1. Several Slides courtesy of Alena Goldman, M.D.
Pericardial Diseases
Several Slides courtesy of Alena Goldman, M.D.
2008
Zoll Firm Lecture Series

2. Zoll Firm Lecture Series
Pericardium
Fibroelastic sack made up of visceral and parietal layers separated by a potential space, pericardial cavity
Forms a sac enclosing the origin of the aorta, pulmonary artery, Pulmonary veins, venae cavae
2008
Zoll Firm Lecture Series

3. Zoll Firm Lecture Series
Categories
3 major categories of pericardial diseases (co-existing, overlaping with one another):
Pericarditis (inflammation of the pericardium)
Pericardial effusion (fluid around the heart causing clinical presentation from asymptomatic to causing tamponade)
Constrictive pericarditis (inelastic sac that impairs filling)
Pericardial effusion and cardiac tamponade really a continuous spectrum of diseases.
2008
Zoll Firm Lecture Series

4. Etiology of pericardial Diseases
Idiopathic pericarditis
Infectious (viral, bacterial, Mycoplasma, fungal, parasitic)
Vasculitis/connective tissue disease (lupus, RA, scleroderma, MCTD, Wegener’s, PAN, sarcoid, IBD, Whipple’s, GCA, Behcet’s)
Hypersensitivity/immunopathies
Diseases of contiguous structures (post-infarction/early, Dressler’s, myocarditis, dissecting aortic aneurism)
Disorders of metabolism (hypothyroidism, uremia, ovarian hyperstimulation syndrome)
Trauma (blunt, penetrating, iatrogenic)
Neoplasms (mets, primary, paraneoplastic)
Other (congenital)
2008
Zoll Firm Lecture Series

5. Acute Pericarditis: Clinical Presentation
Symptoms
Left precordial chest pain (pleuritic, worsens with recumbency; relieved with leaning forward, sudden onset)
Fever
Malaise, myalgias
Symptoms of systemic illness, depending on the etiology
Signs
Pericardial friction rub (easier to hear in an absence of an effusion):
Three phases: correspond to movement of the heart during atrial systole ventricular systole, and in the rapid filling phase of early ventricular diastole
serum biomarkers for myocardial injury: related to the extent of myocardial inflammation
Elevated WBC, CRP
2008
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6. Zoll Firm Lecture Series
ECG Changes
Low Voltage
Electrical Alternans
(“Cardiac Nystagmus” by Littman)
ST Segment Deviation
PR Segment Changes
TWI
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7. Zoll Firm Lecture Series
EKG changes
Stage I- diffuse PR depression, ST elevation except in avR and v1 (the typical pericarditis EKG).
Stage II- (several days later) PR and ST segments normalized, T wave becomes flat.
Stage III- diffuse T wave inversion
Stage IV- resolution (several days to weeks)
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8. Zoll Firm Lecture Series
Typical ECG (stage I)
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9. Zoll Firm Lecture Series
Echocardiography
Acute pericarditis is a clinical diagnosis.
Echocardiogram is often normal in patients with acute syndrome unless it is associated with a pericardial effusion
Finding of a pericardial effusion in a patient with known or suspected pericarditis supports the diagnosis, the absence of a pericardial effusion or other echocardiographic abnormalities does not exclude it
Do not need to order it unless you suspect substantial pericardial effusion.
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10. Zoll Firm Lecture Series
2D Echo
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11. Zoll Firm Lecture Series
Identifying the Cause
In Western countries, most cases of acute pericarditis in immunocompetent patients that are not associated with apparent medical or surgical conditions are due to viral infection (entero-, echo-, adenoviruses; CMV, EBV, HSV, influenza, parvo, HCV, HIV) or are idiopathic
A full diagnostic evaluation is not appropriate in all patients
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12. Zoll Firm Lecture Series
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Zoll Firm Lecture Series
Maisch, B., Heart 2003; 89

13. Zoll Firm Lecture Series
Management
For symptom relieve:
NSAIDs- indomethacin 25-50mg PO TID or ibuprofen mg PO TID for 3 weeks
Cholchicine- 1mg/d for 3 weeks
Steroids- less preferred, patient’s symptoms often rebound when steroids are withdrawn. If needed- prednisone 40-60mg PO qd x 3wks
2008
Zoll Firm Lecture Series

