.5 liters of serosanguinous fluid are
drained. Immediately following pericardiocentesis, the
blood pressure and heart rate normalize.
A catheter is left in the pericardial space, and over
the next 48 hours an insignificant amount of fluid
(< 80 mL) is drained. The catheter is removed. Further
workup to determine the cause of the pericardial effusion does not identify a specific cause. The patient is
treated with nonsteroidal anti-inflammatory medications and is discharged from the hospital. Predischarge
echocardiogram does not reveal further accumulation
of pericardial fluid.
PHYSIOLOGY AND PATHOLOGY
The pericardium is an elastic, closed fibroserous sac
that envelops the entire heart and much of the ascending aorta, the main pulmonary artery, all pulmonary
veins, and portions of the inferior and superior venae
cavae. It consists of an inner serous layer and an external layer composed of fibrous tissue. The pericardial
space between the 2 layers contains a small amount of
ultrafiltrate of plasma that acts as a lubricant and normally drains through the right lymphatic duct via the
right pleural space and through the thoracic duct via
the parietal pericardium.2,3
The pericardium is relatively inextensible and has a
limited ability to expand acutely in the face of rapidly
increasing pericardial contents. The exponential
volume–pressure relationship for the pericardium is
shown in Figure 1. The flat portion of the J-shaped
volume–pressure curve represents intrapericardial
C a r d i a c Ta m p o n a d e : D i a g n o s i s a n d Tr e a t m e n t
pressure when the pericardial content and cardiac volumes are at normal, physiologic levels (ie, pericardial
reserve volume). According to the concept of the pericardial continuum,4 steady increases in pericardial content cause pericardial pressure to increase once the relatively small pericardial volume reserve is filled.
Increases in pericardial content that exceed the rate at
which the pericardium stretches will place the pericardial pressure on the steep portion of the volumepressure curve and cause a parallel increase in intracardiac pressure. In this situation, the cardiac chambers
must compete with pericardial content for relatively
finite intrapericardial volume to avoid progressive cardiac compression and eventual hemodynamic failure.5,6
During the first phase of cardiac tamponade, intrapericardial and ventricular diastolic pressures rise but do
not equilibrate.4 In phase 2, the more rapidly rising
intrapericardial pressure equilibrates with right ventricular diastolic pressure. During this phase, the parallel
rise of the intrapericardial and right ventricular diastolic
pressures continue until they equilibrate with left ventricular diastolic pressure (phase 3). Cardiac chamber
collapse occurs at the moment when the myocardial
transmural pressure (the intracardiac pressure minus
the pericardial pressure)7 becomes transiently negative.
Collapse of the thinner right atrium tends to occur earlier than collapse of the right ventricle.
Like most tamponade-induced abnormalities of pressure and flow, transmural pressures are reciprocally reduced and increased during the respiratory phases (variation in intrathoracic pressure) due to the effect of
respiration on systemic and pulmonary venous pressures.8
These respiratory pressure changes and the phenomenon of ventricular interdependence are mechanisms
underlying the clinical finding of pulsus paradoxus,
defined as an abnormally large (> 10 mm Hg) decrease in
systolic blood pressure on inspiration. The origin of pulsus paradoxus is complex and multifactorial: because
both ventricles share a tight pericardial sac, the inspiratory enlargement of the right ventricle in cardiac tamponade compresses the left ventricle and reduces left ventricular volume. Leftward bulging of the interatrial and
interventricular septa further increases the volume of the
right side of the heart at the expense of the left side,
decreasing left ventricular inflow. Thus, in cardiac tamponade the normal inspiratory augmentation of right
ventricular volume causes an exaggerated reciprocal
reduction in left ventricular volume. In addition, the negative thoracic pressure produced by inspiration is transmitted to the aorta, increasing left ventricular afterload
and reducing stroke volume.9
Pressure
or strain
Pericardial reserve
volume
Volume
or stress
Figure 1. Dimensionless schematic pericardial pressure–
volume curve. (Adapted with permission from Spodick DH,
ed. The pericardium: a comprehensive textbook. New York:
Dekker; 1997:19.)
