Pericardial diseases - Etiopathogenesis, Clinical features, Advances in Management

1. PERICARDIAL DISEASE
CHAIR PERSON: DR.PRASHANTH KUMAR M
STUDENT: DR CHETHAN .Y
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2. Pericardial Anatomy
• Visceral – single layer mesothelial cells
• Parietal- fibrous < 2 mm thick
• Functions
– Limits motion
– Prevents dilatation during volume increase
– Barrier to infection
• 15-50 ml serous fluid
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4. Arterial Supply
• Mainly from the pericardiophrenic artery
Smaller contribution from the
• Musclophrenic artery
• Bronchial artery
• Esophageal
• Superior phrenic artery
• Coronary artery supplies the visceral layer
ONLY

5. Venous drainage
• Pericardiophrenic veins
• Azygos venous system

6. Innervations
• Phrenic nerve (C3-
C5) sensory fibers
• Partial & Fibrous
“Sensitive to pain”
• Vagus nerve &
Sympathetic
(vasomotor)

7. Acute Pericarditis Etiology
• Infectious
– Viral
– Bacterial
– TB
• Noninfeccious
– Post MI (acute and Dresslers)
– Uremia
– Neoplastic disease
– Post radiation
– Drug-induced
– Connective tissue diseases/autoimmune
– traumatic
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8. Infectious
• Viral (idiopathic)
– Echovirus, coxsackie B
– Hepatitis B, influenza, IM, Caricella, mumps
– HIV
Bacterial and fungal(purulent)
• Pneuococcus, staphlococci
• Neisseria, legionella
• Histoplasma, coccididomycosis
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9. Pericarditis post- MI
• Early <5% patients
• Dressler’s 2 weeks – months
– Autoimmune
• Post-pericardiotomy
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10. Neoplastic
• Breast
• Lung
• Lymphoma
• Primary pericardail tumors rare
• Hemmorrhagic and large
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11. • Radiation
– Dose > 4000rads
– Local inflammation
• Autoimmune
– SLE
– RA
• Drugs
– Hydralazine
– Procainamide
– Phenytoin
– Methyldopa
– Isoniazid
– Minoxidil
– Anthracycline antineoplastic agents
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12. Pathogenesis and Pathology
• Inflammatory
– Vasodilation
– Increased vascular permeability
– Leukocyte exudation
• Pathology
– Serous-little cells
– Serofibrinous – rough appearance / scarring
• common
– Purulent – intense inflammation
– Hemmorrhagic – TB or malignancy
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13. Clinical
• Chest pain
– Radiate to back
– Sharp and pleuritic
– Positional – worse lying back
• Fever
• Dyspnea due to pleuritic pain
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14. Examination
• Friction rub
– 1, 2 or 3 components
• Ventricular contraction, relaxaltion, atrial contraction
– intermittent
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15. Diagnostic
• Clinical history
• ECG
– Abn in 90%
– Diffuse ST elevation
– PR depression
• Echocardiography
– Effusion
• Autoimmune antibodies
• Evaluate for malignancy
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16. • Role of hs crp
• Role of troponin I in pericarditis
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17. ECG in Pericarditis

