Acute pericarditis — inflammation of the pericardium. Viral / idiopathic in most developed-world cases. Use the 2025 ESC clinical-plus-objective criteria below. The two jobs: (1) don't miss a STEMI masquerading as pericarditis, and (2) treat with NSAID + colchicine — colchicine roughly halves recurrence.
A

Diagnose: presentation + additional evidence

ESC 2025
  • Presentation typically pleuritic/positional pain, sometimes dyspnea. Exclude ACS and other causes.
  • Certainty definite: ≥2 additional criteria. One additional criterion supports possible pericarditis. Symptoms alone are insufficient.
  • Additional criteria rub, typical ECG changes, elevated CRP, new/worsening effusion, or CMR pericardial edema/LGE.
  • The familiar 2-of-4 rule is the 2015 framework. Troponin elevation prompts assessment for myocardial involvement.
▤

The four ECG stages

evolve over days–weeks
I · EarlyWidespread ST elevation and PR depression
II · TransitionST/PR normalize, T waves flatten
III · RecoveryT inversion after ST normalization
IV · ResolutionT waves normalize

Not every patient passes through all stages. Shape, ST height and troponin magnitude cannot safely distinguish pericarditis from ACS on their own.

B

Pericarditis vs STEMI — the can't-miss call

when in doubt, cath
FeaturePericarditisSTEMI
PainPleuritic, positional (better leaning forward)Pressure/heaviness, exertional, radiates
ST elevationOften widespread and concaveTerritorial, but may also be concave
Reciprocal ↓None (except aVR / V1)Present in opposite leads
PR segmentPR depression (PR ↑ in aVR)Usually normal
Q waves / evolutionNone. Evolves over days–wksQ waves. Evolves over min–hrs
TroponinMay be normal or markedly elevated with myocarditisCan be normal early. Serial values and clinical context determine interpretation
C

Treat — NSAID/ASA + colchicine

avoid steroids first-line
  • NSAID ibuprofen 600 mg TID or ASA 750–1000 mg TID (preferred after MI). Add PPI, check kidney/bleeding risk, then taper after remission.
  • Colchicine 0.5 mg daily (≤70 kg) / BID (>70 kg), as in ICAP, for ≥3 mo first episode and ≥6 mo recurrent disease. Review kidney/liver function and CYP3A4/P-gp interactions.
  • Avoid steroids first-line — ↑ recurrence. Reserve for contraindication / autoimmune, low-dose + slow taper.
  • Refractory / recurrent colchicine-resistant, steroid-dependent inflammatory disease may warrant IL-1 blockade (rilonacept or anakinra) with a specialist. Exclude infection and review drug-specific approvals.
  • Also restrict physical activity during the acute phase. Return after clinical remission. Review anticoagulation indication + bleeding/effusion context — do not stop a necessary anticoagulant automatically. Myopericardial involvement needs LV-fxn + rhythm assessment.
D

Etiology & high-risk features (admit)

triage
  • Causes viral/idiopathic, TB (especially endemic regions), purulent, uremic, post-cardiac-injury (Dressler, post-pericardiotomy), neoplastic, autoimmune (SLE/RA), radiation, drug (hydralazine, ICI).
  • Major risk fever >38°, subacute onset, large effusion / tamponade, no ASA/NSAID response after ≥1 wk.
  • Minor risk myopericarditis, immunodepression, trauma, oral anticoagulant therapy. Any → admit, seek cause.
  • Workup ECG, hsTnI, CRP/ESR, echo, CXR, plus targeted infection/autoimmune/thyroid/renal testing by context. Routine viral serology is not recommended.
Tamponade is a clinical + echo diagnosis, not a size threshold. What matters is the rate of accumulation: a rapidly forming small effusion (post-procedure, dissection, trauma) tamponades on a non-compliant sac, while a slowly growing large effusion may not. Rising intrapericardial pressure equalizes with diastolic chamber pressures → impaired filling → ↓ stroke volume → shock.
▤

