Acute Pericarditis

Acute pericarditis is a condition characterized by the rapid onset of inflammation in the pericardium, the double-walled sac that encloses the heart. This disease, although sometimes self-limited and benign, can present with severe complications if not properly recognized and managed.

Anatomy and Function of the Pericardium

The pericardium consists of two layers: the outer fibrous pericardium and the inner serous pericardium, which itself is subdivided into parietal and visceral layers. The pericardial cavity between these layers contains a small amount of lubricating fluid (normally 15–50 mL) that facilitates frictionless movement of the heart during each beat. The pericardium serves several functions:

• Mechanical Protection: Shields the heart from infection and external trauma.
• Limits Cardiac Distension: Prevents excessive dilation of the heart chambers.
• Reduces Friction: The fluid allows the heart to move smoothly within the thoracic cavity.
• Barrier to Infection: Acts as a physical barrier against infections that could spread from adjacent organs.

Etiology and Risk Factors

Acute pericarditis can have a wide variety of causes. The etiology is classified as either infectious or non-infectious, and in many cases, the cause remains idiopathic.

Infectious Causes

• Viral infections: These are the most common cause in developed countries. Coxsackievirus, echovirus, HIV, cytomegalovirus, influenza, and adenovirus are frequently implicated.
• Bacterial infections: Mycobacterium tuberculosis is a notable cause, especially in areas where tuberculosis is prevalent. Other bacteria such as Staphylococcus, Streptococcus, and Borrelia burgdorferi (Lyme disease) can also contribute.
• Fungal and parasitic infections: These are rare but possible, particularly in immunocompromised individuals.

Non-Infectious Causes

• Autoimmune diseases: Systemic lupus erythematosus, rheumatoid arthritis, scleroderma, and other autoimmune disorders can cause pericardial inflammation.
• Neoplastic disease: Primary tumors of the pericardium are rare, but secondary involvement from metastases (lung, breast cancer, lymphoma, leukemia) is more common.
• Post-myocardial infarction (Dressler’s syndrome): Inflammatory response occurring days to weeks after a heart attack.
• Uremia: Chronic kidney disease can lead to accumulation of toxins that irritate the pericardium.
• Trauma: Both blunt and penetrating injuries, as well as iatrogenic causes such as cardiac surgery or invasive procedures.
• Medications and toxins: Certain drugs (e.g., hydralazine, isoniazid, phenytoin) may induce pericarditis.
• Radiation: Prior chest radiation therapy can lead to chronic irritation and inflammation.

Idiopathic Pericarditis

In up to 90% of cases in developed countries, no specific cause is identified and the condition is termed “idiopathic pericarditis.” These cases are thought to be primarily viral in origin.

Clinical Presentation

The classic presentation of acute pericarditis is sudden-onset, sharp chest pain, but the range of symptoms can be broader.

• Chest pain: Typically pleuritic (worsens with inspiration or coughing) and may improve when sitting up or leaning forward. The pain can radiate to the neck, shoulders, or back.
• Pericardial friction rub: A high-pitched, scratchy sound best heard with the diaphragm of a stethoscope at the left lower sternal border.
• Fever: May accompany infectious or inflammatory pericarditis.
• Dyspnea: Especially when lying flat, due to pain or pericardial effusion.
• Other symptoms: Weakness, palpitations, and in rare severe cases, signs of cardiac tamponade (hypotension, jugular venous distention, muffled heart sounds).

Diagnostic Approach

Diagnosis is based on clinical criteria, supported by laboratory and imaging studies.

Major Diagnostic Criteria

Acute pericarditis is diagnosed when at least two of the following four criteria are present:

• Typical chest pain
• Pericardial friction rub
• Electrocardiographic (ECG) changes—widespread ST-elevation or PR depression
• New or worsening pericardial effusion

Supporting findings include elevated inflammatory markers (ESR, CRP, leukocytosis) and evidence of pericardial inflammation on imaging.

Investigations

• ECG: Shows diffuse concave ST-segment elevation and PR-segment depression in the acute phase; later, T-wave inversions may develop.
• Echocardiogram: Used to detect pericardial effusion and rule out tamponade.
• Chest X-ray: Often normal unless a large effusion is present, in which case a “water bottle” silhouette may be seen.
• Blood tests: CBC, CRP, ESR, troponins (to rule out concomitant myocarditis), renal function, and viral serologies if indicated.
• Other tests: Depending on the clinical context, TB test, autoimmune markers, or pericardial fluid analysis (if pericardiocentesis is performed).

Management

Treatment is aimed at reducing inflammation, relieving symptoms, and addressing the underlying cause if known.

