01Approach to the Critical Patient/attcp58

Immediate stabilization

›Airway and hemodynamic threats

›Obstructive shock physiology recognition

›SBP < 90 mmHg with tachycardia

›Narrow pulse pressure as early marker

›Altered mental status or syncope

›Beck's triad: hypotension, JVD, muffled heart sounds

›Classic triad present in minority of cases

›Absence does not exclude tamponade

›Pulsus paradoxus > 10 mmHg on manual BP measurement

›Most specific clinical sign of tamponade physiology

›May be absent in aortic regurgitation, ASD, severe LV dysfunction, PPV

›Avoid positive-pressure ventilation

›Reduces venous return and precipitates arrest

›If intubation unavoidable, have pericardiocentesis ready immediately

›Avoid IV diuretics and vasodilators

›Reduce preload and precipitate cardiovascular collapse

Monitoring and targets

›Monitoring bundle

›Continuous cardiac monitoring

›Electrical alternans pattern on ECG

›Sinus tachycardia as most common finding

›Arterial line for hemodynamic monitoring

›Beat-to-beat SBP variation with respiration

›Accurate pulsus paradoxus measurement

›Pulse oximetry continuous

›SpO2 target > 94% on supplemental O2

›Desaturation as escalation trigger

02History/hx58

Presenting symptoms

›Core cardiopulmonary symptoms

›Dyspnea

›Most frequently reported symptom

›Orthopnoea without rales distinguishes from heart failure

›Chest pain or fullness

›Pleuritic quality if pericarditis is underlying cause

›Trapezius ridge radiation suggests pericarditic etiology

›Weakness, fatigue, lightheadedness

›Low output symptoms from reduced cardiac output

›Syncope or near-syncope in severe cases

›Symptom timeline

›Acute onset (minutes to hours)

›Trauma or iatrogenic cause

›Type A aortic dissection

›Subacute onset (days to weeks)

›Malignant or inflammatory etiologies

›Viral pericarditis

Risk factors and exposures

›Procedural and surgical history

›Cardiac catheterization, ablation, pacemaker or ICD insertion

›Iatrogenic causes account for 15-20% of tamponade cases

›Cardiac surgery including postpericardiotomy syndrome

›Chest trauma

›Blunt or penetrating mechanism

›Steering wheel or high-velocity impact

›Malignancy history

›Lung, breast, lymphoma, leukemia, melanoma highest risk

03Physical Exam/exam45

Vitals and hemodynamic assessment

›Hemodynamic profile

›Tachycardia

›Most sensitive clinical sign

›HR > 100 bpm compensatory response

›Hypotension

›SBP < 90 mmHg as late finding

›Narrow pulse pressure earlier than frank hypotension

›Pulsus paradoxus measurement

›Inspiratory SBP drop > 10 mmHg

›Measured with manual BP cuff or arterial line

›False negative: AR, ASD, severe LV dysfunction, PPV, regional tamponade

Neck and cardiac exam

›Jugular venous assessment

›Elevated JVP with prominent x-descent

›Absent y-descent distinguishes from constrictive pericarditis

›Kussmaul sign absent (seen in constrictive pericarditis)

