Pericardial effusion and tamponade

(Redirigido desde «Pericardial effusion»)

Background

File:Pericardial anatomy diagram.png
(d) Pericardial cavity, part of the inferior mediastinum, in relation to (a) superior mediastinum; (c) pleural cavities; and (e) diaphragm.
File:Pericardium anatomy.png
Anatomy of the pericardium.
File:Pericardial pressure volume curve.png
Pericardial pressure-volume relationships. Rapid accumulation (left curve) causes tamponade with small volumes; slow accumulation (right curve) allows pericardial stretching.
  • Pericardial effusion: abnormal accumulation of fluid in the pericardial space
  • Cardiac tamponade: hemodynamic compromise from pericardial fluid compressing the heart
    • Rate of accumulation matters more than volume
    • Acute: as little as 100-150 mL can cause tamponade (e.g., trauma)
    • Chronic: up to 1-2 L may accumulate before tamponade (e.g., malignancy, uremia)
  • Pathophysiology: increased pericardial pressure → decreased RV filling → decreased cardiac output
  • Always consider in PEA
  • Always consider in penetrating thoracic trauma within the cardiac box (80% result in tamponade)
    • Gunshot wounds less likely to cause tamponade (larger pericardial defect allows decompression)
    • RV is most commonly injured chamber due to anterior position

Etiology

  • Hemopericardium:
    • Trauma (penetrating or blunt), iatrogenic (central line, pacemaker, post-cardiac surgery)
    • Ventricular free wall rupture (post-MI, typically day 3-5)
    • Aortic dissection (type A with rupture into pericardium)
    • Bleeding diathesis / anticoagulation
  • Non-hemorrhagic:
    • Malignancy (most common cause of large effusions): lung, breast, lymphoma, melanoma
      • Melanoma has particular predilection for cardiac metastasis
    • Pericarditis (viral, bacterial, tuberculous)
    • Uremia (renal failure)
    • HIV (infection, Kaposi sarcoma, lymphoma)
    • Autoimmune (SLE, rheumatoid arthritis, scleroderma)
    • Post-radiation, hypothyroidism/myxedema
    • Idiopathic (up to 50% of large effusions)

Clinical Features

  • Chest pain, dyspnea, cough, fatigue
  • Tachycardia (most reliable sign; bradycardia is ominous/preterminal)
  • Narrow pulse pressure
  • Friction rub (may be absent with large effusion)
  • Pulsus paradoxus: >10 mmHg drop in systolic BP during inspiration
  • Beck's triad (present in only ~33% of cases):
  • Kussmaul sign: paradoxical rise in JVP with inspiration
  • Hepatomegaly, peripheral edema (if chronic)
  • May present as PEA arrest or cardiogenic shock

Differential Diagnosis

Template:Chest pain DDX

Evaluation

ECG

  • Sinus tachycardia (most common finding)
  • Electrical alternans (pathognomonic but insensitive — alternating QRS amplitude)
  • Low voltage:
    • Limb leads: all QRS <5 mm or I+II+III <15 mm[1]
    • Precordial leads: all QRS <10 mm or V1+V2+V3 <30 mm
  • PR depression (if associated pericarditis)

CXR

File:Massive pericardial effusion CXR.jpg
Massive pericardial effusion on chest x-ray
  • Enlarged cardiac silhouette (water bottle sign)
  • May be normal with small or acute effusions
  • Not sensitive for early detection

Pulsus Paradoxus

  • >10 mmHg decrease in systolic BP during inspiration
  • Measure with manual sphygmomanometer (inflate above systolic, slowly deflate noting first Korotkoff sounds in expiration vs inspiration)
  • False negatives: aortic regurgitation, ASD, severe hypotension, positive-pressure ventilation

Bedside Ultrasound (Test of Choice in ED)

