Medical School · Year 1 · Cardiovascular · includes a quiz and discussion video

Lecture 17: Pericardial Disease

Unit 1.7: Cardiovascular System

Learning Objectives

By the end of this lecture, students will be able to:

1. Describe the anatomy and physiology of the pericardium
2. Recognize the clinical presentation of acute pericarditis
3. Describe the pathophysiology and management of cardiac tamponade
4. Explain the features of constrictive pericarditis
5. Differentiate constrictive pericarditis from restrictive cardiomyopathy
6. Describe the management of pericardial diseases

Lecture Content

Pericardial Anatomy and Physiology

The pericardium is a fibroserous sac that encloses the heart and the roots of the great vessels. Understanding its structure explains how various pathological processes affect cardiac function and produce characteristic clinical findings.

The fibrous pericardium forms the outer layer, consisting of dense connective tissue that provides structural support. This tough layer attaches superiorly to the adventitia of the great vessels, inferiorly to the central tendon of the diaphragm, anteriorly to the sternum via the sternopericardial ligaments, and posteriorly to the vertebral column. These attachments anchor the heart within the mediastinum, preventing excessive motion with changes in body position.

The serous pericardium consists of two layers: the parietal layer lines the inner surface of the fibrous pericardium, while the visceral layer (also called the epicardium) adheres directly to the heart surface. These two serous layers are continuous at the reflections around the great vessels, creating the pericardial cavity between them. This potential space normally contains fifteen to fifty milliliters of serous fluid that lubricates the heart during its motion within the pericardial sac.

The physiological functions of the pericardium extend beyond simple containment. The pericardium limits acute cardiac dilation by virtue of its relatively non-compliant nature, preventing excessive stretching during sudden volume loads. It maintains constant transmural cardiac pressures during respiratory variations by providing a stable external environment. The pericardium also facilitates ventricular interdependence, the phenomenon whereby changes in filling of one ventricle affect the other through the shared pericardial space and interventricular septum. Additionally, the pericardium serves as a barrier against infection spreading from adjacent structures and reduces friction during cardiac contraction.

Pericardial pressure normally approximates intrathoracic pressure, remaining slightly negative or near zero. This pressure varies with respiration, becoming more negative during inspiration. Pathological elevation of pericardial pressure through fluid accumulation or fibrosis impairs cardiac filling and produces the hemodynamic abnormalities that characterize pericardial disease.

<image>Panel A: Coronal section through the thorax showing the fibrous pericardium as the outer tough layer and the serous pericardium with parietal and visceral layers, with the pericardial cavity containing straw-colored fluid. Panel B: Inset magnification showing microscopic structure: fibrous pericardium with dense collagen, parietal mesothelium, pericardial space with fluid, and visceral mesothelium over epicardial fat and myocardium. Panel C: Pericardial attachment points superiorly to great vessels, inferiorly to the diaphragm, and anteriorly to the sternum via sternopericardial ligaments. Panel D: Ventricular interdependence demonstrating how pericardial constraint allows filling changes in one ventricle to affect the other through septal shift.</image>

Acute Pericarditis: Etiology and Pathophysiology

Acute pericarditis represents inflammation of the pericardium, producing characteristic clinical findings regardless of the underlying cause. While numerous etiologies exist, the vast majority of cases in developed countries are classified as idiopathic or presumed viral, as extensive diagnostic testing rarely identifies a specific pathogen and would not alter management.

Viral infection represents the most common identifiable cause, with numerous viruses implicated including coxsackievirus, echovirus, Epstein-Barr virus, cytomegalovirus, influenza, HIV, and parvovirus B19. The inflammation may result from direct viral invasion, immune-mediated injury, or both. Most viral pericarditis is self-limited, though some patients develop recurrent episodes.

Bacterial pericarditis (purulent pericarditis) is much less common but far more serious, typically resulting from direct extension of pneumonia, thoracic surgery complications, or hematogenous spread. The mortality rate without prompt drainage and antibiotics exceeds ninety percent. Tuberculous pericarditis remains common in endemic regions and in immunocompromised patients, characteristically presenting with subacute or chronic symptoms and frequently progressing to constrictive pericarditis.

