|Video: Pericarditis Overview|
Overview Pericarditis is the most common form of pericardial disease and a relatively common cause of chest pain. The etiology of pericarditis may be infectious (eg, viral and bacterial) or noninfectious (eg, systemic inflammatory diseases, cancer, and post-cardiac injury syndromes). Tuberculosis is a major cause of pericarditis in developing countries but accounts for less than 5% of cases in developed countries, where idiopathic, presumed viral causes are responsible for 80% to 90% of cases. The diagnosis is based on clinical criteria including chest pain, a pericardial rub, electrocardiographic changes, and pericardial effusion.
Acute pericarditis: An inflammation of the pericardial sac surrounding the heart.
Pericardial friction rub: Harsh, high-pitched, scratchy sound, with variable intensity, usually best heard at the left sternal border by auscultation, due to pericarditis.
Pericardial Effusion: Fluid that fills the pericardial space, which may be due to infection, haemorrhage, or malignancy. A rapidly accumulating effusion may lead to cardiac compromise.
Cardiac Tamponade: Increased pressure within the pericardial space caused by an accumulating effusion, which compresses the heart and impedes diastolic filling.
The pericardium is a membranous layer that covers the heart and helps protect it, fixes the heart in the mediastinum and lubricates the heart.
The pericardium has two layers:
The pericardium has two layers:
|Remember Patients with systemic autoimmune disease can have multiorgan involvement, such as pericarditis, nephritis, pleuritis, arthritis, and skin disorders.|
|Remember Acute Pericarditis triad: chest pain, friction rub and ECG changes|
Pericarditis causing pericardial effusion can show
Remember to differentiate pericarditis from other life-threatening causes of chest pain, including acute coronary syndrome, myocarditis or pulmonary thromboembolism
|Remember Prompt echocardiography may be required to determine the presence and amount of pericardial fluid.|
|PERICARDITIS VS MYOCARDIAL INFARCTION|
|ECG||Acute pericarditis||Acute MI|
|ST-segment elevation||Diffuse in limb leads V2-V6||Depending on area of infarction (inferior, anterior or lateral)|
|QRS complex changes||Absent||Loss of R-wave and development of Q-wave|
In symptomatic pericardial effusion and cardiac tamponade cardiocentesis is performed.
|Remember Constrictive pericarditis and pericardial effusion can mimic heart failure but both of these can themselves be differentiated|
|Constrictive Pericarditis||Cardiac Tamponade||Heart failure|
|Jugular Venous Pressure (JVP)||Increased||Increased||Increased|
|Percardial Knock (third heart sound, due to rapid ventricular filling's being abruptly halted by the restricting pericardium)||Present||Absent||Absent|
|Remember Kusmaul's sign looks at JVP relationship with breathing. This is different to Kusmaul breathing which is air hunger, rapid deep breathing a sign of metabolic acidosis|
|Remember Constrictive pericarditis may show calcifications of the pericardium on chest x-ray or thickened pericardium on echocardiography. Definitive therapy is resection of the pericardium|
|Classical Quatret of Tamponade: hypotension, increased JVP, tachycardia, pulsus paradoxus|
Pathophysiology high intra-pericardial pressure → decreased venous return → decreased diastolic ventricular filling → decreased CO → hypotension and venous congestion