Pericarditis
Pericarditis is inflammation of the pericardium, typically presenting with sharp pleuritic chest pain, pericardial friction rub, and diffuse ST-segment elevation on electrocardiogram.
Pericarditis
Pericarditis literally means inflammation of the pericardium ("peri-" = around, "card-" = heart, "-itis" = inflammation). It refers to inflammation of the pericardial sac surrounding the heart, which can occur as an isolated entity or as a manifestation of a systemic disease [1][2].
Pericarditis is a cardiovascular cause of chest discomfort — this is a key framing to remember for differential diagnosis of chest pain [3].
The condition may present acutely, recurrently, or progress to chronic forms including constrictive pericarditis. It often coexists with myocarditis (termed "myopericarditis" when both are involved) [2][4].
2. Anatomy and Function of the Pericardium
Understanding the anatomy is essential — the clinical features of pericarditis (friction rub, pain with breathing, effusion, tamponade) all follow directly from the structure.
The pericardium is a fibroelastic sac with the following layers (from outermost to innermost) [1]:
| Layer | Description | Key Points |
|---|---|---|
| Fibrous pericardium | Tough outer sac of dense connective tissue | Anchored to the diaphragm inferiorly, the sternum anteriorly, and the great vessels superiorly. Relatively inelastic — this is why rapid fluid accumulation causes tamponade |
| Parietal pericardium | Serous membrane lining the inner surface of the fibrous pericardium | Contains pain fibres (somatic innervation via phrenic nerve C3–C5) — this is why pericardial pain radiates to the trapezius ridge and shoulder |
| Pericardial cavity | Potential space between parietal and visceral layers | Normally contains 15–50 mL of ultrafiltrate (serous fluid) that acts as lubricant to reduce friction during cardiac motion |
| Visceral pericardium (Epicardium) | Serous membrane directly adherent to the heart surface and proximal great vessels | Contains the coronary arteries and fat. Innervated by autonomic fibres (not pain-sensitive) |
- Lubrication: Pericardial fluid reduces friction between the beating heart and surrounding structures
- Mechanical constraint: Limits acute cardiac distension (prevents overdilation of chambers)
- Barrier: Protects the heart from infection spreading from adjacent structures (lungs, mediastinum)
- Ventricular interdependence: The fixed pericardial space means that when one ventricle fills more, the other fills less — this principle underlies pulsus paradoxus in tamponade
- Anchoring: Fixes the heart in the mediastinum
Why does pericardial pain radiate to the trapezius ridge?
The parietal pericardium is innervated by the phrenic nerve (C3, C4, C5). The phrenic nerve also provides sensory innervation to the shoulder (supraclavicular area) and trapezius ridge via the same dermatomes. When the inflamed parietal pericardium irritates the phrenic nerve, the brain "misinterprets" the signal as coming from the shoulder/trapezius — this is referred pain.
Radiation to the trapezius ridge is the characteristic site of pericardial pain [5].
- Incidence: Approximately 27.7 per 100,000 population per year [2]
- Accounts for approximately 5% of non-ischaemic chest pain presentations to the emergency department [2]
- Sex: Males slightly more commonly affected than females (male-to-female ratio approximately 2–3:1 in most series)
- Age: Can occur at any age; most common in young to middle-aged adults (20–50 years)
- Recurrence: Up to 15–30% of patients with a first episode of acute pericarditis develop recurrent pericarditis
- Association with myocarditis: Pericarditis and myocarditis frequently coexist — when troponin is elevated in the context of pericarditis, the term "myopericarditis" is used [4]
| Risk Factor | Mechanism |
|---|---|
| Recent viral illness (URI, gastroenteritis) | Most common identifiable trigger — viral infection directly inflames the pericardium or triggers post-viral immune response |
| Male sex | Unclear; possibly hormonal or healthcare-seeking behaviour differences |
| Young age (20–50) | Higher exposure to viral infections; more vigorous immune response |
| Immunosuppression (e.g. HIV) | ↑Susceptibility to opportunistic pericardial infections (TB, fungal) |
| Autoimmune disease (SLE, RA) | SLE cardiac features include pericarditis, cardiomyopathy, pulmonary hypertension, Libman-Sacks endocarditis [6]. RA: up to 30% have echo evidence of pericardial effusion but < 10% have clinical pericarditis [8] |
| Chronic kidney disease / Uraemia | Uraemic toxins cause a "chemical" (non-infectious) inflammation of the pericardium [9] |
| Malignancy (lung, breast, lymphoma, leukaemia) | Direct pericardial invasion or metastasis |
| Recent cardiac surgery / PCI / pacemaker insertion | Iatrogenic injury to pericardium |
| Recent MI | Early (2–4 days): direct inflammation from transmural infarction. Late (weeks–months): Dressler's syndrome (autoimmune) |
| TB endemic area (e.g. sub-Saharan Africa, parts of Asia including Hong Kong historically) | TB pericarditis — TB is the most common cause of constrictive pericarditis in this locality (Hong Kong) [2] |
| Mediastinal radiation therapy | Radiation-induced pericardial injury and fibrosis |
5. Etiology (with Focus on Hong Kong)
- By definition, no identifiable cause is found
- Most are presumed viral — but we don't routinely test for viruses because it doesn't change management
- In clinical practice, "idiopathic" and "viral" pericarditis are treated synonymously
5.2 Infectious ( < 5% in developed countries, but higher in endemic areas)
- Pathogens: Coxsackie A or B, Echovirus, Adenovirus, Mumps, Measles, Influenza, HIV, VZV, EBV, CMV, HHV-6 [1]
- Pathophysiology: Direct viral cytopathic effect on pericardial mesothelial cells → inflammatory infiltrate → serous exudate. Also involves molecular mimicry and post-viral autoimmune response
- Often occurs together with myocarditis [2] — hence "myopericarditis"
- Flu-like prodrome is a characteristic associated feature [3]
- TB pericarditis: Particularly important in Hong Kong and endemic regions
- TB reaches the pericardium via direct spread from mediastinal lymph nodes, haematogenous spread, or contiguous spread from lungs
- Often causes haemorrhagic effusion and can progress to constrictive pericarditis (the most common cause of constrictive pericarditis in HK [2])
- Pathophysiology: granulomatous inflammation → caseous necrosis → fibrosis → calcification → constriction
- Pyogenic bacteria: Staphylococci, Streptococci, Meningococci [1]
- Purulent pericarditis — rare but rapidly fatal if untreated
- Usually by contiguous spread from pneumonia/empyema or haematogenous
- Borrelia (Lyme disease) [1]
- Histoplasmosis, Coccidioidomycosis, Candidiasis [1]
- Rare; typically in immunocompromised patients
- Entamoeba, Echinococcus, Toxoplasmosis [1]
- Very rare; typically in endemic areas
| Type | Examples |
|---|---|
| Primary (rare) | Mesothelioma, Sarcoma [1] |
| Secondary (more common) | Lung, Breast, Thyroid, Leukaemia, Lymphoma [1] |
- Pathophysiology: Direct pericardial invasion, lymphatic obstruction (preventing drainage of pericardial fluid), or haematogenous metastasis
- Often causes haemorrhagic or exudative effusion
- May present with large effusion and tamponade as first manifestation of malignancy
- SLE: Pericarditis is one of the most common cardiac manifestations (occurs in 20–40% of SLE patients during their disease course [2])
- SLE cardiac features: pericarditis, cardiomyopathy, pulmonary hypertension, Libman-Sacks endocarditis [6]
- Pathophysiology: Immune complex deposition in pericardium → complement activation → inflammation
- RA: Up to 30% have echocardiographic pericardial effusion but only < 10% have clinical pericarditis. Management is related to disease activity — usually treated by steroids/NSAIDs [8]
- Systemic sclerosis, Sjögren's syndrome [1]
- Vasculitis: EGPA (Eosinophilic Granulomatosis with Polyangiitis), GPA (Granulomatosis with Polyangiitis), Polyarteritis nodosa [1]
- Mixed Connective Tissue Disease (MCTD): Cardiac involvement in ~20% including pericarditis, conduction abnormality, cor pulmonale [8]
- Uraemic pericarditis [1][7][9]:
- Occurs in advanced CKD / ESRD (typically GFR < 15 mL/min or on dialysis)
- Pathophysiology: Accumulation of uraemic toxins → direct chemical irritation of pericardial mesothelial cells → "sterile" inflammation → fibrinous pericarditis
- Characteristically does not show the typical ECG changes of acute pericarditis (no diffuse ST elevation) because the inflammation is more "chemical" than inflammatory
- Management: intensification of dialysis is the primary treatment [9]
- Hypothyroidism (Myxoedema) [1]:
- Causes pericardial effusion due to accumulation of mucopolysaccharides (myxoedematous fluid)
- Usually slowly accumulating → rarely causes tamponade
- Resolves with thyroid hormone replacement
- Doxorubicin, Procainamide, Hydralazine, Isoniazid, Cyclosporin A [1]
- Procainamide and hydralazine can cause a drug-induced lupus-like syndrome → serositis including pericarditis [8]
- Immune checkpoint inhibitors (e.g. nivolumab, pembrolizumab) — increasingly recognized in 2024–2026 as a cause of immune-related pericarditis/myocarditis
This is an extremely high-yield distinction:
| Timing | Name | Mechanism |
|---|---|---|
| Early (2–4 days post-MI) | Early post-MI pericarditis | Direct inflammation of pericardium overlying transmural (full-thickness) infarct. Only occurs with STEMI (transmural infarction reaches the epicardium/pericardium) |
| Late (weeks to months post-MI) | Dressler's syndrome (Post-myocardial infarction syndrome) | Autoimmune pericarditis occurring weeks to months after MI. Fever + pleuritic chest pain + pericarditis ± pericardial effusion [1][7] |
- Why does Dressler's syndrome occur? Myocardial necrosis releases intracellular antigens (e.g. cardiac myosin) that are normally hidden from the immune system → the immune system mounts an autoimmune response against these "neo-antigens" → pericardial inflammation
Post-MI Pericarditis – Important Management Note
If recent MI: use aspirin (avoid NSAID/steroid as they increase the risk of ventricular aneurysm formation and impair myocardial healing) [7]. This is because NSAIDs and steroids may thin the infarcted myocardium → ↑risk of ventricular wall rupture or aneurysm.
6. Pathophysiology
Understanding the pathophysiology is the key to understanding every clinical feature:
Why does pericardial effusion cause tamponade only sometimes?
- The pericardium has a pressure-volume curve with an initial flat portion (compliant) and then a steep exponential rise [2]
- Acute ↑volume → no time for pericardium to stretch → rapid ↑pressure [2]
- Chronic ↑volume → gradual ↑compliance → slow ↑pressure → can accumulate up to 2L of fluid without tamponade [2]
- This explains why a post-traumatic haemopericardium of only 150–200 mL can cause tamponade (acute), while a malignant effusion of 1–2L may only cause mild symptoms (chronic)
Why does sitting up and leaning forward relieve pericardial pain?
- This is due to ↓pressure on the parietal pericardium in this position [2] — gravity pulls the heart anteriorly and slightly away from the posterior parietal pericardium, reducing friction and irritation of pain-sensitive nerve endings
Why is the pain pleuritic (worse with inspiration)?
- During inspiration, the diaphragm descends → lung expands → the inflamed pericardium is stretched and moves against the adjacent inflamed pleura → increased friction → increased pain
- The phrenic nerve (which innervates the parietal pericardium) is also stretched during deep inspiration
7. Classification
| Classification | Duration | Key Features |
|---|---|---|
| Acute pericarditis | < 4–6 weeks | New onset; most common presentation |
| Incessant pericarditis | > 4–6 weeks but < 3 months | Symptoms persist without a clear remission |
| Recurrent pericarditis | Recurrence after a symptom-free interval of ≥ 4–6 weeks | Occurs in 15–30% of first episodes; often autoimmune mechanism |
| Chronic pericarditis | > 3 months | Persistent inflammation; may progress to constrictive pericarditis |
| Type | Pathology | Common Causes |
|---|---|---|
| Fibrinous (dry) | Fibrin deposition on pericardial surfaces, no significant effusion | Viral, uraemic, early post-MI, autoimmune |
| Effusive (wet) | Significant fluid accumulation in the pericardial space | Viral, TB, malignancy, hypothyroidism, autoimmune |
| Constrictive | Fibrosis, thickening, ± calcification of pericardium | TB (most common in HK) [2], post-radiation, post-surgical, recurrent pericarditis |
| Effusive-constrictive | Combination of effusion + visceral pericardial constriction | TB, post-radiation, post-surgical |
8. Clinical Features
8.1 Symptoms
High Yield – The Classic Symptom Profile of Acute Pericarditis
This is the hallmark symptom and is described per the SOCRATES framework from the GC lecture slides [3]:
| Feature | Description | Pathophysiological Basis |
|---|---|---|
| Site | Retrosternal or left-sided [3] | Parietal pericardium inflammation; referred via phrenic nerve |
| Onset | Gradual; postural change may suddenly aggravate [3] | Inflammation develops over hours; positional change alters friction between inflamed pericardial surfaces |
| Character | Sharp, "stabbing," pleuritic [3][5] | Somatic pain from phrenic nerve irritation of parietal pericardium (sharp quality = somatic pain, unlike visceral pain of MI which is dull/heavy) |
| Radiation | Left shoulder or back [3], trapezius ridge (characteristic site of pericardial pain) [5] | Phrenic nerve (C3–C5) referred pain to the supraclavicular/trapezius region |
| Associated features | Flu-like prodrome, breathlessness, fever [3] | Viral etiology; effusion causing compression; systemic inflammatory response |
| Timing | Acute presentation; variable duration [3] | Depends on etiology and treatment response |
| Exacerbating/Relieving factors | Sitting up/lying down may affect intensity. NSAIDs help [3]. ↑ by inspiration, movement, postural change, exercise, swallowing. ↓ by sitting up and leaning forward [2] | See pathophysiology above — sitting forward reduces pericardial-pleural friction; NSAIDs suppress prostaglandin-mediated inflammation |
| Severity | Can be severe [3] | Depends on degree of inflammation |
Distinguishing pericardial pain from MI pain: Pericardial pain is sharp and pleuritic (worse with breathing/movement), positional (better sitting forward), and radiates to the trapezius ridge. MI pain is heavy/constricting, not positional, and radiates to the arm/jaw. NSAIDs relieve pericardial pain but not MI pain. Pericardial pain is NOT relieved by GTN.
