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Pericardial Effusion

DDx of Pericardial Disease:

  • Autoimmune: lupus, rheumatoid arthritis, vasculitis, scleroderma, Wegner’s, PAN, sarcoid, IBD, Behcet’s
  • Infectious: viral (coxsackie, HIV), bacterial, fungal, infective endocarditis with ring abscess
  • Malignant: metastatic lung, breast, melanoma; Hodgkin’s dz; leukemia; rhabdomyosarcoma; leiomyoma; paraneoplastic
  • Cardiac: myocarditis, early infarct pericarditis, Dressler’s syndrome, aortic aneurysm
  • Metabolic: hypothyroidism, uremia
  • Idiopathic
  • Trauma, iatrogenic (related to cardiac procedures)
  • Drugs (drug induced lupus, hypersensitivity)

 

 

Analysis of pericardial fluid:

  • Culture
  • Cytology
  • Adenosine deaminase (for tuberculous pericarditis)
  • PCR (viral etc.)
  • Hemorrhagic pericardial effusions are most likely to be malignant, related to cardiac procedure, trauma or TB (less common in US)
  • Cell count, LDH, glucose, TP etc. are LESS helpful in pericardial fluid (c/w pleural fluid)

 

 

Management of Pericardial Effusions: 

  • Depends on the underlying etiology and the hemodynamic consequences
  • If tamponade physiology exists, urgent pericardiocentesis is usually indicated: pericardiocentesis +/- catheter placement vs. surgical (pericardectomy or pericardial window)
  • For recurrent effusions, guidelines suggest surgical pericardiectomy only in patients with symptomatic effusions 
  • Generally, treatment is aimed at the underlying cause (ie. autoimmune, viral, TB etc.)

 

 

Review of pathophysiology and clinical findings in cardiac tamponade:

  • compression of all cardiac chambers as a result of increasing intrapericardial pressure
  • as the cardiac chambers become progressively smaller and diastolic compliance is reduced, cardiac inflow is limited, equalizing mean diastolic pericardial and chamber pressures
  • the right heart increases its filling at the expense of the left heart, especially during inspiration when low intrathoracic pressure facilitates more rapid RA/RV filling
  • Tamponade is a form of cardiogenic shock, and most finding are non-specific: tachycardia, hypotension, renal failure, cool extremities
  • JVP is elevated, but may lack the classic y descent, due to high RV pressures; Kussmaul’s sign is the lack of normal decline in JVP with inspiration
  • pulsus paradoxus: an inspiratory decrease in systolic blood pressure of >10 mm Hg during normal breathing (due to RV bulging into LV during inspiration causing a drop in cardiac output)
  • R cardiac catheterization shows an equalization of intracardiac diastolic pressures (usually between 10 and 30 mmHg) an inspiratory increase in right-sided pressures and reduction in left-sided pressures (responsible for pulsus paradoxus)

 

 

 

**Attached is an article Keo found about the diagnostic accuracy of the clinical exam in diagnosing cardiac tamponade.  The paper, published in JAMA in 2007, is a meta-analysis of 8 studies assessing the clinical findings in patients with known pericardial effusions or echocardiographic signs of cardiac tamponade.  They found that 5 features occur in the majority of patients with tamponade:


* dyspnea (sensitivity ~ 88%)
* tachycardia (sensitivity ~77%)
* elevated JVP (sensitivity ~76%)
* pulsus paradoxus (sensitivity ~ 82%)
* cardiomegaly on CXR (sensitivity ~ 89%)

According to 1 study included in the meta-analysis, a pulsus paradoxus>10mmHg increased the likelihood of cardiac tamponade, with a LR of 3.3, while a pulsus<10mmHg greatly lowers the likelihood of tamponade (LR 0.03).**


 

(Victoria Kelly MD, 10/4/10)