›JVD may be absent with hypovolemia

›Traumatic tamponade with hemorrhage

›Dehydrated patient with existing effusion

›Cardiac auscultation

›Muffled or distant heart sounds

›Insulating effect of pericardial fluid

›Large effusions > 300 mL typically required

›Pericardial rub

›Usually absent with large effusions

›If present suggests concurrent pericarditis with smaller effusion

04Differential Diagnosis/ddx46

Obstructive shock mimics

›Tension pneumothorax

›Unilateral absent breath sounds

›Tracheal deviation away from affected side

›Hyperresonance on percussion

›ICD-10 J93.0

›Distinguished by CXR or POCUS

›Immediate needle decompression if suspected

›Massive pulmonary embolism

›RV strain pattern on ECG

›S1Q3T3 pattern

›Right heart strain on echo

›ICD-10 I26.09

›CT pulmonary angiography for confirmation

›No pericardial effusion on POCUS

›Cardiac tamponade

›ICD-10 I31.4

›SNOMED CT: Cardiac tamponade (disorder) 40549009

›Pericardial effusion with chamber collapse on echo

Cardiogenic and inflammatory mimics

›Acute decompensated heart failure

›Rales present on lung auscultation

›Elevated BNP / NT-proBNP

›Systolic dysfunction on echo rather than effusion

›ICD-10 I50.9

›Volume overload physiology vs obstructive physiology

›Right ventricular infarction

›Inferior ST elevation on ECG

05Laboratory Tests/lt46

Core cardiac and inflammatory labs

›Troponin

›Myopericarditis or concomitant MI evaluation

›Elevated in 30-50% of acute pericarditis

›ST-elevation pattern distinguishes from STEMI

›Post-procedural rise expected in iatrogenic tamponade

›BNP or NT-proBNP

›Differentiation from heart failure

›May be mildly elevated in tamponade from RV stretch

›Markedly elevated favors decompensated heart failure

›ESR and CRP

›Inflammatory markers for pericarditis etiology

›CRP > 3 mg/L supports pericarditis

›Serial trending for treatment response

Metabolic and hematologic labs

›Complete blood count

›Leukocytosis suggests infectious etiology

›Normocytic anemia in malignancy or chronic disease

›Thrombocytopenia in malignancy or autoimmune disease

›Comprehensive metabolic panel

›Renal function for uremic pericarditis

›Creatinine and BUN elevation in uremic etiology

›Electrolyte derangements in ESRD

›Hepatic panel

›Congestion from elevated venous pressure

›Transaminase elevation in severe venous congestion

›Coagulation studies

›INR and aPTT before pericardiocentesis

06Diagnostic Tests/dt96

Scoring Systems

›Clinical tamponade spectrum classification

›Impending tamponade

›Echocardiographic signs present without hemodynamic compromise

›Compensatory tachycardia maintaining cardiac output

›At risk for rapid decompensation with any preload reduction

›Established tamponade

›Hemodynamic compromise with hypotension or shock

›Cardiac arrest (PEA) as extreme presentation

›Tamponade is clinical diagnosis

›Echocardiographic findings alone insufficient without clinical correlation

›2025 ACC Expert Consensus guidance

›Pulsus paradoxus threshold

›> 10 mmHg inspiratory SBP drop

›Sensitivity 98%, specificity 83% for tamponade (JAMA 2007)

›LR+ 5.9, LR- 0.03 for cardiac tamponade

›ACEP Level B supporting evidence

›> 20 mmHg associated with more severe tamponade physiology

›Reduced sensitivity in hypovolemia or tachycardia

MRI

›Cardiac MRI role in pericardial disease

›Not indicated acutely for cardiac tamponade

›Hemodynamic instability precludes MRI suite

›POCUS and echo are first-line

›Useful for recurrent or effusive-constrictive disease

›Pericardial thickness > 4 mm supports constriction

›Late gadolinium enhancement identifies active pericardial inflammation

›T2-weighted imaging for edema

›High T2 signal in active pericarditis

›Guides duration of anti-inflammatory therapy

›CMR protocol (ASE 2013 recommendations)

›SSFP cine sequences for effusion size and chamber collapse

›T1 and T2 mapping for tissue characterization

›Phase-contrast for respirophasic flow variation

CT

›Chest CT indications in tamponade workup

›Secondary cause evaluation

›Malignancy (pulmonary mass, mediastinal adenopathy)

›Aortic dissection (Type A with hemopericardium)

›Loculated effusions not seen on TTE

›CT findings in pericardial effusion

›Hyperdense collection (>30 HU) suggests hemorrhagic effusion

›Low-density effusion suggests transudative or serous

›Pericardial thickening > 4 mm suggests inflammation or malignancy

›CT-guided pericardiocentesis

›Loculated or posteriorly positioned effusions

›When echo window inadequate

›Sensitivity approaches 95% for loculated collections

›CT aortography

›If Type A dissection suspected

›Sensitivity 100%, specificity 98% for aortic dissection

›Immediate surgical consultation if Type A confirmed

Ultrasound

›Echocardiography as first-line imaging (2025 ACC Expert Consensus)

