Pericarditis (Clinical)

Pericarditis is an inflammation of the pericardium, often with fluid accumulation. It

can be caused by infection (often viral), myocardial infarction, drugs, malignancies,
metabolic disorders, autoimmune disorders, or trauma. Acute, subacute, and
chronic forms exist. Acute pericarditis is usually idiopathic and manifests as fever,
pleuritic chest pain, and an audible pericardial rub by auscultation. Diffuse
upwardly concave ST-segment elevations in the initial ECG and pericardial effusion
on echocardiography confirm the diagnosis. Acute pericarditis is usually self-
limiting (2–6 weeks); therefore, management is conservative. If cardiac tamponade
or constrictive pericarditis develops, cardiac output can be severely reduced.
Treatment depends on the cause, but general measures include analgesics, anti-
inflammatory drugs, colchicine, and rarely surgery.

Last updated: January 17, 2024

CONTENTS

Definition and Classification

Epidemiology and Etiology
Pathophysiology
Clinical Presentation and Diagnosis
Management
Differential Diagnoses
References
Definition and Classification
Definition

Pericarditis is an inflammation of the pericardium, the double-layered sac

surrounding the heart.

Classification[1,3,4]

Clinical classification is based on duration.

Acute (< 4‒6 weeks)

Incessant (> 4‒6 weeks, but < 3 months)
Chronic (> 3 months)
Recurrent: new signs and symptoms after 4‒6 week symptom-free interval

Epidemiology and Etiology

Epidemiology[4]
Reported in 0.1%–0.2% of hospitalized patients
Found in 5% of patients admitted to the emergency department (ED) for
nonischemic chest pain

Etiology[1,2,4]
Idiopathic (most After exclusion of other causes
common)

Viral infection Coxsackievirus B

Influenza
HIV
Echovirus

Bacterial infection Tuberculosis (most common cause

worldwide)
Streptococcus species (rheumatic fever)
Lyme disease
Pseudomonas
Staphylococcus species
Mycoplasma

Fungal infection (very Histoplasma

rare) Blastomyces
Coccidioides
Aspergillus

Autoimmune disease Systemic lupus erythematosus

Rheumatoid arthritis
Sarcoidosis
Vasculitides (Behcet’s,
Takayasu’s arteritis)

Metabolic Uremia
Hypothyroidism

Cardiovascular Takotsubo cardiomyopathy

Dressler syndrome
Myocardial infarction
Cardiac injury (e.g., following operation)
Aortic dissection
Chronic heart failure
 Cancer Lung cancer
Breast cancer
Leukemia
Lymphoma
Radiation therapy

Drugs Procainamide
Hydralazine
Penicillin
Isoniazid
Chemotherapy

Pathophysiology
Inflammatory cascade stimulates the release of fluid in the
pericardial space, causing effusion.[3]
Rapid accumulation of large amounts of fluid in the pericardial space can
cause cardiac tamponade, compromising cardiac output and potentially
resulting in obstructive shock.
Constrictive pericarditis is characterized by a thickened and scarred
pericardial sac that lies around the heart and prevents proper diastolic
filling.

Clinical Presentation and Diagnosis

Typical clinical presentation[1,2,4]
Patient presents with central chest pain that worsens during inspiration or
when lying flat. Leaning forward while sitting may relieve the pain.
Fever can be present.
In 50% of cases, a pericardial friction rub (scratching sound during systole
and diastole) can be heard upon auscultation.
Table: Important clinical and diagnostic features of acute, chronic, an
constrictive pericarditis

Features Acute Chronic Constrictive

Features Acute Chronic Constrictive

Pain Severe/sharp Less None

Frequently: severe
pleuritic1 May be
Sometimes: absent if
steady (may developing
get confused slowly
with acute
myocardial
infarction
[MI])
Radiation:
neck,
shoulder(s),
arm(s),
trapezius

