Occurs when fluid accumulates in the pericardial space compressing the heart and compromises cardiac output.
Consequences range from minimal to hemodynamic collapse.
It is a cardiac emergency, in which there is often rapid accumulation of pericardial fluid, resulting in a sudden increase in intra-pericardial pressure.
Intrapericardial, right atrial, pulmonary artery diastolic and pulmonary capillary wedge pressures are all elevated and equalized.
When intrapericardial pressure exceeds intracardiac pressures, the atrial and ventricular walls invert, resulting in a decrease in diastolic filling, and eventually a decrease in cardiac output.
If cardiac tamponade is left untreated, cardiogenic shock occurs and can result in death.
In the absence of other pathology, pericardiocentesis with normalize pressures and improve cardiac output and can confirm diagnosis.
Diagnosis can be challenging because patients can have indolent fluid accumulation.
When clinically suspected echocardiography is the most frequently used diagnostic technique.
The finding of a pericardial effusion does not define the presence of cardiac tamponade.
Findings in echocardiographic studies include right atrial systolic collapse, right ventricular diastolic collapse, inferior vena caval plethora and exaggeration of respiratory related changes in flow velocities across the mitral and tricuspid valves.
Echocardiographic findings of right atrial and right ventricle collapse are characteristic of cardiac tamponade and are specific for diagnosis.
Cardiac CT and magnetic resonance imaging are second line to echocardiography in diagnostic effectiveness.
Occurs on a continuum of hemodynamic effects.
Echocardiography may be overly sensitive and the diagnosis can be suggested with only subtle evidence of hemodynamic compromise.
Pericardial sac normally contains 15-30 ml of fluid.
Pericardial sac has 2 layers: an outer parietal pericardium and an inner visceral pericardium, the epicardium, which reflects over the surface of the heart.
Pericardial pressure approximates that of the pleural pressure which is about 5 mm Hg lower than the central venous pressure.
The finding of a pericardial effusion does not define the presence of cardiac tamponade.
When fluid accumulates in the pericardial sac slowly the parietal pericardium compliance increases.
As fluid increases in the pericardial space the intrapericardial pressure increases and the central venous pressure increases as well to maintain a gradient that allows cardiac filling.
When pericardial compliance reaches its limit the intrapericardial pressure first equalizes with the right ventricle diastolic pressure and then with the left causing drop in cardiac output and circulation is remained by an increased heart rate, contractility and peripheral arterial vasoconstriction.
Patients with the acute idiopathic pericarditis rarely develop constrictive pericarditis at less than .5% or pericardial tamponade at less than 3%.
Life-threatening complications of pericarditis, such as constrictive pericarditis or pericardial tamponade are more associated with bacterial, or tuberculosis infections.
A large amount of fluid may accumulate before hemodynamic changes occur because of pericardial compliance.
In the presence of rapid accumulation of fluid in the pericardial space the ability of the pericardium to stretch may be exceeded and a rapid drop in cardiac output may occur.
Most common diagnoses are acute idiopathic pericarditis, iatrogenic effusion, malignancy, acute myocardial infarction, end stage renal disease, congestive heart failure, collagen vascular diseases, tuberculosis or bacterial infections and valvular heart disease.
Viral infections, metabolic abnormalities, such as uremia and hypothyroidism, autoimmune disorders are common causes of pericardial effusion which lead to transudative and nonhemorrhagic effusions.
Aortic dissection, leading to aortic wall injury, and penetrating, trauma are severe causes of hemorrhagic pericardial, effusion and develop abruptly.
Metastatic disease is a common cause of symptomatic hemorrhagic pericardial effusion with lung, breast, esophageal cancers, being the most common, but melanomas, lymphoma, leukemia, AIDS related Kaposi’s sarcoma may be causes.
Although pericardial effusions are common after cardiac surgery, tamponade in this situation is rare.
Percutaneous cardiac procedures, such as pacemaker implantation, coronary angioplasty procedures that involve interatrial septostomy and transcatheter valve interventions can cause hemorrhagic pericardial effusion.
Symptoms include shortness of breath, chest pain or fullness in the chest.
Beck’s triad of hypertension, jugular venous distention, and muffled heart sounds are unreliable in diagnosing acute cardiac tamponade.
EKG signs of pericardial involvement, including depressed PR segments, diffuse ST segment elevations, T-wave flattening, low-voltage QRS complexes or electrical alternans, are unreliable in making the diagnosis of cardiac tamponade.
May be associated with nausea or abdominal pain from hepatic and visceral congestion or difficulty swallowing from esophageal compression.
May be associated with fever, anorexia, cough, weakness, and heart palpitations.
Diagnosis is a clinical one and requires a high index of suspicion.
The lack of hemodynamic instability does not preclude the diagnosis.
Distensibility of the pericardium, and the rate of fluid accumulation, rather than the amount of fluid in the pericardial sac determines the interaction between pericardial and cardiac filling pressures.
A small amount of pericardial fluid that accumulates rapidly can cause tamponade faster than a large slow-growing to effusion.
Physical examination with pericardial tamponade may reveal tachycardia, hypotension and tachypnea and depends on the degree of hemodynamic compromise.
Chest x-rays have limited ability in diagnosing cardiac tamponade unless the effusion exceeds 300 mL and it provides only a supportive role in diagnosis.
Classic findings, Beck triad, characterized by decreasing arterial blood pressure, increasing jugular venous pressure and a small quiet heart and is typically seen in acute tamponade from trauma, myocardial or aortic rupture.
Increased jugular venous pulse, pulsus paradoxes and tachycardia are the most common findings on clinical exam.
Signs of tamponade include compensatory, tachycardia, elevated, jugular venous pressure, hypertension, and pulsus paradoxus.
Patients should be evaluated for the presence of pulsus paradoxus, which is an exaggeration of the normal inspiratory decreased in blood pressure.
Pulsus paradoxes has a sensitivity of 82% when greater than 10 mmHg.
Muffled heart sounds, electrical alternans on EKG, increased cardiac size on chest x-ray are not sensitive, nor specific for acute tamponade.
In medical patients that develop pericardial effusions slowly the Beck triad may not be seen at all, and in some medical patients with preexisting hypertension may have increased blood pressure.
Fever associated with pericardial effusions suggest an infectious etiology or a connective tissue disease.
Acute process associated with shock.
Hypertensive cardiac tamponade occurs in patients with pre-existing hypertension and is attributed partly due to Beta adrenergic surge.