›TTE standard approach

›Parasternal long axis, subxiphoid, and apical views

›Most sensitive and specific for hemodynamically significant effusion

›ACEP Level A recommendation for POCUS in suspected tamponade

›Echocardiographic findings of tamponade physiology

›Dilated IVC > 2.1 cm with respiratory collapse < 50%

›Most sensitive screening marker

›IVC plethora reflects elevated RA pressure

›Diastolic RV free wall collapse

›Most specific finding for tamponade

›Occurs when pericardial pressure exceeds RV diastolic pressure

›RA inversion > 1/3 of cardiac cycle

›Sensitive and highly specific

›Earliest chamber collapse sign

›Respirophasic Doppler variation

›Transmitral > 30% variation

›Transtricuspid > 60% variation

›Biphasic inspiratory septal bounce

›Ventricular interdependence sign

›POCUS for bedside diagnosis

›Identifies hemodynamically significant effusion rapidly

›Diastolic RV collapse key bedside finding

›IVC assessment for plethora

›Guides needle placement for pericardiocentesis

›Effusion size classification by echo

›Small: < 10 mm circumferential

›Echo-free space in diastole

›Typically does not cause tamponade

›Moderate: 10-20 mm

›Monitor for hemodynamic compromise

›Serial echo surveillance

›Large: > 20 mm circumferential

›High risk for tamponade physiology

›Immediate drainage if hemodynamically significant

›Volume does not determine tamponade

›As little as 250 mL can cause acute tamponade

›Rate of accumulation more important than volume

›Chest X-ray findings

›Enlarged cardiac silhouette (water-bottle heart)

›Only visible with effusions > 300 mL

›Cardiomegaly with clear lung fields

›Low sensitivity for acute tamponade

›CXR utility

›Excludes tension pneumothorax

›Identifies underlying pulmonary cause

›Pulmonary mass or mediastinal widening

07Disposition/dispo43

Admission criteria

›All cardiac tamponade requires hospital admission

›Established hemodynamic tamponade

›ICU or cardiac care unit admission

›Continuous hemodynamic monitoring post-pericardiocentesis

›Serial echo to monitor reaccumulation

›Impending tamponade with hemodynamic stability

›Monitored bed with cardiology consultation

›Serial echocardiography

›Avoid preload-reducing therapies

›Post-pericardiocentesis monitoring

›ICU level monitoring minimum 24-48 hours

›Drain output hourly

›Hemodynamic stability confirmation

›Reaccumulation rate assessment

Transfer and surgical indications

›Surgical consultation triggers

›Type A aortic dissection with hemopericardium

›Immediate cardiothoracic surgery

›Pericardiocentesis contraindicated (may precipitate aortic propagation)

›Ventricular free wall rupture post-MI

›Emergent surgical repair

›Bridge with careful volume and vasopressors

›Penetrating thoracic trauma

›Operative exploration over percutaneous drainage

›ED thoracotomy if arresting

›Purulent pericarditis not controlled percutaneously

›Surgical drainage and decortication

08Treatment/t85

Immediate pericardiocentesis

›Echo-guided pericardiocentesis (first-line definitive treatment)

›Subxiphoid or apical approach

›Target largest, shallowest fluid pocket

›No intervening vital structures in needle path

›2025 ACC Expert Consensus: Class I recommendation for hemodynamic tamponade

›Technique

›18-gauge spinal or pericardiocentesis needle

›Advance under continuous echo guidance

›Confirm placement with agitated saline injection

›Pigtail catheter placement for continued drainage

›Drainage strategy

›Drain slowly to avoid pericardial decompression syndrome

›Acute RV failure from sudden volume shift

›Pulmonary edema from rapid LV preload increase

›Leave pigtail drain in place 3-5 days

›Until drainage < 25-50 mL per 24 hours

›Serial echo to confirm resolution

›Fluid analysis

›Cell count, differential, Gram stain, culture

›Cytology for malignant etiology

›Protein, LDH, glucose, triglycerides

Volume and vasopressor support

›Temporizing hemodynamic support

›Normal saline IV bolus

›250-500 mL as single temporizing bolus

›Augments preload and cardiac output

›Repeat only if reaccumulation delay unavoidable

›Norepinephrine as vasopressor bridge

›0.1-0.3 mcg/kg/min IV infusion

›Titrate to MAP > 65 mmHg

›Increase peripheral resistance to maintain coronary perfusion

›Avoid agents reducing preload or heart rate

›Beta-blockers contraindicated (tachycardia is compensatory)