Tamponade physiology at a glance

compression + pulsus
Pericardial effusion and phase-specific right-heart collapseAnterior schematic, patient right on image left. SVC and IVC enter the RA. RV is anterior, LV has thicker myocardium and forms the apex, LA is posterior. Pericardial fluid surrounds the heart. Animation isolates RA indentation in ventricular systole and RV free-wall collapse in early diastole. Static arrows mark vulnerable free walls. Not a literal echo plane or a quantitative pressure model.ANTERIOR CUTAWAY · SCHEMATICRARVLALVSVCIVCPAAoRLRA indentationventricular systoleRV collapseearly diastoleEffusionoutside the heartArrows: collapse sites
Pericardial effusion and phase-specific right-heart collapseAnterior schematic, patient right on image left. SVC and IVC enter the RA. RV is anterior, LV has thicker myocardium and forms the apex, LA is posterior. Pericardial fluid surrounds the heart. Animation isolates RA indentation in ventricular systole and RV free-wall collapse in early diastole. Static arrows mark vulnerable free walls. Not a literal echo plane or a quantitative pressure model.ANTERIOR CUTAWAY · SCHEMATICRARVLALVSVCIVCPAAoRL
Collapse is pressure-relative. RA indentation: ventricular systole. RV collapse: early diastole. Blue = right-heart blood, red = left-heart blood, violet = pericardial fluid. High right-sided pressure can prevent collapse. Localized clot may compress a different chamber. Schematic, not to scale.
Published paired echocardiograms. Left red arrow marks early-diastolic RV collapse. Right red arrows mark collapse of both atria in a different patient, with visible surrounding pericardial effusion.
Time the collapse. Left: RV collapse in early diastole. Right: atrial collapse in another patient. Read the ECG and integrate the full clinical and echo examination.
Pérez-Casares, Cesar, Brunet-Garcia & Sanchez-de-Toledo (2017), Figure 8. CC BY 4.0. Whole figure, unchanged.
Pulsus paradoxus waveformA schematic arterial waveform has lower systolic peaks during inspiration. The inspiratory fall is greater than 10 mmHg. No absolute blood pressure or respiratory rate is modeled.PULSUS PARADOXUSInspiration: SBP falls >10 mmHgEXPINSPEXP>10mmHgQualitative trace · spontaneous breathing
Pulsus paradoxus waveformQualitative arterial pressure peaks fall during inspiration, with a systolic decrease greater than 10 mmHg.PULSUS PARADOXUSInspiratory SBP fall >10 mmHgEXPINSPEXP>10mmHgQualitative · spontaneous breathing
Ventricular interdependence: spontaneous inspiration increases RV filling, shifts the septum toward the LV and can reduce LV stroke volume.
A

Recognize at the bedside

Beck + pulsus
  • Beck triad hypotension + ↑ JVP + muffled heart sounds (all three in only a minority — don't wait for it).
  • Pulsus paradoxus inspiratory SBP fall >10 mmHg, tachycardia, narrow pulse pressure, dyspnea.
  • JVP elevated with blunted Y descent (vs constriction's prominent Y).
  • ECG sinus tach, low voltage, electrical alternans (swinging heart).
B

Echo & cath signs

sensitive → specific
SignMeaning
RA systolic collapseInterpret with ECG timing. Collapse lasting >⅓ of the entire cardiac cycle is more specific, not one third of systole.
RV diastolic collapseSupports tamponade. May be absent with pulmonary hypertension/high RV pressure or localized postoperative compression.
IVC plethoraDilated IVC, <50% inspiratory collapse — sensitive, ↑ filling pressures.
Respirophasic inflowSpontaneous breathing: mitral E falls and tricuspid E rises. Published thresholds are >25–30% and >40–60%. State denominator and respiratory phase. Ventilation, AF and lung disease confound.
RHCEqualized diastolic pressures (RA ≈ RVEDP ≈ PADP ≈ PCWP), blunted Y, intrapericardial P tracks RA.
C

The effusion itself — size & sampling

tap to diagnose?
Echo size (diastole)Approach
Small <10 mmObserve. Treat the cause.
Moderate 10–20 mmInvestigate cause. Follow with serial echo.
Large >20 mmDrain for tamponade, significant symptoms or diagnostic need (bacterial/TB/neoplastic suspicion). Persistence alone is not an indication. Stable chronic idiopathic noninflammatory effusions may be observed.
  • Noninflammatory causes HF, renal/thyroid disease, low oncotic pressure. Fluid chemistry alone does not assign cause.
  • Inflammatory / malignant integrate fluid studies with imaging and clinical evidence. Do not use pleural Light criteria.
  • Hemopericardium dissection, trauma, post-procedure, free-wall rupture, OAC.
  • Tap to Dx suspected purulent / TB / neoplastic, not for asymptomatic small.
D

Manage

drain it
Hemodynamically significant tamponade requires urgent drainage (percutaneous or surgical, selected by cause, anatomy & expertise). A cautious fluid bolus + norepinephrine may bridge selected hypotensive patients but must not delay drainage. Positive-pressure ventilation can sharply reduce venous return. If unavoidable, use a controlled plan with an experienced resuscitation/procedural team. Type A dissection or post-MI free-wall rupture generally requires immediate surgery. Controlled drainage is a specialist bridge, not routine centesis.
Constrictive pericarditis — a rigid, scarred (± calcified) pericardium fixes total cardiac volume, dissociates intrathoracic from intracardiac pressures, and drives ventricular interdependence. Hallmarks: rapid early-diastolic filling then an abrupt halt (dip-and-plateau / "square-root sign"), Kussmaul sign, and a pericardial knock. Separate it from restrictive cardiomyopathy: inflammatory/transient constriction may improve medically. Chronic permanent constriction may require pericardiectomy.
▤