Post-cardiac injury syndromes represent an important category including Dressler syndrome (occurring two to ten weeks after myocardial infarction), postpericardiotomy syndrome (after cardiac surgery), and post-traumatic pericarditis. These conditions share an autoimmune pathophysiology with antibodies directed against cardiac antigens exposed by the initial injury.

Autoimmune diseases including systemic lupus erythematosus, rheumatoid arthritis, and scleroderma can cause pericarditis as part of their systemic inflammatory process. Uremic pericarditis occurs in patients with end-stage renal disease, typically when blood urea nitrogen exceeds sixty milligrams per deciliter, though dialysis-associated pericarditis can occur even with adequate small-molecule clearance.

Malignancy-related pericarditis most commonly results from metastatic disease, with lung cancer, breast cancer, lymphoma, and melanoma being the most frequent primary tumors. Primary pericardial tumors are rare. Radiation-induced pericarditis can occur acutely during treatment or present years later as constrictive pericarditis. Various medications, including hydralazine, procainamide, and isoniazid, can trigger pericarditis through immune-mediated mechanisms.

<image>Panel A: Central image of inflamed pericardium with thickened hyperemic layers and increased fluid, with idiopathic and viral causes representing over 80% including coxsackievirus, EBV, and CMV. Panel B: Bacterial pericarditis with purulent fluid as an emergency, tuberculous pericarditis with granulomatous inflammation progressing to constriction, and post-cardiac injury syndromes including Dressler syndrome at weeks 2-10 post-MI. Panel C: Autoimmune causes including SLE and rheumatoid arthritis, and uremic pericarditis with BUN above 60 mg/dL in end-stage renal disease. Panel D: Malignancy-related pericarditis with lung, breast, and lymphoma as common primaries producing hemorrhagic effusion, and drug-induced pericarditis from hydralazine, procainamide, and isoniazid.</image>

Clinical Presentation of Acute Pericarditis

The clinical presentation of acute pericarditis is distinctive and, when classic features are present, allows confident diagnosis at the bedside. The diagnosis requires at least two of four criteria: characteristic chest pain, pericardial friction rub, typical ECG changes, and new or worsening pericardial effusion.

Pericarditic chest pain has several characteristic features that distinguish it from other causes of chest pain. The quality is typically sharp or stabbing, contrasting with the pressure or heaviness of ischemic pain. Most distinctively, the pain is pleuritic, worsening with inspiration and often with coughing or swallowing. Positional variation provides another clue: pain typically worsens when lying supine and improves when sitting up and leaning forward, a position that moves the inflamed pericardium away from adjacent structures. Pain may radiate to the trapezius ridge due to phrenic nerve irritation by the inflamed pericardium, a pattern essentially pathognomonic for pericarditis.

The pericardial friction rub is pathognomonic when present but is often transient or subtle and therefore may be missed on a single examination. The classic rub has three components corresponding to atrial systole, ventricular systole, and early ventricular diastole, though one or two component rubs are common. The sound is described as scratchy or squeaky, similar to leather creaking, and is best heard with the diaphragm of the stethoscope at the left lower sternal border with the patient leaning forward at end-expiration. Serial examinations increase detection sensitivity.

Systemic symptoms including low-grade fever, malaise, and myalgias commonly accompany viral and idiopathic pericarditis, reflecting the underlying inflammatory process. High fever exceeding thirty-eight degrees Celsius should raise concern for bacterial infection. Dyspnea may occur due to pain limiting deep breathing or from an associated pericardial effusion.

The ECG evolves through four classic stages, though not all patients demonstrate the complete sequence. Stage 1, occurring within hours to days, shows diffuse ST elevation with concave upward morphology and PR depression, reflecting subepicardial injury. The changes are characteristically diffuse rather than following coronary territories, helping distinguish pericarditis from acute myocardial infarction. PR depression in lead aVR is a subtle but specific finding. Stage 2 shows normalization of ST and PR segments over days. Stage 3 demonstrates diffuse T wave inversions occurring days to weeks after onset. Stage 4 represents normalization, which may take weeks to months.

