Pathophysiology
Summary
Pericarditis is an inflammatory condition affecting the pericardium, the protective sac around the heart. Common etiological factors mirror those of myocarditis and include viral and bacterial infections, toxins, and autoimmune disorders. Notably, it is one of the most common clinical features of systemic lupus erythematosus. Myocardial infarction (MI) can lead to two forms of pericarditis: an initial inflammatory type immediately after the event, and a delayed autoimmune variant known as Dressler syndrome appearing 2-4 weeks later. Additionally, pericarditis can be induced by uremia, as a sequela of metastatic disease to the pericardium, or due to conditions causing hemorrhagic pericarditis, such as uremia or malignancy.
Clinical symptoms of pericarditis include fever, tachycardia, and a characteristic precordial, sharp pain that is intensified by inspiration and decreased when leaning forward. On auscultation, the movement of inflamed pericardial layers against one another produces a distinct friction rub. Diagnostic clues include diffuse ST elevation on ECG and the potential development of pericardial effusion. The severity of an effusion, especially when leading to morbidity in cases like cardiac tamponade, is largely determined by the rate of pericardial filling rather than volume.
If left unchecked, pericardial effusion can escalate to cardiac tamponade, a grave condition that confines the heart's ability to expand and fill during diastole. This is clinically manifested by Beck's triad: muffled heart sounds, hypotension, and jugular vein distension (JVD). A hallmark of tamponade is pulsus paradoxus, a drop in systolic blood pressure of >10 mmHg during inspiration. This phenomenon arises due to all heart chambers experiencing equal pressures due to external compression, leading to the right ventricle bowing into the left ventricle during inspiration, consequently reducing left ventricular chamber size and stroke volume. Immediate intervention via pericardiocentesis becomes imperative in severe cases.
Constrictive pericarditis is as another complication, characterized by the heart's enclosure within a fibrotic, non-distensible pericardium, which hinders diastolic filling. Constrictive pericarditis can lead to diastolic heart, and is further distinguished by a pericardial knock on auscultation, a pronounced Y descent on the jugular venous waveform due to rapid atrial emptying, and increased in JVD during inspiration – known as Kussmaul's sign. Common etiologies of constrictive pericarditis span from scarring following open-heart surgery, infection by Mycobacterium tuberculosis, thoracic radiation, or from scarring following open heart surgery. In chronic stages, calcification of the pericardium becomes discernible as a white rim encircling the heart on CXR or CT.
Lesson Outline
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FAQs
Pericarditis commonly presents with sharp, precordial chest pain that intensifies upon inspiration and is alleviated by leaning forward. Tachycardia is often observed, and fever is a frequent constitutional symptom. Auscultation may reveal a pericardial friction rub, attributable to the inflamed visceral and parietal layers of the pericardium rubbing against each other.
Pericarditis is often indicated by diffuse ST elevation on an ECG. The condition may lead to pericardial effusion, which can hamper cardiac filling and preload if it becomes severe. The rate of pericardial fluid accumulation is a key factor in assessing the severity of the effusion. Underlying conditions such as uremia or malignancies can result in hemorrhagic pericarditis. In severe instances, rapid accumulation of pericardial fluid may precipitate cardiac tamponade, a life-threatening complication that significantly restricts diastolic filling of the heart.
Cardiac tamponade typically presents with Beck's Triad: muffled heart sounds, hypotension, and jugular vein distension (JVD). Another noteworthy feature is pulsus paradoxus, characterized by a decrease in systolic blood pressure of more than 10 mmHg during inspiration. Given its emergent nature, the definitive treatment for severe cardiac tamponade is immediate pericardial drainage via pericardiocentesis.
Constrictive pericarditis is a consequence of scarring and fibrosis of the pericardium, often subsequent to a previous episode of pericarditis. This results in a rigid, non-distensible pericardium that restricts diastolic expansion of the heart. It often presents with jugular vein distension (JVD) due to compromised right atrial filling and Kussmaul’s sign (a paradoxical rise in JVD during inspiration). Additionally, a "pericardial knock" may be heard on auscultation, indicating ventricular expansion against the thickened pericardium.
Constrictive pericarditis may arise from a myriad of causes such as mycobacterium tuberculosis infection, thoracic radiation therapy for malignancies like lung or breast cancer, or postoperative scarring after cardiac surgery. In chronic cases, pericardial calcification may be evident, appearing as a white rim encircling the heart on diagnostic imaging studies like chest X-ray (CXR) or computed tomography (CT).
