Pericardial Disease

Acute Pericarditis

Acute pericarditis is inflammation of the pericardial layers. Pain is typically sharp and pleuritic, worsens with inspiration or positional change, and often improves when the patient sits upright and leans forward. A friction rub results from inflamed pericardial surfaces moving against one another. Diffuse ST-segment elevation and PR depression can occur on ECG (Norris, 2020).

Pericardial inflammation can occur alone or overlap with myocardial inflammation. Contemporary evaluation therefore considers a broader inflammatory myopericardial syndrome when findings suggest myocardial involvement (Schulz-Menger et al., 2025).

Etiology and Disease Course

Pericardial inflammation can be idiopathic or viral, autoimmune, uremic, malignant, post-myocardial injury, post-procedural, traumatic, bacterial, or related to other systemic disease. Acute disease may resolve completely, recur after a symptom-free interval, or evolve into persistent/recurrent inflammation. Chronic inflammation can eventually produce fibrotic constriction in a subset of patients. The etiologic context matters because purulent, malignant, hemorrhagic, uremic, and inflammatory effusions have different risks and management priorities (Norris, 2020; Schulz-Menger et al., 2025).

Pericardial Effusion

Pericardial effusion is abnormal fluid accumulation within the pericardial cavity. Hemodynamic impact depends on volume, accumulation rate, and pericardial compliance. A slowly enlarging pericardium can accommodate substantial fluid, while rapid hemorrhage or fluid accumulation sharply raises intrapericardial pressure (Norris, 2020; Schulz-Menger et al., 2025).

Cardiac Tamponade

Tamponade occurs when intrapericardial pressure restricts cardiac filling. Right-sided chambers, which normally fill at lower pressures, are often affected first. Reduced diastolic filling lowers end-diastolic volume, stroke volume, and cardiac output. Compensatory tachycardia and vasoconstriction may temporarily support perfusion (Norris, 2020; Schulz-Menger et al., 2025).

Pulsus paradoxus reflects exaggerated inspiratory reduction in LV filling: inspiration increases right-heart filling, but the compressed heart cannot expand outward, so the septum shifts toward the LV and systolic pressure falls more than normal (Norris, 2020; Schulz-Menger et al., 2025).

Pericarditis, Effusion, and Tamponade

Feature	Acute pericarditis	Pericardial effusion	Cardiac tamponade
Primary problem	Inflammation	Fluid accumulation	Hemodynamic compression
Pain	Common, pleuritic/positional	Variable	Not defining
Friction rub	May be present	May disappear with large effusion	Not defining
JVD/hypotension	Not typical from uncomplicated disease	Possible if hemodynamically important	Common
Pulsus paradoxus	Not defining	May occur if pressure is significant	Characteristic clue
Echo	May show effusion	Defines fluid burden/distribution	Shows effusion plus chamber/hemodynamic effects

Pleural Effusion Versus Pericardial Effusion/Tamponade

Pleural effusion places fluid around the lung, not around the heart. It primarily impairs lung expansion and causes dyspnea through compression of pulmonary tissue. Pericardial effusion surrounds the heart; tamponade develops only when pericardial pressure rises enough to restrict diastolic filling (Norris, 2020).

Feature	Pleural effusion	Pericardial effusion	Tamponade
Fluid location	Pleural space	Pericardial space	Pericardial space with hemodynamic compression
Primary effect	Restricts lung expansion	Variable	Restricts cardiac filling
Major consequence	Ventilatory impairment/dyspnea	Depends on rate/volume	Low preload, low stroke volume, low CO
Primary imaging	Chest radiograph/ultrasound	Echocardiography	Echocardiography with hemodynamic assessment

Constrictive Pericarditis

Chronic inflammation may produce a rigid fibrotic or calcified pericardium that limits diastolic expansion. Unlike tamponade, the constraint is a fixed scar rather than fluid pressure. Systemic venous congestion, ascites, edema, exertional dyspnea, and Kussmaul sign may result (Norris, 2020; Schulz-Menger et al., 2025).