APPROACH TO DIAGNOSIS
CLINICAL AND PHYSICAL FINDINGS
Cardiac tamponade should be viewed hemodynamically as a continuum ranging from mild to severe. Mild
cardiac tamponade is frequently asymptomatic, whereas moderate and severe tamponade produce precordial
discomfort, dizziness, and dyspnea at rest. Patients frequently complain of palpitations and dyspnea on exertion that progresses to shortness of breath at rest. They
also may complain of general weakness, poor appetite,
abdominal distention, atypical chest pain, and cough.1
When cardiac tamponade complicates a diagnostic procedure, common symptoms include vague discomfort,
generalized uneasiness, and precordial pain. Fluoroscopy may show an enlarged cardiac silhouette and
diminished pulsations.
Similar to the clinical findings, most physical findings in cardiac tamponade are nonspecific.1 Tachycardia and hypotension (which can be profound) are seen
in most patients with clinically significant cardiac tamponade. The triad of hypotension, quiet heart sounds,
and increased jugular venous pressure described by
Beck in 1935 is present in only 30% of patients with
acute cardiac tamponade.10,11 Careful inspection of the
jugular venous pulse waveform is essential for the
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C a r d i a c Ta m p o n a d e : D i a g n o s i s a n d Tr e a t m e n t
Table 1. Conditions That Lead to the Absence of
Diagnostic Pulsus Paradoxus in Cardiac Tamponade
Condition
Comment
Marked LV or RV dysfunction
Decrease myocardial compliance or hypertrophy; heart
failure
Aortic regurgitation
Can produce sufficient regurgitant flow to the left ventricle
to damp respiratory fluctuations
Atrial septal defect
Sufficiently large defects cause
increased venous return to
the right atrium to be balanced by right-to-left shunting of blood
Extreme hypotension
Respiratory pressure changes
become unmeasurable, especially by cuff
Local cardiac adhesions
and compression (eg,
with loculated fluid)
Acute LV myocardial
infarction
May be related to LV stiffness
for uncertain reasons
LV = left ventricular; RV = right ventricular.
Adapted with permission from Swami A, Spodick DH. Pulsus paradoxus
in cardiac tamponade: a pathophysiologic continuum. Clin Cardiol
2003;26:215–7.
diagnosis. In cardiac tamponade, compression of the
heart by pericardial fluid results in a characteristic loss
of the y descent, but the x descent is preserved.
However, the venous pressure may be normal in early
tamponade, and extreme elevations of venous pressure
may go unrecognized in a recumbent or semirecumbent patient. Peripheral venous distention also is noted
in the forehead, scalp, and ocular fundi unless the
patient is hypovolemic. A pericardial rub is a frequent
finding in patients with inflammatory effusions.12 Heart
sounds may be attenuated due to the muffling effects of
the pericardial fluid and reduced cardiac function. An
apical beat is occasionally palpable, and patients with
cardiomegaly or apical pericardial adhesions may have
active pulsations.
An inspiratory decline of systolic arterial pressure
exceeding 10 mm Hg (ie, pulsus paradoxus) may be
quantified with sphygmomanometry as the patient
breathes normally through a respiratory cycle. The size
of the pulsus is the difference between the systolic pres-
4 Hospital Physician Board Review Manual
sure at which Korotkoff sounds are heard only during
expiration and the systolic pressure at which sounds are
heard through the respiratory cycle.9 Although pulsus
paradoxus is neither sensitive nor specific for cardiac
tamponade, in the appropriate clinical setting it is a key
finding that signifies cardiac tamponade. Pulsus paradoxus also may be observed in hypovolemic shock,
acute and chronic obstructive airways disease, and pulmonary embolus. In certain conditions, cardiac tamponade can occur without the presence of pulsus paradoxus (Table 1).13
Hemodynamic changes in the postsurgical period
may delay the appearance of clinical signs of cardiac
tamponade such as jugular venous distention, quiet
heart sounds, and pulsus paradoxus. In these patients,
the appropriate imaging modality is needed for a correct and quick diagnosis.14,15
A high index of suspicion for cardiac tamponade is
required because right ventricular myocardial infarction and constrictive pericarditis can resemble cardiac
tamponade. The differences between these conditions
are shown in Table 2.
