Pericarditis, Effusion and Tamponade

In depth

The one-page summary above is what the PDF prints. These sections go further.

Physiology: the pericardium and tamponade

The pericardium is a fibrous parietal sac lined by a serous layer that continues as the epicardium; it normally holds 10–50 mL of plasma ultrafiltrate (ESC 2015). Its pressure–volume curve rises slowly at first and then almost vertically, so a small bleed arriving in minutes after surgery or a perforation can tamponade the heart, while a slow malignant or uremic effusion stretches the sac over weeks to hold far more before pressure climbs.

Once pericardial pressure reaches right-heart filling pressure, each chamber fills only as far as its pressure exceeds pericardial pressure: CVP, RV diastolic, PA diastolic and wedge pressures rise together and equalize, usually at 15–30 mm Hg (ESC 2015). Total cardiac volume is fixed, so the ventricles compete for it. Inspiration draws more blood into the right heart, the septum bows left, LV filling and stroke volume fall, and systolic pressure drops more than the normal few mm Hg: pulsus paradoxus, the product of exaggerated ventricular interdependence (ESC 2015). Filling is impeded through all of diastole, so the atrial trace keeps its x descent but loses the y descent.

Tachycardia and vasoconstriction hold blood pressure until late, so falling urine output, confusion, a narrowing pulse pressure and rising lactate come before hypotension. In low-pressure tamponade, hypovolemia from bleeding, dialysis or diuresis lets a modest pericardial pressure compress the heart at near-normal filling pressures. Positive-pressure ventilation raises pleural and pericardial pressure and cuts venous return: tamponade appears with smaller effusions, intubation can cause collapse, and respiratory swings in blood pressure and Doppler flow are blunted or reversed (Santangelo 2026).

Acute pericarditis: causes, definitions and triage

Pericarditis accounts for about 5% of emergency visits for chest pain, and an Italian city recorded 27.7 cases per 100,000 people a year (ESC 2015). In high-income countries most cases are idiopathic or presumed viral (85% of 486 patients in Imazio 2013); tuberculosis leads worldwide. Other causes are MI, cardiac surgery and procedures, uremia and dialysis, cancer and radiation, autoimmune disease, bacteria and drugs.

ESC 2025 groups myocarditis and pericarditis as inflammatory myopericardial syndrome (IMPS). Myopericarditis is predominant pericarditis with a troponin rise but no new LV dysfunction; perimyocarditis is predominant myocarditis with new regional or global dysfunction. The pericardium is electrically silent, so ECG changes signal myocardial inflammation, and CRP is raised in 79–90% (ESC 2025). Myopericarditis is admitted for monitoring, with coronary angiography when ACS is possible; the outlook is good, with no deaths and LV function normalized in over 90% in Imazio 2013.

Without colchicine, 15–30% of first episodes recur, and up to 50% after a first recurrence (ESC 2015). Recurrence requires a symptom-free gap of 4–6 weeks (ESC 2015); ESC 2025 calls disease lasting over 4 weeks without remission incessant, and over 3 months chronic. Constriction follows under 1% of idiopathic or viral cases, 2–5% of immune or neoplastic ones and 20–30% of bacterial, especially tuberculous or purulent, pericarditis (ESC 2015).

The ECG and the STEMI question

Subepicardial inflammation produces concave ST elevation across most leads, with PR depression from atrial injury; aVR, which faces the other way, shows ST depression and PR elevation. Classic evolution: stage 1, ST elevation and PR depression (first two weeks); stage 2, ST back to baseline with flat T waves (1–3 weeks); stage 3, T inversion (3 to several weeks); stage 4, normal. Fewer than half of patients pass through all four (LITFL).

STEMI is favored by elevation confined to one territory, convex or horizontal ST, reciprocal depression outside aVR and V1, more elevation in III than II, Q waves, and T inversion while the ST is still raised. Against benign early repolarization, an ST/T amplitude ratio above 0.25 in V6 favors pericarditis (LITFL). Effusions add sinus tachycardia, low QRS voltage and electrical alternans as the heart swings (ESC 2015). When the pattern is uncertain, treat it as possible occlusion: repeat the ECG, compare old tracings, look for regional wall-motion loss on echo and involve cardiology before anticoagulating.

