What is the difference between pericarditis and pericardial effusion

Management of Acute and Recurrent Pericarditis. J Am Coll Cardiol. Acute Cardiac Tamponade. N Engl J Med. Anesthetic challenges for pleuro-pericardial window. Saudi J Anaesth. Rosen's Emergency Medicine. Guidelines on the diagnosis and management of pericardial diseases executive summary. In: Post TW, ed. Last updated: May 4, Accessed: December 27, Imazio M, Adler Y.

Management of pericardial effusion. Cardiac tamponade revisited: a postmortem look at a cautionary case.. Tex Heart Inst J. Pericardial Effusion and Pericardiocentesis: Role of Echocardiography. Korean Circ J. Update on bedside ultrasound diagnosis of pericardial effusion.

Intern Emerg Med. Emergency Medicine E-Book. Elsevier Health Sciences ; Balachandran G. The Pericardium. Pleural, peritoneal and pericardial effusions — a biochemical approach. Biochem Med Zagreb. Current Clinical Medicine E-Book. Practical aspects of the management of pericardial disease.

Purulent pericardial effusions with pericardial tamponade - diagnosis and treatment issues.. This content does not have an English version. This content does not have an Arabic version.

Overview Pericardial effusion per-e-KAHR-dee-ul uh-FU-zhun is the buildup of excess fluid in the sac-like structure around the heart pericardium. Request an Appointment at Mayo Clinic.

Share on: Facebook Twitter. Show references Hoit BD. Etiology of pericardial disease. Accessed Feb. Hoit BD. Prompt recognition of the signs and symptoms of pericardial disease is critical so that appropriate treatments can be initiated.

Acute pericarditis has a classical presentation, including symptoms, physical examination findings, and electrocardiography abnormalities. Early recognition of acute pericarditis will avoid unnecessary invasive testing and prompt therapies that provide rapid symptom relief. Non-steroidal anti-inflammatory drugs NSAIDs remain first-line therapy for uncomplicated acute pericarditis, although colchicine can be used concomitantly with NSAIDS as the first-line approach, particularly in severely symptomatic cases.

Echocardiography is the main diagnostic tool used in the evaluation of pericardial effusion. A pericardial effusion causes an echo-free space between visceral and parietal pericardium; the extent of the space defines the size of the effusion Table 3.

Large effusions can produce the picture of a swinging heart. Although echocardiography is the imaging modality of choice for diagnosing a pericardial effusion, small loculated effusions pose a greater diagnostic challenge.

If there is a high level of clinical suspicion of a pericardial effusion and the TTE is nondiagnostic, alternative tomographic imaging should be considered. This is especially true for patients who have recently undergone open heart surgery, who frequently have echocardiographic studies with suboptimal imaging quality, and effusions which may be loculated and complex.

Cardiac CT and MRI will also aid in differentiating an effusion from pericardial fat, pericardial cysts and pleural effusions, all of which can mimic a pericardial effusion. Laboratory analysis in a patient with a pericardial effusion should include a complete blood count, chemistry panel, and erythrocyte sedimentation rate.

Further testing should be done according to clinical suspicion. The initial inspection should assess whether the fluid is hemorrhagic, purulent, or chylous.

Chylous fluid implies injury to the thoracic duct by trauma or infiltration. The fluid should be sent for a cell count; Gram stain; culture; cytology; acid-fast bacilli; determination of glucose, protein, and lactate dehydrogenase LDH levels; and specific gravity. The parameters listed in Table 4 have a high sensitivity for differentiating exudates versus transudates. An elevated protein level higher than 6.

However, no diagnostic test of pericardial fluid is specific for effusion associated with postpericardiotomy syndrome, radiation or uremic pericarditis, hypothyroidism, or trauma.

The medical management of pericardial effusion is based on treating the underlying cause. Effusions causing pretamponade or tamponade require immediate drainage.

Volume expansion and inotropic support may be used for hemodynamic stabilization pending drainage. In the immediate postoperative setting, surgical management and open drainage are preferred because of the high incidence of loculated effusions. Anti-coagulation should be avoided if possible.

Pericardiocentesis should be performed for diagnostic purposes if the cause of the effusion is unclear, or if malignancy or a purulent effusion is suspected. Therapeutic pericardiocentesis should be performed for effusions amenable to percutaneous drainage that are causing pretamponade or tamponade physiology.

