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Cardiac tamponade, also known as pericardial tamponade, is an emergency condition

in which fluid accumulates in the pericardium (the sac in which the heart is enclosed). If
the fluid significantly elevates the pressure on the heart it will prevent the heart's
ventricles from filling properly. This in turn leads to a low stroke volume. The end result
is ineffective pumping of blood, shock, and often death.

Incidence :

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.

Causes:

Cardiac tamponade occurs when the pericardial space fills up with fluid faster than the
pericardial sac can stretch. If the amount of fluid increases slowly (such as in
hypothyroidism) the pericardial sac can expand to contain a liter or more of fluid prior to
tamponade occurring. If the fluid occurs rapidly (as may occur after trauma or myocardial
rupture) as little as 100 ml can cause tamponade.

Causes of increased pericardial effusion include

hypothyroidism,

physical trauma (either penetrating trauma involving the pericardium or blunt chest
trauma),

pericarditis (inflammation of the pericardium),

iatrogenic trauma (during an invasive procedure),

and myocardial rupture

large or uncontrolled pericardial effusion

cancer, uraemia

Cardiac tamponade can occur due to:

 Dissecting aortic aneurysm (thoracic)


 End-stage lung cancer
 Pericarditis caused by bacterial or viral infections
 Wounds to the heart

Other potential causes include:


 Kidney failure
 Radiation therapy to the chest
 Recent invasive heart procedures
 Recent open heart surgery
 Systemic lupus erythematosus

cardiac surgery

Myocardial rupture is a somewhat uncommon cause of pericardial tamponade. It typically


happens in the subacute setting after a myocardial infarction (heart attack), in which the
infarcted muscle of the heart thins out and tears. Myocardial rupture is more likely to
happen in elderly individuals without any previous cardiac history who suffer from their
first heart attack and are not revascularized either with thrombolytic therapy or with
percutaneous coronary intervention or with coronary artery bypass graft surgery.[6]

One of the most common settings for cardiac tamponade is in the first 24 to 48 hours
after heart surgery. After heart surgery, chest tubes are placed to drain blood. These chest
tubes, however, are prone to clot formation. When a chest tube becomes occluded or
clogged, the blood that should be drained can accumulate around the heart, leading to
tamponade. Nurses will frequently milk clots from the tubes, or strip the tubes, but even
with these efforts chest tubes can become clogged. Thus, after heart surgery it is critical
to be on the watch for chest tube clogging.

Pathophysiology:
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 S 1 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.

 Anxiety, restlessness
 Chest pain
o Radiating to the neck, shoulder, back, or abdomen
o Sharp, stabbing
o Worsened by deep breathing or coughing
 Difficulty breathing
 Discomfort, sometimes relieved by sitting upright or leaning forward
 Fainting, light-headedness
 Pale, gray, or blue skin
 Palpitations
 Rapid breathing
 Swelling of the abdomen or other areas

Additional symptoms that may be associated with this disease:

 Dizziness
 Drowsiness
 Low blood pressure
 Weak or absent pulse

Exams and Tests

There are no specific laboratory tests that diagnose tamponade. Echocardiogram is the
first choice to help establish the diagnosis.

Signs:

 Blood pressure may fall (pulsus paradoxical) when the person inhales
deeply
 Breathing may be rapid (faster than 12 breaths in an adult per minute)
 Heart rate may be over 100 (normal is 60 to 100 beats per minute)
 Heart sounds faint during examination with a stethoscope
 Neck veins may be abnormally extended (distended) but the blood
pressure may be low
 Peripheral pulses may be weak or absent

Other tests may include:

 Chest CT or MRI of chest


 Chest x-ray
 Coronary angiography
 ECG

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