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Morning Report. Steven Hart, MD. History. CC: increasing DOE HPI 49 y/o AAF Increasing SOB over 1-2 weeks Intermittent Chest pain Leg swelling starting to develop. History. Any thing else you like to know?. History. Chest pain Non-exersional Pleuritic in nature

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Morning report l.jpg

Morning Report

Steven Hart, MD

History l.jpg

  • CC: increasing DOE

  • HPI

    • 49 y/o AAF

    • Increasing SOB over 1-2 weeks

    • Intermittent Chest pain

    • Leg swelling starting to develop

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  • Any thing else you like to know?

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  • Chest pain

    • Non-exersional

    • Pleuritic in nature

    • Improves by leaning forward

    • Worsened when laying down

  • Recent URI symptoms, low grade fevers, malaise

  • Recent orthopnea, now PND

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  • PMHx

    • HTN

    • Hyperlipidemia

  • Social

    • Non-smoker

    • Works as secretary

    • Social ETOH (1-2 times per month)

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Physical Exam

What things might you look for?

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Physical Exam

  • VS T 99.1 P 108 R 22 BP 102/64

  • + JVD

  • CV

    • Tachy, distant heart sounds

    • Rub heard intermittently by examiners

    • Lower extremity edema

  • Resp

    • sits up to breath

    • Crackles at bases

    • Mildly increased effort

    • able to speak full sentences sitting up

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Physical Exam

  • Extremities - +1 edema

  • Pulses

    • Exaggerated drop in pulses with inspiration

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  • Cardiac enzymes slightly elevated

  • WBC 12

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Note diffuse ST seg elevations

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  • CXR – any guesses

  • ECHO – any guesses

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  • The Pericardium is a fibroelastic tissue made up of parietal and visceral layers

  • These two layers are separated by the pericardial cavity

  • Pericardial cavity usually contains 15-50 ml of plasma ultrafiltrate in healthy individuals

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Diseases of the Pericardium

  • Acute Fibrinous Pericarditis

  • Pericardial Effusion without major hemodynamic compromise

  • Cardiac Tamponade

  • Constrictive Pericarditis

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Viral Infections

Purulent Pericarditis


Mediastinal radiation


Cardiac surgery


Cardiac procedures

Drugs and Toxins

Metabolic disorders

Malignancies (breast, lung, Hodgkin’s, mesothelioma)

Collagen Vascular Disease


Etiology of Pericardial Diseases

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Etiologies of Pericarditis

  • Neoplastic-35%

  • Immune Mediated- 23%

  • Viral- 21%

  • Bacterial-6%

  • Uremia-6%

  • TB- 4%

  • Idiopathic-4%

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Viral Pericarditis

  • Common bugs

    • Cocksackie A and B

    • Echovirus

    • Adenovirus

  • Viral infections uncommon in patients presenting with pericardial effusion w/o pericarditis

    • Exception is HIV- frequently presents with significant effusion w/o pericaritis

    • seen in 7 % of patients hospitalized with effusions

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Bacterial Pericarditis

  • Staphylococcus

  • Pneumococccus

  • Streptococcus(rheumatic pancarditis)