- Due to pleuritic pain limiting deep inspiration (splinting) and/or pericardial effusion compressing the lungs
- May also indicate concurrent myocarditis with LV dysfunction
- Due to systemic inflammatory response (cytokines such as IL-1, IL-6, TNF-α acting on the hypothalamic thermoregulatory centre)
- High fever ( > 38°C) should raise suspicion for bacterial/purulent pericarditis or autoimmune disease
- Non-specific systemic inflammatory symptoms, particularly with viral or autoimmune etiology
- Flu-like prodrome is characteristic of viral pericarditis [3]
- Dysphagia — oesophageal compression by enlarged pericardial sac
- Hoarseness — recurrent laryngeal nerve compression
- Hiccups — phrenic nerve stimulation [7]
- Dyspnoea — lung compression
- Weight loss, night sweats (TB, malignancy)
- Joint pain, rash (SLE, RA)
- Oliguria, fatigue (uraemia)
8.2 Signs
| Feature | Detail | Why? |
|---|---|---|
| Character | High-pitched, superficial, scratching/grating ("like walking on fresh snow" or "leather rubbing together") | Two roughened, inflamed pericardial surfaces (visceral and parietal) rubbing against each other with each heartbeat |
| Phases | Classically triphasic [2][7]: (1) Atrial systole (presystolic), (2) Ventricular systole, (3) Early diastole (rapid ventricular filling) | Each phase corresponds to a moment when the heart moves maximally within the pericardial sac — friction is generated at each movement |
| Mono/Biphasic | May be mono- or biphasic (especially if atrial fibrillation → loss of atrial systole component) | The triphasic rub is "classic" but often only 1–2 components are heard |
| Best heard | Left sternal border, with patient sitting up and leaning forward, at end-expiration | This position brings the heart closer to the chest wall, maximizing pericardial surface contact |
| Variability | Evanescent — may come and go, can change with position and over hours | As effusion develops, the pericardial surfaces separate → friction rub may disappear (a paradoxically "bad sign" if it disappears as it may indicate increasing effusion) |
Clinical Pearl
The disappearance of a previously heard pericardial friction rub should raise concern for developing pericardial effusion — the fluid separates the inflamed surfaces, reducing friction. Always reassess with echocardiography if the rub disappears and the patient's condition worsens.
- Muffled/distant heart sounds — fluid around the heart dampens sound transmission
- Ewart sign: dullness on percussion over the left angle of the scapula [2][7] — caused by compressive atelectasis of the left lower lobe by the enlarged pericardial sac
- ↓ Pericardial friction rub [2] — fluid separates the inflamed surfaces
Beck's triad = hypotension + distended neck veins + muffled heart sounds [2]
| Sign | Mechanism |
|---|---|
| Hypotension | ↑pericardial pressure > diastolic pressure in ventricles → ↓ventricular filling → ↓preload → ↓SV + CO → obstructive shock [2] |
| Distended neck veins (↑JVP) | ↑RA pressure because blood cannot enter the compressed right heart → backs up into the jugular veins |
| Muffled heart sounds | Fluid around the heart dampens sound transmission to the chest wall |
| Pulsus paradoxus | Exaggerated drop in systolic BP ( > 10 mmHg) during inspiration. Why? During inspiration, ↑venous return to right heart → the septum bulges leftward within the fixed pericardial space (ventricular interdependence) → ↓LV filling → ↓LV stroke volume → ↓systolic BP |
| Tachycardia | Compensatory — to maintain CO in the face of ↓SV (CO = SV × HR) |
| Haemodynamic collapse [2] | End-stage: obstructive shock with cardiovascular collapse |
If pericarditis progresses to constriction (chronic scarring), look for [2]:
- Pericardial knock: early diastolic sound, follows S2 — caused by sudden cessation of ventricular diastolic filling as ventricles slap against the rigid pericardium [2]
- Kussmaul sign (13–21%): paradoxical ↑JVP during inspiration [2] — normally JVP falls with inspiration; in constriction, the rigid pericardium prevents the right heart from expanding to accommodate ↑venous return → pressure rises
- ↑JVP with prominent x and y descents [2]
- Hepatomegaly, ascites, peripheral oedema (right heart failure from impaired RV filling)
- Pulsus paradoxus ( < 20%) — less obvious compared to cardiac tamponade as negative intrathoracic pressure during inspiration is less readily transmitted to the pericardium (due to the rigid pericardial shell) [2]
- Malar rash, oral ulcers → SLE
- Joint deformities → RA
- Lymphadenopathy, cachexia → Malignancy
- Uraemic fetor, asterixis → CKD/Uraemia
| Feature | Acute Pericarditis | Pericardial Effusion | Cardiac Tamponade | Constrictive Pericarditis |
|---|---|---|---|---|
| Pain | Sharp, pleuritic, positional | Dull, constant ache [2] | Absent (often painless) | Absent |
| Friction rub | Present (pathognomonic) | ↓ or absent | Absent | Absent |
| Heart sounds | Normal or rub | Muffled | Muffled | Pericardial knock |
| JVP | Normal or mildly ↑ | ↑ | Markedly ↑ | ↑ with prominent y descent, Kussmaul sign |
| Pulsus paradoxus | Absent | Absent | Present | May be present ( < 20%) |
| Key investigation | ECG | Echo | Echo + urgent pericardiocentesis | Echo/CT/MRI + catheterization |
This is extremely high-yield for exams. The ECG changes in pericarditis are the result of superficial myocardial inflammation (epicarditis) affecting the electrical activity.
ECG: Diffuse ST elevation concaving upwards. Max in V5–V6, II > I/III/aVF. Reciprocal ↓ST in aVR, V1. PR depression in some leads (specific). T wave flattening or inversion (late, after ↑ST resolved) — ST/T changes never occur together [2][7].
| Stage | Timing | ECG Finding | Pathophysiology |
|---|---|---|---|
| Stage 1 | Hours to days | Diffuse concave-up ("saddle-shaped") ST elevation + PR depression + Spodick's sign (downsloping TP segment) [7] | Epicardial inflammation creates an "injury current" → ST elevation. PR depression results from atrial inflammation (atrial injury current is directed opposite to ventricular injury current) |
| Stage 2 | Days to 1 week | ST segments normalize, T waves flatten | Resolution of acute inflammation; transition phase |
| Stage 3 | 1–3 weeks | Diffuse T-wave inversion | Post-inflammatory repolarization abnormality. This occurs after ST returns to baseline (ST/T changes never occur together [2]) |
| Stage 4 | Weeks to months | ECG normalizes (or T-wave inversion may persist) | Recovery |
Key ECG Distinctions: Pericarditis vs. STEMI
| Feature | Pericarditis | STEMI |
|---|---|---|
| ST elevation | Diffuse, concave-up ("smiley face"), widespread leads | Localized to coronary territory, convex-up ("frowning") |
| Reciprocal ST depression | Only in aVR and V1 | Present in reciprocal leads (e.g. inferior ↔ lateral) |
| PR segment | PR depression (specific for pericarditis) [2] | Usually normal or isoelectric |
| Q waves | Absent | Often present (pathological Q waves = necrosis) |
| T-wave inversion | Occurs after ST normalizes | Can occur simultaneously with ST elevation |
| Evolution | Global, all stages happen together across leads | Territorial, evolves in affected leads |
| Spodick's sign | Present (downsloping TP segment) [7] | Absent |
High Yield – ECG Differentiation
The two most specific ECG features of pericarditis (vs. STEMI) are: (1) PR depression and (2) Diffuse concave-up ST elevation without reciprocal changes (except aVR/V1). The presence of PR depression strongly favours pericarditis. In STEMI, you see territorial ST changes with reciprocal depression and Q waves.
Pericarditis often occurs together with myocarditis [2]. This is because many causes (especially viral) affect both the pericardium and the adjacent myocardium.
- Myopericarditis: Primarily pericarditis with minor myocardial involvement (elevated troponin but no wall motion abnormalities)
- Perimyocarditis: Primarily myocarditis with pericardial involvement (wall motion abnormalities present)
- Myocarditis per se is usually asymptomatic and chest pain usually reflects concomitant pericarditis [4]
- DON'T give NSAIDs in isolated myocarditis (↓prostaglandin production → may worsen myocardial function + ↑myocardial necrosis) [4] — but NSAIDs ARE the mainstay of treatment for pericarditis
Why NSAIDs are OK in Pericarditis but NOT in Myocarditis
In pericarditis, the inflammation is primarily on the pericardial surface — NSAIDs reduce this inflammation and pain effectively. In myocarditis, the inflammation is within the myocardium itself — NSAIDs inhibit prostaglandin synthesis, and prostaglandins actually have some protective effects on injured myocytes (limiting necrosis). NSAIDs may also impair myocardial healing and have been shown in animal models to worsen myocardial damage. Therefore: NSAIDs for pericarditis ✓, NSAIDs for isolated myocarditis ✗.
11. Special Considerations: Pericarditis in Specific Diseases
- Pericarditis occurs as part of pancarditis (affects all three layers: endocardium, myocardium, pericardium) [10]
- Characteristically, rheumatic heart disease is the only disease that affects all three layers of the heart [10]
- Usually children 5–15 years old, preceded by GAS pharyngitis 2–3 weeks before
- Pericarditis associated with pericardial effusion is a recognized complication [11]
- Part of the spectrum of pancarditis (pericarditis, myocarditis, endocarditis) in acute KD
- Uraemic pericarditis: Occurs in underdialysed or predialysis patients with advanced CKD
- Management: Intensification of dialysis (not NSAIDs) — because the cause is uraemic toxin accumulation, not a prostaglandin-driven process [9]
From the GC lecture slides, pericarditis appears in several symptom frameworks:
- Chest discomfort — cardiovascular causes include: MI, angina, pericarditis, aortic dissection [3]
- Oedema — cardiovascular causes include: heart failure, constrictive pericarditis [3]
- Why does constrictive pericarditis cause oedema? The rigid pericardium impairs RV filling → ↑systemic venous pressure → ↑hydrostatic pressure in capillary beds → fluid transudation into interstitial space → oedema
- Pericardial effusion is a non-myocardial cause of heart failure [12]
- Constrictive pericarditis is a cause of diastolic dysfunction / HFpEF — impaired ventricular relaxation/filling due to rigid external casing [12]
- Constrictive pericarditis (along with MS/TR) is a cause of cardiac cirrhosis (congestive hepatopathy) [13] — chronic ↑RA pressure → chronic hepatic congestion → centrilobular necrosis → fibrosis → cirrhosis
High Yield Summary
Definition: Inflammation of the pericardium — can be acute, recurrent, or chronic. Often coexists with myocarditis.
Anatomy: Pericardium = fibrous (outer) + parietal (serous) + pericardial cavity (15–50 mL ultrafiltrate) + visceral (epicardium). Parietal pericardium is innervated by phrenic nerve (C3–C5) → explains trapezius ridge radiation.
Epidemiology: 27.7/100k/year; 5% of non-ischaemic chest pain; M > F; young adults.
Etiology: Idiopathic/viral ( > 80%) > malignancy ( < 10%) > infection ( < 5%). In HK: always consider TB. Other causes: autoimmune (SLE, RA), metabolic (uraemia, hypothyroidism), post-MI (early: inflammatory; late: Dressler's), iatrogenic, drug-induced.
Key Clinical Features:
- Chest pain: Sharp, pleuritic, retrosternal → trapezius ridge. ↑inspiration/movement, ↓sitting forward. NSAIDs help.
- Pericardial friction rub: Triphasic (atrial systole, ventricular systole, early diastole). Pathognomonic. Best heard at left sternal border, patient sitting forward.
- Low-grade fever; flu-like prodrome in viral cases.
- ECG: Diffuse concave-up ST elevation + PR depression (most specific features). No reciprocal changes except aVR/V1. T-wave inversion occurs AFTER ST normalizes.
Effusion → Tamponade: Rapid accumulation → tamponade (Beck's triad: hypotension, ↑JVP, muffled HS). Pulsus paradoxus present.
Constriction: Chronic scarring → pericardial knock, Kussmaul sign, ↑JVP. TB is the most common cause in HK.
Post-MI pericarditis: Use aspirin, NOT NSAIDs/steroids (risk of ventricular aneurysm).
Uraemic pericarditis: Treat with intensified dialysis, not NSAIDs.
NSAIDs: OK in pericarditis, CONTRAINDICATED in isolated myocarditis.
Active Recall - Pericarditis (Definition, Etiology, Clinical Features)
[1] Senior notes: MBBS Final MB (Medicine) (Felix PY Lai).pdf — Cardiovascular Diseases, Pericarditis section (p. 427–429) [2] Senior notes: Ryan Ho Cardiology.pdf — Section 3.5 Diseases of Pericardium (p. 172–174) [3] Lecture slides: CFB (MED05) Cardiovascular (I) Physical Examination (History Taking).pdf — Chest Pain table (p. 15) and Cardiac Symptoms table (p. 9) [4] Senior notes: Ryan Ho Cardiology.pdf — Myocarditis section (p. 165) [5] Lecture slides: GC 088. Sudden Severe Chest Pain.pdf — Differential diagnosis (p. 13) [6] Lecture slides: GC 046. Facial rash and painful fingers_SLE.pdf — SLE Cardiac features (p. 36) [7] Senior notes: Maksim Medicine Notes.pdf — Section 1.9 Pericardial disease (p. 38) [8] Senior notes: Ryan Ho Rheumatology.pdf — RA cardiac involvement (p. 49), MCTD cardiac features (p. 86), SLE (p. 69) [9] Senior notes: Ryan Ho Urogenital.pdf — Uraemic pericarditis / Uraemic complications (p. 109) [10] Senior notes: Adrian Lui Pediatrics Notes.pdf — Acute Rheumatic Fever (p. 235) [11] Senior notes: MBBS Final MB (Pediatrics) (Felix PY Lai).pdf — Kawasaki Disease complications (p. 302) [12] Senior notes: Ryan Ho Fundamentals.pdf — Heart Failure etiology (p. 215) [13] Senior notes: MBBS Final MB (Surgery) (Felix PY Lai).pdf — Liver cirrhosis, Cardiac cirrhosis (p. 442)
Differential Diagnosis of Pericarditis
The approach to differential diagnosis here works on two levels simultaneously:
- When a patient presents with chest pain → Is this pericarditis, or one of the other life-threatening/important mimics?
- When pericarditis is confirmed → What is the underlying etiology causing the pericarditis?
We will address both systematically.
A. Differential Diagnosis of Acute Chest Pain (Is This Pericarditis?)
This is the more common exam scenario: a patient walks in with chest pain, and you need to work through the differential. The key is to identify and exclude life-threatening causes first before settling on pericarditis.
