Pericarditis & Cardiac Tamponade

The pericardium is a double-layered fibroelastic sac: a visceral layer (the epicardium) and a richly innervated parietal layer, with a potential space between them holding only 15 to 50 mL of serous fluid. Pericarditis is inflammation of that sac. Whatever the insult — a virus, an immune attack after infarction or surgery, uremic toxins, tuberculosis, a tumor — it activates the inflammasome, with downstream caspase-1, interleukin-1β and inflammatory cytokines. The parietal layer is supplied by the phrenic nerve (C3–C5), while the visceral layer is insensitive to pain, which is why more than 90% of patients have severe retrosternal chest pain and why it can refer to the shoulder and trapezius ridge. The pain is pleuritic (worse with deep inspiration) and positional (worse lying flat, relieved by sitting up and leaning forward). Ischemic pain is the opposite profile: it worsens with exertion or emotional stress, improves with rest or nitroglycerin, and is nonpositional and nonpleuritic.

The pericardial friction rub is the inflamed layers rubbing against each other — or, on a newer reading, inflammation-induced movement of fibrin strands. It is a rasping, scratchy, triphasic sound (atrial systole, ventricular systole, early ventricular diastole), heard in 35 to as many as 85% of patients at some point but in no more than a third at any single examination, because it is intermittent. Listen with the diaphragm over the left sternal border with the patient leaning forward at end-expiration, in several positions and at different times of day; a pericardial rub persists when the patient holds the breath, which is how you separate it from a pleural rub. Its presence does not track effusion size — it may even grow louder as an effusion resolves.

Inflammation of the epicardial surface also writes the ECG: stage I is diffuse, concave ST-segment elevation without a coronary-territory distribution plus PR-segment depression, with reciprocal ST depression and PR elevation in aVR — the discriminator from myocardial infarction. Within the first week the ST and PR segments normalize (stage II), then T waves invert diffusely (stage III) and finally normalize (stage IV); only 50–60% of patients show the full sequence. As StatPearls defines it, pericarditis is acute when it lasts under 4–6 weeks, incessant (subacute) when it persists past 4–6 weeks but resolves within 3 months, chronic past 3 months, and recurrent when it returns after a symptom-free interval of 4–6 weeks. When troponin rises alongside the pericarditis picture the myocardium is involved too — myopericarditis — which happened in about one in five patients in a 2026 cohort.

In developed countries 50–80% of acute cases are idiopathic or presumed viral (coxsackieviruses, echoviruses, adenoviruses, parvovirus B19, HIV, influenza, EBV, CMV, SARS-CoV-2), often with a flu-like prodrome. After a myocardial infarction the pericarditis to know is Dressler syndrome, an immune-mediated pericarditis appearing 1 to 6 weeks after the injury (most in the first month) in which antimyocardial antibodies are elevated. Reperfusion therapy has driven Dressler’s incidence below 1% of infarcts. The same immune mechanism follows cardiac surgery as postpericardiotomy syndrome, with risk tracking the extent of pericardial trauma and bleeding, which occurred in up to 29% of adults in recent prospective studies and typically appears within a month of surgery.

Uremic pericarditis occurs before or within 8 weeks of starting renal replacement therapy, typically with a BUN above 60 mg/dL: accumulated metabolic byproducts drive systemic inflammation through interleukin-1, interleukin-6 and tumor necrosis factor, and the platelet dysfunction of renal failure raises the risk of a hemorrhagic effusion. Pericarditis appearing more than 8 weeks into dialysis is dialysis-associated and often reflects missed or inadequate sessions. The uremic form behaves differently: pleuritic pain is less prevalent, ECG changes are often absent, the aspirate is often bloody, and it is treated with intensified dialysis rather than NSAIDs. Tuberculosis is the most common cause in endemic areas and in HIV-positive patients (the main cause in developing countries, over 60% of cases) and the leading cause of constrictive pericarditis worldwide. Malignancy is present in 12–23% of pericardial effusions, lung cancer most often, and carries a higher tamponade risk; autoimmune disease is another cause; medicines (procainamide, hydralazine, phenytoin, isoniazid, checkpoint inhibitors), chest radiation and hypothyroidism round out the list.

The cause matters because it predicts what comes next. Tamponade after pericarditis is rare with an idiopathic cause, and the constriction risk by etiology per ESC 2015 runs from under 1% for viral or idiopathic disease, to up to 30% for purulent bacterial or tuberculous pericarditis.