Other symptoms Pain May have Weakness

intensifies dyspnea Fatigue
with lying Weight gain
supine Exertional dysp
Pain
improves
with leaning
forward
Features Acute Chronic Constrictive

Physical May have May have Neck vein

examination neck vein neck vein distension
distension distension Pericardial kno
Pericardial X-ray: Kussmaul’s sig
friction rub Large
Paradoxical pu
2 cardiac
Hepatomegaly
silhouette
ascites,
peripheral ede
JVP curve:
prominent x an
descents
X-ray:
small/normal/s
large cardiac
silhouette and
pericardial
calcifications

ECG Diffuse ST- Electrical Low-voltage Q

segment alternans Atrial fibrillation
elevation 7 with a large ⅓ of cases
with upward effusion
concavity
and without
T-wave
inversions6
Electrical
alternans
7 with a large

effusion

Echocardiography Pleural Pleural Pericardial thicke

8 effusion effusion
 Features Acute Chronic Constrictive

Tamponade9 With rapid fluid Uncommon Never

accumulation

Comments Elevated
cardiac
biomarkers
can occur,
further
simulating a
diagnosis of
acute MI.

1. Pleuritic pain: pain that is exacerbated with inspiration or exhalation

and reduced or eliminated by holding respirations
2. Pericardial friction rub: a rasping, scratching, or grating sound with
up to 3 components per cardiac cycle and best heard during
expiration with the patient leaning forward
3. Pericardial knock: an early third heart sound
4. Kussmaul’s sign: absence of normal decline in jugular venous
pressure with inspiration; also seen in tricuspid stenosis, right
ventricular infarction, and restrictive cardiomyopathy
5. Paradoxical pulse: a drop by > 10 mm Hg in systolic blood pressure
(SBP) during inspiration (i.e., difference between the first SBP sound
heard during exhalation and the first SBP sound heard audible
throughout the respiratory cycle > 10 mm Hg)
6. Subsequent ECG changes include: ST-segment elevation returns to
normal after several days (stage 2), followed by T-inversions (stage
3), and complete normalization of ECG after weeks to months (stage
4)
7. Electrical alternans: alternating QRS amplitudes
8. Echocardiography for pericarditis: most widely used modality (CT
and MRI are more accurate for pericardial disease)
9. Tamponade: pericardial effusion, usually of rapid onset, exceeding
ventricular filling pressures and causing collapse of the heart with a
markedly reduced cardiac output

Etiology-specific features[1,2]
Viral or acute idiopathic pericarditis:
Chest pain 1–2 weeks after a viral-like illness is suggestive.
Must exclude acute MI, postcardiac injury, collagen vascular disease,
drugs, pyogenic pericarditis, etc.
Most frequent complication is relapsing pericarditis.
Postcardiac injury acute pericarditis:
1–4 weeks after a cardiac operation or blunt/penetrating trauma
Tuberculous pericarditis:
Common cause of chronic pericardial effusion in developing countries
In a patient with tuberculosis or systemic illness and large cardiac
silhouette: positive fluid culture or pericardial biopsy revealing
caseating granuloma confirms the diagnosis.
Uremic pericarditis:
Seen with severe renal failure or in patients on chronic dialysis
Progression of ECG changes[1, 2]
Stage 1 (hours to days): PR depression and diffuse ST elevation
Stage 2 (~ 1 week): PR and ST segments return to baseline
Stage 3 (subacute phase, highly variable): diffuse T wave inversion
Stage 4: return to baseline
Note: These progressive changes are highly variable, and many patients’
ECG findings normalize after stage 1.

Diagnostic criteria for acute pericarditis[1, 3]

Based on US and UK recommendations, a diagnosis can be made if ≥ 2 of the
following criteria are met:

Chest pain characteristic of acute pericarditis

Presence of a pericardial friction rub
Characteristic ECG changes
Presence of a new or worsening pericardial effusion

Management
Management can be location-specific. The following recommendations are
based on US, European, and UK medical society recommendations.

