Understanding, investigating and managing pericarditis

You’ll hear it described as “sharp chest pain,” “worse when lying flat,” or “relieved by sitting forward.” But what’s actually happening when someone has pericarditis—and how do we reason through it clinically?

Let’s explore the pathophysiology first, then walk through how to spot it, investigate it, and manage it.

🔬 The Pathophysiology: What’s inflamed, and why?

The pericardium is a double-layered sac that surrounds the heart. It has two layers:

• Visceral pericardium (inner layer, touching the heart)

• Parietal pericardium (outer layer, attached to surrounding structures)

Between them is a thin film of lubricating fluid. In pericarditis, this space becomes inflamed—due to infection, autoimmune processes, trauma, or other causes. Inflammation leads to:

• Pain from irritation of nearby structures (especially the pleura)

• Friction rub as the inflamed layers scrape against each other

• Fluid accumulation (pericardial effusion), which can impair cardiac filling if severe.

🧬 Aetiology of Pericarditis: What causes the inflammation?

Pericarditis can be idiopathic, but often has a clear underlying cause. Think in categories—this helps students build differential diagnosis and clinical reasoning:

🦠 1. Infectious

• Viral: Most common in developed settings. Coxsackievirus, echovirus, influenza, HIV.
• → Often self-limiting, but can cause significant discomfort and effusion.
• Bacterial: Rare but serious—TB (especially in endemic areas), pneumococcus, staph.
• → May lead to purulent pericarditis or constrictive sequelae.
• Fungal/parasitic: Uncommon, usually in immunocompromised patients

Clinical clue: Recent viral illness, fever, or systemic symptoms. Ask about travel, exposures, and immune status.

🧬 2. Autoimmune and Inflammatory

• Systemic lupus erythematosus (SLE)
• Rheumatoid arthritis
• Scleroderma, mixed connective tissue disease
• Sarcoidosis

These conditions trigger immune-mediated inflammation of the pericardium.

Clinical clue: Look for joint pain, rashes, serositis, or other systemic features. Pericarditis may be the first sign of autoimmune disease.

💔 3. Post-MI and Post-Procedure

• Dressler’s syndrome: Autoimmune pericarditis occurring weeks after myocardial infarction
• Post-pericardiotomy syndrome: After cardiac surgery
• Post-ablation or catheter-based procedures

Clinical clue: Timing is key—pain and inflammation days to weeks after cardiac insult. Often responds well to NSAIDs and colchicine.

🧪 4. Metabolic

• Uraemia: Seen in advanced renal failure
• → Toxins irritate the pericardium, often causing large effusions
• Hypothyroidism: Can cause serous effusion, usually painless
• Malignancy: Direct invasion or paraneoplastic inflammation

Clinical clue: Look for systemic signs—renal dysfunction, weight loss, fatigue. Effusion may be disproportionate to symptoms.

🧨 5. Trauma and Radiation

• Blunt or penetrating chest trauma
• Radiation therapy to the chest (e.g. for lymphoma or breast cancer)

Clinical clue: History of injury or prior radiotherapy. May lead to chronic inflammation or constrictive pericarditis.

❓ 6. Drug-Induced

• Hydralazine, isoniazid, phenytoin, procainamide
• Immune checkpoint inhibitors (increasingly relevant)

Clinical clue: Always review the medication list. Onset may be delayed and subtle.

🧠 Clinical Reasoning: How do we recognise it?

Recognising pericarditis isn’t just about ticking off symptoms—it’s about understanding the underlying mechanisms and using them to differentiate from other causes of chest pain, like myocardial infarction, pulmonary embolism, or pneumonia. Let’s consider the key features and the reasoning behind them.

Key symptoms:

• Sharp, pleuritic chest pain is the hallmark symptom. It’s typically:
• Worse when lying flat: This position stretches the inflamed pericardial layers, increasing friction.
• Relieved by sitting forward: This reduces contact between the pericardium and surrounding structures, easing irritation.
• Worse with inspiration or coughing: Because the pericardium is adjacent to the pleura, inflammation can mimic pleuritic pain
• This positional and pleuritic nature helps distinguish pericarditis from myocardial infarction, which usually presents with crushing, pressure-like pain unrelated to position or respiration.