DIAGNOSTIC MODALITIES
Electrocardiogram
There are no specific ECG signs in cardiac tamponade. The ECG may show tachycardia, atrial arrhythmias,
low-voltage, P-R segment and ST-T changes of pericarditis, and electrical alternation,16 which may affect
any electrocardiographic waves.17 Occurring in only approximately 20% of cardiac tamponade cases, electrical
alternans is an insensitive sign,17 unless complete alternans is present.18
Chest Radiograph
Similarly, there are no specific signs of cardiac tamponade on chest radiograph. A large cardiac silhouette
in a patient with clear lung fields may suggest the presence of a pericardial effusion. Chest radiographs may
not be helpful early in the course of acute cardiac tamponade because at least 200 mL of fluid must accumulate before the cardiac silhouette is affected.
Computed Tomography/Magnetic Resonance Imaging
Computed tomography scanning can easily detect as
little as 50 mL of pericardial effusion, reflecting better
resolution of boundaries between cardiac, pleural, pericardial, and mediastinal structures. Magnetic resonance
imaging is also a very sensitive tool in the diagnosis of
pericardial effusion. This modality has the same advantages of computed tomography as well as the potential
C a r d i a c Ta m p o n a d e : D i a g n o s i s a n d Tr e a t m e n t
Table2. Features That Distinguish Cardiac Tamponade from Constrictive Pericarditis and Similar Clinical Disorders
Characteristic
Tamponade
Constrictive
Pericarditis
Restrictive
Cardiomyopathy
RVMI
Common
Usually absent
Rare
Rare
Absent
Usually present
Rare
Rare
Clinical
Pulsus paradoxus
Jugular veins
Prominent y descent
Prominent x descent
Kussmaul’s sign
Present
Usually present
Present
Rare
Absent
Present
Absent
Absent
Third heart sound
Absent
Absent
Rare
May be present
Pericardial knock
Absent
Often present
Absent
Absent
Low ECG voltage
May be present
May be present
May be present
Absent
Electrical alternans
May be present
Absent
Absent
Absent
Electrocardiogram
Echocardiography
Thickened pericardium
Absent
Present
Absent
Absent
Pericardial calcification
Absent
Often present
Absent
Absent
Pericardial effusion
Present
Absent
Absent
Absent
RV size
Usually small
Usually normal
Usually normal
Enlarged
Myocardial thickness
Normal
Normal
Usually increased
Normal
Right atrial collapse
and RVDC
Present
Absent
Absent
Absent
Increased early filling,
increased MFV
Absent
Present
Present
May be present
Exaggerated respiratory
variation in flow velocity
Present
Present
Absent
Absent
Absent
Present
Absent
Absent
Usually present
Usually present
Usually absent
Absent or present
No
No
Sometimes
No
CT/MRI
Thickened/calcific pericardium
Cardiac catheterization
Equalization of diastolic
procedures
Cardiac biopsy helpful?
CT = cardiac tamponade; ECG = electrocardiogram; MFV = mitral flow velocity; MRI = magnetic resonance imaging; RV = right ventricle; RVDC
= right ventricular diastolic collapse; RVMI = right ventricular myocardial infarction.
Adapted with permission from Brockington GM, Zebede J, Pandian NG. Constrictive pericarditis. Cardiol Clin 1990;8:645–61.
to characterize the nature of the pericardial content in
certain cases. In a study comparing magnetic resonance
imaging and 2-dimensional echocardiography for diagnosis of pericardial effusion, Mulvagh and colleagues
found that MRI’s ability to easily visualize epicardial borders and pericardial fat pad enabled detection of small
pericardial effusions that were not seen with echocardiography. Despite these advantages, both computed
tomography and magnetic resonance imaging are
often less readily available and more costly and inconvenient in an acutely ill patient. These imaging modalities usually are not required unless echocardiography is
not feasible.
Echocardiography
Echocardiography plays a significant role in the
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C a r d i a c Ta m p o n a d e : D i a g n o s i s a n d Tr e a t m e n t
Table 3. Echocardiographic Features of Cardiac
Tamponade
Swinging heart
Abnormal respiratory changes in ventricular sizes
Dilated inferior vena cava with absence of inspiratory collapse
Late diastolic right or left atrial collapse
Early diastolic right or left ventricular collapse
Paradoxical septal motion
A
peak tricuspid inflow velocity of more than 50% (normal, less than 25%) had a good correlation with clinically significant cardiac tamponade plus a greater sensitivity than right ventricular early diastolic collapse and
greater specificity than right atrial late diastolic collapse.21,22
B
Figure 2. Subcostal long-axis (A) and apical 4-chamber (B)
images from a patient with cardiac tamponade demonstrating the
presence of right ventricular and right atrial collapse. (Adapted
with permission from Alexander RW, Schlant RC, Fuster V, eds.