GC High Yield – Differential Diagnosis of Sudden Severe Chest Pain
From GC 088 lecture slides [5]:
1. Acute pericarditis — aggravated by respiratory movement, sharp, knife-like. Radiates to the trapezius ridge (characteristic site of pericardial pain)
2. Pulmonary embolism — hemoptysis
3. Aortic dissection — radiation to back, ripping or tearing sensation
These three conditions are the key differential diagnoses for sudden severe chest pain that you must distinguish.
The full differential of chest pain is best organized by system [2][7][14]:
| Condition | Key Distinguishing Features | Why You Cannot Miss It |
|---|---|---|
| Acute coronary syndrome (ACS / MI) | Central, tight or heavy sensation, radiates to jaw or left arm [1]. Crushing, constricting. NOT positional. NOT pleuritic. ECG: territorial ST elevation (convex up) with reciprocal depression and Q waves | Immediate reperfusion needed; delay = myocardial death |
| Aortic dissection | Very sudden onset, radiates to the back, ripping or tearing sensation [1][5]. Interscapular. May have BP discrepancy between arms, new AR murmur, limb/mesenteric ischaemia | Surgical emergency; misdiagnosis with anticoagulation can be fatal |
| Pulmonary embolism | Pleuritic pain with hemoptysis [5]. Sudden onset SOB, tachycardia. Risk factors: DVT, immobility, malignancy, OCP. ECG: S1Q3T3 | Anticoagulation / thrombolysis needed urgently |
| Tension / massive pneumothorax | Sudden onset, unilateral, sharp. Absent breath sounds on affected side. Tracheal deviation away | Needle decompression is immediately life-saving |
| Myopericarditis ± cardiac tamponade [14] | Sharp, pleuritic pain (pericarditis component) + haemodynamic compromise (tamponade) + elevated troponin (myocarditis) | Tamponade requires emergency pericardiocentesis |
Pericarditis is listed alongside pneumothorax, PE, acute pancreatitis, and AMI as a differential diagnosis of aortic dissection [15][16] — this tells you they occupy the same diagnostic "space" in acute chest pain presentations.
| System | Condition | Key Distinguishing Features |
|---|---|---|
| Cardiac | Stable angina | Exertional, constricting, relieved by rest and GTN within 2–10 minutes [14] |
| Pleuro-pericardial | Myocarditis | Recent flu-like syndrome accompanied by fever, arthralgia, and malaise. ECG: ventricular arrhythmias or heart block, or mimic AMI or pericarditis [4]. Troponin elevated. AVOID NSAIDs (contrast with pericarditis) |
| Pleuro-pericardial | Pleurisy / Pneumonia | Pleuritic pain, fever and SOB [1]. Productive cough. CXR: consolidation |
| GI | GERD | Unrelated to exertion, worsen when lies down, relieved by swallowing (warm water) [1]. Retrosternal burning. May respond to nitrates (mimics angina) |
| GI | Oesophageal spasm | Can mimic MI — retrosternal, may be relieved by nitrates. Distinguished by relation to swallowing, warm water relief |
| GI | Acute pancreatitis | Epigastric pain radiating to back, worse after meals, ↑amylase/lipase |
| Chest wall | Muscle strains | Worsen with movement [1]. Localized tenderness. Often preceded by trauma or exertion |
| Chest wall | Thoracic zoster | Thoracic nerve root distribution, precedes typical vesicular rash of herpes zoster [1] |
| Chest wall | Rib fracture / Rib tumour | Localized tenderness [1] |
| Mediastinal | Mediastinitis / Lymphoma | Central pain, systemic features |
| Psychiatric | Panic attacks [1][14] | Anxiety, hyperventilation, perioral tingling, young patient, no objective findings |
This table is derived directly from the CFB (MED05) lecture slide [3] and is extremely high-yield for exams:
| Feature | Pericardial Pain | Angina | MI | Aortic Dissection | Oesophageal Pain |
|---|---|---|---|---|---|
| Site | Retrosternal or left-sided | Retrosternal | Retrosternal | Interscapular / retrosternal | Retrosternal or epigastric |
| Onset | Gradual; postural change may suddenly aggravate | Progressive ↑ over 1–2 min | Rapid over a few min | Very sudden | Over 1–2 min; can be sudden |
| Character | Sharp, "stabbing", pleuritic | Constricting, heavy | Constricting, heavy | Tearing or ripping | Gripping, tight or burning |
| Radiation | Left shoulder or back | Sometimes arm(s), neck | Often to arm(s), neck, jaw | Back, between shoulders | Often to back |
| Associated | Flu-like prodrome, breathlessness, fever | Breathlessness | Sweating, nausea, vomiting, angor animi | Sweating, syncope, neurological signs | Heartburn, acid reflux |
| Timing | Acute presentation; variable duration | Intermittent, 2–10 min episodes | Acute, prolonged | Acute, prolonged | Intermittent, variable |
| Exacerbating / Relieving | Sitting up/lying down may affect intensity. NSAIDs help | Triggered by exertion. Relieved by rest, GTN | Not relieved by rest or GTN | Spontaneous. No manoeuvres relieve | Lying flat may trigger. Nitrates sometimes relieve |
| Severity | Can be severe | Mild to moderate | Usually severe | Very severe | Usually mild (spasm can mimic MI) |
This is one of the most commonly tested differentials in exams because both cause ST elevation. The distinction is critical because the management is opposite — pericarditis gets NSAIDs while STEMI gets anticoagulation/reperfusion, and giving the wrong treatment can be catastrophic.
Note that STEMI is NOT the only cause of ST elevation [2]:
| Cause of ST Elevation | Key ECG Distinguishing Features |
|---|---|
| Acute STEMI | Localized, convex ↑ST, usually III > II, associated with Q waves [2] |
| Acute pericarditis | Transient PR depression ( > 0.5–0.8 mm), diffuse concave ↑ST (max in V5–V6, II > I/III/aVF, never in aVR), J/T > 25% in V6, shorter QTc [2] |
| LVH with strain pattern | Usually concave up and especially in V1–V3, associated with other LVH features [2] |
| Early repolarization ("high takeoff") | J point elevation immediately follows S wave, concave ↑ST (highest at V2–V3 up to 3 mm, rarely > 0.5 mm at V5–V6, rarely > 2 mm if age > 45y, drops with tachycardia), no reciprocal ↓ST [2] |
| LBBB | Can be distinguished using Sgarbossa criteria [2] |
| Ventricular aneurysm | Usually ≤ 3 mm at V1–V3, may have QS pattern, T wave flat or inverted. Confirm by cTn negative and echo positive [2] |
| SAH (or ↑ICP) | Due to cardiac stunning from adrenaline surge [2] |
High Yield – ECG DDx of ST Elevation
The DDx of ST elevation [2][7] is:
- STEMI — convex, territorial, reciprocal changes, Q waves
- Acute pericarditis — diffuse concave ST elevation + PR depression [7]
- LVH with strain pattern
- Early repolarization
- LBBB (use Sgarbossa criteria)
- Ventricular aneurysm
- SAH / ↑ICP
This list is directly from the Ryan Ho Cardiology notes and Maksim notes and is extremely commonly tested.
Once you've established that the clinical picture is pericarditis (rather than ACS, PE, etc.), the next step is to determine the etiology. Most cases ( > 80%) are idiopathic/viral and self-limiting, but you must identify the minority with a treatable or dangerous underlying cause.
The key etiological differentials to consider [1][7]:
| Category | Specific Diagnosis | Key Clues to Distinguish |
|---|---|---|
| Idiopathic / Viral | Idiopathic ( > 80%), Coxsackie, Echo, Adeno, EBV, CMV, HIV | Young patient, viral prodrome, self-limiting, no red flags |
| TB | TB pericarditis | Endemic area (HK relevant), subacute, weight loss, night sweats, haemorrhagic effusion, positive IGRA |
| Bacterial (purulent) | Staph, Strep, Meningococcus | High fever, septic, purulent effusion, rapid deterioration |
| Autoimmune | SLE: pericarditis, cardiomyopathy, pulmonary hypertension, Libman-Sacks endocarditis [6] | Malar rash, oral ulcers, arthritis, positive ANA/anti-dsDNA, young female |
| Autoimmune | RA | Known RA, joint deformities, positive RF/ACPA |
| Autoimmune | Diffuse SSc — cardiac involvement more severe including pericarditis, arrhythmia [17] | Skin thickening, Raynaud, sclerodactyly, anti-Scl70 |
| Autoimmune | MCTD — cardiac involvement in ~20% including pericarditis [8] | Mixed features of SLE + SSc + PM, anti-U1 RNP |
| Metabolic | Uraemic pericarditis | Known CKD/ESRD, uraemic symptoms, elevated urea/creatinine |
| Metabolic | Hypothyroidism (myxoedema) | Slow accumulating effusion, weight gain, cold intolerance, elevated TSH |
| Malignancy | Lung, breast, lymphoma, leukaemia | Weight loss, constitutional symptoms, haemorrhagic effusion, malignant cytology |
| Post-MI | Early (2–4d) vs Dressler's (weeks–months) | Temporal relationship to recent MI; Dressler's: fever + pleuritic pain + effusion |
| Drug-induced | Procainamide, hydralazine, isoniazid, doxorubicin | Temporal relationship to drug initiation |
| Iatrogenic | Post-pericardiotomy, post-PCI, post-pacemaker | Recent cardiac procedure |
These two conditions commonly coexist but have different management implications, making their differentiation essential.
| Feature | Pericarditis | Myocarditis | Myopericarditis |
|---|---|---|---|
| Pain | Sharp, pleuritic, positional | Usually absent or dull (chest pain usually reflects concomitant pericarditis [4]) | Sharp, pleuritic (from pericarditis component) |
| Friction rub | Present | Absent | May be present |
| Troponin | May be mildly elevated (32% of viral/idiopathic) [1] | Elevated | Elevated |
| ECG | Diffuse ST elevation + PR depression | Ventricular arrhythmias or heart block, or mimic AMI or pericarditis [4] | Pericarditis pattern |
| Echo | ± Effusion, normal LV function | Regional/global LV dysfunction, wall motion abnormalities | ± Effusion, normal or mildly ↓ LV function |
| MRI | Pericardial enhancement | Myocardial oedema, early enhancement, late gadolinium enhancement | Both pericardial and myocardial involvement |
| Key Mx difference | NSAIDs + colchicine | AVOID NSAIDs (↓PG → may worsen myocardial function + ↑myocardial necrosis) [4] | Treat as pericarditis if no significant LV dysfunction |
| Biopsy | Not typically needed | Endomyocardial biopsy: gold standard but carries perforation risk (1%) [4] | Not typically needed |
Critical Management Distinction
NSAIDs are the mainstay of pericarditis treatment but are CONTRAINDICATED in isolated myocarditis [4]. This is because prostaglandins have protective effects on injured myocytes, and blocking them with NSAIDs worsens myocardial damage. If both are present (myopericarditis) with preserved LV function, treat as pericarditis. If LV function is significantly impaired (perimyocarditis), treat as myocarditis — avoid NSAIDs and manage heart failure.
This is a classic exam differential because both present with diastolic heart failure and elevated JVP. The distinction is critical because constrictive pericarditis is surgically curable (pericardiectomy) while restrictive cardiomyopathy is not.
Major d/dx of RCMP = constrictive pericarditis → similar clinical and haemodynamic features [2]:
| Feature | Restrictive Cardiomyopathy | Constrictive Pericarditis |
|---|---|---|
| History | Hx of infiltrative disease [2] (amyloidosis, sarcoidosis, haemochromatosis) | Hx of pericarditis [2] (TB, radiation, cardiac surgery) |
| Auscultation | Audible S3 [2] | Pericardial knock (slightly before S3) [2] |
| ECG | BBB, L/RVH, pathological Q wave, AV blocks [2] | Low voltage, isolated repolarization abnormalities [2] |
| CXR | Normal heart size or mild cardiomegaly | Calcified pericardium [2] (strongly suggestive) |
| BNP | ↑BNP due to myocardial stretching [2] | Normal or mildly elevated |
| Echo | Ventricular wall thickening, abnormal echotexture [2] | ↑thickness of pericardium [2] |
| Definitive Dx | Endomyocardial biopsy [2] | Pericardial biopsy [2] |
| Kussmaul sign | Present | Present |
| Treatment | Medical (treat underlying cause) | Pericardiectomy in late disease [2] |
| Feature | Pericarditis | ACS/MI | Aortic Dissection | PE | Pneumothorax |
|---|---|---|---|---|---|
| Pain quality | Sharp, pleuritic | Heavy, crushing | Tearing, ripping | Sharp, pleuritic | Sharp, unilateral |
| Radiation | Trapezius ridge | Jaw, left arm | Between shoulder blades | None specific | None |
| Positional | ↓sitting forward | No | No | No | No |
| Pleuritic | Yes | No | No | Yes | Yes |
| NSAIDs | Help | Don't help | Don't help | Don't help | Don't help |
| GTN | Doesn't help | Helps (angina) / Doesn't (MI) | Doesn't help | Doesn't help | Doesn't help |
| ECG | Diffuse concave ST↑, PR↓ | Territorial convex ST↑, Q waves | Often normal or LVH | S1Q3T3, RV strain | Normal |
| Key Ix | Echo | Troponin, coronary angiography | CTA aorta | CTPA, D-dimer | CXR |
High Yield Summary — Differential Diagnosis of Pericarditis
-
Life-threatening DDx of chest pain: ACS, aortic dissection, PE, tension pneumothorax, tamponade — must be excluded first.
-
Pericarditis vs. STEMI (ECG): Pericarditis = diffuse concave-up ST elevation + PR depression, no territorial reciprocal changes. STEMI = territorial convex-up ST elevation + reciprocal depression + Q waves.
-
Pericarditis vs. Myocarditis: NSAIDs are the mainstay for pericarditis but CONTRAINDICATED in myocarditis. Troponin elevation with wall motion abnormalities = myocarditis. Troponin elevation without = myopericarditis (treat as pericarditis).
-
Constrictive pericarditis vs. RCMP: Constriction has pericardial knock, calcification on CXR, low voltage ECG, history of pericarditis, and is surgically curable. RCMP has S3, BBB/AV block on ECG, infiltrative history, ↑BNP, and requires biopsy.
-
Etiological DDx of pericarditis: Idiopathic/viral ( > 80%) > malignancy > infection. In HK always consider TB. Red flags (high fever, large effusion, tamponade, immunosuppression, NSAID failure) warrant further investigation.