<image>Panel A: Characteristic chest pain features showing sharp stabbing quality, pleuritic worsening with inspiration, positional variation worse when supine and improved sitting forward, and trapezius ridge radiation from phrenic nerve irritation. Panel B: Pericardial friction rub examination with patient leaning forward at end-expiration, stethoscope at left lower sternal border, showing three components timed to atrial systole, ventricular systole, and early diastole. Panel C: Four ECG stages: Stage 1 with diffuse concave ST elevation and PR depression, Stage 2 with normalization, Stage 3 with diffuse T wave inversions, and Stage 4 with return to baseline. Panel D: ECG comparison contrasting pericarditis with diffuse concave ST elevation and no reciprocal changes versus STEMI with territorial convex ST elevation and reciprocal depression.</image>

Workup and Management of Acute Pericarditis

The evaluation of acute pericarditis aims to confirm the diagnosis, assess for complications (particularly pericardial effusion and tamponade), and identify high-risk features that would warrant hospitalization and more extensive investigation for specific etiologies.

Initial laboratory testing includes inflammatory markers (C-reactive protein and erythrocyte sedimentation rate), which are elevated in most cases and provide a baseline for monitoring treatment response. Cardiac troponin may be mildly elevated when inflammation extends to the myocardium (myopericarditis), which occurs in a subset of patients and does not necessarily indicate worse prognosis when the elevation is modest. Complete blood count and basic metabolic panel help assess for infection and establish renal function. Additional testing guided by clinical suspicion might include antinuclear antibody, thyroid function tests, or HIV testing.

Echocardiography should be performed in all patients to evaluate for pericardial effusion and assess for tamponade physiology. While many cases of acute pericarditis occur without significant effusion, identification of effusion affects prognosis and monitoring. Chest radiography may show an enlarged cardiac silhouette with large effusions but is often normal.

High-risk features warranting hospitalization include fever exceeding thirty-eight degrees Celsius (suggesting bacterial cause), subacute onset (raising concern for tuberculosis or malignancy), large pericardial effusion or tamponade, immunosuppressed state, oral anticoagulation (risk of hemopericardium), failure to respond to initial anti-inflammatory therapy, and elevated troponin suggesting significant myocardial involvement.

First-line treatment for idiopathic and viral pericarditis combines nonsteroidal anti-inflammatory drugs with colchicine. NSAIDs, typically ibuprofen 600 milligrams three times daily or aspirin 750 to 1000 milligrams three times daily, provide symptomatic relief and reduce inflammation. Treatment continues until symptom resolution plus an additional one to two weeks, then tapers gradually rather than stopping abruptly. Colchicine 0.5 milligrams twice daily (or once daily for patients under seventy kilograms) is added for all patients, typically for three months for a first episode. Colchicine reduces the recurrence rate by approximately fifty percent, representing a major advance in pericarditis management.

Corticosteroids should generally be avoided as first-line therapy because they increase recurrence risk. However, they may be necessary when NSAIDs and colchicine are contraindicated or ineffective, using the lowest effective dose with very slow taper. Recurrent pericarditis, occurring in fifteen to thirty percent of patients after a first episode, should be treated with prolonged colchicine (at least six months) and gradual NSAID taper. For refractory recurrent pericarditis, interleukin-1 blockers such as anakinra or rilonacept have shown efficacy.

<image>Panel A: Diagnostic criteria checklist requiring 2 or more of 4: characteristic chest pain, pericardial friction rub, ECG changes with ST elevation and PR depression, and new or worsening pericardial effusion on echocardiogram. Panel B: High-risk features requiring hospitalization including fever above 38 degrees, subacute onset, large effusion or tamponade, immunosuppression, anticoagulation, elevated troponin, and failure to respond to NSAIDs. Panel C: Initial workup showing labs including CRP, ESR, troponin, CBC, and BMP; ECG with Stage 1 changes; echocardiogram with effusion measurement; and chest X-ray. Panel D: Treatment algorithm: first-line NSAID plus colchicine for 3 months, if contraindicated or refractory then low-dose corticosteroids with slow taper, if refractory recurrent then IL-1 blockers such as anakinra, with colchicine reducing recurrence by approximately 50%.</image>

Pericardial Effusion

Pericardial effusion refers to the accumulation of fluid within the pericardial space beyond the normal fifteen to fifty milliliters. The clinical significance of an effusion depends not only on its size but critically on the rate of accumulation and the compliance of the pericardium.