Drug therapy and the evidence

Aspirin or an NSAID at full dose continues until pain resolves and CRP normalizes, usually 1–2 weeks, then tapers, with gastroprotection throughout (ESC 2015); ACC 2025 lists aspirin 500–1,000 mg, ibuprofen 600–800 mg or indomethacin 25–50 mg three times daily. Colchicine starts with them, weight-based and without a loading dose, runs 3 months after a first episode and at least 6 months for recurrences, and is the last drug stopped. ESC 2025 rates aspirin or an NSAID plus colchicine Class I and corticosteroids IIa after first-line failure (SEC 2026).

Corticosteroids relieve pain within days, but ESC 2015 keeps them second line because they favor chronic evolution, and high doses bring more recurrences (Imazio 2008); the likely reasons are prolonged viral replication and rebound as the dose falls (Merck 2026). When they are needed (contraindication to or failure of first-line drugs, autoimmune disease), give prednisone 0.2–0.5 mg/kg/day after infection is excluded, keep colchicine going and taper slowly.

Recurrence with fever, high CRP and effusion is an autoinflammatory, IL-1–driven phenotype. Anakinra (1–2 mg/kg/day, up to 100 mg SC daily) and rilonacept (320 mg SC, then 160 mg weekly; FDA-labeled for recurrent pericarditis) prevent flares while given. ESC 2025 rates IL-1 blockade IIa for refractory recurrence and Class I when CRP is raised (SEC 2026), and ACC 2025 prefers it to steroids for this phenotype. Injection-site reactions are common; serious infection and live vaccines are label warnings.

Colchicine toxicity is life-threatening with strong CYP3A4 or P-gp inhibitors such as clarithromycin, ketoconazole, ritonavir or cyclosporine, and with renal failure (CrCl under 15) or severe hepatic impairment (label); GI symptoms are often the first sign, and myelosuppression and myopathy are rarer. Exercise: ACC 2025 restricts strenuous exercise for at least 1 month and until remission, with a heart rate under 100; ESC 2025 starts at 1 month and individualizes; ESC 2015 asked athletes to wait at least 3 months, or 6 with myocardial involvement.

Recognizing tamponade

In Roy 2007's review, dyspnea was present in 87–89% of patients with tamponade, tachycardia in 77%, pulsus paradoxus in 82%, a raised JVP in 76% and cardiomegaly on chest film in 89%. A pulsus over 10 mm Hg raised the probability (LR 3.3), and 10 mm Hg or less nearly excluded tamponade (LR 0.03). Beck's triad is late and often incomplete.

Pulsus with a manual cuff (Merck 2026): with the patient breathing quietly, inflate above systolic, deflate no faster than about 2 mm Hg per beat, note the pressure where Korotkoff sounds first appear (expiration only), keep deflating until every beat is heard, and subtract. On an arterial line, systolic pressure falls with each spontaneous inspiration. Pulsus also occurs with severe asthma or COPD, massive PE and hypovolemia and is rare in constriction; it can be absent despite tamponade during positive-pressure ventilation, with a localized clot, or with a high LV diastolic pressure, aortic regurgitation or an atrial septal defect.

After cardiac surgery the picture is often atypical. Of 29 postoperative tamponades (Chuttani 1994), 66% were localized posterior collections; only 24% of patients were hypotensive and 48% had pulsus, RA and RV collapse were often absent while LV diastolic collapse was common, and pressures equalized in 81%. About half of postoperative effusions sit posteriorly where TTE misses them, so TEE comes early (Santangelo 2026).

Bridging, drainage and the pericardial drain

Bridging buys minutes, not a cure. In Sagristà-Sauleda 2008, 500 mL of saline over 10 minutes raised the cardiac index by more than 10% in 47% of 49 patients, left it unchanged in 22% and lowered it in 31%, while intrapericardial and right atrial pressures rose; an SBP under 100 mm Hg predicted benefit. Give a modest bolus to the hypotensive or dry patient, not liters, and use a pressor or inotrope only until drainage; never slow the compensatory tachycardia with a β-blocker. If intubation cannot wait, have the drainage team at the bedside, keep spontaneous breathing as long as possible, use small tidal volumes and low PEEP, and expect collapse at induction.