Active Recall - Differential Diagnosis of Pericarditis
References
[1] Senior notes: MBBS Final MB (Medicine) (Felix PY Lai).pdf — Pericarditis (p. 427–429) and Differential diagnosis of chest pain (p. 399) [2] Senior notes: Ryan Ho Cardiology.pdf — Diseases of Pericardium (p. 172–174), ST segment and DDx of ST elevation (p. 36, 129), Chest Pain (p. 54–58), RCMP vs Constrictive Pericarditis (p. 170) [3] Lecture slides: CFB (MED05) Cardiovascular (I) Physical Examination (History Taking).pdf — Chest Pain SOCRATES table (p. 15), Cardiac Symptoms table (p. 9) [4] Lecture slides: Three Cases SOB 20211.pdf — Myocarditis: Diagnosis (p. 32) [5] Lecture slides: GC 088. Sudden Severe Chest Pain.pdf — Differential diagnosis (p. 13) [6] Lecture slides: GC 046. Facial rash and painful fingers_SLE.pdf — SLE Cardiac features (p. 36) [7] Senior notes: Maksim Medicine Notes.pdf — Pericardial disease (p. 38–40), Clinical approach to chest pain (p. 3–5), DDx of ST elevation (p. 10) [8] Senior notes: Ryan Ho Rheumatology.pdf — MCTD cardiac features (p. 86–87) [14] Senior notes: Ryan Ho Fundamentals.pdf — Approach to Acute Chest Pain (p. 203) [15] Senior notes: MBBS Final MB (Medicine) (Felix PY Lai).pdf — Aortic Dissection DDx (p. 607) [16] Senior notes: MBBS Final MB (Surgery) (Felix PY Lai).pdf — Aortic Dissection DDx (p. 906) [17] Senior notes: Maksim Medicine Notes.pdf — Scleroderma/Systemic Sclerosis (p. 318)
Diagnostic Criteria, Diagnostic Algorithm and Investigations for Pericarditis
The diagnosis of acute pericarditis is fundamentally clinical — there is no single "gold-standard" laboratory test. The most widely used criteria are from the 2015 ESC Guidelines for Pericardial Diseases (reaffirmed by the 2024 ESC update). The diagnosis requires at least 2 of 4 criteria:
High Yield – ESC Diagnostic Criteria for Acute Pericarditis (≥ 2 of 4)
- Pericarditic chest pain — Sharp, pleuritic, retrosternal pain radiating to the trapezius ridge. ↑ by inspiration, movement, postural change. ↓ by sitting up and leaning forward [2][7]
- Pericardial friction rub — High-pitched superficial scratching noise. Classically triphasic (atrial systole, ventricular systole, rapid filling phase of early diastole) [2][7]
- ECG changes — Diffuse ST elevation concaving upwards + PR depression [2][7]
- Pericardial effusion — New or worsening, detected on echocardiography
Supporting features (not required for diagnosis but strengthen it): Elevated inflammatory markers (CRP, ESR), elevated cardiac troponin (suggests myopericarditis), evidence of pericardial inflammation on CT or cardiac MRI (pericardial enhancement, thickening).
Why ≥ 2 of 4? Because no single feature is present in every case:
- The friction rub is evanescent (comes and goes) and may be absent if effusion develops
- ECG changes occur in ~60% but may be absent or atypical (especially in uraemic pericarditis)
- Pericardial effusion is NOT always present — "dry" fibrinous pericarditis has no effusion
- Therefore, requiring at least 2 features ensures adequate sensitivity while maintaining specificity
Important Nuances
| Criterion | Sensitivity | Specificity | Pitfalls |
|---|---|---|---|
| Pericarditic chest pain | Very high ( > 95%) | Moderate (pleurisy, PE, and MSK pain also pleuritic) | May be absent in uraemic or malignant pericarditis; immunosuppressed patients may have blunted symptoms |
| Pericardial friction rub | ~33% (often missed) | Very high (essentially pathognomonic) | Evanescent; may disappear when effusion develops; requires careful auscultation with patient leaning forward |
| ECG changes | ~60% | High (PR depression is most specific) | Absent in uraemic pericarditis; may be confused with STEMI or early repolarization |
| Pericardial effusion | ~60% | Low (many causes of effusion besides pericarditis) | Absent in dry/fibrinous pericarditis; isolated effusion without other features is NOT pericarditis |
Once the diagnosis of acute pericarditis is made, the next critical step is to identify patients who need hospital admission and further investigation versus those who can be managed as outpatients. This is because > 80% of cases are idiopathic/viral and self-limiting, but a minority have dangerous underlying causes.
High-risk features (any one → admit and investigate further):
| Category | Feature | Rationale |
|---|---|---|
| Major | Fever > 38°C | Suggests bacterial/purulent or TB pericarditis |
| Major | Subacute onset (symptoms over days–weeks) | Suggests TB, malignancy, or autoimmune rather than viral |
| Major | Large pericardial effusion ( > 20 mm on echo) | Risk of tamponade; suggests non-idiopathic cause |
| Major | Cardiac tamponade | Requires emergency pericardiocentesis |
| Major | Failure of NSAID therapy after ≥ 1 week [2][7] | Suggests resistant or non-viral etiology |
| Minor | Myopericarditis (elevated troponin) | Indicates myocardial involvement |
| Minor | Immunosuppression | Higher risk of opportunistic infections (TB, fungal) |
| Minor | Anticoagulant therapy | Risk of haemorrhagic effusion/tamponade |
| Minor | Acute trauma | Consider haemopericardium |
D. Investigation Modalities — Detailed Interpretation
D1. Electrocardiography (ECG) — The First-Line Investigation
The ECG is performed stat in any patient with chest pain and is the single most useful initial investigation for pericarditis. Understanding the ECG findings from first principles is essential.
Why does pericarditis cause ECG changes? The visceral pericardium (epicardium) sits directly on the myocardial surface. Inflammation of the epicardium causes superficial myocardial injury ("epicarditis"), which produces a current of injury detectable on the ECG. Because the pericardium wraps around the entire heart, the changes are diffuse (all leads), unlike STEMI where changes are territorial (only leads facing the infarcted segment).
| Stage | Timing | ECG Findings | Pathophysiology |
|---|---|---|---|
| Stage 1 (most diagnostic) | Hours–days | Diffuse concave-up ST elevation (max V5–V6, II > I/III/aVF). Reciprocal ↓ST in aVR, V1. PR depression in some leads (specific). Spodick's sign (downsloping TP segment) [2][7] | Epicardial inflammation → diffuse epicardial injury current. PR depression from atrial epicardial inflammation (atrial injury vector opposite to ventricular) |
| Stage 2 | Days–1 week | ST segments normalize, T waves flatten | Acute inflammation subsiding |
| Stage 3 | 1–3 weeks | T wave flattening or inversion (late, after ↑ST resolved) [2] — ST/T changes never occur together [2] | Post-inflammatory repolarization abnormality |
| Stage 4 | Weeks–months | ECG normalizes (or T inversion may persist) | Full recovery |
| Finding | Mechanism |
|---|---|
| Low QRS voltage (limb leads < 5 mm, precordial leads < 10 mm) [7] | Pericardial fluid acts as an electrical insulator, attenuating the QRS signal reaching the body surface |
| Electrical alternans (alternating QRS axis) [2][7] | Constantly changing electrical axis as the heart swings from side to side within large pericardial volume [2] — this is nearly pathognomonic for large pericardial effusion |
| Tachycardia [7] | Compensatory — ↓SV from effusion → reflex ↑HR to maintain CO |
| Finding | Mechanism |
|---|---|
| Non-specific ST/T changes, low voltage, AF [2] | Thickened pericardium attenuates signals (low voltage); chronic atrial stretching/fibrosis → AF |
ECG in shock evaluation: ECG: arrhythmia, ST changes (ischaemia, pericarditis), low-voltage (pericardial effusion), S1Q3T3/RV strain (PE) [19] — this is the systematic approach to ECG interpretation in the acute setting.
D2. Blood Tests
| Test | Expected Finding | Why? |
|---|---|---|
| CRP / ESR | ↑ ESR and CRP [1][7] | Systemic inflammatory response. CRP is more useful than ESR for monitoring because it rises and falls more quickly. CRP is also used to guide treatment duration — treatment is continued until CRP normalizes |
| White cell count | Variable | Leukocytosis with neutrophilia → bacterial. Lymphocytosis → viral. Leukopenia → SLE |
| Test | Expected Finding | Significance |
|---|---|---|
| Cardiac troponin (cTn) | Elevated in ~32% of idiopathic/viral pericarditis [1] | Indicates inflammatory damage of subepicardial myocardium close to the visceral pericardium (myopericarditis) or myocarditis with pericardial involvement (perimyocarditis) [1]. Does NOT necessarily indicate ACS — must correlate with clinical picture and ECG pattern |
| CK-MB [7] | May be mildly elevated | Less specific than troponin; also rises with skeletal muscle injury |
Troponin in Pericarditis — Don't Panic
Cardiac troponin levels may be elevated in 32% of patients with idiopathic or viral pericarditis [1]. This does NOT mean they are having an MI. The elevation reflects subepicardial myocardial inflammation (the epicardium is the visceral pericardium, so inflammation easily extends a few millimetres into the underlying myocardium). If the troponin is elevated but the clinical picture is classic pericarditis (diffuse ST elevation, PR depression, no territorial changes, pleuritic positional pain), the diagnosis is myopericarditis, not ACS. However, if there is significant LV wall motion abnormality on echo, this tips toward perimyocarditis/myocarditis, which changes management (avoid NSAIDs).
DDx of elevated troponin: any ischaemic damage (e.g. tachyarrhythmia, HF), myocarditis, pericarditis, Takotsubo cardiomyopathy, CKD (renally excreted) [7].
| Test | What It Screens For | When to Order |
|---|---|---|
| CBC with differential count [7] | Leukocytosis (bacterial), lymphocytosis (viral), leukopenia (SLE), eosinophilia (eosinophilic/parasitic), thrombocytopenia (SLE) | All patients |
| RFT (urea, creatinine) | Uraemic pericarditis (GFR < 15, elevated urea) | All patients |
| TFT | Hypothyroidism (myxoedema pericardial effusion) | If hypothyroidism suspected |
| ANA [1][7] | SLE, drug-induced lupus | If autoimmune features present |
| Anti-dsDNA | SLE (more specific than ANA) | If ANA positive |
| RF [7] | RA | If arthritis features present |
| IGRA (QuantiFERON TB) or tuberculin skin test [1][7] | TB pericarditis | Useful in patients who are immunocompromised or HIV positive and in regions where TB is endemic [1] — always consider in Hong Kong |
| HIV serology | HIV-associated pericarditis, immunosuppression | All patients with unclear etiology (per guidelines) |
| Blood cultures | Bacterial/purulent pericarditis | If high fever, septic features |
Important — Viral Serology NOT Recommended Routinely
Routine viral studies such as serology, culture or PCR is NOT recommended except HIV serology since the yield is low and the management is NOT altered for the vast majority of patients [1].
Why? Because (1) most viral pericarditis resolves with the same anti-inflammatory treatment regardless of the specific virus, (2) the yield is low (virus often cleared by the time of presentation), and (3) it adds cost without changing management. The only exception is HIV — because HIV status changes the differential (opportunistic infections, need for ART).
The CXR is part of the baseline workup for any patient with chest pain, but its findings in pericarditis vary depending on whether effusion is present.
| Scenario | CXR Findings | Interpretation |
|---|---|---|
| Acute pericarditis without effusion | Often normal | A normal CXR does NOT exclude pericarditis |
| Pericardial effusion ( > 250 mL) | Globular-shaped heart / water bottle appearance [7]. Clear lung fields (cf. CHF) [7]. Oreo-cookie sign on lateral film [7] | The key distinction from CHF: in pericardial effusion the lung fields are clear (no pulmonary congestion), whereas in CHF you see upper lobe diversion, Kerley B lines, pleural effusions |
| Constrictive pericarditis | Pericardial calcification (strongly suggestive) [2] | Calcification is best seen on lateral CXR or CT. Not always present — absence does not exclude constriction |
Why is the heart "globular" in effusion? The pericardial sac is a roughly flask-shaped structure. When fluid accumulates uniformly, it expands the sac symmetrically in all directions, producing a rounded/globular silhouette rather than the normal asymmetric cardiac shadow with distinct chamber borders.
Echocardiography is essential in all patients with suspected pericarditis. It is the most important imaging tool because it can:
- Detect and quantify pericardial effusion
- Assess for tamponade physiology
- Evaluate LV function (to differentiate myopericarditis from perimyocarditis)
- Detect pericardial thickening (constrictive pericarditis)
- Guide pericardiocentesis
GC High Yield — Echocardiography in Suspected Heart Failure
Echocardiography for suspected acute and chronic HF can detect pericardial disease including constrictive pericarditis and pericardial effusion, as well as valvular heart diseases, congenital heart diseases, and myocardial disorders including HFrEF and HFpEF [20].
| Finding | What It Means | Pathophysiology |
|---|---|---|
| Echo-free space around heart | Pericardial effusion | Fluid accumulation between visceral and parietal pericardium |
| Size grading: small ( < 10 mm), moderate (10–20 mm), large ( > 20 mm) | Guides management decisions | Large effusion ( > 20 mm) is a high-risk feature |
| Chamber collapse — RA most prone [7] | Early sign of tamponade | RA has the lowest intracavitary pressure → first to collapse when intrapericardial pressure rises |
| Distended IVC [7] | Elevated RA pressure (tamponade or constriction) | Fluid cannot drain into the compressed RA → backs up into IVC |
| Respiratory variation in mitral/tricuspid inflow velocities ( > 25%/40%) | Tamponade physiology | Ventricular interdependence → respiratory variation in filling |
| Thickened, bright pericardium with abrupt termination of ventricular filling [2] | Constrictive pericarditis | Fibrosed, rigid pericardium prevents further diastolic filling → the "septal bounce" pattern |
| Normal LV systolic function | Confirms pericarditis rather than myocarditis | Myocarditis causes ↓LVEF and wall motion abnormalities |
| Regional/global LV dysfunction, RWMA, ↓LVEF [4] | Suggests myocarditis ± pericarditis (perimyocarditis) | Myocardial inflammation impairs contractility |
D5. Pericardiocentesis and Pericardial Fluid Analysis
Pericardiocentesis: usually reserved for large effusions or tamponade [2].
Image-guided insertion of needle medial to cardiac apex or below xiphoid directed upward towards left shoulder [2]
Why the subxiphoid approach? The subxiphoid (subcostal) approach avoids the lungs and internal mammary arteries. The needle is directed toward the left shoulder, which aligns it with the long axis of the heart and the area of maximal fluid accumulation.
