Pericardial Disease¶

Part 6 | Pericardial Disease · Part 6 – Cardiovascular Disorders · Chapter 281

Key Clinical Points¶

Acute pericarditis is characterized by chest pain, pericardial friction rub, ECG changes (diffuse ST elevation/PR depression), and pericardial effusion.
Distinguishing acute pericarditis from AMI relies on the shape of ST elevation (concave vs. convex) and the presence of reciprocal changes.
Cardiac tamponade presents with Beck's triad (hypotension, JVD, muffled heart sounds) and pulsus paradoxus (>10 mmHg).
Constrictive pericarditis is identified by an M-shaped jugular venous pulse (prominent x and y descents) and a 'square root' sign in ventricular pressure pulses.
Acute idiopathic pericarditis treatment: NSAIDs (aspirin, ibuprofen, indomethacin) plus colchicine for 3 months.
Pericardial effusion volume to cause tamponade varies from 200 mL (rapid) to >2000 mL (slow).
Echocardiography is the primary imaging modality for detecting pericardial fluid and evaluating hemodynamic impact.
Kussmaul's sign (failure of venous pressure to drop on inspiration) is common in constrictive pericarditis but absent in tamponade.
Pericardial knock is a hallmark of constrictive pericarditis, reflecting the abrupt cessation of ventricular filling.
Uremic pericarditis may occur in patients with severe renal dysfunction or during chronic dialysis.

DEFINITION & CLASSIFICATION¶

• Pericardium: A double-layered sac (visceral and parietal) containing 15–50 mL of ultrafiltrate fluid. • Normal Functions: ◦ Restraining force: Prevents sudden dilation of cardiac chambers (especially right atrium/ventricle). ◦ Anatomical restriction: Maintains the heart's position. ◦ Infection barrier: Retards spread of infections from lungs/pleura to the heart. • Clinical Classification (Table 281-1): ◦ I. Acute pericarditis (<6 weeks): Fibrinous or Effusive (serous/sanguineous). ◦ II. Subacute pericarditis (6 weeks to 6 months): Effusive-constrictive or Constrictive. ◦ III. Chronic pericarditis (>6 months): Constrictive or Adhesive (nonconstrictive). • Etiologic Classification (Table 281-1): ◦ I. Infectious: Viral (e.g., Coxsackievirus, HIV, COVID), Pyogenic, Tuberculous, Fungal. ◦ II. Noninfectious: Idiopathic, Renal failure, Neoplasia, Trauma, Aortic dissection, AMI, Postirradiation, Metabolic. ◦ III. Autoimmune-related: Rheumatic fever, Collagen vascular disease (SLE, RA, Scleroderma), Drug-induced, Postcardiac injury (Dressler's syndrome).

EPIDEMIOLOGY¶

• Demographics: Most common in young adult males. • Associations: Often associated with pleural effusion and pneumonitis. • Course: Typically resolves in a few days to 4 weeks. • Recurrence: Approximately 1/4 of patients with acute idiopathic pericarditis experience relapsing episodes.

ETIOLOGY & PATHOPHYSIOLOGY¶

• Acute Pericarditis Pathophysiology: ◦ Pain: Often retrosternal, left precordial, or referred to neck/arms; frequently pleuritic. ◦ Positioning: Pain intensified by lying supine; relieved by sitting up and leaning forward. ◦ Clinical Context: Viral/idiopathic cases often follow respiratory infections but lack specific serologic markers.

Cardiac Tamponade¶

• Mechanism: Accumulation of fluid in the pericardial space causing obstruction of blood inflow to ventricles. ◦ Fluid Volume: 200 mL (rapid accumulation) to >2000 mL (slow accumulation). ◦ Beck's Triad: Hypotension, soft/absent heart sounds, and jugular venous distention (prominent x descent, absent y descent). ◦ Pulsus Paradoxus: Present in approximately 1/3 of patients with constrictive pericarditis; also seen in RV infarction or pulmonary embolism.

Constrictive Pericarditis¶

• Mechanism: Formation of a rigid, thickened, and potentially calcified pericardial scar following inflammation/effusion. ◦ Filling Dynamics: Ventricular filling is unimpeded in early diastole but stops abruptly when the elastic limit of the pericardium is reached. ◦ Jugular Venous Pulse: M-shaped contour with prominent x and y descents; y descent reflects rapid early filling followed by abrupt cessation. ◦ Square Root Sign: Ventricular pressure pulses show a characteristic 'square root' shape during diastole.