Classification by size uses echocardiographic criteria: small effusions (less than 100 milliliters) typically appear only posterior to the heart in systole, moderate effusions (100 to 500 milliliters) distribute circumferentially around the heart, and large effusions (more than 500 milliliters) create substantial echo-free space surrounding the heart. However, these volumes are approximations, and the hemodynamic impact depends heavily on acuity.

The pericardium exhibits limited acute distensibility but can stretch considerably with chronic, gradual fluid accumulation. An acute effusion of 150 to 200 milliliters can cause tamponade because the pericardium cannot accommodate the sudden volume. In contrast, chronic slow accumulation allows pericardial stretching, and patients may tolerate effusions exceeding one liter without significant hemodynamic compromise. This distinction between acute and chronic effusion has profound implications for management urgency.

The etiologies of pericardial effusion overlap substantially with those of pericarditis but also include conditions that produce effusions without significant pericardial inflammation. Transudative effusions occur with heart failure, hypoalbuminemia, and hypothyroidism. Exudative effusions accompany inflammatory conditions, infection, and malignancy. Hemorrhagic effusions suggest malignancy, uremia (due to platelet dysfunction), coagulopathy, trauma, or aortic dissection with intrapericardial rupture.

Clinical features depend on effusion size and acuity. Small and many moderate effusions are asymptomatic. Larger effusions may cause dyspnea from compression of surrounding structures or vague chest discomfort. Physical findings include muffled heart sounds when fluid insulates the heart from the chest wall, Ewart sign (dullness to percussion and bronchial breathing below the left scapular angle due to lung compression), and signs of tamponade when present.

<image>Panel A: Three echocardiographic views comparing effusion sizes: small with posterior crescent below 100 mL, moderate with circumferential distribution 100-500 mL, and large with substantial echo-free space above 500 mL. Panel B: Acute versus chronic distinction showing rapid accumulation of 150-200 mL with steep pressure-volume rise causing tamponade, versus gradual accumulation exceeding 1 L with pericardial stretching maintaining low pressure. Panel C: Physical examination findings including muffled heart sounds, Ewart sign with dullness below the left scapula from lung compression, and neck vein distension when tamponade develops. Panel D: Effusion etiology categorized as transudative from heart failure, hypoalbuminemia, and hypothyroidism; exudative from infection, inflammation, and malignancy; and hemorrhagic from malignancy, uremia, trauma, and dissection.</image>

Cardiac Tamponade

Cardiac tamponade occurs when pericardial fluid accumulation raises intrapericardial pressure sufficiently to compress the cardiac chambers and impair diastolic filling. This condition represents a medical emergency that, if untreated, progresses to circulatory collapse and death.

The pathophysiology centers on the relationship between pericardial pressure and cardiac filling. As fluid accumulates and pericardial pressure rises, it eventually equals and then exceeds the normally low filling pressures of the cardiac chambers. Because the right heart operates at lower pressures, the right atrium and right ventricle are compressed first. Impaired diastolic filling reduces stroke volume, initially compensated by tachycardia and increased contractility. As tamponade worsens, these compensatory mechanisms fail, cardiac output drops, and hypotension develops. The final stage involves equalization of diastolic pressures across all cardiac chambers as the pericardium constrains filling uniformly.

Beck's triad describes the classic findings of tamponade: hypotension (from decreased cardiac output), elevated jugular venous pressure (from impaired right heart filling), and muffled heart sounds (from the insulating fluid layer). However, this triad is present in only a minority of patients and typically indicates advanced tamponade.

Pulsus paradoxus represents an exaggerated version of normal respiratory variation in blood pressure. Normally, systolic pressure falls slightly during inspiration as negative intrathoracic pressure increases pulmonary venous capacitance and transiently reduces left ventricular filling. In tamponade, the constrained pericardial space amplifies ventricular interdependence: inspiration augments right ventricular filling at the direct expense of left ventricular filling because total cardiac volume is fixed. Pulsus paradoxus is defined as a fall in systolic blood pressure exceeding ten millimeters of mercury during normal inspiration and is assessed using a sphygmomanometer by noting the pressure at which Korotkoff sounds are first heard (only during expiration) versus when they become audible throughout the respiratory cycle. Notably, Kussmaul sign (inspiratory rise in JVP) is characteristically absent in tamponade but present in constrictive pericarditis.