When NOT to Perform Pericardiocentesis
NOT done when cardiac rupture or aortic dissection → do emergency surgery instead (because it may precipitate ↑bleeding) [2]. Removing the tamponading blood removes the only thing containing the haemorrhage — the patient may exsanguinate.
Diagnostic pericardiocentesis: order Gram stain, C/ST, AFB + TB culture, PCR, cytology ± biopsy for histology [7]
| Test | What It Detects | Key Interpretations |
|---|---|---|
| Appearance | Gross assessment | Straw-coloured (viral/idiopathic), bloody/haemorrhagic (TB, malignancy, trauma), purulent (bacterial) |
| Cell count and differential | Type of inflammation | Neutrophils → bacterial; Lymphocytes → TB, viral, autoimmune |
| Gram stain | Bacteria | Quick bedside test; low sensitivity |
| Culture and sensitivity | Bacterial pathogen + antibiotic susceptibility | Takes days; essential for purulent pericarditis |
| AFB stain + TB culture [7] | Mycobacterium tuberculosis | Culture is the gold standard but takes weeks; PCR gives faster result |
| TB PCR | Rapid TB detection | Higher sensitivity than smear; result in hours |
| Adenosine deaminase (ADA) | TB pericarditis | ADA > 40 U/L is highly suggestive of TB in the appropriate clinical context |
| Cytology [7] | Malignant cells | Sensitivity ~60–90%; multiple samples increase yield |
| Protein, LDH, glucose | Exudate vs transudate (Light's criteria) | Exudate: high protein ( > 30 g/L), high LDH ( > 200 IU/L), low glucose. Transudate: low protein, low LDH |
| Pericardial biopsy | Histological diagnosis | For TB granulomas, malignancy, or other specific pathology; higher sensitivity than fluid cytology alone for malignancy |
Cardiac MRI is the most comprehensive non-invasive imaging modality for pericardial disease. It provides anatomical AND functional information.
| Finding | What It Means | When to Use |
|---|---|---|
| Pericardial thickening ( > 4 mm) | Inflammation or constriction | When constrictive pericarditis is suspected but echo is non-diagnostic |
| Pericardial enhancement with gadolinium | Active pericardial inflammation | Helps confirm diagnosis when clinical criteria are borderline |
| Late gadolinium enhancement (LGE) of myocardium | Myocardial involvement (myopericarditis) | When troponin is elevated — LGE consistent with necrosis or scar [1][21] |
| T1/T2 mapping — increased signal | Increase in T1 and T2 signal intensity consistent with inflammatory oedema [1][21] | Myocarditis/myopericarditis assessment (Lake Louise criteria) |
| Effusion quantification | More accurate than echo for loculated effusions | Complex or loculated effusions not well characterized by echo |
| Septal bounce | Constrictive pericarditis — ventricular interdependence | Dynamic assessment during real-time cine imaging |
Cardiac MRI — When Is It Indicated?
CMR is NOT needed for every case of acute pericarditis. It is indicated when:
- Diagnosis is uncertain (borderline clinical criteria)
- Myocardial involvement is suspected (elevated troponin) — to differentiate myopericarditis from perimyocarditis
- Constrictive pericarditis is suspected but echo is non-diagnostic
- Assessment of pericardial thickness and activity of inflammation
| Finding | What It Means |
|---|---|
| Pericardial calcification | Strongly suggestive of constrictive pericarditis [2] — CT is more sensitive than CXR for detecting calcification |
| Pericardial thickening | Inflammation or constriction |
| Pericardial effusion | Can characterize density (blood vs serous vs chylous) |
CT is particularly useful for constrictive pericarditis — CT/MRI done if echo non-diagnostic, to show calcification and thickened pericardium [2].
Reserved for cases where constrictive pericarditis is suspected and non-invasive imaging is inconclusive.
Cardiac catheterization: characteristic sharp y descent in RA pressure with rapid termination [2]
| Haemodynamic Finding | What It Means | Why? |
|---|---|---|
| "Square root" sign / "dip-and-plateau" pattern | Characteristic of constriction | Rapid early diastolic filling (dip) followed by abrupt cessation (plateau) when the ventricle hits the rigid pericardium — like a ball bouncing in a box |
| Equalization of diastolic pressures | All four chambers have similar end-diastolic pressures (within 5 mmHg) | The rigid pericardium transmits pressure equally to all chambers |
| Prominent x and y descents on RA pressure tracing | Sharp y descent = rapid early diastolic filling before abrupt halt | Venous blood rushes into the RA/RV during early diastole (y descent), but filling is abruptly curtailed by the rigid pericardium |
| Discordant ventricular pressure changes with respiration | Distinguishes constriction from restriction | In constriction: when RV systolic pressure rises with inspiration, LV systolic pressure falls (ventricular interdependence within rigid sac). In restriction: concordant changes |
Constrictive vs Restrictive — Catheterization Differentiation
Functional resemblance to constrictive pericarditis. Differentiating the two is mandatory because of the potential for successful surgical treatment of constriction [22].
| Feature | Constrictive Pericarditis | Restrictive Cardiomyopathy |
|---|---|---|
| End-diastolic pressures | Equalized (within 5 mmHg) | LV > RV (usually > 5 mmHg difference) |
| Respiratory variation | Discordant (RV ↑, LV ↓ in inspiration) | Concordant (both ↑ or ↓ together) |
| RVEDP/RVSP ratio | > 1/3 | < 1/3 |
| Pulmonary artery systolic pressure | Usually < 50 mmHg | Often > 50 mmHg |
| Investigation | Acute Pericarditis | Pericardial Effusion | Cardiac Tamponade | Constrictive Pericarditis |
|---|---|---|---|---|
| ECG | Diffuse concave ↑ST + PR depression [2] | Low voltage + electrical alternans [2][7] | Sinus tachycardia + low voltage ± electrical alternans | Low voltage, non-specific ST/T changes, AF [2] |
| CXR | Often normal | Globular heart, clear lungs [7] | Globular heart | Pericardial calcification [2] |
| Echo | ± Small effusion, normal LV function | Quantify effusion, RA collapse, distended IVC [7] | Chamber collapse, respiratory variation, IVC plethora | Thickened bright pericardium, abrupt halt of filling [2] |
| Bloods | ↑CRP/ESR, ± ↑troponin [1][7] | Variable (depends on cause) | Variable | Variable |
| CT/MRI | Pericardial enhancement (if needed) | Characterize effusion | Not first-line (unstable patient) | Calcification + thickened pericardium [2] |
| Catheterization | Not needed | Not first-line | Not first-line (do pericardiocentesis) | Sharp y descent, dip-and-plateau, equalized pressures [2] |
| Pericardiocentesis | Usually not needed | Diagnostic when dx unknown; therapeutic when tamponade [2] | Emergency — life-saving | Not typically needed |
High Yield Summary — Diagnosis of Pericarditis
Diagnostic Criteria (ESC): ≥ 2 of 4: (1) Pericarditic chest pain, (2) Pericardial friction rub, (3) ECG changes (diffuse concave ↑ST + PR depression), (4) New/worsening pericardial effusion on echo.
ECG is the most important initial investigation: Stage 1 = diffuse concave-up ST elevation + PR depression (most diagnostic). Distinguish from STEMI (territorial, convex-up, reciprocal changes, Q waves). ST/T changes never occur simultaneously in pericarditis.
Echo is essential in all patients: Detect effusion, assess tamponade physiology, evaluate LV function (r/o myocarditis), detect pericardial thickening.
Blood tests: CRP/ESR (monitor treatment response), troponin (32% elevated in viral pericarditis — indicates myopericarditis, not ACS), RFT (uraemia), ANA (SLE), IGRA (TB in HK).
Viral serology NOT routinely recommended — low yield and does not change management (except HIV).
Pericardiocentesis: Reserved for tamponade (therapeutic) or unknown diagnosis with large effusion (diagnostic). Send for Gram stain, C/ST, AFB + TB culture, PCR, cytology. NOT done in cardiac rupture or aortic dissection.
Cardiac MRI: For uncertain diagnosis, suspected myocardial involvement, or suspected constriction when echo non-diagnostic.
Catheterization: For constrictive pericarditis — equalized diastolic pressures, dip-and-plateau, discordant respiratory variation. Differentiating constriction from restriction is mandatory because constriction is surgically curable.
Active Recall - Diagnostic Criteria and Investigations for Pericarditis
References
[1] Senior notes: MBBS Final MB (Medicine) (Felix PY Lai).pdf — Pericarditis, Diagnosis section (p. 427–429) [2] Senior notes: Ryan Ho Cardiology.pdf — Diseases of Pericardium (p. 172–174), ST Segment and DDx of ST elevation (p. 36, 129), RCMP vs Constrictive Pericarditis (p. 170), Peri-infarction pericarditis (p. 140) [4] Senior notes: Ryan Ho Cardiology.pdf — Myocarditis evaluation (p. 165) [5] Lecture slides: GC 088. Sudden Severe Chest Pain.pdf — Differential diagnosis (p. 13) [7] Senior notes: Maksim Medicine Notes.pdf — Pericardial disease, Investigations column (p. 38–40), Cardiac investigations overview (p. 4–6) [18] Senior notes: Ryan Ho Fundamentals.pdf — ST Segment and DDx of ST elevation (p. 457) [19] Senior notes: Ryan Ho Critical Care.pdf — Shock evaluation, early investigations (p. 17) [20] Lecture slides: GC 084. Shortness of breath on exertion.pdf — Echocardiography for Suspected HF (p. 38) [21] Senior notes: MBBS Final MB (Medicine) (Felix PY Lai).pdf — Myocarditis, Cardiac MRI features (p. 426); MBBS Final MB (Pediatrics) (Felix PY Lai).pdf — Myocarditis diagnosis (p. 294) [22] Lecture slides: GC 069. Inherited Cardiac conditions.pdf — Restrictive Cardiomyopathy, differentiating from constrictive pericarditis (p. 23)
Management of Pericarditis
The management of pericarditis follows a logical, stepwise approach that is entirely driven by three questions:
- Is there haemodynamic compromise? (i.e. tamponade → emergency drainage)
- What is the underlying etiology? (treat the cause)
- Is this a first episode or a recurrence? (escalate therapy accordingly)
B. General Principles
Reversal of underlying cause, e.g. uraemia [2] — this is the first and most important principle. Anti-inflammatory therapy treats the symptoms, but if the underlying cause is not addressed, the pericarditis will persist or recur.
Strenuous physical activity may trigger recurrence of symptoms and thus activity should be avoided until symptom resolution and normalization of biomarkers [1]
Avoid strenuous activity [2]
Why? Exercise increases heart rate and myocardial motion → increased friction between inflamed pericardial surfaces → worsens pain and inflammation → delays healing and increases recurrence risk. The ESC 2015/2024 guidelines recommend:
- Non-athletes: Restrict strenuous activity until symptoms resolve AND CRP normalizes
- Athletes: Complete restriction from competitive sport for at least 3 months (or 6 months if myopericarditis with elevated troponin or LV dysfunction)
Symptomatic active pericarditis / myocarditis is listed as a contraindication for resumption of activity / exercise in the early mobilisation guidelines [23].
Whenever NSAIDs are prescribed, always co-prescribe a proton pump inhibitor (PPI) — gastroprotective agents should be prescribed as adjuncts [1]. Why? NSAIDs inhibit COX-1 → ↓prostaglandin synthesis → ↓gastric mucosal protection → increased risk of peptic ulcer and GI bleeding.
C. First-Line Therapy: NSAIDs + Colchicine
NSAIDs ("non-steroidal anti-inflammatory drugs") work by inhibiting cyclooxygenase (COX) enzymes → ↓prostaglandin and thromboxane synthesis → ↓inflammation, pain, and fever. They are the cornerstone of pericarditis treatment because pericardial inflammation is driven largely by prostaglandin-mediated pathways.
NSAIDs choices include aspirin, ibuprofen and indomethacin [1]
| Drug | Dose | Duration | Notes |
|---|---|---|---|
| Aspirin | 750–1000 mg TDS (every 8 hours) | Taper by 250–500 mg every 1–2 weeks over 2–4 weeks | Preferred in post-MI pericarditis because it does not interfere with myocardial healing and has antiplatelet benefit |
| Ibuprofen | 600 mg TDS | Taper by 200–400 mg every 1–2 weeks over 2–4 weeks | Preferred in idiopathic/viral pericarditis — best side-effect profile among NSAIDs, fewer coronary and GI side effects |
| Indomethacin ("indo-" = within, "methacin" from methyl acetic acid) | 25–50 mg TDS | Taper similarly over weeks | Very effective anti-inflammatory but more GI side effects; avoid in elderly (↑risk of renal impairment) |
How to taper: The principle is guided by CRP normalization. Do NOT taper NSAIDs until CRP has normalized — premature tapering is the most common cause of recurrence. The approach is:
- Full-dose NSAIDs until symptoms resolve AND CRP normalizes
- Then taper every 1–2 weeks
- Only taper one drug at a time (taper NSAIDs first, then colchicine)
Contraindications to NSAIDs:
- Active peptic ulcer disease / GI bleeding
- Severe renal impairment (NSAIDs → afferent arteriole vasoconstriction → ↓GFR)
- Known NSAID allergy / aspirin-exacerbated respiratory disease
- Pregnancy (3rd trimester — risk of premature closure of ductus arteriosus)
- Concurrent anticoagulation with high bleeding risk
Colchicine (from the autumn crocus plant, Colchicum autumnale) is an anti-inflammatory agent that works by a completely different mechanism from NSAIDs:
Mechanism: Binds to tubulin → inhibits microtubule polymerization → disrupts:
- Neutrophil chemotaxis and adhesion (they can't migrate to the inflamed pericardium)
- Inflammasome (NLRP3) activation → ↓IL-1β release
- Mitotic spindle formation (at high doses, but not relevant at therapeutic doses)
The landmark COPE and ICAP trials demonstrated that adding colchicine to NSAIDs significantly reduces recurrence rates (from ~30% to ~15%) and speeds symptom resolution.