Goals of treatment[1‒3]
Goals include:

Pain relief
Reducing inflammation
Resolution of pericardial effusion (if present)
Preventing recurrence

In addition, the clinician should look for and treat underlying etiologies.

Acute pericarditis
Treatment recommendations: anti-inflammatory agents are the mainstay of
management[1‒4]
 Oxygen and analgesia
High-dose aspirin/nonsteroidal anti-inflammatory drugs (NSAIDs) (e.g.,
ibuprofen, indomethacin) plus gastric protection
Options include:
Aspirin 750‒1000 mg every 8 hours (often preferred in
individuals with coronary artery disease)
Ibuprofen 600‒800 mg every 8 hours
Indomethacin 25‒50 mg every 8 hours
Treat at these higher doses until symptoms resolve (typically 1‒2
weeks) before beginning a taper
Some prefer to treat until symptoms resolve AND C-reactive
protein (CRP) normalizes
Taper over 2‒4 weeks
Gastric protection: typically a PPI
Adjuvant therapy with colchicine enhances response and reduces the
recurrence rate.
Colchicine 0.5‒0.6 mg twice daily x 3 months
Adjust dose based on weight and renal insufficiency
Short-term glucocorticoids can be used if NSAIDs/colchicine are
ineffective or contraindicated: E.g., Prednisone 0.2‒0.5 mg/kg/day
Avoid strenuous exercise (minimum 3 months)
General population: until symptoms resolve
Athletes: until symptoms and diagnostic tests normalize
Most individuals may be managed outpatient.

Indications for hospitalization:[1, 3]

Fever > 38℃ (100.4℉)

Subacute onset
The presence of a large pericardial effusion
Pericardial tamponade
Unresponsive to 1 week of anti-inflammatory treatment
Myocardial involvement (myopericarditis, typically identified by elevated
troponins)
Other risk factors to consider:
Immunosuppression
Anticoagulation
Trauma
Management checklist:

Does the individual meet criteria for hospitalization?

Antiinflammatory agent (NSAID or aspirin)
Gastroprotection (e.g., PPI)
Colchicine
Consider short-term glucocorticoids (if NSAIDs/colchicine are ineffective or
contraindicated)
Activity restriction
Pericarditis due to infection → antibiotics aimed at specific pathogen

Recurrent pericarditis[1, 2, 4]
Pericarditis occurring at least 4‒6 weeks following a first episode of
acute pericarditis.

Much less common when colchicine is used during initial treatment

Treatment for months
Options include:
Corticosteroids (Prednisone 0.2‒0.5 mg/kg/day) → may result in
adrenal suppression
IL-1 blockade with Anakinra 1‒2 mg/kg (up to 100 mg) once daily
Other immunosuppressive agents (weak evidence):
Azathioprine 1‒3 mg/kg/day
IV immunoglobulin 400–500 mg/kg/day x 5 days
Methotrexate 10‒15 mg weekly
Mycophenolate mofetil 2000 mg daily
Consider pericardiocentesis

Constrictive pericarditis[1, 2]
If active inflammation is noted on imaging, a trial of anti-inflammatory
therapy is indicated.
Complete pericardial resection (pericardiectomy) is the only definitive
treatment and is best performed as early as possible (as an option of last
resort for refractory cases)
Diuretics can be used cautiously in individuals with heart failure symptoms.
Consider β-blockers in patients with tachycardia

Specific treatments[1]
 Cardiac tamponade requires immediate pericardiocentesis.
Pericardial window may also be considered.
Initiation or intensification of dialysis in addition to NSAIDs in
uremic pericarditis
Antibiotics if an underlying infection is found
Antituberculous therapy ± pericardiectomy