The dip-and-plateau ("square-root sign")

ventricular pressure
Constrictive pericardium and respiratory ventricular interactionShort-axis schematic viewed from the apex, anterior up and patient right on image left. Crescentic RV lies anterior to the thick-walled LV. A constrained pericardial envelope limits expansion. During spontaneous inspiration the septum moves toward the LV as RV filling increases and LV filling falls. Expiration reverses the change. This motion is supportive and is not unique to constriction.SHORT AXIS · VIEWED FROM APEXRVLVRLANTERIORConstrained envelopeInspirationRV filling ↑ · LV filling ↓ExpirationReciprocal changeRespiratory septal shift · qualitative, not a cardiac beat
Constrictive pericardium and respiratory ventricular interactionShort-axis schematic viewed from the apex, anterior up and patient right on image left. Crescentic RV lies anterior to the thick-walled LV. A constrained pericardial envelope limits expansion. During spontaneous inspiration the septum moves toward the LV as RV filling increases and LV filling falls. Expiration reverses the change. This motion is supportive and is not unique to constriction.SHORT AXIS · VIEWED FROM APEXRVLVRLANTERIORInspiration: RV ↑ · LV ↓Expiration: reciprocal change
Ventricular pressure dip and plateauQualitative ventricular pressure waveform. After the systolic fall, an early-diastolic dip is followed by an elevated plateau as filling is abruptly limited. A moving marker follows the trace. No pressure values or heart rate are calculated.VENTRICULAR PRESSURE · SCHEMATICDipPlateauRapid early fillingthen an abrupt limitQualitative waveform · no numeric scale

The respiratory loop shows septal interaction inside a constrained envelope. The pressure loop shows early filling followed by an abrupt limit. Neither sign alone separates constriction from its mimics.

A

Constriction vs restriction

curable vs myocardial
DiscriminatorConstriction (pericardial)Restriction (myocardial)
InterdependencePresent — RV/LV systolic pressures discordant with respirationAbsent — concordant
Mitral e′ (tissue Dop.)Medial e′ often ≥9 cm/s. Medial > lateral e′ = annulus reversusUsually reduced. Mixed myocardial/pericardial disease can blur the distinction
Septal bounceRespiratory septal shift supports constrictionUsually absent. Postoperative bounce alone is nonspecific
PericardiumMay be thickened/calcified, but normal thickness does not exclude constrictionUsually normal thickness
BNPOften lower than in restrictionOften higher. Overlap and kidney function limit diagnostic use
Hepatic veinExpiratory diastolic flow reversalOften more inspiratory reversal. Interpret the full Doppler pattern
Exam & Rx Kussmaul sign (JVP fails to fall / rises on inspiration), pericardial knock (early diastolic, after S2), prominent Y descent. Causes: post-viral/idiopathic, post-cardiac surgery, mediastinal radiation, TB. Persistent symptomatic constriction may need pericardiectomy. Inflammatory/transient disease may improve with 3–6 months of therapy. Annulus paradoxus means E/e′ loses its usual relation to filling pressure.
B

Pericardiocentesis

echo-guided
StepDetail
IndicationsTamponade (emergent), large symptomatic effusion, diagnostic sampling (purulent / neoplastic / TB suspected).
ApproachImage-guided drainage by a trained team — choose the safest window from real-time effusion distribution + adjacent structures. A landmark-only needle instruction is not a substitute for imaging and local procedural protocol.
ConfirmAgitated-saline contrast → bubbles in pericardial space (not RV). Leave a pigtail drain.
DrainageAvoid abrupt excessive decompression (usually <500 mL initially when feasible). Leave a drain for controlled completion and monitor for decompression syndrome.
ComplicationsRV/cardiac puncture, coronary / internal-mammary laceration, pneumothorax, arrhythmia, hepatic injury, vagal.
Choose surgeryDissection, free-wall rupture, purulence, or inaccessible/loculated clot may require surgery. Controlled rescue drainage can bridge selected collapsing patients. Correct coagulopathy when time permits.
C