ESC 2015 advises draining tamponade without delay in unstable patients, preferably by needle pericardiocentesis under echo or fluoroscopic guidance, and surgically for purulent pericarditis or urgent bleeding into the pericardium; stable patients are timed by clinical and echo assessment, and the ESC working-group triage score rests on expert consensus. Aortic dissection needs the operating room, with needle drainage limited to small, controlled volumes if surgery is delayed. Recurrent malignant effusions, loculated or posterior fluid and clot are treated with a subxiphoid or thoracoscopic window or extended catheter drainage.

At Mayo, 1,127 echo-guided pericardiocenteses succeeded in 97%, with major complications in 1.2% and minor in 3.5%; extended catheter drainage rose from 23% to 75% of procedures over 21 years (Tsang 2002). Echo picks the entry point where fluid is deepest and closest to the skin; the blind subxiphoid route is for arrest. Complications include RV or coronary laceration, arrhythmia, pneumothorax, liver injury, vagal reactions, infection and pericardial decompression syndrome, an uncommon ventricular failure after a large effusion is drained.

• Before: bedside echo, coagulation tests and platelets when time allows, atropine and fluid ready for vagal reactions, defibrillator pads on.
• During: continuous ECG and arterial pressure; new ectopy as the needle advances suggests myocardial contact.
• After: echo for residual fluid; vital signs and drain output every 15 minutes at first, then hourly, recording volume and color.
• A drain that stops while BP falls or CVP rises means clot, kink or reaccumulation until proven otherwise: check the line and get an echo.
• Removal: usually once output falls below about 25–50 mL/day and echo shows no reaccumulation (practice varies).
• Fluid studies as ordered: cell count, glucose, protein, Gram stain and culture, cytology, TB tests.

After cardiac surgery and MI

Early tamponade, within about 48 hours, is bleeding and clot: chest tube output stops or falls while CVP and PA diastolic pressure rise, CI, SvO₂ and urine output fall, pulse pressure narrows and pressor needs climb. The fix is re-exploration. Arrest follows 0.7–8% of cardiac operations; because external compressions cannot fill a tamponaded heart, STS 2017 makes resternotomy within 5 minutes a standard part of the arrest protocol for 10 days after surgery.

Late tamponade is quieter. Among 4,561 operations (Kuvin 2002), it followed 0.2% of isolated CABG and 0.6% of valve operations, was diagnosed at a mean of day 10, and 84% of patients had received aspirin, heparin or warfarin within 3 days of surgery; half the effusions were posterior. Fatigue, dyspnea, nausea, tachycardia or falling urine output on warfarin, or after pacing-wire removal, needs an echo.

Postpericardiotomy syndrome is immune pericarditis after pericardial injury, appearing days to weeks later and mostly in the first month, in up to 29% of patients in prospective studies; female sex and pleural incision raise the risk (Imazio 2026). It presents with fever, pleuritic pain, a rub, pericardial and pleural effusions and raised CRP, and is treated like acute pericarditis. Colchicine for 1 month from postoperative day 3 cut it from 21.1% to 8.9% (COPPS 2010); started 48–72 h before surgery it cut it from 29.4% to 19.4% but caused more adverse effects (20.0% vs 11.7%) and did not reduce effusions (COPPS-2 2014).

Early post-infarction pericarditis appears within days of a large transmural MI and is treated with aspirin (ACCF/AHA 2013, Class I); other NSAIDs and steroids are Class III: Harm because they impair scar healing and have been linked to rupture. Dressler syndrome, immune pericarditis weeks to months after MI, has fallen from up to 3% to under 1% with early revascularization (Imazio 2026). A new effusion with hypotension or PEA days after MI suggests free-wall rupture, a surgical emergency. Pericarditis also follows about 10% of AF ablations, 1–2% of device implants and 0.2% of catheterizations (Imazio 2026).

Anticoagulants raise the risk of hemopericardium and are generally avoided in acute pericarditis, although they may be given in early post-MI pericarditis (Merck 2026). Uremic and dialysis-related pericarditis is treated by starting or intensifying dialysis with little or no heparin, as the effusion is often bloody; colchicine is contraindicated in severe renal impairment (ESC 2015).