Colchicine is indicated for patients with acute idiopathic or viral pericarditis. Effective for systemic inflammatory diseases and post-cardiac injury syndrome. NOT effective for bacterial pericarditis and malignancy-related pericarditis [1]
| Parameter | Detail |
|---|---|
| Dose | 0.5 mg daily PO ( < 70 kg) or 0.5 mg BD PO ( > 70 kg) [23] |
| Duration | 3 months for first episode; 6 months for recurrent pericarditis |
| When to start | From diagnosis, together with NSAIDs |
| Tapering | Taper colchicine AFTER NSAIDs have been tapered and stopped. Do not stop abruptly — can reduce to 0.5 mg daily or alternate days before stopping |
| Side effects | GI (diarrhoea, nausea — most common, dose-dependent), myelosuppression (rare at therapeutic doses), hepatotoxicity |
| Contraindications | Severe hepatic impairment, severe renal impairment (GFR < 10 — dose reduction needed), pregnancy/breastfeeding |
| Drug interactions | CYP3A4 and P-glycoprotein inhibitors (e.g. clarithromycin, ketoconazole, cyclosporin) → ↑colchicine levels → toxicity risk. Also interacts with statins |
Why Colchicine Works in Pericarditis but NOT in Bacterial/Malignant Pericarditis
Colchicine targets the inflammatory component of pericarditis by inhibiting neutrophil chemotaxis and IL-1β. In idiopathic/viral/autoimmune pericarditis, inflammation IS the disease. In bacterial pericarditis, the problem is active infection — you need antibiotics and drainage, not just anti-inflammatory therapy. In malignant pericarditis, the problem is tumour invasion/fluid production — colchicine cannot address this. Hence: colchicine is an adjunct for inflammation-driven pericarditis only.
D. Second-Line Therapy: Low-Dose Corticosteroids
Glucocorticoids can be used as 2nd line treatment to substitute NSAIDs in patients who are contraindicated to aspirin/NSAIDs [1]
Low-dose steroids if autoimmune cause or C/I to NSAIDs [2]
| Indication | Rationale |
|---|---|
| Contraindication to NSAIDs (e.g. renal failure, GI bleeding, allergy) | Need an alternative anti-inflammatory |
| Autoimmune pericarditis (SLE, RA, MCTD) | Steroids address the underlying autoimmune process |
| Failure of NSAID + colchicine after 1–2 weeks | Escalation of therapy |
| Post-cardiac injury syndrome (Dressler's) — if aspirin/NSAID insufficient | Add steroid cautiously |
| Parameter | Detail |
|---|---|
| Dose | Prednisone 0.2–0.5 mg/kg/day (typically 15–25 mg/day) |
| Duration | Until symptom resolution + CRP normalization |
| Tapering | Very slow taper — decrease by 2.5–5 mg every 2 weeks once CRP normalized. Always maintain colchicine during taper |
Steroids in Pericarditis — The Double-Edged Sword
Why are steroids second-line and not first-line, despite being potent anti-inflammatories?
Steroids actually increase the risk of recurrent pericarditis. The mechanism is likely:
- Steroids enhance viral replication (in viral pericarditis) → more pericardial damage
- Rapid steroid taper → rebound inflammation → recurrence
- Steroids suppress the immune response that would normally clear the inciting agent
The COPE trial showed that corticosteroid use was an independent risk factor for recurrence (OR 4.3). Therefore: use steroids only when truly needed, at the lowest effective dose, and taper very slowly while maintaining colchicine.
E. Management of Specific Etiologies
This is one of the most commonly tested management scenarios because of the important contraindications.
| Type | Timing | Management | Key Contraindications |
|---|---|---|---|
| Peri-infarction pericarditis (PIP) | 2–4 days post-MI | Paracetamol ± aspirin (650 mg Q6–8h) ± opiate-based analgesia (usually self-limited) [2] | Avoid NSAIDs/steroids 7–10 days after acute MI due to ↑risk of aneurysm/rupture [2] |
| Post cardiac injury (Dressler) syndrome | Weeks–months post-MI | High-dose aspirin/NSAID (e.g. indomethacin 25–50 mg TDS × 1–2 days), colchicine ± steroid [2] | Use with more caution; Dressler's occurs later when myocardial healing is more advanced, so NSAIDs are safer |
Need to differentiate post-cardiac injury syndrome (Dressler's syndrome) from peri-infarct pericarditis [23]. High dose aspirin with colchicine or NSAID with colchicine for post-cardiac injury syndrome (but not peri-infarct pericarditis) [23].
If recent MI: aspirin (avoid NSAID/steroid: ↑risk of aneurysm) [7]
Why are NSAIDs dangerous early post-MI? NSAIDs inhibit COX-2 → ↓prostaglandin production → prostaglandins are involved in the healing/scarring process of infarcted myocardium. Without prostaglandins, the infarcted area thins and weakens → ↑risk of:
- Ventricular free wall rupture (fatal)
- Ventricular aneurysm formation
- Ventricular septal defect
This risk is highest in the first 7–10 days when the necrotic myocardium is being replaced by granulation tissue (the "weakest" phase of healing). Aspirin at analgesic doses is safer because it preferentially inhibits COX-1 (platelet aggregation) with less effect on COX-2-mediated healing at the doses used.
Tx: usually dialysis, pericardiocentesis ± pericardiectomy if large size ± tamponade [9]
| Principle | Detail |
|---|---|
| Primary treatment | Intensify dialysis — daily haemodialysis until pericarditis resolves (usually within 1–2 weeks). The logic: uraemic toxins cause the inflammation, so removing them addresses the root cause |
| Heparin-free dialysis | Preferred — anticoagulation during dialysis increases risk of haemorrhagic pericardial effusion in the setting of inflamed pericardium |
| NSAIDs | Generally not effective in uraemic pericarditis (the mechanism is chemical irritation, not prostaglandin-driven inflammation) and are nephrotoxic |
| Pericardiocentesis | If large effusion or tamponade |
| Pericardiectomy | If recurrent or refractory despite intensive dialysis |
Uraemia: features of uraemia, e.g. pericarditis, neuropathy, ↓mental status is listed as an indication for haemodialysis [24].
Patients become symptomatic of uraemia — presents as anorexia, nausea, vomiting, pericarditis, peripheral neuropathy [25].
| Principle | Detail |
|---|---|
| Anti-TB therapy | Standard 6-month regimen (2RHZE/4RH) — same as pulmonary TB |
| Adjunctive corticosteroids | Prednisolone for 6–8 weeks with gradual taper — reduces mortality, reduces need for repeat pericardiocentesis, and may prevent progression to constriction |
| Pericardiocentesis | Therapeutic if large effusion/tamponade; diagnostic for fluid analysis |
| Pericardiectomy | For established constrictive pericarditis that does not respond to anti-TB therapy + steroids |
| Principle | Detail |
|---|---|
| IV antibiotics | Empiric broad-spectrum (e.g. vancomycin + ceftriaxone/meropenem) → narrow based on culture. Prolonged course (4–6 weeks) |
| Surgical drainage | Essential — purulent fluid must be drained. Options: pericardiocentesis (if simple), subxiphoid pericardiostomy, pericardial window, or open surgical drainage. NSAIDs and colchicine are NOT effective here |
| Mortality | Very high (20–40%) even with treatment — emphasizes the need for early aggressive management |
The approach varies by disease but follows the principle of treating the underlying autoimmune condition:
SLE pericarditis [8]:
- Asymptomatic: conservative treatment
- Symptomatic: HCQ, short course NSAIDs or low to medium dose steroids
- Colchicine may be used if unresponsive
- Percutaneous drainage with echocardiographic guidance if cardiac tamponade
RA pericarditis [8]: Related to disease activity → usually treated by steroids/NSAIDs
Scleroderma pericarditis [8]: NSAIDs + avoid steroids for pericarditis (high-dose steroids risk precipitating scleroderma renal crisis)
MCTD pericarditis [8]: Classically very responsive to steroid
| Principle | Detail |
|---|---|
| Pericardiocentesis | Therapeutic + diagnostic (cytology) |
| Pericardial window / pericardiostomy | Prevents re-accumulation of effusion |
| Intrapericardial therapy | Instillation of sclerosing agents (e.g. tetracycline, bleomycin) or chemotherapy to prevent recurrence |
| Systemic chemotherapy / radiation | Address the underlying malignancy |
Pericardiocentesis if fluid output more than 50 mL/hour [7]
| Situation | Management |
|---|---|
| Small, asymptomatic effusion | Observe with serial echo; treat underlying cause |
| Moderate effusion without tamponade | Anti-inflammatory therapy for the underlying cause; serial echo |
| Large effusion or symptomatic | Pericardiocentesis (diagnostic + therapeutic) |
| Cardiac tamponade | Emergency pericardiocentesis — life-saving [2] |
| Cardiac rupture or aortic dissection | Do emergency surgery instead — pericardiocentesis NOT done (may precipitate ↑bleeding) [2] |
Pericardiocentesis technique: Image-guided insertion of needle medial to cardiac apex or below xiphoid directed upward towards left shoulder [2]
Recurrent pericarditis occurs in 15–30% of first episodes and is a major clinical challenge. The approach escalates through the following steps:
| Line | Therapy | Details |
|---|---|---|
| 1st | NSAIDs + colchicine (6 months) | Same as acute episode but longer colchicine course. CRP-guided tapering |
| 2nd | Low-dose corticosteroids + colchicine | Add prednisone 0.2–0.5 mg/kg/day if NSAID-refractory. Very slow taper |
| 3rd | Steroid-sparing immunosuppressants | Azathioprine, IVIG, or anakinra (anti-IL-1 receptor antagonist — emerging evidence from AIRTRIP trial) |
| 4th (last resort) | Pericardiotomy, pericardial window, pericardiectomy — if frequent, highly symptomatic recurrence resistant to medical Tx [2] |
Anakinra (anti-IL-1 receptor antagonist): This is the most important emerging therapy for colchicine-resistant/steroid-dependent recurrent pericarditis. It blocks IL-1, a key cytokine in pericardial inflammation. The AIRTRIP trial (2016) showed dramatic efficacy in reducing recurrences. It is given as a daily subcutaneous injection (100 mg/day) and is now recommended by ESC guidelines as a preferred option for corticosteroid-dependent recurrent pericarditis.
Rilonacept (IL-1α and IL-1β trap) was FDA-approved in 2021 specifically for recurrent pericarditis, based on the RHAPSODY trial. It is given as a weekly subcutaneous injection — more convenient than daily anakinra.
Anti-inflammatory agent in early disease, pericardiectomy in late disease [2]
| Phase | Management | Rationale |
|---|---|---|
| Early / transient constriction | Trial of anti-inflammatory therapy (NSAIDs + colchicine ± steroids) for 2–3 months | Some cases of "constrictive" pericarditis are actually transient constriction — inflamed, oedematous pericardium that mimics true fibrotic constriction. These resolve with anti-inflammatory therapy |
| Established constriction | Pericardiectomy [2] | Definitive treatment — surgical removal of the fibrosed, calcified pericardium to allow free ventricular filling |
| TB constriction | Anti-TB therapy + steroids + consider pericardiectomy if no improvement | Some cases improve with medical therapy alone |
Pericardiectomy ("peri-" = around, "card-" = heart, "-ectomy" = surgical removal): Complete surgical removal of the pericardium. It is a major operation with significant perioperative mortality (6–12%) but is the only curative treatment for established constrictive pericarditis.
| Scenario | First-Line | Second-Line | Key Points |
|---|---|---|---|
| Idiopathic/Viral | NSAIDs + colchicine | Low-dose steroids | Outpatient if no red flags |
| Post-MI (early, 2–4 days) | Aspirin + paracetamol | Opiates | AVOID NSAIDs/steroids [2][7] |
| Dressler's syndrome | Aspirin/NSAID + colchicine | ± Steroid | NSAIDs safer because healing is more advanced |
| Uraemic | Intensify dialysis | Pericardiocentesis ± pericardiectomy | NSAIDs not effective and nephrotoxic |
| TB | Anti-TB therapy + adjunctive steroids | Pericardiectomy for constriction | Always consider in HK |
| Bacterial/Purulent | IV antibiotics + surgical drainage | — | Colchicine NOT effective; high mortality |
| SLE | HCQ + NSAIDs/steroids | Colchicine, drainage if tamponade | Part of overall SLE management |
| RA | NSAIDs/steroids | — | Related to disease activity |
| Scleroderma | NSAIDs | Avoid steroids (renal crisis risk) [8] | Key contraindication |
| Malignant | Pericardiocentesis ± window | Systemic chemo/RT | Intrapericardial sclerosing agents |
| Recurrent | NSAIDs + colchicine (6 months) | Steroids → anakinra/rilonacept → pericardiectomy | Escalation ladder |
| Constrictive | Anti-inflammatory trial (early) | Pericardiectomy (established) [2] | TB most common cause in HK |
| Tamponade | Emergency pericardiocentesis [2] | Surgical window | NOT in cardiac rupture/aortic dissection |
High Yield Summary — Management of Pericarditis
General principles: Treat the underlying cause first. Restrict activity until symptoms resolve + CRP normalizes. Always co-prescribe PPI with NSAIDs.
First-line: NSAIDs + colchicine (colchicine 0.5 mg OD if < 70 kg, 0.5 mg BD if > 70 kg). Taper NSAIDs guided by CRP; taper colchicine after NSAIDs stopped.
Second-line: Low-dose corticosteroids if C/I to NSAIDs or autoimmune cause. Use lowest effective dose and taper very slowly — steroids increase recurrence risk.
Post-MI (early): Aspirin + paracetamol ONLY. AVOID NSAIDs and steroids (risk of ventricular aneurysm/rupture). Dressler's: NSAIDs + colchicine are acceptable.
Uraemic: Intensify dialysis (heparin-free). NSAIDs not effective.
TB: Anti-TB therapy + adjunctive steroids.
Bacterial: IV antibiotics + surgical drainage. Colchicine/NSAIDs NOT effective.
Scleroderma: NSAIDs but avoid steroids (renal crisis risk).
Tamponade: Emergency pericardiocentesis. NOT done in cardiac rupture or aortic dissection.
Recurrent: Escalate: NSAIDs + colchicine (6 months) → steroids → anakinra/rilonacept → pericardiectomy.
Constrictive: Anti-inflammatory trial for early/transient constriction; pericardiectomy for established constriction.