Electrical alternans on ECG, reflecting the heart swinging within a large effusion, is specific for tamponade but present in only a subset of cases. The QRS complexes alternate in amplitude on a beat-to-beat basis.

Echocardiography provides the definitive diagnosis, demonstrating the effusion and characteristic findings of elevated intrapericardial pressure. Right atrial collapse in late diastole represents an early and sensitive sign. Right ventricular diastolic collapse is more specific, indicating that intrapericardial pressure exceeds right ventricular diastolic pressure. Inferior vena cava plethora (dilation greater than 2.1 centimeters without respiratory variation) indicates elevated right atrial pressure. Exaggerated respiratory variation in mitral and tricuspid inflow velocities (more than 25% for mitral, more than 40% for tricuspid) reflects the hemodynamic consequences of ventricular interdependence.

Treatment of tamponade requires drainage of the pericardial fluid. Pericardiocentesis, typically performed under echocardiographic guidance using a subxiphoid approach, is the standard technique. In unstable patients, even partial drainage produces dramatic hemodynamic improvement because the pressure-volume relationship is steep in tamponade. Surgical drainage via pericardial window or pericardiectomy may be necessary for loculated effusions, recurrent effusions, or when tissue diagnosis is required.

<image>Panel A: Pathophysiology showing pressure-volume diagram with steep relationship where small volume increases cause large pressure rises, and four-chamber heart view showing progressive right atrial then right ventricular compression with ventricular interdependence during inspiration. Panel B: Beck's triad showing hypotension, elevated JVP with distended neck veins, and muffled heart sounds, with pulsus paradoxus measurement showing greater than 10 mmHg systolic drop during inspiration. Panel C: Echocardiographic findings including right atrial collapse in late diastole, right ventricular diastolic collapse, IVC plethora above 2.1 cm without respiratory variation, and greater than 25% respiratory variation in mitral inflow on Doppler. Panel D: Pericardiocentesis procedure showing subxiphoid approach with echocardiographic guidance, needle trajectory toward the left shoulder, and drainage catheter placement.</image>

Constrictive Pericarditis

Constrictive pericarditis results from chronic pericardial inflammation leading to a thickened, fibrotic, and often calcified pericardium that encases the heart and restricts diastolic filling. Unlike tamponade where fluid causes compression, in constriction the rigid pericardial shell prevents normal cardiac expansion during diastole.

The etiology varies geographically. In developed countries, idiopathic or viral pericarditis, post-cardiac surgery, and post-radiation therapy are the most common causes. Tuberculosis remains the leading cause in developing countries and endemic regions. Other causes include connective tissue diseases, uremia, malignancy, and prior purulent pericarditis. The progression from acute inflammation to chronic fibrosis typically occurs over months to years, though the timeline varies substantially.

The pathophysiology reflects the consequences of a rigid pericardial constraint. Early diastole proceeds relatively normally because the heart has not yet reached the limits imposed by the pericardium. However, once the ventricles fill to the point where they contact the rigid pericardium, filling abruptly ceases. This produces the characteristic "square root sign" on ventricular pressure tracings: rapid early filling followed by a diastolic plateau. Ventricular interdependence is markedly enhanced because the fixed pericardial volume means any increase in filling of one ventricle must come at the expense of the other. This produces exaggerated respiratory variation with septal shift toward the left ventricle during inspiration (septal bounce).

Clinical features predominantly reflect elevated systemic venous pressure and reduced cardiac output. Right heart failure symptoms predominate: peripheral edema, ascites (often out of proportion to peripheral edema), hepatomegaly with pulsatile liver, and elevated jugular venous pressure. The JVP waveform characteristically shows a prominent y descent (rapid early diastolic filling) followed by rapid rise as filling halts. Kussmaul sign (paradoxical rise in JVP with inspiration) occurs because the rigid pericardium prevents the normal inspiratory enhancement of right heart filling, and the increased venous return actually elevates right atrial pressure. A pericardial knock, an early diastolic sound similar to but earlier than an S3, reflects the abrupt cessation of ventricular filling. Fatigue and exercise intolerance result from the inability to augment cardiac output.