Constrictive pericarditis

A scarred, sometimes calcified pericardium fixes the heart’s volume. The ventricles fill rapidly in early diastole and then stop abruptly, producing a pericardial knock, a steep y descent and the dip-and-plateau (square root) ventricular pressure, with diastolic pressures roughly equal in all chambers; the rigid shell also keeps inspiration from lowering venous pressure (Kussmaul sign). Pulsus paradoxus is rare and milder than in tamponade (Merck 2026).

In high-income countries the causes are idiopathic or viral (42–49%), cardiac surgery (11–37%), radiation (9–31%) and connective tissue disease (3–7%) (ESC 2015). Patients have right heart failure with preserved ventricular function: edema, ascites, hepatomegaly, pleural effusions and fatigue. Echo shows respirophasic septal shift, a medial mitral annular e′ normal or higher than the lateral (annulus reversus) and expiratory hepatic vein flow reversal; septal shift with a medial e′ ≥9 cm/s or a hepatic vein reversal ratio ≥0.79 gave 87% sensitivity and 91% specificity (Xu 2018). About 20% of surgically proven cases have a normal-thickness pericardium (ESC 2015), so a thin pericardium on CT does not exclude it.

Transient constriction (10–20% of cases, ESC 2015) usually resolves within a few months, so a stable patient with new constriction and raised CRP or imaging inflammation gets a 2–3-month anti-inflammatory trial before surgery. In effusive-constrictive pericarditis, right atrial pressure stays high after the effusion is drained because the visceral layer constricts. Chronic constriction needs pericardiectomy, which carries an operative mortality of 6–12% (ESC 2015).

Nursing care, monitoring and teaching

• Cardiovascular: HR, BP and pulse pressure trends, JVP and heart sounds; pulsus whenever tamponade is possible; telemetry for AF and ST changes.
• Respiratory: work of breathing, SpO₂, breath sounds for pleural effusion; sit upright; splinting and incentive spirometry after surgery.
• Renal and labs: urine output; CRP to guide tapering; creatinine, potassium and CBC on NSAIDs and colchicine; liver tests on anakinra.
• GI: PPI with full-dose NSAIDs; diarrhea on colchicine; signs of bleeding.
• Pain: positional pleuritic pain that settles on treatment is expected; new constant pain, fever or breathlessness needs review.
• Transport: keep preload, avoid positive pressure and sedatives where possible, and confirm where drainage can happen on arrival.

Teach patients to take colchicine for the full course even when well, to check any new medicine for interactions (clarithromycin, antifungals, some HIV and transplant drugs), to report severe diarrhea, muscle weakness, fever or easy bruising, to avoid strenuous exercise until cleared, and to return for worsening breathlessness, dizziness or fainting. Document CRP trends, doses and taper dates, pulsus values, drain output and echo results.

Exam pearls

• Pericarditis: diffuse concave ST elevation and PR depression with reciprocal change only in aVR and V1; STEMI: one territory, reciprocal depression, III > II.
• First line: aspirin or an NSAID plus colchicine; colchicine for 3 months (6 if recurrent) halves recurrence (ICAP 16.7% vs 37.5%).
• Steroids are second line at 0.2–0.5 mg/kg/day; high doses mean more recurrence.
• After MI or CABG, use aspirin; after MI, avoid other NSAIDs and steroids.
• Pulsus paradoxus: inspiratory SBP fall >10 mm Hg, measured from expiration-only to every-beat Korotkoff sounds.
• Tamponade: Beck's triad, electrical alternans, equal CVP, PAD and PAOP, RA and RV diastolic collapse on echo.
• Treat tamponade by drainage; fluid bridges; no diuretics, vasodilators, β-blockers or positive pressure if avoidable.
• Postoperative tamponade: tubes stop, filling pressures rise and equalize, output falls; often a posterior clot; TEE; resternotomy in arrest.
• Postpericardiotomy and Dressler syndromes: fever, pleuritic pain and effusions days to weeks after injury; aspirin plus colchicine.
• Constriction: Kussmaul sign, pericardial knock, dip-and-plateau; pericardiectomy.