Active Recall - Management of Pericarditis
References
[1] Senior notes: MBBS Final MB (Medicine) (Felix PY Lai).pdf — Pericarditis, Treatment section (p. 430–432) [2] Senior notes: Ryan Ho Cardiology.pdf — Diseases of Pericardium, Management (p. 172–174), Pericardial complications post-MI (p. 140) [4] Senior notes: Ryan Ho Cardiology.pdf — Myocarditis management (p. 165) [7] Senior notes: Maksim Medicine Notes.pdf — Pericardial disease, Management column (p. 38–40) [8] Senior notes: Ryan Ho Rheumatology.pdf — SLE pericarditis management (p. 77), Scleroderma pericarditis management (p. 85), MCTD (p. 87), RA cardiac involvement (p. 49) [9] Senior notes: Ryan Ho Urogenital.pdf — Uraemic pericarditis treatment (p. 109) [23] Lecture slides: Handbook of Internal Medicine 2024.pdf — Pericarditis post-MI (p. 30), Early mobilisation contraindications (p. 375) [24] Senior notes: Ryan Ho Critical Care.pdf — Haemodialysis indications (p. 26) [25] Senior notes: MBBS Final MB (Surgery) (Felix PY Lai).pdf — Dialysis indications, uraemic symptoms (p. 863)
Complications of Pericarditis
The complications of pericarditis form a natural continuum — they follow directly from the pathophysiology. Inflammation → fluid accumulation → haemodynamic compromise → chronic scarring. Understanding this progression makes the complications intuitive rather than a memorized list.
1. Pericardial Effusion
Inflammation of the pericardium leads to increased permeability of pericardial capillaries → exudation of fluid (plasma, protein, fibrin, cells) into the pericardial space. The amount and rate of accumulation depend on the etiology and severity.
Range from asymptomatic to cardiac tamponade — determined by rate of accumulation [7]
- Dull, constant ache on left side of chest [2]
- Compression symptoms: dysphagia, SOB, hoarseness, hiccups (phrenic nerve stimulation) [2][7]
- P/E: muffled heart sound, Ewart sign (dullness over left angle of scapula: compressive atelectasis) [2][7]
Why hoarseness? The recurrent laryngeal nerve runs between the aorta/pulmonary artery and the oesophagus. A large pericardial effusion can compress this nerve → left vocal cord paralysis → hoarseness.
Why hiccups? The phrenic nerve (C3–C5) runs along the lateral border of the pericardium. Distension of the pericardial sac stretches and irritates the phrenic nerve → involuntary diaphragmatic contractions (hiccups).
| Modality | Finding | Mechanism |
|---|---|---|
| CXR | Globular-shaped heart / water bottle appearance (if > 250 mL). Clear lung fields (c.f. CHF). Oreo-cookie sign on lateral film [7] | Pericardial fluid expands the sac symmetrically; lungs remain clear because the problem is external compression, not pulmonary congestion |
| ECG | Tachycardia. Low QRS voltage (limb leads < 5 mm, precordial leads < 10 mm). Electrical alternans (alternating QRS axis due to swinging heart) [7] | Fluid insulates electrical signals (↓voltage); heart swings freely within large fluid volume (alternans) |
| Echo | Chamber collapse (RA most prone), distended IVC [7] | RA has lowest intracavitary pressure → first to collapse when intrapericardial pressure rises. IVC distension reflects elevated RA pressure |
- Small effusions are very common with any cause of pericarditis and are often clinically insignificant
- Post-MI pericardial effusion: common, occurs in ~1/3 of acute STEMI, often minimal. Usually asymptomatic and detected incidentally [2]
- The critical determinant is rate of accumulation, not volume — this is what determines whether tamponade develops
2. Cardiac Tamponade
This is the most acute and immediately life-threatening complication of pericarditis. Tamponade ("tampon" = plug; the fluid "plugs" or compresses the heart) occurs when pericardial fluid accumulates to the point where intrapericardial pressure exceeds intracardiac diastolic pressures.
High Yield – Cardiac Tamponade
Cardiac tamponade is defined as a pericardial effusion compressing one or more cardiac chambers and leading to haemodynamic compromise. In acute conditions, the pericardium cannot distend, and its pressure rises markedly with small volume changes. This explains how tamponade develops with a small acute effusion (~200 mL) [23].
Mechanism: rapid accumulation of pericardial fluid under pressure ( < 200 mL). ↑pericardial pressure > diastolic pressure in ventricles → ↓ventricular filling → ↓preload → ↓SV + CO → obstructive shock [2]
Common causes: neoplastic, pericarditis (infective or non-infective), uraemia, iatrogenic (e.g. cardiac instrumentation), traumatic, acute pericarditis treated with anticoagulants, idiopathic [23]
This is an important point — acute pericarditis treated with anticoagulants can precipitate tamponade. Why? Anticoagulants promote haemorrhagic conversion of the pericardial effusion → rapid accumulation of blood → tamponade. This is clinically relevant when pericarditis is initially misdiagnosed as ACS and the patient is started on heparin/anticoagulation.
Tamponade can also occur from free wall rupture, myocarditis, pericarditis, or iatrogenic causes as an acute mechanical complication from MI [26].
AMI complications include: heart failure, arrhythmias, VSD (anterior MI), mitral regurgitation complicating papillary muscle dysfunction (inferior MI), pericarditis [5]. Tamponade in this context usually results from free wall rupture.
Cardiac tamponade is a clinical diagnosis, i.e. it is diagnosed when a pericardial effusion is associated with haemodynamic compromise [23].
Signs and symptoms: Tachypnoea, tachycardia, small pulse volume, pulsus paradoxus. Raised JVP with prominent x descent, Kussmaul's sign. Absent apex impulse, faint heart sound, hypotension, clear chest [23].
| Sign | Mechanism |
|---|---|
| Beck's triad: hypotension + distended neck vein + muffled heart sounds [2][7] | ↓CO (hypotension), ↑RA pressure (distended neck veins), fluid dampening sound (muffled HS) |
| Pulsus paradoxus (↓ > 10 mmHg in SBP during inspiration) [7] | During inspiration, ↑venous return to RV → interventricular septum bulges leftward within the fixed pericardial space → ↓LV filling → ↓LV stroke volume → exaggerated drop in SBP |
| Kussmaul's sign (rare) [7] | Paradoxical ↑JVP during inspiration — because the compressed right heart cannot accommodate the increased venous return |
| Tachycardia | Compensatory: CO = SV × HR → if SV is critically ↓, the body tries to maintain CO by ↑HR |
| Absent apex impulse [23] | Fluid around the heart prevents the apex from contacting the chest wall |
Pulsus Paradoxus — Explained from First Principles
Normal physiology: During inspiration, intrathoracic pressure becomes more negative → ↑venous return to right heart → RV fills slightly more → slight bulging of interventricular septum towards LV → LV filling decreases slightly → systolic BP drops by ≤ 10 mmHg. This is a normal phenomenon (a small drop).
In tamponade: The pericardial sac is already maximally distended. The right heart cannot expand outward (no room in the rigid, fluid-filled sac). So all the extra inspiratory venous return pushes the septum much further leftward → much greater reduction in LV filling → SBP drops by > 10 mmHg. This is an exaggerated version of normal physiology.
Pulsus paradoxus is less obvious in constrictive pericarditis compared to cardiac tamponade as negative intrathoracic pressure during inspiration is less readily transmitted to the pericardium (due to the rigid pericardial shell) [2].
Management: (1) Expand intravascular volume — D5 or NS or plasma, full rate if in shock. (2) Positive pressure mechanical ventilation should be avoided, if possible, because the positive thoracic pressures can further impair cardiac filling. (3) Pericardiocentesis with echo guidance — apical or subcostal approach, risk of damaging epicardial coronary artery or cardiac perforation. (4) Open drainage under LA/GA [23].
Do not misdiagnose as CHF: AVOID vasodilators / diuretics (↓preload) and positive airway pressure (↓cardiac filling) [7]
| Principle | Rationale |
|---|---|
| IV fluid expansion | The compressed heart needs maximum preload to maintain any forward flow. Reducing preload (diuretics) would be catastrophic |
| Avoid positive pressure ventilation | Positive intrathoracic pressure further compresses the already compressed heart → worsens tamponade |
| Echo-guided pericardiocentesis | Approaches: apical or subcostal. Complications: cardiac perforation, damage to epicardial coronary artery [7][23] |
| Pericardial window [7] | Prevents recurrent tamponade by creating a permanent drainage path |
| NOT done when cardiac rupture or aortic dissection → emergency surgery instead [2] | Draining the tamponading blood removes the only containment of the haemorrhage |
3. Recurrent Pericarditis
Recurrent pericarditis is the most common complication of a first episode, occurring in approximately 15–30% of cases.
The mechanism is thought to be autoimmune in most cases:
- The initial episode (usually viral) damages pericardial mesothelial cells → release of intracellular antigens
- The immune system develops antibodies against these pericardial "neo-antigens"
- Once the acute treatment is stopped, the autoimmune response reactivates → recurrence
- This explains why colchicine (which dampens the NLRP3 inflammasome and reduces IL-1β) is so effective at preventing recurrence
| Factor | Mechanism |
|---|---|
| Corticosteroid use (strongest risk factor, OR 4.3) | Steroids may enhance viral replication; rapid taper causes rebound inflammation; impair immune clearance |
| Premature NSAID taper (before CRP normalizes) | Inflammation is still active but symptoms have resolved → treatment withdrawal allows re-flare |
| Not using colchicine | Colchicine blocks the inflammasome-driven autoinflammatory cycle |
| Non-viral etiology (TB, autoimmune, malignant) | Persistent antigenic stimulation from the underlying disease |
- Recurrent episodes are often equally or more severe than the first
- Significantly impairs quality of life (repeated hospitalizations, activity restriction, medication side effects)
- May eventually progress to incessant or constrictive pericarditis
4. Constrictive Pericarditis
This is the most feared long-term complication. "Constriction" refers to the pericardium becoming a rigid shell that prevents normal diastolic filling.
Constrictive pericarditis: progressive thickening, fibrosis and calcification of the pericardium [2]
Epidemiology: develops in 0.48% of viral/idiopathic pericarditis and 8.3% of non-viral pericarditis [2]
Classically TB pericarditis — most common cause in this locality (Hong Kong) [2][7]
- Chronic or recurrent pericardial inflammation → fibrin deposition
- Fibrin organizes into dense fibrous tissue (fibrosis)
- Calcium deposits within the fibrotic pericardium (calcification)
- The result: a rigid, inelastic shell encasing the heart
Rigid casing outside heart → abrupt arrest of ventricular filling during diastole [2]
Diastolic dysfunction results in: LV → ↓SV + CO + S/S of LV failure. RV → S/S of RV failure [2]
Why does this cause biventricular failure? The rigid shell limits filling of both ventricles equally. The LV cannot fill properly → ↓stroke volume → ↓cardiac output → forward failure symptoms (fatigue, hypotension). The RV cannot fill properly → blood backs up into the systemic venous system → backward failure symptoms (↑JVP, hepatomegaly, ascites, peripheral oedema).
| Feature | Pathophysiology |
|---|---|
| ↓CO: fatigue, hypotension, reflex tachycardia [2] | ↓Ventricular filling → ↓stroke volume → ↓cardiac output |
| ↑Venous pressure: ↑JVP with ↑x and y descents, hepatomegaly, ascites, oedema [2] | Blood cannot enter the rigid heart → backs up into systemic veins |
| Pericardial knock (47%): early diastolic, follows S2 [2] | Sudden cessation of ventricular diastolic filling as ventricles slap against the rigid pericardium [2] — this is slightly earlier than S3 because filling halts earlier than in RCMP |
| Kussmaul sign (13–21%): paradoxical ↑JVP during inspiration [2] | Rigid pericardium prevents RV from expanding to accommodate ↑venous return during inspiration |
| Pulsus paradoxus ( < 20%) [2] | Less obvious than in tamponade as negative intrathoracic pressure during inspiration is less readily transmitted to the pericardium (due to rigid pericardial shell) [2] |
- Cardiac cirrhosis (congestive hepatopathy): Chronic elevation of RA pressure → chronic hepatic venous congestion → centrilobular necrosis → progressive fibrosis → cirrhosis. Constrictive pericarditis (along with MS/TR) is a cause of cardiac cirrhosis [13]
- Protein-losing enteropathy: Elevated systemic venous pressure → increased intestinal capillary hydrostatic pressure → loss of protein into the gut lumen → hypoalbuminaemia → worsening oedema and ascites
- Atrial fibrillation: Chronic atrial stretching and fibrosis from elevated atrial pressures
- Renal impairment: ↓CO → ↓renal perfusion → pre-renal AKI; chronic venous congestion → congestive nephropathy
| Modality | Finding |
|---|---|
| CXR | Pericardial calcification (strongly suggestive) [2][7] |
| ECG | Non-specific ST/T changes, low voltage, AF [2] |
| Echo | Thickened, bright pericardium with abrupt termination of ventricular filling [2] |
| CT/MRI | Done if echo non-diagnostic, to show calcification and thickened pericardium [2] |
| Cardiac catheterization | Characteristic sharp y descent in RA pressure with rapid termination [2] — "dip-and-plateau" or "square root" sign |
Anti-inflammatory agent in early disease, pericardiectomy in late disease [2]
5. Myopericarditis / Perimyocarditis
Pericarditis often occurs together with myocarditis [2]. When the inflammation extends from the pericardium into the adjacent myocardium, we get myopericarditis (predominantly pericarditis with some troponin elevation) or perimyocarditis (predominantly myocarditis with pericardial involvement).
