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1. PERICARDIAL DISEASES-1
Ajay Kumar Yadav
PGY3,Medicine
IOM-TUTH, Kathmandu
2075/06/07

2. LAYOUT
• Anatomy and physiology of pericardium
• Pericarditis
• Pericardial effusion and tamponade
• Constrictive pericarditis
• Effusive-constrictive pericarditis

3. Anatomy and Physiology of the Pericardium
• Two layers
• Visceral pericardium :
• Mesothelial cells + collagen + elastin fibers
• Adherent to the epicardial surface of the heart
• Reflects back near the origins of the great vessels
• Fibrous parietal layer :
• About 2 mm thick and surrounds most of the heart
• Largely acellular and contains collagen and elastin fibers.
• Pericardial fluid : 15-50 ml , Small reserve volume.

5. Functions of Pericardium
1) Maintain the heart at a relatively constant position within the thorax.
2) Barrier to infection.
3) The pericardium is well innervated with mechanoreceptors and chemoreceptors
1) Bezold-Jarisch reflex
2) Transmission of pericardial pain
4) Mechanical function : restraining effect on cardiac volume.
5) Diastolic interaction : transmission of intracavitary filling pressure to adjoining Chambers.

6. PRESENTATIONS
• Diseases of the pericardium present clinically in one of several ways :
 Acute and recurrent pericarditis
 Pericardial effusion without major hemodynamic compromise
 Cardiac tamponade
 Constrictive pericarditis(Vs Restrictive pericarditis)
 Effusive-constrictive pericarditis.

7. PERICARDITIS

8. INTRODUCTION
• At autopsy, the frequency is approximately 1%.
• Accounts for up to 5% of pts with nonischemic chest pain in ER.
• As many as 15% of pericarditis cases are associated with myocarditis(↑troponin)
• With normal ventricular function : Myopericarditis
• With impaired ventricular function : Perimyocarditis.
• Cause
• Presumed viral and idiopathic forms are most common in developed countries.
• Tb is the most common cause in developing countries.

9. Classification of Pericarditis

10. Etiological Classification

14. TB Pericarditis
• EPIDEMIOLOGY
• Tuberculous pericarditis occurs in approx. 1 to 2 pc. of patients with PTB.
• Constrictive pericarditis occurs in 30 to 60 pc. of pts, despite prompt ATT and use of
corticosteroids.(1)
• 1 - Sagrista-Sauleda J, Permanyer-Miralda G, Soler-Soler J. Tuberculous pericarditis: ten
year experience with a prospective protocol for diagnosis and treatment. Journal of the
American College of Cardiology. 1988 Apr 1;11(4):724-8.

15. PATHOGENESIS
• Extension of infection from the lung or tracheobronchial tree, adjacent lymph nodes, spine,
sternum, or via miliary spread.
• Mostly reactivation disease, and the primary focus of infection may be inapparent.
• Four pathological stages of tuberculous pericarditis have been described
Fibrinous exudation with PMN leukocytosis, abundant mycobacteria, and early granuloma
formation with loose organization of macrophages and T cells
Serosanguineous effusion with lymphocytic exudate and high protein concentration; tubercle bacilli
present in low concentrations
Absorption of effusion with granulomatous caseation and pericardial thickening with subsequent
fibrosis
Constrictive scarring; fibrosing visceral and parietal pericardium contracts on the cardiac chambers
and may become calcified, leading to constrictive pericarditis, which impedes diastolic filling

16. Clinical Presentation of TB Pericarditis
• Patients with TB pericarditis generally present with clinical findings typical of pericarditis or
cardiac tamponade.
• In most cases, tuberculous pericarditis is insidious; the onset is acute in up to 25 percent of cases
• In one series, the following frequency of symptoms was noted (Fowler NO, Manitsas GT.
Infectious pericarditis. Progress in cardiovascular diseases. 1973 Nov 1;16(3):323-36.)
 Cough – 94 percent
 Dyspnea – 88 percent
 Chest pain (often pleuritic) – 76 percent
 Night sweats – 56 percent
 Orthopnea – 53 percent
 Weight loss – 48 percent

17. Clinical Presentation
• CHEST PAIN : > 90%
 Often severe , retrosternal, and left precordial
 Radiation : To neck, arms, or left shoulder
 The trapezius ridge is a classic radiation.
 Pain is pleuritic
 Characteristically relieved by sitting up and leaning forward and is intensified by lying supine.
 Pain is often absent in slowly developing tuberculous, post-irradiation, and neoplastic, uremic,
and constrictive pericarditis.