<image>Panel A: Pathological progression from normal thin pliable pericardium through chronic inflammation to thickened fibrotic calcified pericardium, with lateral chest X-ray showing pericardial calcification and CT/MRI showing thickness above 4 mm. Panel B: Square root sign on ventricular pressure tracings showing rapid early filling then abrupt plateau, compared to normal gradual diastolic filling, and septal bounce on M-mode echocardiogram. Panel C: Clinical features including elevated JVP with prominent y descent, Kussmaul sign with JVP rising on inspiration, pericardial knock earlier than S3, peripheral edema, and disproportionate ascites. Panel D: Comparison box distinguishing constriction from tamponade: Kussmaul sign present versus absent, JVP y descent prominent versus blunted, and pulsus paradoxus variable versus consistently present.</image>

Diagnosis and Differentiation from Restrictive Cardiomyopathy

The diagnosis of constrictive pericarditis requires integration of clinical findings, imaging, and often hemodynamic assessment. A critical challenge is distinguishing constriction from restrictive cardiomyopathy, as both present with similar clinical features of heart failure with preserved systolic function.

Imaging plays a central role. Chest radiography may reveal pericardial calcification, particularly on the lateral view, which is essentially diagnostic when present. However, calcification occurs in only a subset of patients. Computed tomography and magnetic resonance imaging provide direct visualization of pericardial thickness, with thickness exceeding four millimeters supporting the diagnosis. Importantly, constrictive physiology can occur with normal pericardial thickness, and thickened pericardium does not guarantee constrictive hemodynamics.

Echocardiography demonstrates several characteristic findings. The septal bounce (abrupt early diastolic septal motion) reflects the enhanced ventricular interdependence. Exaggerated respiratory variation in mitral inflow velocity (more than 25% variation) indicates the respiratory-dependent filling changes characteristic of constriction. Tissue Doppler imaging provides particularly useful information: the mitral annular e' velocity is normal or increased in constriction (reflecting preserved myocardial relaxation despite impaired filling) but reduced in restriction (reflecting abnormal myocardial relaxation). "Annulus paradoxus" describes the finding that medial e' equals or exceeds lateral e', the opposite of the normal relationship, and reflects tethering of the lateral annulus by the constricting pericardium.

Cardiac catheterization may be required when non-invasive testing is inconclusive. Classic findings include equalization of diastolic pressures across all cardiac chambers (right atrial, right ventricular end-diastolic, pulmonary artery diastolic, and pulmonary capillary wedge pressures within five millimeters of mercury), the square root sign on ventricular pressure tracings, and discordance of right and left ventricular systolic pressures with respiration. In constriction, inspiration decreases left ventricular systolic pressure while increasing right ventricular systolic pressure (discordance), reflecting the enhanced ventricular interdependence. In restriction, both ventricles move in the same direction with respiration (concordance).

BNP levels help differentiate the conditions: typically normal or mildly elevated in constriction (because the myocardium itself is normal) but significantly elevated in restriction (because the myocardial disease causing restriction also stimulates BNP release).

<image>Panel A: Imaging comparison showing CT with thickened calcified pericardium in constriction versus normal pericardium but abnormal myocardium in restriction, and echocardiographic findings with septal bounce present versus absent and e-prime velocity normal or high versus low. Panel B: Catheterization tracings showing diastolic pressure equalization in both conditions, but respiratory pressure discordance in constriction with RV and LV moving opposite directions versus concordance in restriction with both moving together. Panel C: Additional differentiating features: annulus paradoxus present in constriction versus absent in restriction, mitral inflow respiratory variation above 25% versus below 25%, and BNP normal or mildly elevated in constriction versus significantly elevated in restriction. Panel D: Diagnostic algorithm proceeding from clinical suspicion to echocardiography, if inconclusive to MRI or CT, and if still uncertain to cardiac catheterization with hemodynamic assessment.</image>

Treatment of Constrictive Pericarditis and Special Scenarios

Medical therapy has limited effectiveness in established constrictive pericarditis because the fundamental problem is mechanical constraint by fibrotic tissue that cannot be reversed pharmacologically. Diuretics provide symptomatic relief by reducing the congestion resulting from elevated filling pressures, but they cannot address the underlying restriction.