A pericardial effusion is excess fluid in the sac; its spectrum runs from a clinically irrelevant incidental finding to life-threatening tamponade. Echo sizes it by the end-diastolic echo-free space — small under 10 mm, moderate 10–20 mm, large over 20 mm (ESC 2015 criteria, as reported by the Italian Society of Cardiology 2024). Effusion accompanies 60–80% of acute pericarditis, about 80% of them small. Cardiac tamponade is life-threatening compression of the heart by fluid or blood in the pericardial sac — hemodynamically significant accumulation that impairs cardiac filling and reduces cardiac output.

The rule that organizes everything is the pressure–volume curve of the parietal pericardium. In an acute setting only 100 to 150 mL of fluid is needed to cause tamponade, because the sac has no time to stretch: rapid bleeding from a ventricular free-wall rupture 3–5 days after an MI, an aortic dissection, penetrating or blunt trauma, or a procedural perforation (including central-line placement) causes swift deterioration with a small volume. In a chronic setting the effusion may reach 1 to 2 liters before tamponade, because gradual accumulation from malignancy, infection or uremia lets the parietal pericardium stretch. That is also why a large effusion is not the same as tamponade: chronic large effusions may be well tolerated, and tamponade is ultimately a clinical diagnosis that requires both a hemodynamically unstable patient and pericardial fluid.

After cardiac surgery the sac can fill with blood rather than serous fluid. The confined pericardial space puts the heart at risk of tamponade when a hematoma compresses it, and chest-tube clogging — which occurs in up to 36% of patients — leaves shed mediastinal blood retained around the heart and lungs, contributing to tamponade; milking and stripping the tubes have been shown to be ineffective and potentially harmful. Delayed tamponade (more than 48 hours post-op) presents insidiously: hypotension not explained by hypovolemia, arrhythmia, ventricular dysfunction or vasoplegia, with rising filling pressures. Echo sensitivity in the first 24 hours after surgery is poor (36.8%), so a high clinical suspicion may prompt immediate re-exploration rather than waiting for the image.

As intrapericardial pressure rises it first impairs diastolic filling of the right atrium and right ventricle, whose walls are thinner and more compressible, and eventually equalizes diastolic pressures across the chambers (right atrium, right ventricle, pulmonary artery diastolic and wedge pressure). Venous return and stroke volume fall. The sympathetic nervous system compensates with tachycardia and arterial vasoconstriction, which is why the earliest bedside cues are a heart rate above 100, tachypnea, anxiety and restlessness, and a narrowed pulse pressure, while blood pressure is still held. When compensation fails the picture becomes obstructive shock: hypotension, distended neck veins from impaired right-heart filling, muffled or distant heart sounds, cool extremities, falling urine output, confusion — and, in the severest cases, pulseless electrical activity. Untreated tamponade is universally fatal. Beck’s triad (hypotension, jugular venous distension, muffled heart sounds) is the classic description, but it is found in only a minority of patients, so its absence never excludes tamponade.

Pulsus paradoxus is the exam’s favorite sign because it is pure physiology. The stiff, pressurized sac stops the right ventricular free wall from expanding to accept the extra venous return of inspiration, so the interventricular septum bows into the left ventricle instead; left ventricular end-diastolic volume, stroke volume and systolic pressure all fall on each inspiration. A systolic drop of more than 10 mmHg during inspiration is the definition (the normal inspiratory fall is under 10 mmHg). In a patient with an effusion it has a sensitivity above 80% for tamponade — yet its absence does not exclude it, and it is not specific: severe asthma, a COPD exacerbation, tension pneumothorax, a large pleural effusion, pulmonary embolism and right ventricular infarction all produce it, while intracardiac shunts, significant valvular regurgitation, severe hypertension or aortic stenosis, dissection-related tamponade and hypovolemia can hide it. Electrical alternans comes from a large effusion letting the heart swing within the sac, changing its position relative to the ECG leads beat to beat, so the QRS amplitude, axis or morphology alternates; it is specific but not sensitive (17–23% of tamponade) and may precede tamponade.

Constrictive pericarditis is the scarred end of the same story: granulation tissue replaces the sac’s elasticity, so a rigid, noncompliant pericardium restricts ventricular filling, reduces cardiac output and produces systemic venous congestion with preserved systolic function — fatigue, breathlessness, peripheral edema, hepatomegaly, ascites, a raised JVP and, in almost half of patients, a pericardial knock. Its hallmark distinction from tamponade is that intrathoracic and intracardiac pressures become dissociated (in tamponade they are transmitted normally). That is why the Kussmaul sign — a paradoxical rise in jugular venous pressure on inspiration — points to constriction and is typically absent in pure tamponade; pulsus paradoxus can occur in constriction but is less common. TB is the leading cause worldwide, pericardiectomy is the only definitive treatment, and misdiagnosed untreated constriction carries mortality in excess of 90%.