General Approach

• Non-steroidal anti-inflammatory drugs (NSAIDs): Mainstay of therapy for pain and inflammation. Common agents include ibuprofen and aspirin, typically continued until symptoms and CRP normalize (1–2 weeks).
• Colchicine: Added to NSAIDs to reduce recurrence rates and hasten symptom resolution. Dose is generally weight-adapted and continued for 3–6 months.
• Corticosteroids: Reserved for patients who cannot tolerate NSAIDs/colchicine or those with autoimmune or uremic pericarditis. Use with caution as corticosteroids are associated with a higher recurrence rate.
• Treatment of underlying causes: Antibiotics for bacterial pericarditis, antitubercular drugs for TB, immunosuppressants for autoimmune conditions, and dialysis for uremic pericarditis.
• Pericardiocentesis: Indicated if a large effusion causes cardiac tamponade or if purulent/bloody fluid is suspected.
• Hospitalization: Required for high-risk patients (fever >38°C, large effusions, immunosuppression, trauma, or suspected myocarditis).

Lifestyle and Monitoring

• Rest is advised during the acute phase until fever and chest pain subside.
• Gradual return to activities, especially for athletes, after complete symptom resolution and normalization of inflammatory markers.
• Close follow-up is essential to monitor for complications or recurrence.

Complications

While most cases resolve without issue, complications can be serious:

• Cardiac tamponade: Accumulation of fluid in the pericardial space compresses the heart, leading to impaired cardiac output, hypotension, and shock. This is a medical emergency requiring urgent drainage.
• Constrictive pericarditis: Chronic inflammation can cause fibrosis and thickening of the pericardium, restricting diastolic filling of the heart and leading to heart failure symptoms.
• Recurrent pericarditis: Up to 15–30% of patients may experience relapses, highlighting the importance of colchicine in treatment.

Prognosis

The majority of patients with idiopathic or viral acute pericarditis recover fully with appropriate treatment. Prognosis worsens if complications develop or if the underlying cause is malignant or tuberculous. Close monitoring and adherence to therapy minimize risks of recurrence and chronic sequelae.

When to Seek Immediate Attention

• Patients should seek urgent medical attention if they experience:
• Signs of cardiac tamponade (rapid heart rate, low blood pressure, confusion)
• Severe or worsening chest pain
• Shortness of breath at rest
• Dizziness or fainting
• Palpitations or irregular heartbeats

Nursing Care of Patients with Acute Pericarditis

Symptom Management

• Pain Relief: Administer prescribed analgesics (e.g., NSAIDs such as ibuprofen) and monitor their effectiveness. Educate the patient on the importance of reporting persistent or worsening pain.
• Positioning: Assist the patient to sit upright or lean forward to relieve chest discomfort. Avoid positions that exacerbate pain.
• Temperature Control: Monitor and manage fever with antipyretics as prescribed.

Monitoring and Prevention of Complications

• Fluid Balance: Monitor intake and output, as fluid overload or deficit can aggravate cardiac function.
• Observe for Pericardial Effusion: Watch for increasing shortness of breath, hypotension, or decreasing urine output, which may suggest effusion or tamponade.
• Electrocardiogram (ECG) Monitoring: Observe for changes such as widespread ST elevation or PR depression, which are common in pericarditis.

Patient Education and Psychosocial Support

• Educate the Patient and Family: Explain the nature of the disease, treatment plan, and warning signs that require immediate medical attention (e.g., sudden severe chest pain, breathlessness, fainting).
• Medication Adherence: Emphasise the importance of completing the full course of prescribed medications and attending follow-up appointments.
• Emotional Support: Offer reassurance and address anxiety related to chest pain and hospitalisation. Involve family members in care and education.

Infection Control and General Care

• Aseptic Techniques: Maintain strict aseptic precautions during invasive procedures (e.g., pericardiocentesis) to prevent secondary infections.
• Rest and Activity: Encourage adequate rest during the acute phase, gradually increasing activity as tolerated. Avoid strenuous exertion until complete recovery.
• Nutritional Support: Provide a balanced diet and adequate hydration unless contraindicated.

Coordination with Multidisciplinary Team

• Collaborative Care: Work closely with physicians, cardiologists, physiotherapists, and dieticians to ensure holistic management.
• Documentation: Maintain accurate records of assessments, interventions, and patient responses to guide ongoing care.

REFERENCES

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6. Health Education & Content Services. Pericarditis: Symptoms, diagnosis and treatment. Mayo Clinic; 2023.
7. Melendo-Viu M, et al. A systematic review and meta-analysis of randomized controlled trials evaluating pharmacologic therapies for acute and recurrent pericarditis. Trends in Cardiovascular Medicine. 2022; doi:10.1016/j.tcm.2022.02.001.
8. Ismail TF. Acute pericarditis: Update on diagnosis and management. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6964178/. Clin Med (Lond). 2020;20(1):48-51.
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