
Hyperlipidaemia
Cardiology | Endocrinology
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:
Risk Factors
Patients with systemic autoimmune disease can have multiorgan involvement, such as pericarditis, nephritis, pleuritis, arthritis, and skin disorders.
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.
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) |
PR-segment depression | Present | Absent |
QRS complex changes | Absent | Loss of R-wave and development of Q-wave |
In symptomatic pericardial effusion and cardiac tamponade cardiocentesis is performed.
Constrictive pericarditis and pericardial effusion can mimic heart failure but both of these can themselves be differentiated.
Constrictive Pericarditis | Cardiac Tamponade | Heart failure | |
Kusmaul’s sign | Present | Absent | Absent |
Pulsus paradoxus | Uncommon | Present | Absent |
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 |
Hypotension | Variable | Severe | Variable |
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.
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 Investigation
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Toronto Essential Notes
Oxford handbook of Clinical Medicine
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