• Dyspnoea. Often mild unless there’s a significant pericardial effusion. In that case, dyspnoea results from:
• Reduced cardiac filling due to external compression
• Decreased stroke volume, leading to compensatory tachypnoea
• Impaired pulmonary venous return, especially if tamponade develops
• Dyspnoea in pericarditis isn’t due to lung pathology—it’s a consequence of impaired cardiac mechanics. If breathlessness is disproportionate to pain, consider effusion or tamponade.

• Fever: Common in viral or autoimmune pericarditis, reflecting systemic inflammation.
• Fever may be low-grade or spiking, depending on the cause.
• Fever helps differentiate inflammatory causes from ischaemic ones. Always ask about recent viral illness, autoimmune symptoms, or renal disease.

On examination:

• Pericardial friction rub. A scratchy, triphasic sound heard best at the left lower sternal border with the patient leaning forward. It reflects:
• Rubbing of inflamed pericardial layers during systole, diastole, and atrial contraction
• Absence of fluid—once effusion accumulates, the rub may disappear
• It’s pathognomonic but fleeting. If you hear it, document it—it may be gone by the next review. Use diaphragm of the stethoscope and listen during held expiration.

• Tachycardia: Often present due to:
• Pain and anxiety
• Fever
• Compensatory response to reduced stroke volume if effusion is present
• Tachycardia is non-specific but supports the picture. If persistent despite analgesia and antipyretics, consider evolving tamponade.

• Signs of tamponade (if effusion is large):
  
• Beck’s triad:
• Hypotension: Due to reduced cardiac output from impaired ventricular filling
• Raised JVP: Reflects elevated right atrial pressure
• Muffled heart sounds: Fluid dampens transmission of sound
• Other signs:
• Pulsus paradoxus: >10 mmHg drop in systolic BP during inspiration
• Tachypnoea and restlessness: Early signs of poor perfusion
• Tamponade is a clinical emergency. Recognising these signs early can be life-saving. Always correlate with echo findings and act promptly

📈 Investigations: What do we look for—and why?

When you suspect pericarditis, your investigations should help you confirm inflammation, rule out mimics (like MI or PE), and assess for complications like effusion or tamponade. Here’s how each test contributes to your reasoning:

🫀 ECG (Electrocardiogram)

This is often the first clue. In pericarditis, you’ll typically see:

• Diffuse ST elevation across multiple leads—not localised like in myocardial infarction. This reflects widespread inflammation of the epicardial surface.

• PR segment depression, especially in limb leads, due to atrial involvement and pericardial irritation.

Why it matters:

These changes help distinguish pericarditis from STEMI. In MI, ST elevation is regional and often accompanied by reciprocal changes. In pericarditis, the ST elevation is more global and concave (“saddle-shaped”), and PR depression is a subtle but telling sign.

more great content here https://www.ecgbook.com/pericarditis/

and here https://litfl.com/pericarditis-ecg-library/ 

🧪 Blood tests

• CRP and ESR: Elevated inflammatory markers support the diagnosis and help track response to treatment.

• Troponin: May be mildly elevated if there’s concurrent myocarditis (myopericarditis). A significantly raised troponin should prompt you to reconsider MI or myocarditis as primary.

Why it matters:

Inflammatory markers confirm systemic inflammation. Troponin helps you assess myocardial involvement—important because treatment and prognosis differ if the myocardium is affected

🪞 Echocardiogram

This is essential to:

• Detect pericardial effusion—fluid accumulation between the pericardial layers (which will be an anechoic dark space in the usually bright echogenic line)

• Assess for tamponade physiology—compression of the heart that impairs filling and reduces cardiac output

Why it matters:

Effusion can be silent or dramatic. If tamponade is present, urgent pericardiocentesis may be life-saving. Echo also helps rule out other structural causes of chest pain or dyspnoea.

📷 Chest X-ray

Often normal in early or mild cases. But if the effusion is large, you may see:

• Enlarged cardiac silhouette (“water bottle” heart)
• Clear lung fields, unless there’s a concurrent pulmonary process

Why it matters:

CXR is less sensitive than echo but can hint at significant effusion. It’s also useful for excluding pneumonia or other thoracic causes of chest pain.