Diagnostic Approach

• Initial assessment may include history, examination, ECG, biomarkers, chest imaging, and echocardiography (Norris, 2020; Schulz-Menger et al., 2025).
• Echocardiography is central when effusion or tamponade is suspected (Norris, 2020; Schulz-Menger et al., 2025).
• Cardiac MRI has an important role when inflammatory myocardial or pericardial involvement requires further characterization (Schulz-Menger et al., 2025).

Clinical Manifestations

Acute pericarditis typically produces sharp pleuritic and positional chest pain, often relieved by sitting forward, and may produce a pericardial friction rub. Effusion may be asymptomatic or cause pressure/dyspnea. Tamponade produces impaired filling and may present with tachycardia, hypotension, elevated jugular venous pressure, pulsus paradoxus, and shock (Norris, 2020; Schulz-Menger et al., 2025).

Findings That Alter the Differential

Diffuse ST elevation with PR depression supports acute pericarditis, while territorial ischemic changes and a compatible biomarker pattern raise concern for myocardial infarction. A large effusion can reduce or eliminate a friction rub by separating the inflamed surfaces. Pericardial inflammation may also overlap with myocardial inflammation, so findings suggesting myocardial injury should prompt evaluation for a broader inflammatory myopericardial syndrome (Norris, 2020; Schulz-Menger et al., 2025).

Differential Diagnosis

Major alternatives include acute coronary syndrome, pulmonary embolism, aortic pathology, pneumonia/pleuritis, pneumothorax, and musculoskeletal chest pain. Constrictive pericarditis and restrictive cardiomyopathy can both impair diastolic filling and may require multimodality imaging or hemodynamic assessment to distinguish them (Norris, 2020; Schulz-Menger et al., 2025).

Treatment Principles

Treatment is directed at the mechanism and cause. Uncomplicated inflammatory pericarditis is treated with anti-inflammatory therapy and cause-specific management. Effusions are observed or drained according to etiology, size, symptoms, and hemodynamic effect. Cardiac tamponade requires urgent relief of pericardial pressure, typically with pericardial drainage; preload-reducing interventions can worsen hypotension before decompression (Norris, 2020; Schulz-Menger et al., 2025).

Red Flags

• Hypotension or shock with a known or suspected pericardial effusion (Norris, 2020; Schulz-Menger et al., 2025).
• Elevated JVP with pulsus paradoxus or echocardiographic chamber compression (Norris, 2020; Schulz-Menger et al., 2025).
• Rapidly enlarging, traumatic, hemorrhagic, purulent, or malignant effusion (Norris, 2020; Schulz-Menger et al., 2025).
• Evidence of myocardial involvement, severe arrhythmia, or hemodynamic deterioration (Schulz-Menger et al., 2025).

High-Yield Distinctions

• Pericarditis = inflammation; pericardial effusion = fluid; tamponade = impaired filling from pericardial pressure.
• Rate of accumulation matters as much as volume.
• Pleural effusion primarily compromises lung expansion; tamponade primarily compromises cardiac filling.
• Tamponade is preload dependent because external compression already limits diastolic filling.

Related YourDNP Resources

• Cardiac Pathophysiology Foundations
• Coronary Artery Disease and Acute Coronary Syndromes
• Heart Failure

---

---

References

Norris, T. L. (2020). Porth’s essentials of pathophysiology (5th ed.). Wolters Kluwer.

Schulz-Menger, J., Collini, V., Gröschel, J., Adler, Y., Brucato, A., Christian, V., Ferreira, V. M., Gandjbakhch, E., Heidecker, B., Kerneis, M., Klein, A. L., Klingel, K., Lazaros, G., Lorusso, R., Nesukay, E. G., Rahimi, K., Ristić, A. D., Rucinski, M., Sade, L. E., … Imazio, M. (2025). 2025 ESC guidelines for the management of myocarditis and pericarditis. European Heart Journal, 46(40), 3952–4041. https://doi.org/10.1093/eurheartj/ehaf192