Hurst’s the heart. 9th ed. New York: McGraw-Hill; 1998:2184.)
diagnosis and hemodynamic assessment of cardiac tamponade (Figure 2). There are multiple M-mode and
2-dimensional signs of cardiac tamponade (Table 3),
but the 2 most suggestive of the presence of hemodynamic compromise are late diastolic collapse of the
right atrium and an early diastolic right ventricular
compression. Right ventricular collapse is a less sensitive
but more specific finding. Transesophageal echocardiography can assist with the diagnosis of posterior loculated effusions, which occasionally produce left atrial
and left ventricular diastolic collapse.20
Pulsed wave doppler echocardiography has been
used to measure exaggerated respiratory variation of
transvalvular blood flow through the left and right heart
valves in patients with cardiac tamponade. An inspiratory decrease in peak mitral inflow of more than 30%
(normal, less than 10%) and inspiratory increase of
6 Hospital Physician Board Review Manual
Cardiac Catheterization
Cardiac catheterization can be used to confirm the
diagnosis of cardiac tamponade. Catheterization shows
equilibration of average diastolic pressure and characteristic respiratory reciprocation of cardiac pressures: an
inspiratory increase in right-sided pressures and a concomitant decrease in left-sided pressures, the proximate
cause of pulsus paradoxus. On hemodynamic tracings
during cardiac catheterization in patients with cardiac
tamponade, the right atrial, pulmonary capillary wedge,
pulmonary artery diastolic, and pericardial pressures are
elevated, usually between 15 and 30 mm Hg, and are
equal within 5 mm Hg. The right atrial and wedge pressure tracings reveal an attenuated or absent y descent
(Figure 3) secondary to impaired late diastolic filling of
the ventricles. Neither Kussmaul sign (ie, abscence of
decline in jugular venous pressure with inspiration) nor
the early ventricular diastolic dip and plateau (ie, the
square root sign) characteristic of pericardial constriction are seen in cardiac tamponade. Cardiac output is
reduced, despite the presence of compensatory tachycardia, and systemic vascular resistance is usually elevated.
Vasoconstriction can be a prominent part of the
hemodynamic response in some patients due to severe
activation of the adrenergic system. In these patients,
blood pressure may be normal or even elevated despite
hemodynamics consistent with tamponade.23 In the
rare cases of low-pressure cardiac tamponade, which
can be observed in the presence of significant volume
depletion, all the hemodynamic signs of cardiac
C a r d i a c Ta m p o n a d e : D i a g n o s i s a n d Tr e a t m e n t
A
B
tamponade may be seen with intrapericardial pressures
below 15 mm Hg.4,24
TREATMENT
Before making decisions on the selection and timing
of therapy in patients with cardiac tamponade, the
physician must assess the clinical status of the patient
and consider the source of the pericardial content. One
may consider close observation and medical therapy if
hemodynamics are not significantly compromised and
the etiology of pericardial content is responsive to medical therapy. However, once hemodynamic deterioration is obvious, the physician must determine how to
quickly and safely relieve intrapericardial pressure with
the equipment that is available and prevent subsequent
hemodynamic collapse.
MEDICAL TREATMENT
Inotropic support, vasodilators, and volume infusion
have a limited role in the medical treatment of cardiac
tamponade, especially in normovolemic and hyper-
Figure 3. Tracings obtained during cardiac catherization from a patient with cardiac tamponade before (A)
and after (B) pericardiocentesis. (Adapted with permission from Hoit BD. Pericardial disease and pericardial heart disease. In: O’Rourke RA, ed. Stein’s
internal medicine, 5th ed. Mosby-Year Book; 1998:
276.)
volemic patients, because volume infusion can decrease
transmural pressures, resulting in worsened hemodynamics.25 On the other hand, blood volume expansion to
maintain the venoatrial gradients may be effective in patients suffering from low-pressure cardiac tamponade.