›Nitroglycerin contraindicated

›Diuretics contraindicated

Anticoagulation reversal

›Reversal strategies by agent

›Heparin reversal

›Protamine sulfate 1 mg per 100 units heparin

›Maximum 50 mg slow IV over 10 minutes

›Monitor aPTT post-reversal

›Warfarin reversal

›4-factor PCC (25-50 units/kg) for urgent reversal

›Vitamin K 10 mg IV concurrent

›Target INR < 1.5 before drainage

›DOAC reversal

›Idarucizumab (Praxbind) 5 g IV for dabigatran

›Andexanet alfa for apixaban or rivaroxaban (400-800 mg IV)

›4-factor PCC as alternative if reversal agents unavailable

Post-drainage anti-inflammatory therapy

›NSAIDs for non-malignant, non-uremic, non-purulent etiologies

›Ibuprofen 400-600 mg orally three times daily

›Duration: 2-4 weeks then taper

›Gastric protection with PPI

›Avoid in renal failure or post-MI (first 4 weeks)

›Aspirin 750-1000 mg orally three times daily

›Alternative, preferred post-MI

›Same duration and taper approach

›Weight-based dosing for gradual taper

›Colchicine adjunct therapy

›Colchicine 0.5 mg orally twice daily (> 70 kg)

›0.5 mg once daily if < 70 kg or intolerance

›Reduces recurrence risk by 50%

›Duration: 3 months for pericarditis

›Contemporary practice: used in 46% of cases (CATEO study 2025)

›Contraindications

›Severe renal or hepatic impairment

›Drug interactions (cyclosporine, clarithromycin)

›Corticosteroids (second-line)

›Prednisone 0.2-0.5 mg/kg/day

›Reserved for NSAID failure or autoimmune/idiopathic cases

›Avoid in infectious etiology

›Taper slowly over 3 months to prevent rebound

›Used in 24% of contemporary cases (CATEO study 2025)

›Anakinra (IL-1 inhibitor) for recurrent refractory cases

›100 mg subcutaneous daily

›Class IIb evidence base

›Specialist guidance for initiation

Surgical drainage

›Surgical pericardial window

›Recurrent tamponade after percutaneous drainage

›Subxiphoid or video-assisted thoracoscopic approach

›Pleuro-pericardial window for malignant effusions

›Indications for primary surgical approach

›Traumatic hemopericardium with instability

›Type A aortic dissection

›Post-MI free wall rupture

›Purulent pericarditis

›Loculated effusion not accessible percutaneously

09Special Populations/sp69

Pregnancy

›Physiologic considerations in pregnancy

›Hemodynamic changes affecting tamponade presentation

›Increased blood volume (40-50%) may initially compensate

›Aortocaval compression in supine position worsens venous return

›Left lateral decubitus positioning during assessment and drainage

›Causes in pregnancy

›Peripartum cardiomyopathy with effusion

›Preeclampsia-related pericarditis

›Lupus flare in pregnancy

›Postpartum myocarditis

›Management in pregnancy

›Echo-guided pericardiocentesis preferred

›Apical approach favored in gravid uterus

›Fetal monitoring during procedure

›Neonatology and obstetrics standby

›Medication safety

›Colchicine: avoid (teratogenic, category D/X)

›Ibuprofen: avoid after 20 weeks (premature ductus closure)

›Aspirin: low dose relatively safe in second trimester

›Prednisone: relatively safe, crosses placenta minimally

›Delivery planning

›Tamponade in third trimester may require delivery first

›Multidisciplinary team: cardiology, MFM, anesthesia, NICU

Geriatric

›Age-related considerations

›Atypical presentation common

›Dyspnea and fatigue without classic Beck's triad

›Blunted tachycardia response from chronotropic incompetence or beta-blocker use

›Pulsus paradoxus less reliable with high prevalence of AF

›Comorbidity burden

›Multiple anticoagulation indications (AF, VTE, mechanical valves)

›Anticoagulation reversal required in most hemorrhagic cases

›Higher prevalence of malignancy-related tamponade

›Procedural considerations in elderly

›Pericardiocentesis remains first-line regardless of age

›Higher procedural risk with frailty and coagulopathy

›Use smallest effective needle and real-time echo guidance

›Medication adjustments

›Colchicine dose reduction with renal impairment (GFR-based)

›NSAIDs with caution: renal and GI toxicity higher

›PPI prophylaxis mandatory with NSAID use

›Mortality risk

›3-month mortality 29% overall; higher in malignant etiology (49%)

›Functional status and goals of care discussion important

Pediatrics

›Epidemiology and etiology in children

›Pericarditis most common cause in developed countries

›Viral etiology predominant (Coxsackie, adenovirus, EBV)