18. Physical Examination
• UNCOMPLICATED ACUTE PERICARDITIS
 Low-grade fever (<38°C)
 Sinus tachycardia.
 Pericardial friction rub : pathognomic ( 1/3rd )
 The classic rub consists of three components corresponding to ventricular systole, early
diastole, and atrial contraction.
 Described as rasping ,scratching and grating.
 Likened to the sound made when walking on crunchy snow.
 Usually loudest at the lower left sternal border and best heard with the patient leaning
forward.

20. Laboratory Testing
• ECG
• Pericardium is electrically silent ,ECG changes reflective of concomitant myocardium
involvement(>90%)
 Classic finding : “diffuse” ST-segment elevation (except aVR and often V1) with concavity upward
 Diff. Vs transmural ischemia
 Extensive lead involvement Vs Regional.
 Lack of evolution to pathologic Q waves in pericarditis
 Reciprocal ST depression in ischemia.
 Concave elevation in pericarditis Vs Convex elevation in STEMI.

21. ECG cont..
• PR-segment depression : Common
 Earliest ECG sign of acute pericarditis, reflecting pericardial involvement overlying the atria
 Can occur w/out STE and may be the initial or sole ECG manifestation.
 The typical ECG evolution follows four stages:
(1) PR depression and/ or diffuse ST-segment elevation.
(2) Normalization of the ST segment.
(3) T-wave inversion with or without ST segment depression.
(4) Normalization.

24. Lab diagnosis cont..
• Modest Leukocytosis
• hsCRP : Elevated in 3/4th
• Usually normalizes within 1 wk and in almost all case by 4 wks.
• Significance : Duration of therapy , Independent risk factor for recurrence.
• CXR :
• Usually normal in uncomplicated pericarditis
• Flask shaped appearance in moderate to severe pericardial effusion.
• Echocardiographic-Doppler examination
• Completely normal in approximately 40% of patients with acute pericarditis.
• Performed mainly to determine if an effusion is present (about 60% of cases of acute pericarditis)
• Mild (< 10 mm) or Moderate or larger effusions (> 20 mm)

25. Approach To Diagnosis

26. ESC guidelines for diagnosis
According to the guidelines, the clinical diagnosis of acute pericarditis can be made based on two of
the following criteria:
(1) Chest pain,
(2) Pericardial friction rub,
(3) ECG changes consisting of typical ST elevation and/ or PR depression, and
(4) Pericardial effusion

28. MANAGEMENT

29. • ACUTE IDIOPATHIC PERICARDITIS
• Self-limited disease without significant complications or recurrence in 70% to 90% 0f pts.
• Occurs at all ages but is more common in young adults
• Often associated with pleural effusions and pneumonitis.
• The almost simultaneous development of fever and precordial pain, often 10–12 days after a
presumed viral illness, constitutes an important feature in the differentiation of acute
pericarditis from AMI, in which chest pain precedes fever.
• Other recommendations include
• Restriction of physical activity beyond a sedentary level until resolution of symptoms and
normalization of hsCRP.
• For athletes, a return to sports is recommended after an arbitrary term of 3 months

30. Empirical Anti-inflammatory Therapy

31. What is the role of steroids ??
• Corticosteroid use should be minimized in patients with acute pericarditis because it may impair the
clearance of infectious agents.
• However, there are selected indications for corticosteroid use:
1) contraindications to or failure of an NSAID and colchicine,
2) underlying conditions (e.g., autoimmune diseases) whose primary treatment is corticosteroids,
3) concomitant diseases (e.g., renal failure),
4) pregnancy, and
5) concomitant therapies constituting relative contraindications to NSAIDs and/or colchicine (e.g ,oral
anticoagulants).
• Relatively low doses of corticosteroids are recommended (e.g., prednisone 0.2 to 0.5 mg/kg daily) with
concurrent colchicine.
• Tapering should be gradual, typically over 6 to 12 weeks, and guided by the symptomatic response and
hsCRP levels.

32. COMPLICATIONS
• Recurrent Pericarditis : M/C common complication(15-30%)
• Pericardial effusion
• Tamponade
• Constrictive Pericarditis
• Over an average 31-month follow-up, tamponade developed in 3.1% and constriction in
1.5%.