CLINICAL FEATURES¶

• General Symptoms: Weakness, fatigue, weight gain, increased abdominal girth, and edema. ◦ Advanced cases: Anasarca, skeletal muscle wasting, and cachexia. • Physical Examination: ◦ Jugular Veins: Distended; Kussmaul's sign (no decrease in pressure on inspiration) is common in chronic pericarditis. ◦ Heart Sounds: May be distant; 'pericardial knock' (abrupt cessation of filling) may be heard at the apex. ◦ Specific Signs: ◦ Ewart's sign: Dullness/increased fremitus under left scapula due to lung base compression by fluid. ◦ Broadbent's sign: Reduced and retracting apical pulse in systole. • Imaging/ECG Findings: ◦ ECG: Low QRS voltage, diffuse T-wave flattening/inversion. ◦ Chest X-ray: 'Water bottle' configuration of the cardiac silhouette.

Acute Pericarditis Symptoms¶

• Pain Characteristics: ◦ Location: Retrosternal/left precordial; often pleuritic. ◦ Radiation: To neck, arms, or left shoulder. ◦ Position Effect: Worse when supine; better sitting up and leaning forward. ◦ Absence of Pain: Common in slowly developing cases (tuberculous, postirradiation, neoplastic, uremic).

Physical Examination Findings¶

• Pericardial Friction Rub: ◦ Prevalence: Heard in ~85% of acute pericarditis patients. ◦ Description: Rasping, scratching, or grating; heard best at end-expiration while upright/leaning forward. ◦ Clinical Significance: Indicates inflammation of the pericardial layers.

DIFFERENTIAL DIAGNOSIS¶

• Acute Pericarditis vs. AMI: ◦ Biomarkers: Pericarditis may show modest troponin rise (epi-myocarditis) but less than AMI. ◦ ST Elevation Shape: Pericarditis = upwardly concave; AMI = upwardly convex. ◦ Reciprocal Changes: Pericarditis = less prominent; AMI = more prominent. • Tamponade vs. Constriction: ◦ Pulsus Paradoxus: Present in both, but much more pronounced (+++) in tamponade. ◦ Kussmaul's Sign: Absent in tamponade (-); present in constrictive pericarditis (+++). ◦ Pericardial Knock: Absent in tamponade (-); present in constrictive pericarditis (++). ◦ Y Descent: Absent/diminished in tamponade; prominent in constrictive pericarditis. ◦ Calcification: Absent in tamponade; common in constrictive pericarditis.

Table 281-2 Summary¶

• Key Differentiators: ◦ Pulsus Paradoxus: Tamponade (+++) vs. Constriction (+). ◦ Kussmaul's Sign: Tamponade (-) vs. Constriction (+++). ◦ Pericardial Knock: Tamponade (-) vs. Constrictive (++). ◦ Pericardial Calcification: Tamponade (-) vs. Constrictive (++) ◦ Pericardial Effusion: Present in Tamponade (+++); absent in Constriction (-).

DIAGNOSTIC APPROACH¶

Echocardiography: Primary noninvasive tool to identify pericardial fluid, estimate volume, and assess hemodynamic impact. → Identify 'echo-free' space between heart and pericardium. → Assess for 'pericardial knock' or 'pulsus paradoxus'.
Advanced Imaging (CT/MRI): Used when echocardiography is insufficient. → CT/MRI: Superior for detecting loculated effusions, pericardial thickening, or masses. → MRI: Specifically useful for identifying pericardial inflammation.
Electrocardiogram (ECG): Initial screening for acute pericarditis. → Look for diffuse ST-segment elevation and PR-segment depression.
Pericardial Fluid Analysis: Performed if effusion is present. → Analyze for: RBCs, WBCs, cytology (neoplasm), culture (infection). → Specific tests: PCR for M. tuberculosis or elevated adenosine deaminase to support diagnosis of tuberculous pericarditis.

MANAGEMENT & TREATMENT¶

Acute Pericarditis Treatment: → Initial therapy: NSAIDs (aspirin, ibuprofen, indomethacin). → Adjunctive therapy: Colchicine for 3 months to reduce recurrence. → Refractory cases: Glucocorticoids (only if NSAIDs/colchicine are contraindicated or fail).
Cardiac Tamponade Management: → Immediate action: Pericardicentesis. → Preferred approach: Subxiphoid.
Constrictive Pericarditis Treatment: → Definitive therapy: Pericardiectomy (surgical removal of the pericardium).
Uremic Pericarditis Management: → Intensified dialysis for renal failure cases. → Pericardial window if necessary.

