Pericarditis, Tamponade & Constrictive Pericarditis
Inflamed, filled, or scarred: three ways the pericardium squeezes the heart
Acute pericarditis: causes
Viral and idiopathic. Most cases in developed countries are idiopathic and presumed viral. Coxsackievirus B is the classic identified cause, with echovirus and adenovirus less often, typically in a young adult 1–2 weeks after a viral illness. The adjacent myocardium is often inflamed as well, and a troponin rise marks myopericarditis. Where TB is endemic, tuberculosis is the leading cause.
| Cause | Clue | Note |
|---|---|---|
| Viral / idiopathic | Young adult after a viral illness | Coxsackie B; troponin rise = myopericarditis |
| Peri-infarction | 1–3 days after a transmural MI | Inflammation extends from necrotic myocardium |
| Dressler / post-pericardiotomy | Weeks to months after MI or cardiac surgery | Autoimmune; fever, pleuritis, ± effusion |
| Uremia | Usually BUN >60 mg/dL | Fibrinous; ECG may be atypical; intensify dialysis |
| Autoimmune | SLE, rheumatoid arthritis | Serositis |
| Drug-induced lupus | Hydralazine, procainamide, isoniazid | Anti-histone antibodies; spares kidneys and CNS; resolves when the drug is stopped |
| Tuberculosis | Endemic regions, HIV | Effusion that often scars into constriction |
| Malignancy | Lung and breast cancer, lymphoma, melanoma | Hemorrhagic effusion; tamponade |
| Radiation | Mediastinal irradiation (e.g., Hodgkin lymphoma) | Acute pericarditis or constriction years later |
After myocardial injury. Peri-infarction (fibrinous) pericarditis appears 1–3 days after a transmural infarct as inflammation spreads to the overlying pericardium. Dressler syndrome, weeks to months later, is an autoimmune reaction to myocardial antigens exposed by necrosis. Post-pericardiotomy syndrome after cardiac surgery is the same process. Aspirin is the preferred anti-inflammatory early after MI, because other NSAIDs and glucocorticoids may impair healing of the infarct scar.
Presentation, ECG, and treatment
Pain. The pain is sharp, pleuritic, and retrosternal. It worsens when lying flat or breathing in and eases when sitting up and leaning forward. Radiation to the trapezius ridge is fairly specific, because the phrenic nerve (C3–C5) supplies the parietal pericardium and shares spinal segments with the skin over the trapezius.
Friction rub. A scratchy, high-pitched rub with up to three components (atrial systole, ventricular systole, and early diastole) is heard best at the left sternal border with the patient leaning forward at end-expiration.
ECG. Pericarditis inflames the entire epicardium and the atria. The result is concave (saddle-shaped) ST elevation across most limb and precordial leads with PR depression, and the mirror image in aVR (ST depression with PR elevation). Reciprocal ST depression and Q waves are absent, unlike a STEMI, whose changes follow one coronary territory. Over days to weeks, the ST segments normalize and T waves may invert before recovering.
Treatment. First-line therapy is high-dose aspirin or an NSAID such as ibuprofen plus colchicine for about 3 months, which roughly halves recurrences. Colchicine binds tubulin and blocks microtubule polymerization, impairing neutrophil migration and degranulation; diarrhea is its main side effect. Glucocorticoids are reserved for contraindications to NSAIDs or for autoimmune causes, because they increase the recurrence rate.
Cardiac tamponade
Physiology. Tamponade is a physiologic state, not a volume. Fluid raises intrapericardial pressure above the chambers' filling pressures, so the heart cannot fill in diastole. Stroke volume and blood pressure fall despite reflex tachycardia, producing obstructive shock. The thin-walled right atrium and right ventricle collapse first. The pericardial pressure-volume curve is flat and then nearly vertical, so the rate of accumulation matters most. As little as 150–200 mL collecting suddenly (trauma, ventricular free-wall rupture, aortic dissection into the pericardium) can tamponade, whereas slow effusions stretch the sac to more than 1 L. For the same reason, removing a small volume can be lifesaving.
Findings. Beck triad is hypotension, distended neck veins, and muffled heart sounds, accompanied by tachycardia. Diastolic pressures equalize across the chambers (RA ≈ RV diastolic ≈ PA diastolic ≈ pulmonary capillary wedge pressure). The jugular venous pulse keeps its x descent but loses the y descent, because the compressed ventricle cannot fill in early diastole.
Pulsus paradoxus. Inspiration increases venous return to the right ventricle. Within a fixed pericardial space, the septum bows into the left ventricle, reducing LV filling and stroke volume, so systolic pressure falls more than 10 mmHg (ventricular interdependence). The sign also occurs in severe asthma or COPD exacerbations and croup, and occasionally in constrictive pericarditis.
ECG, echo, and chest film. Electrical alternans is a beat-to-beat alternation of QRS amplitude, with low voltage, as the heart swings within a large effusion. It differs from pulsus alternans, the alternating pulse strength of severe LV failure. Echocardiography confirms the diagnosis: an effusion with right atrial and early-diastolic RV collapse and a plethoric IVC. The chest film may show an enlarged "water-bottle" heart with clear lungs.
Treatment. Treat with emergency echo-guided pericardiocentesis, or surgical drainage for trauma or rupture, while IV fluids support preload. Recurrent malignant effusions are managed with a pericardial window.
Diuretics, nitrates, and positive-pressure ventilation reduce preload and can precipitate cardiovascular collapse in tamponade.
Constrictive pericarditis
Pathology and causes. A thickened, fibrotic, often calcified pericardium encases the heart like a rigid shell. Tuberculosis is the leading cause worldwide. In developed countries, the usual causes are prior idiopathic or viral pericarditis, cardiac surgery, and mediastinal radiation. Chronic right-heart congestion dominates, with jugular venous distension, hepatomegaly, ascites, and edema. Pericardiectomy is curative.
Signs. Early diastolic filling is rapid and then stops abruptly when the ventricle meets the shell. This produces a steep y descent, a dip-and-plateau ("square-root") ventricular pressure tracing, and a pericardial knock, an early diastolic sound that occurs earlier than an S3. The shell also blocks transmission of inspiratory pressure changes to the heart, so the extra venous return cannot be accommodated and the JVP rises on inspiration (Kussmaul sign). Kussmaul sign also occurs with restrictive cardiomyopathy and right ventricular infarction but is typically absent in tamponade. Imaging shows pericardial thickening or calcification.
| Feature | Tamponade | Constrictive pericarditis | Restrictive cardiomyopathy |
|---|---|---|---|
| Problem | Fluid under pressure | Rigid, thick pericardium | Stiff, infiltrated myocardium (amyloid, sarcoid, hemochromatosis) |
| y descent | Absent | Steep (dip-and-plateau) | Steep |
| Kussmaul sign | Usually absent | Present | Often present |
| Pulsus paradoxus | Prominent | Occasional | Rare |
| Distinctive clue | Electrical alternans; chamber collapse on echo | Knock; calcification; septal bounce; near-normal BNP | Biatrial enlargement; normal pericardium; high BNP |
| Treatment | Pericardiocentesis | Pericardiectomy | Treat the cause |
Constriction versus restrictive cardiomyopathy. Both cause diastolic heart failure with a preserved ejection fraction, high filling pressures, and steep y descents. Constriction shows a thick or calcified pericardium, exaggerated respiratory variation in ventricular filling with a septal bounce on echo, a knock, and a near-normal BNP because the myocardium itself is not stretched. It is surgically curable. Restrictive cardiomyopathy has a normal pericardium, stiff infiltrated walls, biatrial enlargement, and a high BNP, and its treatment targets the underlying disease.