Subxiphoid pericardiostomy, also known as a pericardial window, may be done under local anesthesia. It has a high success rate, with few complications, and recurrence of fluid accumulation is rare. Percutaneous balloon pericardiotomy is the least invasive of the surgical procedures. It is used primarily as palliative treatment for neoplastic effusions with a poor prognosis. It may be performed in the catheterization laboratory under fluoroscopy using a balloon-dilating catheter. Cardiac tamponade occurs when fluid accumulation in the finite serous pericardial space causes an increase in pressure, with subsequent cardiac compression and hemodynamic compromise.

Elevated intrapericardial pressure leads to progressive limitation of diastolic ventricular filling, resulting in lowered cardiac output. Symptoms resulting from decreased cardiac output and congestion include dyspnea, chest discomfort, weakness, restlessness, agitation, drowsiness, oliguria, and anorexia. If the tamponade develops acutely as a complication of an acute MI free wall rupture or trauma, the presentation is usually catastrophic, with shock or sudden death.

Tachycardia and tachypnea are common. Pulsus paradoxus is defined as an inspiratory decline in systolic blood pressure of more than 10 mmHg resulting from compression and poor filling of the left ventricle. Pulsus paradoxus is nonspecific and insensitive and can occur with extracardiac disease, such as severe chronic obstructive pulmonary disease or asthma. The ECG may be unremarkable. Abnormal findings on ECG include tachycardia, electrical alternans Figure 9 , low voltage, and may include changes associated with acute pericarditis Figure 6.

Usually, a moderate-size or large pericardial effusion is present and leads to increasing compression and subsequent diastolic compression of the cardiac chambers, usually in the sequence right atrium, right ventricle, left atrium with the lowest pressure chamber being affected first.

The most sensitive finding for tamponade physiology on the echocardiogram is inferior vena cava plethora, with absent inspiratory collapse; however this is not very specific. Right ventricular diastolic inversion may also been seen. Absent diastolic flow from the hepatic views suggests tamponade physiology.

The most typical finding on right heart catheterization is equalization of mean right atrial, right ventricular and pulmonary artery diastolic, and mean pulmonary capillary wedge pressures. The symptoms of pericardial tamponade can mimic those of right-sided heart failure, right ventricular infarction, constrictive pericarditis, and pulmonary embolism.

However, with the use of echocardiography and occasionally right heart catheterization, these may be distinguished. Patients with pretamponade and tamponade require immediate hospital admission and prompt pericardial drainage by pericardiocentesis. The drain catheter may be left in place for up to 48 hours if drainage is slow or reaccumulation likely. If follow-up echocardiography documents fluid reaccumulation, a pericardial window should be considered, because the infection risk associated with a pericardial drain increases after 48 hours.

Constrictive pericarditis refers to an abnormal scarring and loss of elasticity of the pericardium, resulting in impaired ventricular filling and decreased cardiac output. The frequency of different causes of constrictive pericarditis depends on the population and geography in question.

In developed countries, cardiac surgery and idiopathic constriction are the leading cause, while in certain developing countries tuberculous remains the number one etiology.

The initiating event results in a chronic inflammatory pericardial process, resulting in fibrinous scarring and occasionally calcification of the pericardium Figure As the heart becomes encased with a non-compliant pericardium, ventricular interdependance and dissociation between the intrathoracic and intracardiac pressure occurs.

In constriction, normal expansion of the right heart is restricted by the pericardium and the septum shifts to the left to accommodate the increase in venous return with inspiration; the opposite movement occurs with expiration.

Normally, there is a reduction in intrathoracic and intracardiac pressure with inspiration. The rigid pericardium impedes normal ventricular expansion and therefore venous return and pulmonary venous pressure. Because intrathoracic pressure drops but left ventricular pressure does not decrease with inspiration there is a reduction in the transpulmonary gradient.

This leads to impaired ventricular filling and decreased cardiac output. Ultimately, right and then left ventricular heart failure develop. Distinguishing heart failure caused by constrictive physiology from diastolic restrictive physiology is a classic diagnostic dilemma. Symptoms are often vague and their onset is insidious; they include malaise, fatigue, and decreased exercise tolerance.

With progression of constrictive pericarditis, symptoms of right-sided heart failure eg, peripheral edema, nausea, abdominal discomfort, ascites become apparent and usually precede signs of left-sided failure eg, exertional dyspnea, orthopnea, paroxysmal nocturnal dyspnea.

Increased ventricular filling pressures cause jugular venous distention and Kussmaul's sign paradoxical rise in jugular venous pressure on inspiration , which is sensitive but not specific for constrictive pericarditis. Constrictive effusive pericarditis consists of a tense pericardial effusion in the presence of pericardial constriction, and both tamponade and constrictive signs and symptoms are present.