Differential Diagnoses
Stable and unstable angina: paroxysmal chest pain or discomfort caused
by myocardial ischemia. Stable angina is characterized by a short duration
of the complaints that are often associated with triggers like physical
activity or stress. In unstable angina, symptoms are present even at rest.
Most individuals with angina have coronary heart disease.
Acute myocardial infarction (AMI): myocardial cell death due to ischemia
of the myocardial tissue caused by a complete obstruction or drastic
constriction of the coronary artery. Typical symptoms include chest pain
that may radiate to the left arm, jaw, neck, and upper back, as well as
nausea and vomiting. ST-elevation on ECG can be present (STEMI) or
absent (NSTEMI). In a STEMI, the ECG typically differs in:
Morphology: The ST elevations (STEs) are convex (dome-shaped) and
may be
> 5 mm in height.
Distribution: The STEs correspond to the localized vascular area of
the infarct. (This does not happen in acute pericarditis because the
pericardium encloses the heart, so the STEs are present in most
leads.)
Reciprocal ST-segment changes: seen in STEMI, but not pericarditis
(except in leads aVR and V1).
Concurrent ST and T-wave changes: a common occurrence in STEMI
Absence of PR segment depressions or PR elevation in aVR: this is
typical of acute pericarditis, not STEMI.
Hyperacute T waves: common in STEMI, not pericarditis
New pathologic Q waves: common in STEMI, not pericarditis
QT prolongation: common in STEMI, not pericarditis
Aortic stenosis: a narrowing of the aortic valve aperture, characterized by
a narrowed left ventricular outflow tract and obstruction of blood flow into
the aorta
Esophagitis: an inflammation of the esophageal lining, which can be
caused by gastroesophageal reflux disease (GERD), infections, drugs, and
allergic reactions.
Pancreatitis: an inflammation of the pancreas that typically causes
epigastric pain that radiates to the back
Pneumonia: acute or chronic inflammation of lung tissue most commonly
caused by infection with bacteria, viruses, or fungi
Pleuritis: also known as pleurisy, an inflammation of the pleura that lines
the lungs. May be caused by a viral infection (most common), pneumonia,
lung cancer, autoimmune disease, or pulmonary embolism
 Tuberculosis: a disease caused by Mycobacterium tuberculosis, which
usually attacks the lungs but can also damage other parts of the body.
Presents with fever, weight loss, night sweats, and a productive cough
Pneumothorax: a collection of air in the pleural space that causes the lung
to collapse due to the loss of negative pressure. Presents with pleuritic
chest pain, dyspnea, tachycardia, and reduced breath sounds on the
ipsilateral side
Herpes zoster: a dermatomal rash with painful blistering, preceded by
sharp burning pain, caused by the reactivation of the varicella-zoster virus.
It usually affects dermatomes T3 through L3.

References

1. Chiabrando, J.G., Bonaventura, A., et al. (2020). Management of acute and recurrent
pericarditis: JACC state-of-the-art review. Journal of American College of Cardiology. 75(1):76-
92. https://www.jacc.org/doi/10.1016/j.jacc.2019.11.021?
_ga=2.37075616.1474680231.1646330634-1222112325.1645077917

2. Little, W.C., and Freeman, G.L. (2006). Pericardial disease. Circulation. 113:1622-1632.
https://www.ahajournals.org/doi/10.1161/circulationaha.105.561514
3. Ismail, T.F. (2020). Acute pericarditis: Update on diagnosis and management. In Clinical
Medicine Journal. 20(1):48-51. https://www.rcpjournals.org/content/clinmedicine/20/1/48
4. Adler Y, Charron P, Imazio M, et al; ESC Scientific Document Group. 2015 ESC Guidelines for the
diagnosis and management of pericardial diseases: The Task Force for the Diagnosis and
Management of Pericardial Diseases of the European Society of Cardiology (ESC) Endorsed by:
The European Association for Cardio-Thoracic Surgery (EACTS). Eur Heart J. 2015 Nov
7;36(42):2921-2964. doi.org/10.1093/eurheartj/ehv318. Epub 2015 Aug 29. PMID: 26320112;
PMCID: PMC7539677.