Constrictive Pericarditis Diagnostic Pathway (Figure 281-4)¶

• Step 1: Assess Mitral Valve (MV) Inflow. → Observe for respirophasic changes. → Identify flow patterns during inspiration vs. expiration. • Step 2: Assess Tricuspid Valve (TV) Inflow. → Observe for respirophasic changes. • Step 3: Evaluate Reciprocity. → If MV and TV show reciprocal changes (e.g., MV flow increases while TV flow decreases during inspiration) → supports diagnosis of Constrictive Pericarditis. → Note: This distinguishes it from other causes of heart failure or pulmonary hypertension.

KEY PEARLS & HIGH-YIELD POINTS¶

• Ewart's Sign: Look for dullness/egophony under the left scapula in large effusions. • Kussmaul's Sign: Key differentiator; absent in tamponade, present in constriction. • Pericardial Knock: Hallmark of constrictive pericarditis (abrupt cessation of filling). • Symmetry of ST Elevation: Pericarditis is typically diffuse/concave; AMI is localized/convex. • Fluid Volume: Tamponade can occur with as little as 200 mL of fluid.

Reference Tables¶

TABLE 281-1 Classification of Pericarditis Clinical Classification I. Acute pericarditis (<6 weeks)¶

Harrison's 22e, p.2079

Clinical Classification
I. Acute pericarditis (<6 weeks)
A. Fibrinous
B. Effusive (serous or sanguineous)
II. Subacute pericarditis (6 weeks to 6 months)
A. Effusive-constrictive
B. Constrictive
III. Chronic pericarditis (>6 months)
A. Constrictive
B. Adhesive (nonconstrictive)
Etiologic Classification
I. Infectious pericarditis
A. Viral (coxsackievirus A and B, echovirus, herpesviruses, mumps,
adenovirus, hepatitis, HIV, post-acute COVID, mpox)
B. Pyogenic (pneumococcus, Streptococcus, Staphylococcus, Neisseria,
Legionella, Chlamydia)
C. Tuberculous
D. Fungal (histoplasmosis, coccidioidomycosis, Candida, blastomycosis)
E. Other infections (syphilitic, protozoal, parasitic)
II. Noninfectious pericarditis
A. Acute idiopathic
B. Renal failure
C. Neoplasia
1. Primary tumors (benign or malignant, mesothelioma)
2. Tumors metastatic to pericardium (lung and breast cancer, lymphoma,
leukemia)
D. Trauma (penetrating chest wall, nonpenetrating)
E. Aortic dissection (with leakage into pericardial sac)
F. Acute myocardial infarction
G. Postirradiation
H. Familial Mediterranean fever and other autoinflammatory syndromes
I. Familial pericarditis
1. Mulibrey nanisma
J. Metabolic (myxedema, cholesterol)
III. Pericarditis presumably related to autoimmunity
A. Rheumatic fever
B. Collagen vascular disease (systemic lupus erythematosus, rheumatoid
arthritis, ankylosing spondylitis, scleroderma, acute rheumatic fever,
granulomatosis with polyangiitis, IgG4 disease)
C. Drug-induced (e.g., procainamide, hydralazine, phenytoin, isoniazid,
minoxidil, anticoagulants, methysergide)
D. Postcardiac injury
1. Postpericardiotomy
2. Posttraumatic
3. Postmyocardial infarction (Dressler’s syndrome)

TABLE 281-2 Features That Distinguish Cardiac Tamponade from Constrictive Pericarditis and Similar Clinical Disorders…¶

Harrison's 22e, p.2081

CHARACTERISTIC	TAMPONADE	CONSTRICTIVE PERICARDITIS	RESTRICTIVE CARDIOMYOPATHY	RIGHT VENTRICULAR MYOCARDIAL INFARCTION	EFFUSIVE CONSTRICTIVE PERICARDITIS
Clinical
Pulsus paradoxus	+++	+	+	+	+++
Jugular veins
Prominent y descent	–	++	+	+	–
Prominent x descent	+++	++	+++	+	+++
Kussmaul’s sign	–	+++	+	+++	++
Third heart sound	–	–	+	+	+
Pericardial knock	–	++	–	–	–
Electrocardiogram
++	++	+	–
++	–	–	–
Echocardiogram
Thickened pericardium	–	+++	–	–	++
Pericardial calcification	–	++	–	–	_
Pericardial effusion	+++	–	–	–	++
RV size	Usually small	Usually normal	Usually normal	Enlarged	Usually normal
Exaggerated respiratory variation in flow velocity	+++	+++	–	+++	+
CT/MRI
–	+++	–
+++	+++	–	++