33. RECURRENT PERICARDITIS
• Recurrences occur in 15% to 30% of patients with idiopathic acute pericarditis.
• Most common complication
• Never been associated with evolution to constrictive pericarditis.
• The risk of constriction is associated with the etiology, not the number of recurrences.
• Recommended therapy
• NSAIDs plus colchicine and a PPI for an initial episode.
• Therapy s/b continued until complete resolution of S/S, and laboratory findings, including hsCRP if elevated.
• At this point the NSAID should be gradually tapered.
• If this therapy fails, corticosteroids may replace the NSAID or may be added as “triple therapy.”
• Doses of 0.2 to 0.5 mg/ kg/day of prednisone or its equivalent are recommended for at least 2 to 4 weeks
until S/S resolve and hsCRP normalizes, followed by gradual tapering every 2 to 4 weeks.
• Colchicine should always be included for at least 6 months.

34. Cont..
• For patients with recurrences who are resistant to colchicine and corticosteroids : 5% to 10% of
recurrent pericarditis cases.
• Azathioprine (2 mg/kg/day orally for several months with gradual dose increases and
monitoring of WBCs, transaminases, and amylases),
• Human IVIG(400 to 500 mg/ kg/day for 5 days with a possible repeat course after 1
month),or
• Anakinra, an interleukin 1 antagonist (1 to 2 mg/kg/day up to 100 mg daily subcutaneously
for several months).
• The optimal duration of therapy for these treatments is not established.
• Refractory to medical therapy : Pericardiectomy(last resort)

36. PERICARDIAL EFFUSION AND CARDIAC TAMPONADE

37. Pathophysiology and hemodynamics
• Formation of an effusion is a generic response to inflammatory, infectious, or
neoplastic diseases involving the pericardium.
• Lymphomas : enlarged mediastinal LNs obstruct lymph drainage.
• Effusion  compression and collapse of the right heart and caval vessels 
reduced right heart output  underfilling of the left heart  decreased CO.
• The limited pericardial reserve volume dictates that modest amounts of rapidly
accumulating fluid (as little as 150 to 200 mL) can impair cardiac function. In
contrast, large, slowly accumulating effusions are often well tolerated.

38. Cont..
• As fluid accumulates, left- and right-sided atrial and ventricular diastolic
pressures rise, and in severe tamponade they equalize at a pressure similar to
that in the pericardial sac, typically 20 to 25 mm Hg
• Equalization is closest during inspiration.
• Characteristics of Tamponade
• Elevated and equal intracavitary filling pressures,
• Low transmural filling pressures,
• Small cardiac volumes,
• Loss of the y descent of the RA or systemic venous pressure.

39. Before Pericardiocentesis After Pericardiocentesis

40. • The 2nd characteristic finding is the paradoxical pulse.
• Abnormally large decline in systemic arterial pressure during inspiration (defined as a drop of
> 10 mm Hg in SBP).
• The arterial pulse may be impalpable during inspiration.
• Cause : Exaggerated Ventricular interaction.
• In tamponade, in contrast to constriction, the normal inspiratory increase in SVR is present and
the normal inspiratory decline in SVP is retained (Kussmaul sign is absent).

44. Low Pressure Tamponade
• Although mean left- and right-sided filling pressures are typically 20 to 25 mm Hg, tamponade can
occur at lower filling pressures, termed low-pressure tamponade.
• Low-pressure tamponade may be observed during hemodialysis, in pts. with blood loss and
volume depletion, and when diuretics are administered to patients with effusions.
• Low-pressure patients were less often critically ill and signs of tamponade were less prominent.
• Echocardiographic findings were similar and benefit was derived from pericardiocentesis.

45. Clinical Presentation
• Without tamponade :
 Usually asymptomatic; although pts. may have pain due to pericarditis.
 Ewart’s sign
• With tamponade
 Dyspnea : mechanism of which is uncertain (no pulmonary congestion)
 Impalpable apex
 Muffled heart sounds
 Pericardial rub
 Tubular breath sounds : may be heard in the left axilla or base due to bronchial compression.
 Beck’s triad : hypotension muffled heart sounds, and elevated JVP
 S/S of reduced CO and shock including tachypnea, diaphoresis, cool extremities, peripheral cyanosis, depressed
sensorium, and, rarely, yawning.
 The JVP is markedly elevated except in low-pressure tamponade, and the y descent is usually absent

46. Laboratory Examination
• ECG abnormalities : Reduced voltage and Electrical alternans
 Reduced voltage is nonspecific
 Electrical alternans is specific but relatively insensitive
 Caused by anteroposterior swinging of the heart with each contraction.
• Chest radiograph
 Normal cardiac silhouette until effusions are at least moderate in size.
 With larger effusions
 PA view : flask-like appearance
 Lateral views : fat pad sign
 The lungs are oligemic.

