Pericardial Disease

Question 1

Common causes of acute pericarditis

Answer 1

Idiopathic (most common)
Infectious
• Viral (echovirus, Coxsackie virus group B)
• Tuberculosis (especially in immunosuppressed)
• Requires prolonged multidrug antituberculous therapy
• Pyogenic bacteria
Noninfectious
1) Post-MI
• Early form: within first few days
o Inflammation extending from epicardial surface
o More common with transmural infarctions
• Dressler’s syndrome
o 2 weeks to several months after MI
o Unknown cause; likely autoimmune
o Ab’s directed against antigens from necrotic tissue
o Similar form of pericarditis after heart surgery
2) Uremia
• Complication of chronic renal failure
• Usually resolves following dialysis
3) Neoplastic disease
• Usually from metastatic spread by cancer of lung, breast, or lymphoma
• Usually large
• Hemorrhagic
• Frequently lead to cardiac tamponade
• Pallative therapy only
4) Radiation induced
• Causes local inflammatory response that can lead to pericardial effusions and fibrosis
5) Connective tissue diseases
• Ex: SLE, rheumatoid arthritis, progressive systemic sclerosis
6) Drug-induced (procainamide, hydralazine, methyldopa, isoniazid, phenytoin, anthracycline, minoxidil)

Question 2

Pathogenesis (stages) of acute pericarditis

Answer 2

o Local vasodilation and transudate in pericardial space
o Increased vascular permeability → protein leak
o Leukocyte exudation
• First neutrophils, then mononuclear cells
• Contain or eliminate offending agent
• BUT metabolic products may prolong inflammation → tissue damage, fever

Question 3

Clinical features of acute pericarditis

Answer 3

o Fever
o Pleuritic chest pain
• Sharp
• Aggravated by inspiration and coughing
• Positional = sitting and leaning forward lessen discomfort
o Pericardial rub
• Auscultation using diaphragm
• Patient leaning forward while exhaling (brings pericardium closer to chest wall)
o Diffuse ST elevation (in multiple leads)
o Often see PR segment depression (due to atrial epicardial inflammation)

Question 4

Diagnose acute pericarditis

Answer 4

o ECG findings
o Echo = evaluate presence and hemodynamic significance of pericardial effusion
o Purified protein derivative (PPD) skin test for Tb
o Serologic tests for CT diseases (antinuclear ab’s and rheumatoid factor)
o Careful search for malignancies

Question 5

Management of acute pericarditis

Answer 5

o Idiopathic and viral caused = self-limited; runs its course in 1-3 weeks
o Rest
o NSAIDs x 1 month (except in MI)
o Colchicine x 3 months
o Avoid steroids due to potential side effects; withdrawal often leads to recurrent symptoms
• Only use in severe or recurrent cases
o Pericardiectomy for relapsing pericarditis

Question 6

Serous pericarditis

Answer 6

o Scant polymorphonuclear leukocytes, lymphocytes, histiocytes
o Thin liquid exudate
o Early inflammatory response common to all types of acute pericarditis

Question 7

Serofibrinous pericarditis

Answer 7

o Most commonly observed pattern
o Exudate with plasma proteins, including fibrinogen → “bread and butter” appearance (rough and shaggy)
o Pericardium may be thickened and fused
o Can lead to dense scar, restricting movement and diastolic filling

Question 8

Suppurative (purulent) pericarditis

Answer 8

o Intense inflammatory response
o Associated with bacterial infection
o Serosal surfaces are erythematous and coated with purulent exudate

Question 9

Hemorrhagic pericarditis

Answer 9

o Grossly = bloody

o Often due to tuberculosis or malignancy

Question 10

Etiology of pericardial effusion

Answer 10

o Result of any of causes of acute pericarditis
o Trauma
o Hypothyroidism (increased capillary permeability)
o Non-inflammatory causes:
• Increased capillary permeability
• Increased capillary hydrostatic pressure
• Decreased plasma oncotic pressure
o Chylous effusions = lymphatic obstructions due to neoplasms and Tb

Question 11

Pathophysiology components of pericardial effusion

Answer 11

o Volume of fluid
• Pericardium = relatively stiff
• Relationship between volume and pressure is not linear
• When intrapericardial volume expands beyond critical level → minor increase in volume = large compressive force on heart
o Rate at which the fluid accumulates
• Sudden increase in volume (chest trauma with hemorrhage) → rapid elevation of pericardial pressure
o Compliance characteristics of the pericardium
• If slow accumulation = pericardium gradually stretches (volume-pressure curve shifts right) = able to accommodate more volume