NEEDLE PERICARDIOCENTESIS
Percutaneous needle pericardiocentesis under echocardiographic guidance is the preferred therapy for cardiac tamponade that is causing hemodynamic compromise (Figure 4).24,26 The first needle pericardiocentesis
was performed in 1840 by Franz Shuh, a physician from
Vienna, and the method has undergone multiple modifications since then. It is best to perform the procedure
in the cardiac catheterization laboratory under echocardiographic guidance so that cardiac hemodynamics
can be monitored. Real-time cardiac ultrasound imaging allows one to track the needle tip and assure correct
location by following the injection of normal saline into
the pericardial space. It also allows the physician to
assess the cardiac response to drainage and measure the
volume of the residual pericardial content after drainage. When the cause of accumulation of the pericardial
Cardiology Volume 10, Part 3 7
C a r d i a c Ta m p o n a d e : D i a g n o s i s a n d Tr e a t m e n t
30°–45°
Figure 4. Technique for emergency pericardiocentesis. (Adapted with permission from Aikat S, Ghaffari S. A review of pericardial diseases: clinical, ECG and hemodynamic features and management. Clev Clin J Med 2000;67:911.)
content is uncertain, fluid obtained at pericardiocentesis should be sent for diagnostic studies. A study by
Ziskind et al showed that percutaneous pericardial
biopsy at the time of pericardiocentesis significantly
increased diagnostic yield in malignant and nonmalignant pericardial effusion.27
Removal of fluid by pericardiocentesis in patients
with cardiac tamponade usually leads to normalization
of intracardiac pressures and cardiac output, returns
pericardial pressure to the intrapleural pressure level,
and normalizes the right atrial waveform with reappearance of the diastolic y descent wave. If the right
atrial pressure remains elevated and prominent y
descent appears after pericardiocentesis, the diagnosis
of effusive constrictive pericarditis must be considered.28,29
Due to the high reoccurrence rate of pericardial
effusion after initial pericardiocentesis, it is recommended that an indwelling pigtail drainage catheter be
left in the pericardial space to monitor the rate of accumulation of pericardial content. If the drained amount
is less than 50 mL over 24 hours, the catheter can be
removed. Otherwise, the catheter should be kept in
8 Hospital Physician Board Review Manual
place so it can be used for intrapericardial delivery of
sclerosing agents.30,31
In certain clinical presentations of cardiac tamponade, percutaneous balloon pericardiotomy (PBP) is
used in order to avoid the morbidity and discomfort of
surgical drainage of the pericardial content.27 With the
PBP method, a pericardial “window” is created between
the pericardium and the absorbing surface of the pleura or peritoneum.32,33 Typically performed in the cardiac catheterization laboratory, PBP is safe and effective
and is usually well tolerated by patients. This procedure
may be especially useful for patients with malignant
pericardial effusion and a short life expectancy.
SURGICAL DRAINAGE
Open surgical drainage offers several advantages,
including complete drainage of the pericardial contents, access to pericardial tissue for histopathologic
and microbiologic diagnoses, and the ability to drain
loculated effusions. The 3 most common surgical approaches to treating cardiac tamponade include the
subxiphoid pericardial window, thoracostomy with creation of a pericardial window, and thoracotomy with
C a r d i a c Ta m p o n a d e : D i a g n o s i s a n d Tr e a t m e n t
complete pericardiectomy. A pericardial window is the
most commonly used technique and may be performed
through subxiphoid median sternotomy or left thoracotomy. The subxiphoid approach provides the same
degree of long-term survival as other approaches with
significantly less operative morbidity and mortality.34
Recently, camera-assisted thoracic surgical techniques
have been introduced, where a pericardial window is created under direct thoracoscopic vision.35,36 This method
provides effective drainage of loculated pericardial effusions complicated by cardiac tamponade.
SUMMARY POINTS
• The fibrous pericardium envelops the entire heart
and much of the ascending aorta, the main pulmonary artery, all pulmonary veins, and portions of
the inferior and superior venae cavae.
• Cardiac tamponade is a life-threatening compression of the heart caused by accumulation of contents
in the pericardium.
• The 4 most common causes of accumulation of fluid
in the pericardium in an amount sufficient to cause
serious obstruction to the cardiac inflow of blood are
infectious and neoplastic diseases, idiopathic pericarditis, and uremia.