File:Pericardial effusion echo.jpg
Transthoracic echo of pericardial effusion showing "swinging heart"
File:Pericardial effusion US.jpg
Pericardial effusion on ultrasound
  • POCUS is the fastest and most reliable bedside diagnostic tool
  • Key views: subxiphoid (most sensitive), parasternal long axis (PLAX), apical 4-chamber
  • Distinguish from pleural effusion on PLAX: pericardial effusion tracks anterior to descending aorta; pleural effusion tracks posterior[2]

Classic Findings of Tamponade

  • Diastolic collapse of RA (earliest sign; >1/3 of cardiac cycle = significant)
  • Diastolic collapse of RV (more specific)
  • Plethoric (non-collapsing) IVC (>2 cm, <50% collapse — sensitive but nonspecific)
  • Swinging heart within large effusion

Advanced Echo Assessment

  • M-mode: position through RV free wall on PLAX to identify diastolic collapse timing
  • Doppler — valvular pulsus paradoxus[3][4]:
    • Mitral inflow variation >25% → likely tamponade
    • Tricuspid inflow variation >40% → likely tamponade
    • Helpful when RV is thickened (chronic pulmonary hypertension)

Management

Immediate Stabilization

  • IV fluid bolus 500-1000 mL NS (patient is preload-dependent)
  • Avoid preload-reducing medications: nitroglycerin, diuretics, morphine
  • Avoid positive-pressure ventilation if possible (reduces preload further)
  • Vasopressors as temporizing bridge (norepinephrine preferred)
  • Position patient upright or leaning forward if tolerated

Pericardiocentesis (Definitive for Non-hemorrhagic Tamponade)

  • Indications: hemodynamic compromise, suspected purulent pericarditis
  • Ultrasound-guided approach preferred (reduces complications)
  • Subxiphoid approach:
    • Insert needle 1-2 cm inferior to left xiphosternal junction, aimed toward left shoulder
    • Advance at 30-45° angle under US guidance
    • As little as 30-50 mL removal can dramatically improve hemodynamics
  • Send fluid for: cell count, protein, LDH, glucose, cytology, gram stain/culture, AFB
  • Complication rate <2% with US guidance (vs ~20% blind)

Traumatic Tamponade

  • Pericardiocentesis is a temporizing measure only — definitive treatment is thoracotomy
  • Hemorrhagic tamponade will reaccumulate
  • IV fluid resuscitation and emergent surgical consultation
  • Can occur if ECG read as STEMI and heparin started inadvertently

Specific Etiologies

  • Uremic tamponade: emergent dialysis
  • Malignant effusion: pericardiocentesis + consider pericardial window for recurrent effusions[5]
  • Post-MI free wall rupture: emergent cardiac surgery

Disposition

  • Unstable traumatic tamponade: emergent OR for thoracotomy
  • All patients with tamponade physiology: ICU admission
  • Large effusion without tamponade: admit with cardiology consultation
  • Small effusion, stable, known etiology: may be managed as outpatient with close follow-up
  • Consult: cardiology and/or CT surgery

See Also

External Links

References

  1. ↑ Mattu A, Brady W. ECGs for the Emergency Physician 2. BMJ Books. 2008.
  2. ↑ Randazzo MR et al. Acad Emerg Med. 2003. PMID 12957982
  3. ↑ Spodick DH. Acute cardiac tamponade. N Engl J Med. 2003;349(7):684-690. PMID 12917306
  4. ↑ Rajagopalan N, et al. Comparison of new Doppler echocardiographic methods. Am J Cardiol. 2001;87(1):86-94. PMID 11137840
  5. ↑ Adler Y, et al. 2015 ESC Guidelines for the diagnosis and management of pericardial diseases. Eur Heart J. 2015;36(42):2921-2964. PMID 26320112
  • Adler Y, et al. 2015 ESC Guidelines for the diagnosis and management of pericardial diseases. Eur Heart J. 2015;36(42):2921-2964. PMID 26320112
  • Spodick DH. Acute cardiac tamponade. N Engl J Med. 2003;349(7):684-690. PMID 12917306
  • Ristic AD, et al. Triage strategy for urgent management of cardiac tamponade: a position statement of the ESC. Eur Heart J. 2014;35(34):2279-2284. PMID 25002085
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