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19. Early repolarisation
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20. Treatment
• ASA or NSAIDs
– Avoid NSAID in MI
• Colchicine
• Steroids - avoid
– May increase reccurance
• TB – Rx TB
• Purulent – drainage of fluid + antibiotics
• Neoplastic- drainage
• Uremic - dialysis
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21. Pericardial Effusion
• From any acute pericarditis
• Hypothyriodism- increased capillary
permeability
• CHF- increased hydrostatic pressure
• Cirrhosis- decreased plasma oncotic pressure
• Chylous effusion- lymphatic obstruction
• Aortic Dissection
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22. Effusion Pathophysiology
• Pericardium is stiff- PV curve not flat
• Above critical volume – rapid increase in
pressure
• Factors that determine compression
– Volume
– Rate of accumulation
– Pericardial compliance
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25. Clinical
• Asymptomatic
• Symptoms
– Chest pain,
– dyspnea,
– dysphagia,
– hoarseness,
– hiccups
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26. • Examination
– Muffled heart sounds
– Absence of rub
– Ewarts sign-dullness L lung at scapula(atelectasis)
– Tubular breath sounds in the left axilla
– Becks triad
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27. Diagnostic studies
• CXR - > 250 ml fluid globular cardiomegaly
• ECG low voltage and electrical alternans
• Echocardiogram most helpful
– Identify hemodynamic compromise
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28. ECG low voltage and electrical alternans
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35. Treatment
• If known cause- treat that
• If unknown- may need pericardiocentesis or
pericardial window
• Cardiac tamponade is emergency-
pericardiocentesis drainage or window
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36. Tamponade
• Any cause of effusion may lead to
• Diastolic pressures elevate and = pericardial
pressure
• Impaired LV/RV filling
• Increased systemic venous pressure
• Decreased stroke volume and C.O.
• Shock
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38. • Have right side failure with edema and fatigue only if
occurs slowly
• Key physical findings:
– JVD
– Hypotension
– Small quiet heart
• Sinus tachycardia
• Pulsus paradoxus
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39. Pulsus Paradoxus
• Exaggeration of normal
• Normally septum moves toward LV with
inspiration, with decrease in LV filling
• With compression and fixed volume, there is
even greater limitation in LV filling and
reduced stroke volume
• PP also seen in COPD/asthma
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40. Tamponade
• Echocardiography
– Compression of RV and RA in diastole
– Can have localized effuison with localized
compression of one chamber (RA,LV)
• Effusion post cardiac surgery
– Differentiate other causes of low cardiac output
• Cardiac catheterization- definitive
– Measure pressures- chamber and pericardial
equal, and all elevated.
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Tamponade- external compression blunts filling
throughout cardiac cycle

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44. Pericardial Fluid
• Stained and cultured
• Cytologic exam
• Cell count
• Protein level
– pp/sp> 0.5 - exudate
• LDH level
– p LDH/ s LDH > 0.6 - exudate
• Adenosine Deaminase level - sensitive and specific
for TB
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45. Tamponade Constricitive
pericarditis
Restrictive
cardiomyopathy
RVMI
Pulsus paradoxus Common Usually
absent
Rare Rare
JVP
Prominent y descent
Prominent x descent
Absent
Present
Present
Present
Rare
Present
Rare
Rare
Kussmauls sign Absent Present Present Present
Third heart sound Absent Absent Rare Present
Pericardial knock Absent Present Absent Absent
Low voltage ECG present May be
present
May be Absent
Electrical alternans present absent absent absent
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46. Constrictive Pericarditis
• Most common etiology is idiopathic (viral)
• Any cause of pericarditis
• Post cardiac surgery
• Pathology
– Organization of fluid, scarring, fusion of pericardial
layers, calcification
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47. Constrictive Pericarditis
• Impaired diastolic
filling of the chambers
• Elevated systemic
venous pressures
• Reduced cardiac
output
• Dip and plateau curve
on catheterization
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48. 48
Fredrichs sign

49. Constrictive Pericarditis
Clinical
• Symptoms
– Fatigue
– weight gain
– increased abdominal girth
– Anasarca
– Cachexia
– Exertional dysnea
– JVD, hepatomegaly and ascites, edema
• Can confuse with cirrhosis- look for JVD
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50. • Examination
Pericardial knock
Broadbent sign
JVD
Kussmaul’s sign- JVD with inspiration
pulsus paradoxus(1/3rd)
• Congestive hepatomegaly
• Ascites
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51. • Differential diagnosis
• Corpulmonale
• Tricuspid stenosis
• Restrictive cardiomyopathy
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52. • Diagnosis
• ECG: low voltage complexes
Atrial fibrillation (1/3rd )
• CXR: pericardial calcification
• 2D echo: pericardial thickening
dilated IVC and hepatic veins
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53. Constrictive vs restrictive
cardiomyopathy
CP RC
Prominent y descent
in venous pressure
Present variable
Paradoxical pulse Less than 1/3rd absent
Pericardial knock present absent
Equal right- and
left-sided filling
pressure
Present Left at least 2-3 more than
right
Filling pressure
>25 mm Hg
Rare common
Square root” sign present absent
Respiratory variation
in left-right
pressure/flow
exagarated normal
Ventricular wall
thickness
normal Usually increased
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54. Atrial size Left atrial enlargement Biatrial enlargement
Septal bounce present absent
Speklele tracing Normal longitudinal and
secreased circumferential
restoration
Decresed longitudinal and
circumferential restoration
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55. 55
Am Heart J 1999;138:219-32

56. 56
(Circulation. 2006;113:1622-1632
Normal pericardium < 2 mm

57. • THANK YOU
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58. REFERNCES
• HARRISONS 19TH EDITION
• BRAUNWALDS 5TH EDITION
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