Send the fluid · effusive-constrictive

what to order
Pericardial fluid panel
  • Core cell count + diff, glucose, protein/LDH, Gram stain + bacterial/fungal culture if infection suspected, cytology if cancer suspected.
  • TB risk AFB smear/culture + PCR, ADA or interferon-γ using validated diagnostic guidance.
  • Targeted hematocrit (hemo), triglycerides (chylo). Tumor markers do not confirm malignant disease.
  • Do not apply pleural Light criteria to pericardial fluid — frequent false exudate classification.
Effusive-constrictive
  • Persistent constrictive physiology after drainage. The invasive definition is failure of RA pressure to fall by ≥50% or below 10 mmHg after intrapericardial pressure normalizes.
  • Exclude RV failure and severe TR as causes of persistent RA pressure. Treat active inflammation, reserve surgery for persistent constriction.
Integrate the syndrome: pericarditis requires compatible symptoms and objective evidence. Tamponade depends on pressure, rate and distribution, not size alone. Constriction requires multiple findings and an assessment of reversibility before surgery.
Cancer-associated ≠ malignant. An effusion in a patient with cancer remains etiology undetermined until the evidence supports tumor involvement, therapy toxicity, infection, or a non-cancer cause. Cancer therapy accounts for <30% of effusions in oncology cohorts. Name the syndrome, measure hemodynamic impact, then decide whether surveillance or tissue diagnosis will change care.
A

Name it correctly

association → suspicion → proof
Cancer-associated
  • Any effusion in a patient with active/prior cancer. Cause not yet established.
  • Common alternatives: renal/thyroid/HF, infection, autoimmune, post-procedure.
Suspected neoplastic
  • Active metastatic/high-burden cancer + growth/recurrence or pericardial/mediastinal nodularity, mass, lymphatic obstruction.
  • Imaging raises probability but may not prove malignant infiltration.
Confirmed malignant
  • Positive pericardial-fluid cytology or pericardial/epicardial biopsy.
  • Negative cytology does not fully exclude involvement if suspicion remains high.
B

Triage, phenotype, find the cause

same-day questions
StepMinimum
HemodynamicsSymptoms, BP/HR, JVP, pulsus. Urgent TTE if dyspnea, presyncope/syncope, hypotension, tachycardia or rapid interval growth.
TTE phenotypeLargest end-diastolic separation, circumferential vs loculated, RA/RV collapse, IVC, respiratory inflow, RV/LV fxn. Compare by the same modality when possible.
Cause mapCancer trajectory + therapy timing. CT/CMR for nodules/mass, thickening, inflammation, loculation, pleural/mediastinal disease. CBC, renal/liver panel, CRP/ESR, TSH. hsTnI if chest pain/ECG change or myopericarditis concern.
C

Observe vs sample vs drain

ESC cardio-oncology
PresentationAction
Stable >4 to <20 mmRepeat TTE in 7–14 d, then every 4–6 wk while evolving. Shorten for symptoms, growth or high-risk anatomy.
Moderate–large, uncertainConsider diagnostic pericardiocentesis when multimodality imaging cannot establish cause and the result will change cancer therapy or procedural strategy.
Tamponade / unstableImmediate image-guided pericardiocentesis. Surgery if percutaneous access is not feasible, bleeding/purulence requires operation, or anatomy is loculated.
If neoplastic drainedLeave extended drainage for 3–6 d to reduce recurrence. Send cytology. Remove when clinically stable and drainage is low (often <30 mL/d under a validated drainage plan).
Recurrent / refractoryPleuro-pericardial window for relapsing effusion. Systemic antineoplastic therapy is first-line when malignancy is confirmed. Intrapericardial therapy or biopsy is selected with oncology/CT surgery when diagnosis or control remains unresolved.
D

Therapy-associated disease — do not over-attribute

timing + inflammation + culprit
  • Known exposures chest RT, anthracycline, bleomycin, cyclophosphamide, cytarabine, ATRA/arsenic, dasatinib, IL-2/interferon, ICI.
  • Isolated effusion no pain/ECG/CRP inflammation → do not empirically give NSAID/colchicine. Treat the cause. Do not reflexively stop an unrelated cancer therapy.
  • ICI pericarditis severe disease or moderate/large effusion → hold ICI + high-dose steroid ± colchicine. Drain tamponade. Uncomplicated disease may use NSAID/colchicine with MDT-guided continuation/rechallenge.
  • Anticoagulation reassess indication, platelet count, bleeding and procedure plan. OAC is a risk feature, not an automatic stop.
E

Decision traps

avoid the wrong label / wrong delay
  • Hemorrhagic ≠ malignant blood raises concern but does not replace cytology/biopsy.
  • CT ≠ TTE ruler do not call growth from cross-modality size labels alone.
  • Negative cytology does not close the case when imaging/suspicion remains high and tissue would change care.
  • Biomarkers CRP/hsTnI phenotype inflammation or myocardial overlap. They do not diagnose malignant fluid.
  • Tamponade first do not delay drainage for staging or perfect diagnostic imaging.
  • After drainage use the P.3 fluid panel. Alert cytopathology to the known cancer + send a cell block when feasible.
Cardio-onc one-liner: stable >4 to <20 mm → TTE 7–14 d then q4–6 wk. Tamponade → urgent image-guided drainage. Suspected/definite neoplastic drainage → cytology + drain 3–6 d. Call it malignant only after tissue/fluid proof. If sampling will not change care, surveillance may be the better procedure.