48. ECHOCARDIOGRAPHY
• Small effusions are usually first evident over the posterobasal left ventricle. Fluid then spreads
anteriorly, laterally, and behind the left atrium.
• Ultimately, the separation becomes circumferential.
• Circumferential effusions are graded as
• Small (echo-free space in diastole < 10 mm)
• Moderate (10 to 20 mm)
• Large (> 20 mm)

50. • Frond-like or shaggy-appearing structures in the pericardial space detected by echocardiography
suggest clots, chronic inflammation, or neoplastic pericardial processes.
• CT and MRI are more precise than TTE for estimating pericardial thickness.
• TEE however, is comparable.
• CT attenuation coefficients
• Thickness of more than 4.1 mm : Metastatic involvement
• Echo findings s/o tamponade severe enough to cause hemodynamic compromise
• Early diastolic collapse of the right ventricle
• Late diastolic indentation or collapse of the right atrium, and
• Exaggerated respiratory variation in RV and LV size and interventricular septal shifting during
inspiration causing a bulge or “bounce.”

55. Approach to a patient with pericardial
effusion

56. Cont..
• Patients with actual or threatened tamponade
 Medical emergency.
 Closed pericardiocentesis ( sub-xiphoid approach under echo guidance ; needle should be
directed toward the left shoulder)
 Success rate of more than 95% and a rate of serious complications of less than 2%
 Some exceptions.
 Pts with acute, apparently idiopathic pericarditis with no more than mild tamponade
 Pts with known inflammatory/autoimmune diseases.
 Patients with suspected bacterial infections or hemopericardium with small effusions (< 10
mm) .

58. • CLOSED Vs OPEN PERICARDIOCENTESIS
 The danger of closed approach is that lowering intrapericardial pressure will allow more bleeding
without affording an opportunity to correct its source.
 In cases of trauma or post-MI LV rupture, closed pericardiocentesis should usually be avoided.
 Closed pericardiocentesis in pts with hemopericardium due to type A aortic dissection has been
considered relatively contraindicated.
• PERICARDIAL DECOMPRESSION SYNDROME
 Poorly understood but life-threatening syndrome
 Characterized by combinations of cardiogenic pulmonary edema and shock.

59. Analysis of Pericardial fluid
• Plasma ultrafiltrate , lymphocyte predominant cell.
• Appearance
• Sanguineous fluid is nonspecific and does not necessarily indicate active bleeding : 3’T’s
• Chylous effusions can occur after traumatic or surgical injury to the thoracic duct or obstruction by
neoplasms.
• Cholesterol-rich (“gold paint”) effusions occur in hypothyroidism.
• Tests
• TC ,DC , hematocrit, and protein content.
• Gram and AFB stain
• Culture of bacteria, including MTB , and fungi
• Malignant cytology
• In suspected tuberculous pericardial disease : IFN-γ, ADA, lysozyme levels, and PCR.

60. Role of Pericardial Biopsy ??
• Generally performed as
 A part of a therapeutic procedure (surgical drainage) in patients with recurrent
pericardial effusions and cardiac tamponade after prior pericardiocentesis
(therapeutic biopsy), and
 A diagnostic procedure in patients with an illness lasting more than three weeks
despite treatment without a definite diagnosis.

61. Treatment of TB Pericarditis
• ATT for 12 months
• Indications of steroids :
• Pts with constrictive tuberculous pericarditis
• Pts at high risk of constrictive tuberculous pericarditis.
• Does not appear to be beneficial in the setting of TB pericarditis that is not constrictive, particularly
among HIV-infected patients)
• Dose and tapering : Prednisone 60 mg/day (or the equivalent dose of prednisolone) given for four weeks
followed by 30 mg/day for four weeks 15 mg/day for two weeks 5 mg/day for one week.
• A shorter course of 60 mg of prednisone daily, tapering by 10 mg/day each week over a six-week period, has
demonstrated efficacy in HIV-infected patients with TB pericarditis

62. TAKE HOME MESSAGE
• Pericarditis : Chest pain + Pericardial rub + ECG changes
• Echocardiography : To R/O pericardial effusion and tamponade
• Tamponade – Medical Emergency
• Pericardiocentesis : Diagnostic + Therapeutic
• See if medical management can alleviate need for pericardiocentesis

64. REFERENCE
• Braunwald’s Heart Disease 11th Edition
•
• Harrison 19th Edition
• UpToDate 2018
• Davidson’s 23rd Edition

65. THANK YOU