›Bacterial (Staphylococcus, Streptococcus, Haemophilus) in younger children

›Other pediatric causes

›Post-cardiac surgery (postpericardiotomy syndrome)

›Rheumatic disease (JIA, SLE)

›Kawasaki disease with coronary aneurysm

›Trauma (child abuse consideration)

›Clinical features in children

›Pulsus paradoxus may be harder to measure in young children

›POCUS-derived respirophasic variation more practical

›Doppler mitral inflow variation > 30% threshold

›Tachycardia more pronounced as compensatory mechanism

›Normal HR range higher in children; adjust thresholds by age

›Treatment in pediatrics

›Echo-guided pericardiocentesis with pediatric cardiology

›Subxiphoid approach preferred

›Conscious sedation with ketamine (preserves sympathetic tone)

›Avoid propofol and high-dose benzodiazepines (reduce preload)

›Ibuprofen weight-based dosing

›5-10 mg/kg orally every 6-8 hours

›Maximum 40 mg/kg/day

›Colchicine in children

›Approved > 6 years of age at 0.5 mg daily (< 40 kg)

›1 mg daily in two divided doses (> 40 kg)

10Background/b81

Epidemiology

›Incidence and etiology distribution

›Malignancy leading cause in many series

›32-47% of tamponade cases are malignant

›Lung cancer most common; breast, lymphoma, leukemia, melanoma follow

›CATEO study 2025: contemporary real-world cohort data

›Iatrogenic cause

›15-20% of tamponade cases from cardiac procedures

›Cardiac catheterization, ablation, pacemaker insertion

›Cardiac surgery including postpericardiotomy syndrome

›Idiopathic or viral pericarditis

›Most common in younger patients without malignancy

›Often self-limited with anti-inflammatory therapy

›Mortality data

›3-month mortality overall 29%

›Malignant etiology: 49% 3-month mortality

›Non-malignant etiology: 11% 3-month mortality

›Sánchez-Enrique et al., Am J Cardiol 2016

›Recurrence rates

›Overall recurrence ~10%

›Neoplastic group: 62% recurrence rate

›Inflammatory: lower recurrence with colchicine therapy

Pathophysiology

›Pericardial pressure-volume relationship

›Pericardial space normally contains 15-50 mL fluid

›Thin sac with limited compliance

›Small acute additions rapidly raise intrapericardial pressure

›Rate of accumulation determines hemodynamic impact

›As little as 250 mL can cause acute tamponade

›Slowly developing effusions may tolerate > 1 L before decompensation

›Steep pericardial pressure-volume curve beyond reserve volume

›Hemodynamic cascade

›Rising intrapericardial pressure compresses cardiac chambers

›RV compressed first (thinner, lower pressure chamber)

›RA inversion earliest sign; diastolic RV collapse most specific

›LV compression leads to reduced stroke volume

›Ventricular interdependence

›Fixed total pericardial volume

›RV filling in inspiration reduces LV volume

›Causes inspiratory SBP drop (pulsus paradoxus)

›Compensatory mechanisms

›Sympathetic activation (tachycardia, vasoconstriction)

›Maintain cardiac output until decompensation

›Frank hemodynamic collapse when compensatory reserve exhausted

›Equalization of pressures

›Diastolic pressure equalization across all chambers

›RA, RV diastolic, PCWP, pericardial pressure all equalize

›Pathognomonic on right heart catheterization

›Loss of y-descent on RA pressure tracing

Therapeutic Considerations

›Drainage approach selection

›Echo-guided percutaneous pericardiocentesis

›First-line for most etiologies

›Subxiphoid approach: anterior effusions, emergent access

›Apical approach: posterior or lateral effusions

›Success rate > 90% in experienced hands

›Surgical drainage indications

›Type A aortic dissection: pericardiocentesis contraindicated

›Purulent pericarditis: requires aggressive drainage

›Loculated effusions not accessible percutaneously

›Recurrent tamponade: pericardial window

›CT-guided pericardiocentesis

›Loculated or atypically positioned effusions

›Posterior effusions difficult on echo approach

›Anti-inflammatory evidence base

›NSAIDs as first-line for idiopathic and viral etiologies

›Reduce inflammation and prevent recurrence

›Avoid in post-MI first 4 weeks (impair healing)