📦 Myopericarditis: When the Pericardium Isn’t Alone

Sometimes, pericarditis doesn’t come solo. In myopericarditis, inflammation affects both the pericardium and the adjacent myocardium.

The clinical picture still includes chest pain and a pericardial rub, but now there's myocardial involvement—which means you may see:

• Elevated troponin (reflecting myocardial injury)
• ECG changes beyond the classic pericarditis pattern (AF, conduction defects etc)
• Occasionally, impaired ventricular function on echocardiogram

The key distinction is that myocarditis predominates in terms of myocardial dysfunction, while myopericarditis presents more like pericarditis but with biochemical or imaging evidence of myocardial inflammation.

Why it matters:
Troponin elevation in pericarditis doesn’t always mean infarction. If the echo shows preserved function and the clinical picture fits, it’s likely myopericarditis. Management is still anti-inflammatory—but with closer cardiac monitoring.

💊 Management: What do we do?

Managing pericarditis isn’t just about relieving pain; it’s about controlling inflammation, preventing complications, and addressing the underlying cause. Here's how each intervention fits into the bigger picture.

🧯 NSAIDs (e.g. ibuprofen)

Non-steroidal anti-inflammatory drugs are the first-line treatment for most cases of acute pericarditis, especially when viral or idiopathic. They work by:

• Inhibiting cyclooxygenase (COX) enzymes ..... my precious.... reducing prostaglandin synthesis
• Dampening the inflammatory response in the pericardial layers
• Relieving pain and fever, which are often the most distressing symptoms

Why it matters:

Pericarditis is fundamentally an inflammatory process. NSAIDs target that mechanism directly, and their rapid symptom relief helps confirm the diagnosis

🔄 Colchicine

Colchicine is added to reduce the risk of recurrence, which is common in idiopathic and viral pericarditis. It:

• Disrupts microtubule formation, impairing leukocyte migration and inflammatory signalling
• Modulates the innate immune response, especially in serosal inflammation

Why it matters:

Recurrence can be debilitating and difficult to manage. Colchicine has strong evidence for reducing relapse rates, especially when used early and alongside NSAIDs.

🧬 Steroids

Corticosteroids are reserved for autoimmune pericarditis (e.g. SLE, RA) or refractory cases where NSAIDs and colchicine fail. They:

• Suppress the broader immune response, not just local inflammation (remember how?)
• Reduce cytokine production, which drives systemic and pericardial inflammation

Why it matters:

Steroids can mask infection and increase recurrence if used too early or inappropriately. They’re powerful—but should be used with clear indication and caution.

💉 Pericardiocentesis

This is a procedural intervention used when pericardial effusion leads to tamponade physiology—compression of the heart that impairs filling and cardiac output. It involves:

• Needle aspiration of pericardial fluid, often guided by echocardiography
• Relieving pressure to restore haemodynamic stability

Why it matters:

Tamponade is life-threatening. Pericardiocentesis is both diagnostic (fluid analysis) and therapeutic. Recognising when it’s needed is a critical skill.

🔍 Treat the Underlying Cause

Pericarditis is often a symptom of something deeper. Management must include:

• Dialysis for uraemic pericarditis, where toxins irritate the pericardium
• Antivirals or immunosuppression if the cause is infectious or autoimmune
• Oncologic treatment if malignancy is involved

Why it matters:

Without addressing the root cause, inflammation may persist or recur. Aetiology guides not just treatment, but prognosis and follow-up.

Clinical cases to consider

🩺 Clinical Vignette

A 24-year-old medical student presents with sharp, central chest pain that worsens when lying flat and improves when sitting forward. She reports feeling unwell for the past week with low-grade fever, sore throat, and general fatigue. She had a mild dry cough and myalgia, which she initially attributed to a viral upper respiratory infection.

On auscultation, you hear a faint pericardial rub. Her ECG shows diffuse ST elevation and PR depression. Echocardiogram reveals a small pericardial effusion but preserved ventricular function.

