Pericardial diseases or other conditions affecting the pericardium can lead to pericardial exudation and pericardial effusion. When the effusion accumulates rapidly or reaches a significant volume, the increased pericardial pressure can result in a marked reduction in cardiac output and venous return, leading to clinical symptoms known as cardiac tamponade.
Etiology
Pericardial effusion can accompany pericarditis of various causes. Common causes include tumors, idiopathic pericarditis, and infectious pericarditis. In recent years, there has been an increasing trend in pericardial effusion caused by tuberculous pericarditis. Severe systemic congestion can lead to transudative pericardial effusion. Hemorrhagic pericardial effusion can result from penetrating injuries, myocardial rupture after infarction, cardiac surgery, or coronary artery perforation during interventional procedures. Rapid or large pericardial effusion can lead to cardiac tamponade.
Pathophysiology
Under normal conditions, the mean pressure within the pericardial cavity is close to zero or slightly below atmospheric pressure, with mild negative pressure during inspiration and near-positive pressure during expiration. Small amounts of pericardial effusion generally do not affect hemodynamics. However, a rapid increase in fluid volume, even as little as 200 mL, can sharply raise pericardial pressure due to the limited ability of the pericardium to stretch, leading to cardiac compression. This results in impaired diastolic filling of the ventricles, elevated central venous pressure, a significant reduction in cardiac output, and hypotension, manifesting as acute cardiac tamponade. In contrast, chronic pericardial effusion allows gradual adaptation of the pericardium, enabling it to accommodate up to 2,000 mL of fluid without significant hemodynamic compromise.
Clinical Manifestations
The clinical hallmark of cardiac tamponade is Beck's triad: hypotension, muffled heart sounds, and jugular venous distension.
Symptoms
Dyspnea is the most prominent symptom of pericardial effusion, potentially caused by pulmonary congestion due to compression of the bronchi, lungs, or major blood vessels. Severe dyspnea may result in orthopnea, with the patient leaning forward, exhibiting shallow and rapid breathing, pallor, and cyanosis. Compression of the trachea or esophagus may cause dry cough, hoarseness, and dysphagia. Additional symptoms may include upper abdominal pain, hepatomegaly, generalized edema, pleural effusion, or ascites. In severe cases, shock may occur.
Signs
Cardiac apex beat may be weakened, located medially to the left cardiac dullness border, or undetectable. Percussion may reveal an enlarged cardiac dullness area extending bilaterally, with the entire area being absolutely dull. Heart sounds may be muffled and distant. Large effusions may cause dullness on percussion below the left scapula, accompanied by bronchial breath sounds, known as Ewart's sign, which results from compression of lung tissue. In rare cases, a pericardial knock may be heard at the left sternal border in the 3rd-4th intercostal space (as seen in constrictive pericarditis). Large effusions may reduce systolic blood pressure with minimal changes in diastolic pressure, leading to a narrowed pulse pressure. Depending on the severity of tamponade, pulses may weaken or pulsus paradoxus may occur. Large effusions can impair venous return, causing systemic venous congestion, including jugular venous distension, hepatomegaly, a positive hepatojugular reflux sign, ascites, and lower extremity edema.
Cardiac Tamponade
Acute cardiac tamponade is caused by the rapid accumulation of large amounts of pericardial fluid, presenting with sinus tachycardia, hypotension, narrowed pulse pressure, and markedly elevated venous pressure. Severe reductions in cardiac output can lead to acute circulatory failure and shock. Slower fluid accumulation may result in subacute or chronic cardiac tamponade, characterized by systemic venous congestion, including jugular venous distension and Kussmaul's sign (increased jugular venous pressure during inspiration). Pulsus paradoxus may also occur, characterized by a noticeable weakening or disappearance of the radial pulse during inspiration, which returns during expiration. This can be confirmed by a drop in systolic blood pressure of 10 mmHg or more during inspiration.
Auxiliary Examinations
X-ray
X-ray imaging may reveal an enlarged cardiac silhouette with a flask shape and reduced or absent cardiac motion. A clear lung field with a significantly enlarged cardiac opacity strongly suggests pericardial effusion and helps differentiate it from heart failure.
Electrocardiography (ECG)
ECG findings in pericardial effusion may include low-voltage QRS complexes in limb leads. With large effusions, electrical alternans of the P wave, QRS complex, and T wave may be observed, often accompanied by sinus tachycardia.
Echocardiography
Echocardiography is a simple, rapid, and reliable method for diagnosing pericardial effusion. Features of cardiac tamponade include the presence of pericardial effusion throughout the cardiac cycle, right atrial collapse during late diastole, early diastolic collapse of the right ventricular free wall, shortened aortic valve opening time, reduced stroke volume, and altered Doppler flow patterns of the mitral, tricuspid, and hepatic veins. Additional findings may include an inspiratory increase in right ventricular diameter, a decrease in left ventricular diameter, and leftward displacement of the interventricular septum. Echocardiography can quantify and localize pericardial effusion and guide pericardiocentesis.
Cardiac Magnetic Resonance Imaging (MRI)
Cardiac MRI provides clear visualization of the location, extent, and volume of pericardial effusion. The signal intensity of the effusion can help infer its nature. MRI can also identify associated pathological changes, such as pericardial thickening or tumors within the pericardial cavity.
Pericardiocentesis
Pericardiocentesis allows for the collection of pericardial fluid for routine, biochemical, bacterial culture, acid-fast bacilli, and cytological analyses, aiding in determining the nature and etiology of the effusion.
Diagnosis and Differential Diagnosis
Diagnostic Criteria
For patients with dyspnea, the presence of hypotension, jugular venous distension, pulsus paradoxus, an enlarged cardiac dullness area, and distant heart sounds should raise suspicion. A definitive diagnosis can be made through echocardiographic detection of pericardial effusion. Determining the etiology of pericardial effusion requires clinical evaluation, laboratory tests, pericardial fluid analysis, and assessment for associated diseases.
Differential Diagnosis
Differentiation is primarily required for clinical conditions causing dyspnea, particularly heart failure. The history of underlying cardiac diseases such as coronary artery disease, hypertension, valvular disease, congenital heart disease, or cardiomyopathy, along with findings like pulmonary crackles, heart sounds, murmurs, or pericardial friction rub, can aid in differentiation. Echocardiography is crucial for confirming the diagnosis.
Prognosis
The prognosis of pericardial effusion varies with its etiology. Malignant tumors are associated with poor outcomes, while infectious pericarditis can resolve with timely and effective treatment, although some cases may result in myocardial damage or constrictive pericarditis.
Treatment
Pericardiocentesis is the simplest and most effective method for relieving cardiac tamponade. Emergency pericardiocentesis or surgical pericardial window drainage is required for all patients with hemodynamically unstable acute cardiac tamponade. Patients with shock require immediate volume expansion and vasopressor therapy. For hemodynamically stable patients with pericardial effusion, efforts should focus on identifying the etiology, treating the primary disease, and monitoring hemodynamic status. Pericardial decompression and laboratory analysis of the drained fluid may be necessary.
Prevention
Pericardial effusion is typically a complication of other diseases. Prevention primarily involves the proactive treatment of underlying conditions.