Cardiac Tamponade

Background
Cardiac tamponade is a clinical syndrome caused by the accumulation of fluid in the pericardial
space, resulting in reduced ventricular filling and subsequent hemodynamic compromise.
Cardiac tamponade is a medical emergency. The overall risk of death depends on the speed of
diagnosis, the treatment provided, and the underlying cause of the tamponade. (See image
below.)
This anteroposterior-view chest radiograph shows a massive bottle-shaped heart and

conspicuous absence of pulmonary vascular congestion. Reproduced with permission from
Chest, 1996: 109:825.
[ CLOSE WINDOW ]
This anteroposterior-view chest radiograph shows a massive bottle-shaped heart and
conspicuous absence of pulmonary vascular congestion. Reproduced with permission from
Chest, 1996: 109:825.
Pathophysiology
The pericardium, which is the membrane surrounding the heart, is composed of 2 layers. The
parietal pericardium is the outer fibrous layer; the visceral pericardium is the inner serous layer.
The pericardial space normally contains 20-50 mL of fluid. Pericardial effusions can be serous,
serosanguineous, hemorrhagic, or chylous.
Reddy et al describe 3 phases of hemodynamic changes in tamponade.1
 Phase I: The accumulation of pericardial fluid causes increased stiffness of the ventricle,
requiring a higher filling pressure. During this phase, the left and right ventricular filling
pressures are higher than the intrapericardial pressure.
 Phase II: With further fluid accumulation, the pericardial pressure increases above the
ventricular filling pressure, resulting in reduced cardiac output.
 Phase III: A further decrease in cardiac output occurs, which is due to equilibration of
pericardial and left ventricular (LV) filling pressures.
The underlying pathophysiologic process for the development of tamponade is markedly

diminished diastolic filling because transmural distending pressures are insufficient to overcome
the increased intrapericardial pressures.
Systemic venous return is also altered during tamponade. Because the heart is compressed
throughout the cardiac cycle due to the increased intrapericardial pressure, systemic venous
return is impaired and right atrial and right ventricular collapse occurs. Because the pulmonary
vascular bed is a vast and compliant circuit, blood preferentially accumulates in the venous
circulation, at the expense of LV filling. This results in reduced cardiac output and venous return.
The amount of pericardial fluid needed to impair the diastolic filling of the heart depends on the
rate of fluid accumulation and the compliance of the pericardium. Rapid accumulation of as little
as 150 mL of fluid can result in a marked increase in pericardial pressure and can severely
impede cardiac output, whereas 1000 mL of fluid may accumulate over a longer period without
any significant effect on diastolic filling of the heart. This is due to adaptive stretching of the
pericardium over time. A more compliant pericardium can allow considerable fluid accumulation
over a longer period without hemodynamic insult.
Frequency
United States
The incidence of cardiac tamponade is 2 cases per 10,000 population in the United States.
Approximately 2% of penetrating injuries are reported to result in cardiac tamponade.
Mortality/Morbidity
Cardiac tamponade is a medical emergency. Early diagnosis and treatment are crucial to reduce
morbidity and mortality. Untreated, it is rapidly and universally fatal.
Sex
In children, cardiac tamponade is more common in boys than in girls, with a male-to-female ratio
of 7:3. In adults, cardiac tamponade appears to be slightly more common in men than in women.
The male-to-female ratio of 1.25:1 observed at author's referral center based on the International
Classification of Diseases (ICD) code 423.9. However, a male-to-female ratio of 1.7:1 is
observed at another level 1 trauma center.
Age
Cardiac tamponade related to trauma or HIV is more common in young adults, whereas
tamponade due to malignancy and/or renal failure occurs more frequently in elderly individuals.
Clinical
History
Symptoms vary with the underlying cause and the acuteness of the tamponade. Patients with
acute tamponade may present with dyspnea, tachycardia, and tachypnea. Cold and clammy
extremities from hypoperfusion are also observed in some patients.
A comprehensive review of the patient's history usually helps identify the probable etiology of a
pericardial effusion, which may result in cardiac tamponade.
 Patients with systemic or malignant disease present with weight loss, fatigue, or anorexia.
 Chest pain may be the presenting symptom in patients with pericarditis or myocardial
infarction.
 Musculoskeletal pain or fever may be present in patients with an underlying connective
tissue disorder.
 A history of renal failure can lead to a consideration of uremia as a cause of pericardial
effusion.
 Careful review of a patient's medications may indicate drug-related lupus leading to a
pericardial effusion.
 Recent cardiovascular surgery, coronary intervention, or trauma can lead to the rapid
accumulation of pericardial fluid and tamponade.2
 Recent pacemaker lead implantation or central venous catheter insertion can lead to the
rapid accumulation of pericardial fluid and tamponade.3
 Consider HIV-related pericardial effusion and tamponade if the patient has a history of
intravenous drug abuse or opportunistic infections.
 Inquire about chest wall radiation (ie, for lung, mediastinal, or esophageal cancer).
 Inquire about symptoms of night sweats, fever, and weight loss, which may be indicative
of tuberculosis.
Physical
Distended neck veins are a common feature in patients with tamponade. Evidence of chest wall
injury may be present in trauma patients. Tachycardia, tachypnea, and hepatomegaly are
observed in more than 50% of patients with cardiac tamponade, and diminished heart sounds and
a pericardial friction rub are present in approximately one third of patients.
 The Beck triad or acute compression triad