›Colchicine reduces recurrence by 50%

›COPE and ICAP trials established benefit

›3-month course standard

›Steroids increase recurrence risk when used first-line

›Reserve for NSAID failure or specific indications

›Slowly taper to prevent rebound pericarditis

›IL-1 inhibition for recurrent corticosteroid-dependent pericarditis

›Anakinra 100 mg subcutaneous daily

›Rilonacept approved for recurrent pericarditis (RHAPSODY trial)

›Malignant effusion management

›Systemic treatment of underlying malignancy first priority

›Chemotherapy, immunotherapy, radiation as appropriate

›Sclerosing agents (bleomycin, doxycycline) for malignant effusions

›Pericardial window preferred over repeated pericardiocentesis

›Lower recurrence rate in malignant etiology

›Surgical or VATS approach depending on patient status

11Patient Discharge Instructions/pdi35

copy discharge instructions

›Cardiac Tamponade Discharge Instructions

›Diagnosis overview

›Fluid accumulated around your heart, compressing it and affecting its ability to pump

›Treatment involved draining the fluid with a needle or tube

›Underlying cause is being treated; follow-up is essential

›Activity restrictions

›No strenuous activity, heavy lifting, or vigorous exercise for 4-6 weeks

›Gradually increase activity as tolerated under cardiology guidance

›No contact sports until cleared by cardiologist

›Medications

›Take all anti-inflammatory medications as prescribed (ibuprofen or aspirin plus colchicine)

›Do not stop anti-inflammatory medications early even if feeling better

›Take ibuprofen with food or milk to protect stomach

›Stomach-protecting medication (PPI) prescribed: take daily as directed

›Fluid and dietary precautions

›Stay well hydrated; do not restrict fluids unless told otherwise

›Avoid dehydration (especially in hot weather or with exercise)

›No specific dietary restrictions unless for underlying kidney disease or heart failure

›Follow-up appointments

›Cardiology appointment within 1-2 weeks (sooner if malignant cause)

›Repeat echocardiogram (heart ultrasound) scheduled to check fluid has not returned

›Keep all scheduled oncology, rheumatology, or nephrology appointments

›Return to emergency department immediately if

›Worsening shortness of breath or inability to lie flat

›May indicate fluid re-accumulation

›Chest pain or pressure

›New or worsening pericarditis or ischemia

12References/r36

Guidelines and key sources

›2025 ACC Expert Consensus Statement on Pericarditis

›Wang TKM, Klein AL, Cremer PC, et al. J Am Coll Cardiol. 2025

›Updated tamponade diagnostic criteria and management algorithm

›Echocardiographic tamponade physiology classification

›Nature Reviews Disease Primers: Cardiac Tamponade 2023

›Adler Y, Ristić AD, Imazio M, et al. Nat Rev Dis Primers. 2023; PMID 37474539

›Comprehensive review of pathophysiology, diagnosis, treatment

›Drainage approach selection and post-pericardiocentesis care

›JAMA Rational Clinical Examination: Pericardial Effusion with Tamponade 2007

›Roy CL, Minor MA, Brookhart MA, Choudhry NK. JAMA. 2007;297(16):1810-1818

›Pulsus paradoxus: sensitivity 98%, specificity 83%

›LR+ 5.9, LR- 0.03 for cardiac tamponade

›American Journal of Emergency Medicine: POCUS Tamponade Review 2022

›Alerhand S, Adrian RJ, Long B, Avila J. Am J Emerg Med. 2022; PMID 35696801

›Emergency POCUS protocol for tamponade diagnosis

›Echo-guided pericardiocentesis technique guidance

Landmark trials and cohort studies

›CATEO Study: Contemporary Analysis of Cardiac Tamponade 2025

›Del Buono MG, Brecciaroli M, Saponara G, et al. J Cardiovasc Pharmacol. 2025; PMID 40261953

›Anti-inflammatory use: NSAIDs 22%, colchicine 46%, steroids 24%

›Contemporary real-world etiology and outcomes data

›Sánchez-Enrique et al.: Long-Term Outcomes 2016

›Am J Cardiol. 2016; PMID 26718232

›3-month mortality 29% overall; malignant 49% vs non-malignant 11%

›Recurrence 10% overall; 62% in malignant group

›Spodick DH: Acute Cardiac Tamponade (NEJM 2003)

›N Engl J Med. 2003; DOI 10.1056/NEJMra022643

Evidence & Review

Evidence & Review