An important exception is transient constrictive pericarditis, which can occur in the weeks following acute pericarditis when the inflamed, edematous pericardium causes constrictive physiology before fibrosis develops. This condition may resolve with anti-inflammatory therapy, making a trial of NSAIDs, colchicine, and potentially corticosteroids reasonable before considering surgery. Serial imaging and hemodynamic assessment can document resolution.

Pericardiectomy (surgical removal of the pericardium) represents the definitive treatment for established symptomatic constrictive pericarditis. The procedure involves resection of as much pericardium as possible, ideally from phrenic nerve to phrenic nerve, to fully relieve the constraint. Operative mortality ranges from five to ten percent in experienced centers but can be higher in advanced cases. Improvement may not be immediate because the underlying myocardium may require time to recover from prolonged constraint, and epicardial fibrosis (which cannot be fully removed) may limit diastolic function. Most patients experience significant improvement, though complete normalization is not universal. Factors associated with poor outcome include prior radiation (which may cause concomitant myocardial and coronary damage), advanced NYHA class, renal impairment, and low preoperative serum sodium.

Effusive-constrictive pericarditis represents a combination of pericardial effusion and underlying constriction. Patients initially present with tamponade physiology from the effusion, but after pericardiocentesis, elevated filling pressures persist because of the constrictive component. Tuberculous pericarditis commonly produces this pattern. Recognition is important because pericardiocentesis alone will not resolve the hemodynamic abnormality, and pericardiectomy is typically required.

Several clinical scenarios merit specific consideration. Post-cardiac injury syndromes (Dressler syndrome, postpericardiotomy syndrome) result from autoimmune inflammation triggered by cardiac antigen exposure and respond to NSAIDs and colchicine. Uremic pericarditis in dialysis-dependent patients often responds to intensified dialysis. The ECG may not show typical ST elevation because the pericarditis is often fibrinous rather than inflammatory. Malignant pericardial disease typically presents with large, often hemorrhagic effusions that recur after drainage. Management involves drainage for tamponade, with pericardial window or systemic therapy for recurrence. Prognosis is generally poor, reflecting the underlying malignancy.

<image>Panel A: Treatment algorithm showing transient constriction in inflammatory phase treated with anti-inflammatory therapy versus established fibrotic constriction requiring pericardiectomy with median sternotomy and resection from phrenic nerve to phrenic nerve. Panel B: Pericardiectomy details showing operative mortality of 5-10% and outcome predictors including radiation history, advanced NYHA class, and renal impairment. Panel C: Effusive-constrictive pericarditis showing pre-drainage tamponade physiology and post-drainage persistent elevated pressures revealing underlying constriction requiring pericardiectomy. Panel D: Clinical scenarios including Dressler syndrome responding to NSAIDs post-MI, uremic pericarditis treated with intensified dialysis, and malignant pericardial disease with hemorrhagic effusion and poor prognosis.</image>

Summary

The pericardium consists of fibrous and serous layers surrounding the heart, normally containing fifteen to fifty milliliters of lubricating fluid and serving functions including limiting acute dilation, facilitating ventricular interdependence, and providing a barrier against infection. Acute pericarditis presents with characteristic pleuritic positional chest pain, pericardial friction rub, diffuse ST elevation with PR depression on ECG, and often pericardial effusion. First-line treatment combines NSAIDs with colchicine, which reduces recurrence by approximately fifty percent. Pericardial effusions are classified by size and acuity, with acute accumulation causing hemodynamic compromise at much smaller volumes than chronic accumulation due to limited pericardial compliance. Cardiac tamponade represents compression of cardiac chambers by pericardial fluid, presenting with Beck's triad (hypotension, elevated JVP, muffled sounds) and pulsus paradoxus, with echocardiographic findings of chamber collapse and IVC plethora requiring urgent pericardiocentesis. Constrictive pericarditis results from chronic inflammation producing a thickened, fibrotic pericardium that restricts diastolic filling, presenting with right heart failure, Kussmaul sign, and prominent JVP y descent. Differentiation from restrictive cardiomyopathy relies on imaging of pericardial thickness, echocardiographic findings (septal bounce, normal e' velocity, respiratory variation), and catheterization demonstrating respiratory discordance. Treatment of established constriction requires pericardiectomy.

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