14. Zoll Firm Lecture Series
Complications
Recurrent in 20-30% of the cases.
Infrequently, can progress to tamponade or constriction.
None of the medical therapy has been vigorously proven to prevent complications.
2008
Zoll Firm Lecture Series

15. Zoll Firm Lecture Series
Pericardial effusion
Can be asymptomatic or present as life-threatening cardiogenic shock (tamponade). Can also present in between the above two polar opposites.
Symptoms occur when increase in pericardial fluid raises the intrapericardial pressure and impairs diastolic filling.
The presenting syndrome depends on the:
Volume (bigger worse)
rate of accumulation (faster worse)
Characteristic (thicker worse)
2008
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16. Zoll Firm Lecture Series
Cardiac Tamponade
Tamponade is at one extreme of the of the syndrome and is characterized by:
Progressive increase in intrapericardial pressure first becoming equal to the RV then later the LV filling pressures (equalization of diastolic pressure)
Continual elevation of intracardiac filling pressure.
Impairment of diastolic filling
Lack of filling leads to fall in cardiac output.
At first, the body compensates through tachycardia and vasoconstriction. As the syndrome progresses, this mechanism becomes inadeqaute and shock ensues.
Needs to be treated by urgent pericardiocentisis.
2008
Zoll Firm Lecture Series

17. Zoll Firm Lecture Series
Relationship Between Intracardiac Filling Pressures and Intrapericardial Pressure and Cardiac Output in Cardiac Tamponade
Slide 2
Roy, C. L. et al. JAMA 2007;297:
2008
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18. Clinical presentation
Symptoms
Mostly relates to low cardiac output and high filling pressure.
Mental status changes
Dypsnea
Signs:
Low BP
Tachycardia
Tachypnea
Diminished heart sounds
Low urine output
Pulsis paradoxus- inspiratory decline in SBP >10mmHg.
2008
Zoll Firm Lecture Series

19. Measurement and Mechanism of Pulsus Paradoxus
Roy, C. L. et al. JAMA 2007;297:
2008
Zoll Firm Lecture Series
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20. Echocardiography in cardiac tamponade
Visualizes the effusion
Impairment of diastolic filling causes the cardiac chambers to be “squashed”
1st RA collapse (lowest pressure chamber, more sensitive, less specific)
2nd RV collapse (fairly specific)
False negative in the presence of substantial pulmonary hypertension.
variation in mitral and tricuspid inflow.
Ultimately, cardiac tamponade is a clinical diagnosis though echocardiogram is very useful in this setting
2008
Zoll Firm Lecture Series

21. Zoll Firm Lecture Series
Echocardiogram of a 62-Year-Old Woman With Advanced Lung Cancer and Malignant Pericardial Effusion Causing Cardiac Tamponade
Roy, C. L. et al. JAMA 2007;297:
2008
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Copyright restrictions may apply.

22. Zoll Firm Lecture Series
Diastolic RA collapse
2008
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23. Constrictive Pericarditis
Typically, long delay between onset of constriction and pericardial inflammation
Common etiologies includes radiation, TB…etc. Although many pericardial diseases can lead to constriction.
Presents with R>L sided failure symptoms
Insidious symptoms at first, followed by dypsnea with exertion, orthopnea, edema…etc.
Diagnosed by a combination of
Echocardiography (pericardium, filling patterns, interventricular dependence…etc)
chest CT/MRI (better at defining pericardium)
RHC (gold standard for hemodynamic assessment)
Pericardiectomy is the only therapy for a permanent constriction
2008
Zoll Firm Lecture Series

24. Constrictive Pericarditis - Pathophysiology
Fibrosed or calcified pericardium restricts diastolic filling of all 4 chambers
constriction leads to elevated and equilibrium of the diastolic pressures
In early diastole filling is unimpaired => abnormally rapid filling
filling is abruptly halted when cardiac volume meets the limits determined by the stiff pericardium
Virtually all filling occurs during early diastole
2008
Zoll Firm Lecture Series

25. Zoll Firm Lecture Series
CXR
dense circumferential calcification of pericardium
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26. Zoll Firm Lecture Series
Chest CT demonstrating extent and severity of pericardial calcification
Circulation. 2005;112:e137-e139
2008
Zoll Firm Lecture Series