The visceral pericardium (epicardium) is directly adherent to the myocardial surface. Inflammatory mediators do not respect anatomical boundaries — they diffuse from the inflamed epicardium into the superficial myocardium (subepicardium). Many viral agents (Coxsackie, Echovirus) also have tropism for both pericardial and myocardial cells.
| Feature | Myopericarditis | Perimyocarditis |
|---|---|---|
| Predominant disease | Pericarditis | Myocarditis |
| Troponin | Mildly elevated | Significantly elevated |
| LV function | Normal or mildly ↓ | Regional/global LV dysfunction, ↓LVEF [4] |
| ECG | Pericarditis pattern | Ventricular arrhythmias, heart block, ACS-like changes [4] |
| NSAIDs | Safe to use | AVOID — ↓PG production → may worsen myocardial function + ↑myocardial necrosis [4] |
| Prognosis | Good (benign) | Variable — progressive DCMP and HF in complicated disease; fulminant myocarditis (arrhythmia, ADHF, death) [4] |
ECG changes in pericardial diseases: widespread upwardly concave ST elevation with PR depression (reciprocal changes in aVR possible), T wave flattened later followed by inversion, low voltage [27]
ECG changes in myocarditis: sinus tachycardia, non-specific ST/T changes, prolonged QRS/QTc, bundle branch block, progressive AV block, PVC/NSVT, can be associated with pericarditis [27]
Pericarditis itself can cause arrhythmias through several mechanisms:
| Arrhythmia | Mechanism |
|---|---|
| Sinus tachycardia | Compensatory — pain, fever, systemic inflammation, ↓CO if effusion |
| Atrial fibrillation/flutter | Atrial inflammation (from pericarditis extending into the atrial epicardium) → atrial electrical remodelling → ectopic foci → AF. Also common in chronic constrictive pericarditis from atrial stretching |
| Ventricular arrhythmias | More common when myocarditis is coexistent (perimyocarditis). Myocardial inflammation → electrical instability → VT/VF → sudden cardiac death |
| Heart block | Rare; occurs if inflammation extends into the conduction system (interventricular septum or AV node area) |
As pericardiocentesis is both a diagnostic and therapeutic intervention, its complications are themselves complications of pericardial disease management:
Complications: cardiac perforation, damage to epicardial coronary artery [7][23]
| Complication | Mechanism | Prevention |
|---|---|---|
| Cardiac perforation | Needle punctures the myocardial wall (especially thin-walled RV) | Echo-guided approach; subxiphoid route preferred (only RV at risk, not LV) |
| Coronary artery laceration | Needle damages an epicardial coronary vessel | Echo guidance; careful technique |
| Pneumothorax | Needle traverses the pleural space or lung | Subxiphoid approach avoids the lung |
| Arrhythmia | Needle irritates the myocardium → ectopic beats or VT | Continuous ECG monitoring during procedure |
| Infection | Introduction of bacteria into the pericardial space | Aseptic technique |
| Recurrent tamponade due to catheter blockage or reaccumulation [23] | Drain clots off or fluid reaccumulates faster than it drains | Prolonged catheter drainage; consider pericardial window for recurrent effusions |
Subcostal (safer as only RV at risk, but more difficult as crosses diaphragm) vs Apical (higher risk as LV at risk) [7]
| Treatment | Complication | Mechanism |
|---|---|---|
| NSAIDs | GI bleeding, peptic ulcer | ↓COX-1 → ↓prostaglandin-mediated gastric mucosal protection |
| NSAIDs | Renal impairment | ↓Prostaglandin → afferent arteriole vasoconstriction → ↓GFR (especially in pre-existing CKD) |
| NSAIDs in acute MI | ↑Risk of ventricular aneurysm/rupture [2][7] | ↓Prostaglandin → impaired myocardial healing during granulation tissue phase |
| Corticosteroids | ↑Recurrence of pericarditis | Enhanced viral replication, rebound inflammation on taper |
| Corticosteroids | Osteoporosis, DM, infections, cushingoid features | Long-term immunosuppressive and metabolic effects |
| Colchicine | GI side effects (diarrhoea) | Inhibition of tubulin polymerization in rapidly dividing GI epithelial cells |
| Colchicine | Myelosuppression (rare at therapeutic doses) | Inhibition of mitotic spindle formation in haematopoietic cells |
| Pericardiectomy | Perioperative mortality (6–12%) | Major cardiac surgery; risk of bleeding, infection, low cardiac output |
| Complication | Frequency | Risk Factors | Key Features | Management |
|---|---|---|---|---|
| Pericardial effusion | ~60% of pericarditis cases | All causes; especially viral, TB, malignant, hypothyroid | Muffled HS, Ewart sign, globular heart on CXR | Anti-inflammatory therapy; pericardiocentesis if large/tamponade |
| Cardiac tamponade | Uncommon in viral/idiopathic; common in TB, malignant, purulent | Rapid accumulation, haemorrhagic effusion, anticoagulant use | Beck's triad, pulsus paradoxus, obstructive shock | Emergency pericardiocentesis; IV fluids; avoid diuretics/PPV |
| Recurrent pericarditis | 15–30% | Steroid use, premature NSAID taper, no colchicine, non-viral etiology | Repeated episodes of chest pain/rub/ECG changes after symptom-free interval | NSAIDs + colchicine (6 months); escalate to steroids → anakinra → pericardiectomy |
| Constrictive pericarditis | 0.48% viral, 8.3% non-viral | TB, radiation, recurrent pericarditis, haemorrhagic effusion | Pericardial knock, Kussmaul sign, ↑JVP, ascites, hepatomegaly | Anti-inflammatory trial (early); pericardiectomy (established) |
| Myopericarditis | ~32% troponin elevation in viral | Viral etiology, concurrent infection | ↑Troponin + pericarditis features ± LV dysfunction | If preserved LV function: treat as pericarditis. If ↓LVEF: treat as myocarditis (avoid NSAIDs) |
| Arrhythmia | Variable | Myocardial involvement, atrial inflammation | AF, VT/VF (if myocarditis), heart block | Antiarrhythmics; treat underlying inflammation |
| Cardiac cirrhosis | Rare (chronic constriction) | Chronic constrictive pericarditis | Hepatomegaly, ascites, jaundice, coagulopathy | Pericardiectomy to relieve venous congestion |
High Yield Summary — Complications of Pericarditis
Pericardial effusion: Most common complication. Range from asymptomatic to tamponade — depends on rate of accumulation. CXR: globular heart, clear lungs. ECG: low voltage, electrical alternans.
Cardiac tamponade: Life-threatening. Beck's triad (hypotension, ↑JVP, muffled HS) + pulsus paradoxus. Management: IV fluids, emergency pericardiocentesis. AVOID diuretics, vasodilators, positive pressure ventilation. NOT done in cardiac rupture/aortic dissection.
Recurrent pericarditis: 15–30% of first episodes. Strongest risk factor = corticosteroid use. Prevention: colchicine for 3–6 months, CRP-guided NSAID tapering.
Constrictive pericarditis: Chronic scarring/calcification. TB is most common cause in HK. Develops in 0.48% viral vs 8.3% non-viral pericarditis. Features: pericardial knock, Kussmaul sign, ↑JVP. Treatment: pericardiectomy for established constriction.
Myopericarditis: Troponin elevated in ~32%. If LV function preserved → treat as pericarditis. If LV dysfunction → treat as myocarditis (avoid NSAIDs).
Tamponade as AMI complication: Can result from free wall rupture, pericarditis, or iatrogenic causes post-MI.
Active Recall - Complications of Pericarditis
References
[2] Senior notes: Ryan Ho Cardiology.pdf — Diseases of Pericardium: pericardial effusion (p. 173), cardiac tamponade (p. 173), constrictive pericarditis (p. 174), pericardial complications post-MI (p. 140) [4] Senior notes: Ryan Ho Cardiology.pdf — Myocarditis evaluation and management (p. 165) [5] Lecture slides: GC 088. Sudden Severe Chest Pain.pdf — AMI complications (p. 56) [7] Senior notes: Maksim Medicine Notes.pdf — Pericardial disease: effusion, tamponade, constrictive pericarditis (p. 38–40) [13] Senior notes: MBBS Final MB (Surgery) (Felix PY Lai).pdf — Cardiac cirrhosis (p. 442) [23] Lecture slides: Handbook of Internal Medicine 2024.pdf — Cardiac tamponade definition, causes, diagnosis, management (p. 43), Pericarditis post-MI (p. 30) [26] Lecture slides: Cardiac Surgery Tutorial_Prof. D Chan.pdf — Acute mechanical complications from MI (p. 31) [27] Lecture slides: General Clerkship_Introduction to CVS Investigations_2026 Yiu (2 Feb 2026).pdf — ECG changes in pericardial diseases and myocarditis (p. 7)
High Yield Summary
Definition: Inflammation of the pericardium — can be acute, recurrent, or chronic. Often coexists with myocarditis.
Anatomy: Pericardium = fibrous (outer) + parietal (serous) + pericardial cavity (15–50 mL ultrafiltrate) + visceral (epicardium). Parietal pericardium is innervated by phrenic nerve (C3–C5) → explains trapezius ridge radiation.
Epidemiology: 27.7/100k/year; 5% of non-ischaemic chest pain; M > F; young adults.
Etiology: Idiopathic/viral ( > 80%) > malignancy ( < 10%) > infection ( < 5%). In HK: always consider TB. Other causes: autoimmune (SLE, RA), metabolic (uraemia, hypothyroidism), post-MI (early: inflammatory; late: Dressler's), iatrogenic, drug-induced.
Key Clinical Features:
- Chest pain: Sharp, pleuritic, retrosternal → trapezius ridge. ↑inspiration/movement, ↓sitting forward. NSAIDs help.
- Pericardial friction rub: Triphasic (atrial systole, ventricular systole, early diastole). Pathognomonic. Best heard at left sternal border, patient sitting forward.
- Low-grade fever; flu-like prodrome in viral cases.
- ECG: Diffuse concave-up ST elevation + PR depression (most specific features). No reciprocal changes except aVR/V1. T-wave inversion occurs AFTER ST normalizes.
Effusion → Tamponade: Rapid accumulation → tamponade (Beck's triad: hypotension, ↑JVP, muffled HS). Pulsus paradoxus present.
Constriction: Chronic scarring → pericardial knock, Kussmaul sign, ↑JVP. TB is the most common cause in HK.
Post-MI pericarditis: Use aspirin, NOT NSAIDs/steroids (risk of ventricular aneurysm).
Uraemic pericarditis: Treat with intensified dialysis, not NSAIDs.
NSAIDs: OK in pericarditis, CONTRAINDICATED in isolated myocarditis.
High Yield Summary — Differential Diagnosis of Pericarditis
-
Life-threatening DDx of chest pain: ACS, aortic dissection, PE, tension pneumothorax, tamponade — must be excluded first.
-
Pericarditis vs. STEMI (ECG): Pericarditis = diffuse concave-up ST elevation + PR depression, no territorial reciprocal changes. STEMI = territorial convex-up ST elevation + reciprocal depression + Q waves.
-
Pericarditis vs. Myocarditis: NSAIDs are the mainstay for pericarditis but CONTRAINDICATED in myocarditis. Troponin elevation with wall motion abnormalities = myocarditis. Troponin elevation without = myopericarditis (treat as pericarditis).
-
Constrictive pericarditis vs. RCMP: Constriction has pericardial knock, calcification on CXR, low voltage ECG, history of pericarditis, and is surgically curable. RCMP has S3, BBB/AV block on ECG, infiltrative history, ↑BNP, and requires biopsy.
-
Etiological DDx of pericarditis: Idiopathic/viral ( > 80%) > malignancy > infection. In HK always consider TB. Red flags (high fever, large effusion, tamponade, immunosuppression, NSAID failure) warrant further investigation.
High Yield Summary — Diagnosis of Pericarditis
Diagnostic Criteria (ESC): ≥ 2 of 4: (1) Pericarditic chest pain, (2) Pericardial friction rub, (3) ECG changes (diffuse concave ↑ST + PR depression), (4) New/worsening pericardial effusion on echo.
ECG is the most important initial investigation: Stage 1 = diffuse concave-up ST elevation + PR depression (most diagnostic). Distinguish from STEMI (territorial, convex-up, reciprocal changes, Q waves). ST/T changes never occur simultaneously in pericarditis.
Echo is essential in all patients: Detect effusion, assess tamponade physiology, evaluate LV function (r/o myocarditis), detect pericardial thickening.
Blood tests: CRP/ESR (monitor treatment response), troponin (32% elevated in viral pericarditis — indicates myopericarditis, not ACS), RFT (uraemia), ANA (SLE), IGRA (TB in HK).
Viral serology NOT routinely recommended — low yield and does not change management (except HIV).
Pericardiocentesis: Reserved for tamponade (therapeutic) or unknown diagnosis with large effusion (diagnostic). Send for Gram stain, C/ST, AFB + TB culture, PCR, cytology. NOT done in cardiac rupture or aortic dissection.
Cardiac MRI: For uncertain diagnosis, suspected myocardial involvement, or suspected constriction when echo non-diagnostic.
Catheterization: For constrictive pericarditis — equalized diastolic pressures, dip-and-plateau, discordant respiratory variation. Differentiating constriction from restriction is mandatory because constriction is surgically curable.
High Yield Summary — Management of Pericarditis
General principles: Treat the underlying cause first. Restrict activity until symptoms resolve + CRP normalizes. Always co-prescribe PPI with NSAIDs.
First-line: NSAIDs + colchicine (colchicine 0.5 mg OD if < 70 kg, 0.5 mg BD if > 70 kg). Taper NSAIDs guided by CRP; taper colchicine after NSAIDs stopped.
Second-line: Low-dose corticosteroids if C/I to NSAIDs or autoimmune cause. Use lowest effective dose and taper very slowly — steroids increase recurrence risk.
Post-MI (early): Aspirin + paracetamol ONLY. AVOID NSAIDs and steroids (risk of ventricular aneurysm/rupture). Dressler's: NSAIDs + colchicine are acceptable.
Uraemic: Intensify dialysis (heparin-free). NSAIDs not effective.
TB: Anti-TB therapy + adjunctive steroids.
Bacterial: IV antibiotics + surgical drainage. Colchicine/NSAIDs NOT effective.
Scleroderma: NSAIDs but avoid steroids (renal crisis risk).
Tamponade: Emergency pericardiocentesis. NOT done in cardiac rupture or aortic dissection.
Recurrent: Escalate: NSAIDs + colchicine (6 months) → steroids → anakinra/rilonacept → pericardiectomy.
Constrictive: Anti-inflammatory trial for early/transient constriction; pericardiectomy for established constriction.
High Yield Summary — Complications of Pericarditis
Pericardial effusion: Most common complication. Range from asymptomatic to tamponade — depends on rate of accumulation. CXR: globular heart, clear lungs. ECG: low voltage, electrical alternans.
Cardiac tamponade: Life-threatening. Beck's triad (hypotension, ↑JVP, muffled HS) + pulsus paradoxus. Management: IV fluids, emergency pericardiocentesis. AVOID diuretics, vasodilators, positive pressure ventilation. NOT done in cardiac rupture/aortic dissection.
Recurrent pericarditis: 15–30% of first episodes. Strongest risk factor = corticosteroid use. Prevention: colchicine for 3–6 months, CRP-guided NSAID tapering.
Constrictive pericarditis: Chronic scarring/calcification. TB is most common cause in HK. Develops in 0.48% viral vs 8.3% non-viral pericarditis. Features: pericardial knock, Kussmaul sign, ↑JVP. Treatment: pericardiectomy for established constriction.
Myopericarditis: Troponin elevated in ~32%. If LV function preserved → treat as pericarditis. If LV dysfunction → treat as myocarditis (avoid NSAIDs).
Tamponade as AMI complication: Can result from free wall rupture, pericarditis, or iatrogenic causes post-MI.
NSTEMI
Non-ST-elevation myocardial infarction (NSTEMI) is an acute coronary syndrome characterized by myocardial necrosis with elevated cardiac biomarkers but without persistent ST-segment elevation on electrocardiography.
Stable Angina
Stable angina is a predictable pattern of chest pain or discomfort caused by myocardial ischemia that occurs with exertion or emotional stress and is relieved by rest or nitroglycerin.