• Patients with cardiac tamponade may complain of
severe shortness of breath accompanied by chest
tightness and dizziness.
• Cardiac tamponade should be considered in any
patient with tachycardia, hypotension, and elevation
of jugular venous pressure with a prominent x descent
and absence of the y wave. The latter finding differentiates cardiac tamponade from constrictive pericarditis, where the y descent is prominent. Kussmaul’s
sign is generally not seen in pure cardiac tamponade.
• Pulsus paradoxus is a key diagnostic finding of cardiac tamponade. It is defined as an inspiratory fall in
systolic arterial pressure greater than 10 mm Hg during normal breathing.
• There are no specific electrocardiogram signs of cardiac tamponade, although low voltage and other
signs of pericarditis, including electrical alternans,
may be present.
• There are no specific signs of cardiac tamponade on
chest radiograph, although cardiomegaly in the
presence of clear lung fields may be suggestive.
• Computed tomography and magnetic resonance
imaging are inconvenient techniques in patients with
acute cardiac tamponade.
• Echocardiographic signs of cardiac tamponade are
right atrial and ventricular collapse and significant
respiratory variation in tricuspid inflow (> 50%) and
mitral inflow (> 30%).
• On hemodynamic tracings during cardiac catheterization in patients with cardiac tamponade, elevation
of cardiac diastolic pressures and equalization of
those with elevated mean pericardial pressure can be
seen. In addition, right atrial and pulmonary capillary wedge pressure tracings show an attenuated or
absent y wave.
• The treatment of cardiac tamponade is urgent percutaneous or surgical drainage of the pericardial
content.
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Alexander RW, editors. Hurst’s the heart: arteries and
veins. 6th ed. Vol 1. New York: McGraw-Hill; 1994:
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2. Fowler NO. Pericardium in health and disease. Mount
Kisco (NY): Futura Publishing Company; 1985.
3. Holt JP. The normal pericardium. Am J Cardiol 1970;
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4. Reddy PS, Curtiss EI, Uretsky BF. Spectrum of hemodynamic changes in cardiac tamponade. Am J Cardiol 1990;
66:1487–91.
5. Spodick DH. Threshold of pericardial constraint: the
pericardial reserve volume and auxiliary pericardial
functions. J Am Coll Cardiol 1985;6:296–7.
6. Santamore WP, Li KS, Nakamoto T, Johnston WE. Effects
of increased pericardial pressure on the coupling
between the ventricles. Cardiovasc Res 1990;24:768–76.
7. Boltwood CM Jr. Ventricular performance related to
transmural filling pressure in clinical cardiac tamponade.
Circulation 1987;75:941–55.
8. Spodick DH. Pathophysiology of cardiac tamponade.
Chest 1998;113:1372–8.
9. Spodick DH. Cardiac tamponade: clinical characteristics,
diagnosis and management. In: Spodick DH, editor. The
pericardium: a comprehensive textbook. New York:
Marcel Dekker; 1997:153–79.
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C a r d i a c Ta m p o n a d e : D i a g n o s i s a n d Tr e a t m e n t
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10 Hospital Physician Board Review Manual
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Cardiology Board Review Manuals
TOPICS COVERED IN THE
CARDIOLOGY BOARD REVIEW MANUALS
Volume 7
Part 1
Chronic Stable Angina I: Risk Factors and Evaluation
Part 2
Chronic Stable Angina II: Treatment and Case Studies
Part 3
Management of Atrial Fibrillation
Part 4
Atrial Fibrillation: Case Studies and Treatment
Volume 8
Part 1
Diagnosis and Treatment of Primary Hypertension
Part 2
Update on Fibrinolytic Therapy: Mega-Trials
Part 3
Update on Fibrinolytic Therapy: New Treatment Regimens
Part 4
Cardiovascular Sources of Embolic Stroke: I
Part 5
Risk Stratification and Treatment for Sudden Cardiac Death
Volume 9
Part 1
Case Studies in Primary Hypertension
Part 2
Constrictive Pericarditis: A Case Study
Part 3
Cardiovascular Sources of Embolic Stroke: II
Part 4
Hormone Replacement Therapy and Coronary Heart Disease
Part 5
Infective Endocarditis
Part 6
Cholesterol and Cardiovascular Risk: Review and Case Studies
Cardiology Volume 10, Part 3 11
NOTES
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