What’s going on?

This is classic pericarditis, likely viral in origin. The preceding flu-like illness suggests a self-limited viral infection—possibly Coxsackievirus or another enterovirus—that has triggered pericardial inflammation. 

🧠 Reasoning Prompts

• How does the viral prodrome help narrow the differential?
• What distinguishes myopericarditis from myocarditis in terms of function and risk?
• Why is echo essential even when the ECG and troponin suggest inflammation

🩺 Clinical Vignette

A 32-year-old woman presents with sudden-onset palpitations and chest discomfort. She describes the pain as sharp and positional—worse when lying flat, relieved by sitting forward. She’s also experiencing fatigue, low-grade fever, and joint stiffness.

Her heart rate is irregularly irregular at 130 bpm. On further questioning, she mentions a history of photosensitive rash and intermittent oral ulcers.

On auscultation, you hear a faint pericardial rub. ECG shows atrial fibrillation with rapid ventricular response and diffuse ST elevation. Troponin is elevated. Echocardiogram reveals a small pericardial effusion and mildly reduced left ventricular function.

What’s going on?

This is myopericarditis, likely secondary to systemic lupus erythematosus (SLE). The chest pain and rub point to pericardial inflammation; the elevated troponin and reduced LV function suggest myocardial involvement. The new-onset atrial fibrillation reflects atrial irritation—either from inflammation, effusion-related stretch, or systemic inflammatory burden.

AF in pericarditis isn’t common, but when present, it signals more extensive cardiac involvement. It may worsen symptoms, reduce cardiac output, and complicate management. In autoimmune cases, rhythm disturbances often resolve with control of the underlying inflammation—but rate control and anticoagulation may be needed acutely.

🧠 Reasoning Prompts 

• What mechanisms could explain AF in this context?
• How does autoimmune myopericarditis differ from viral causes in presentation and management?
• What are the priorities: rate control, rhythm, inflammation, or underlying disease

🩺 Clinical Vignette

A 19-year-old man presents to the emergency department with progressive fatigue, exertional dyspnoea, and chest tightness. He reports a recent viral illness—fever, sore throat, and body aches about ten days ago—but didn’t seek medical attention.

Over the past 48 hours, he’s developed orthopnoea and palpitations. On examination, he’s tachycardic at 120 bpm, hypotensive (BP 88/60), and has elevated JVP. Auscultation reveals a soft S3 gallop and bibasal crackles.

ECG shows sinus tachycardia with non-specific ST changes. Troponin is markedly elevated. Echocardiogram reveals global hypokinesis and an ejection fraction of 30%.

What’s going on?

This is severe acute myocarditis, likely viral in origin. The initial infection triggered an inflammatory response that has now extended into the myocardium, impairing contractility and leading to early heart failure. Unlike pericarditis, where the pain is positional and the ECG shows diffuse ST elevation, myocarditis presents with subtle ECG changes, marked troponin rise, and ventricular dysfunction on echo.

 

Myocarditis can masquerade as a benign viral illness until the patient decompensates. In severe cases, it leads to cardiogenic shock, arrhythmias, and even sudden death. Management includes supportive care (oxygen, diuretics, inotropes if needed), cardiac monitoring, and sometimes immunosuppression or mechanical support in fulminant cases.

🧠 Reasoning Prompts

• What distinguishes myocarditis from pericarditis and myopericarditis?
• How does viral history guide your differential—and what other causes must you consider?
• What investigations help assess severity and guide management?

🧵 Putting It All Together

Pericarditis is a great case for integrating anatomy, physiology, and clinical reasoning:

• Anatomy: Know your layers—visceral vs parietal
• Physiology: Understand how effusion impairs preload and cardiac output
• Clinical reasoning: Use positional pain, ECG changes, and echo findings to differentiate from MI or PE

And always ask:

Is this isolated pericarditis, or part of a systemic process?

🩺 Final Thought

Pericarditis is more than just chest pain—it’s a window into how inflammation affects cardiac function, and how careful reasoning helps us distinguish it from more dangerous differentials. Keep your ears tuned for the rub, your eyes on the ECG, and your mind on the mechanism.