Question 12

Clinical features of pericardial effusion

Answer 12

o May be asymptomatic or may present with signs of tamponade
o Ewart’s sign = dull constant ache over posterior left lung
o Soft heart sounds (fluid buffers sound)
o Reduced intensity of friction rub

Question 13

Diagnosis of pericardial effusion

Answer 13

o Chest radiograph
• Small effusion = may be normal
• If >250 ml = globular, symmetric cardiac silhouette
o ECG:
• Reduced voltage
• Large effusion: height of QRS varies beat to beat (electrical alternans) as axis changes as heart swings side to side within large pericardial volume
o Echo:
• Can identify effusions as small as 20 ml

Question 14

Treatment of pericardial effusion

Answer 14

o Treat underlying disorder
o If unknown cause:
• If symptomatic → pericardiocentesis
• If asymptomatic → observed for months to years
• Pericardiocentesis if large rise in pericardial volume or hemodynamic compression of cardiac chambers

Question 15

Etiology of cardiac tamponade

Answer 15

• Pericardial fluid accommodates under high pressure
• Compresses cardiac chambers
• Limits filing of heart (decreased ventricular SV and CO)
• Etiology
o Any cause of acute pericarditis
o Common causes: neoplastic, postviral, uremic pericarditis
o Acute hemorrhage from chest trauma, LV rupture after MI, complication of dissecting aortic aneurysm

Question 16

Pathophysiology of cardiac tamponade

Answer 16

o	Heart is compressed → increased diastolic pressures in each chamber
•	Equal to pericardial pressure
o	Decreased venous return to heart
o	Results in increased systemic and pulmonary venous pressures
•	Signs of right sided HF
•	Pulmonary congestion
o	Reduced ventricular filling → decreased SV and CO
o	Failure to compensate
•	Inadequate perfusion
•	Hypotension
•	Shock
•	Death

Question 17

Clinical features of cardiac tamponade

Answer 17

o Beck’s triad
1) JVD (jugular venous distension)
2) Hypotension
3) Quiet heart
o Pulmonary rales (congestion)
o Sinus tachycardia (compensatory measure from decreased CO and hypotension)
o Pulsus paradoxus
• Cyclical decrease of systolic BP (>10 mmHg) during normal inspiration
• An exaggeration of normal cardiac physiology
• Inspiration = increased venous return to RA and RV
• Results in shift of ventricular septum toward LV
• Limitation in LV filling and decreased CO
o Y descent of RA pressure recording is blunted due to pericardial fluid compressing heart and impairing filling

Question 18

Diagnosis of cardiac tamponade

Answer 18

o	Chest x-ray: globular heart
o	ECG: electrical alternans
o	TTE: effusion
o	Cath: equalization of chamber pressures to pericardial pressure
o	Echo: 
•	RV early diastolic collapse (specific)
•	RA early systolic collapse (sensitive)
•	Ventricular interdependence
•	Respiratory variation in mitral and tricuspid inflow velocities

Question 19

Treatment of cardiac tamponade

Answer 19

o Watchful waiting
o Treat underlying cause
o Pericardiocentesis or pericardial window

Question 20

Etiology of Constrictive pericarditis

Answer 20

o Same as acute pericarditis and pericardial effusion
o Common now: idiopathic
o Historically: tuberculosis

Question 21

Pathology of Constrictive pericarditis

Answer 21

o If fluid not resorbed → organize and fuse the pericardial layers
o Fibrous scar formation = rigid pericardium
o Problems with filling → inhibits normal filling of cardiac chambers
o Signs of right sided heart failure, dyspnea; decreased SV, CO, BP
o No increase in right sided filling during inspiration (so no pulsus paradoxus)

Question 22

Clinical features of Constrictive pericarditis

Answer 22

o Dyspnea
o Systemic venous congestion
o Cardiac cirrhosis
o Pericardial knock
• Early diastolic knock after S2 if have severe calcific constriction
• Due to sudden cessation of ventricular diastolic filling from rigid sac
o Kussmaul’s sign
• Increased venous return accumulated in intrathoracic veins → jugular veins distend during inspiration (opposite of normal physiology)
o JVP tracing

Question 23

Diagnosis of Constrictive pericarditis

Answer 23

o Chest x-ray: pericardial calcification
o ECG: non-specific ST and T wave abnormalities; atrial arrhythmias are common
o CT/MRI (pericardial thickening)
o Echo: septal balance/movement
o Cardiac catheterization:
• Confirms diagnosis
• Elevation and equalization of diastolic pressures in cardiac chambers
• Square root sign (dip and plateau during early diastolic filling on pressure vs time plot)
• RA pressure tracing shows prominent y descent

Question 24

Treatment of Constrictive pericarditis

Answer 24

Surgical removal of pericardium