 Described in 1935, this complex of physical findings refers to increased jugular
venous pressure, hypotension, and diminished heart sounds.
 These findings result from a rapid accumulation of pericardial fluid. However,
this classic triad is usually observed in patients with acute cardiac tamponade.
 Pulsus paradoxus or paradoxical pulse
 This is an exaggeration (>12 mm Hg or 9%) of the normal inspiratory decrease in
systemic blood pressure.
 To measure the pulsus paradoxus, patients are often placed in a semirecumbent
position; respirations should be normal. The blood pressure cuff is inflated to at
least 20 mm Hg above the systolic pressure and slowly deflated until the first
Korotkoff sounds are heard only during expiration. At this pressure reading, if the
cuff is not further deflated and a pulsus paradoxus is present, the first Korotkoff
sound is not audible during inspiration. As the cuff is further deflated, the point at
which the first Korotkoff sound is audible during both inspiration and expiration
is recorded. If the difference between the first and second measurement is greater
than 12 mm Hg, an abnormal pulsus paradoxus is present.
 The paradox is that while listening to the heart sounds during inspiration, the
pulse weakens or may not be palpated with certain heartbeats, while S1 is heard
with all heartbeats.
 A pulsus paradoxus can be observed in patients with other conditions, such as
constrictive pericarditis, severe obstructive pulmonary disease, restrictive
cardiomyopathy, pulmonary embolism, rapid and labored breathing, and right
ventricular infarction with shock.
 A pulsus paradoxus may be absent in patients with markedly elevated LV
diastolic pressures, atrial septal defect, pulmonary hypertension, and aortic
regurgitation.
 Kussmaul sign
 This was described by Adolph Kussmaul as a paradoxical increase in venous
distention and pressure during inspiration.
 This sign is usually observed in patients with constrictive pericarditis but
occasionally is observed in patients with effusive-constrictive pericarditis and
cardiac tamponade.
 Ewart sign
 Also known as the Pins sign, this is observed in patients with large pericardial
effusions.
 It is described as an area of dullness, with bronchial breath sounds and
bronchophony below the angle of the left scapula.
 The y descent
 The y descent is abolished in the jugular venous or right atrial waveform.
 This is due to an increase in intrapericardial pressure, preventing diastolic filling
of the ventricles.
 Dysphoria: Behavioral traits such as restless body movements, unusual
facial expressions, restlessness, sense of impending death were reported by Ikematsu in
about 26% patients with cardiac tamponade.4
 Low-pressure tamponade: In severely hypovolemic patients, classical physical findings
such as tachycardia, pulsus paradoxus, and jugular venous distension were infrequent.
Sagrista-Sauleda et al identified low-pressure tamponade in 20% of patients with cardiac
tamponade.5 They also reported low-pressure tamponade in 10% of large pericardial
effusions.
Causes
For all patients, malignant diseases are the most common cause of pericardial tamponade.
Among etiology of tamponade, Merce et al reported malignant diseases in 30-60% of cases,
uremia in 10-15% of cases, idiopathic pericarditis in 5-15%, infectious diseases in 5-10%,
anticoagulation in 5-10%, connective tissue diseases in 2-6%, and Dressler or
postpericardiotomy syndrome in 1-2%. Tamponade can occur as a result of any type of
pericarditis.6
 HIV infection
 Infection - Viral, bacterial (tuberculosis), fungal
 Drugs - Hydralazine, procainamide, isoniazid, minoxidil
 Postcoronary intervention (ie, coronary dissection and perforation)
 Trauma
 Cardiovascular surgery (postoperative pericarditis)2
 Postmyocardial infarction (free wall ventricular rupture, Dressler syndrome)
 Connective tissue diseases -Systemic lupus erythematosus, rheumatoid arthritis,
dermatomyositis
 Radiation therapy
 Iatrogenic7 - After sternal biopsy, transvenous pacemaker lead implantation,
pericardiocentesis, or central line insertion
 Uremia
 Idiopathic pericarditis
 Complication of surgery at the esophagogastric junction such as antireflux surgery
 Pneumopericardium (due to mechanical ventilation or gastropericardial fistula)

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Background

This anteroposterior-view chest radiograph shows a massive bottle-shaped heart and

Reddy et al describe 3 phases of hemodynamic changes in tamponade.1

The underlying pathophysiologic process for the development of tamponade is markedly

 The Beck triad or acute compression triad

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