  • Haemophilus

  • M.Tuberculosis

  • Can occur as systemic spread or direct extension

  • Frequently purulent

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Fungal Pericarditis

  • Histoplasma- most common fungus in immunocompetent patients

    • Especially the Ohio River Valley

  • In immunocompromised

    • Aspergillus

    • Candida

    • Coccidoides

  • Frequently purulent

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Other Infectious Etiologies

  • Rickettsia Ricketsii

  • Chlamydia Psittaci

  • Borrelia burgdorferi

  • Treponema Pallidum

  • Actinomycosis

  • Mycoplasma Pneumonia

  • Nocardia

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Post MI

  • Pericardial involvement is related to infarct size

  • Early stage - inflammatory etiology

  • Late stage

    • Immune mediated weeks to months out

    • Known as Post Cardiac Injury syndrome (PCIS) or Dressler’s syndrome

    • Rare in modern time due to reperfusion therapies

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Iatrogenic Causes

  • Mediastinal Radiation-wide spectrum of diseases seen

  • Cardiac Surgeries

  • Cardiac Procedures

  • Traumatic

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  • Lupus like sydromes

    • Procainamide

    • Hydralazine

    • Phenytoin

    • INH

  • Penicillins- Hypersensitivity Pericarditis

  • Chemotherapy

    • Doxorubicin/Daunorubicin-cardiomyopathy/pericardiopathy

  • Bleomycin - sclerosing agent

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  • Asbestosis can cause pericardial lesions

  • Scorpion fish venom can cause pericarditis

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Metabolic Disorders

  • Uremia-

    • Most common metabolic cause

    • 6-10 % of ESRD patients not on HD can have Pericarditis

    • Dialysis related Pericardial Effusions (seen in 13% of patients)

  • Severe Hypothyroidism

    • effusion – usually not significant

    • rarely pericarditis

  • Ovarian hyperstimulation syndrome

    • complication of gonadotropin therapy

    • Due to fluid shifts

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  • Responsible for 6% of acute pericardial disease (pericarditis and tamponade)

  • Accounts for 15-20% of moderate to large pleural effusions

  • Mets - Lung, Breast, Hodgkin’s metastases

  • Primary - Mesotheliomas and lipomas

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Collagen Vascular Disease

  • SLE- pericardial involvement in up to 50%

  • Rheumatoid Arthritis

  • Progressive Systemic Sclerosis

  • MCTD

  • Polyarteritis

  • Giant Cell Arteritis

  • Inflammatory Bowel Disease

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  • In two large series (331 patients), only 16 % had an identifiable cause of pericarditis

  • Many of these cases are presumed viral

  • Only 7-29% of patients have idiopathic pericardial effusions

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Clinical Presentation of Pericarditis

  • Chest Pain-

    • sudden onset over anterior chest

    • sharp and pleuritic

    • Improves by leaning forward

    • Radiates commonly to trapezius ridges

  • Pericardial Friction Rub

  • EKG – findings depend on stage

  • 2 of 3 needed to make diagnosis +/- effusion.

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Search for systemic disorders



ANA in selected cases



BCx if febrile

No routine viral cultures

Workup for malignancy if history suggests

Echo-Class Ia

Diagnostic evaluation

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Pericardial Friction Rub

  • Auscutation

    • Scratchy or squeaky sound

    • LLSB most frequent site

    • Use the diaphragm

    • suspended respiration

  • Highly specific for pericarditis (up to 85%).

  • Intermittent – sensitivity can vary.

  • Heard better in patients without effusion.

  • Result of friction from 2 inflamed layers of pericardium

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EKG Findings

  • Stage I

  • ST elevation in most leads

    • Exceptions aVR and V1

  • Depression of PR segment

  • Low voltage QRS – usually assoc with tampanode

  • Stage IITransition or “pseudonormalization” or ST/PR segments

  • Stage IIIT wave inversions.

  • Stage IVNormalization vs persistent changes

  • *No changes in metabolic causes

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EKG changes

  • Arrhythmias uncommon. Arryhthmias suggest myocarditis or ischemia

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Distinction From AMI

  • ST elevations in pericarditis: begin at J point, rarely exceed 5 mm, and retain normal concavity

  • ST elevations / T wave changes are more generalized

  • No reciprocal lead changes

  • ST elevations and T wave inversions do not occur at the same time

  • PR segment changes common

  • Q waves/QT prolongation/Hyperacute T waves uncommon

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Cardiac Biomarkers

  • Can see elevation in CK, MB, TpnI

  • 22% of patients with Acute Pericarditis in one trial were above TpnI threshold

  • Transient rise, resolving within the first 7 days

  • Patients with higher TpnI did not have higher complication rates

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CXR findings

  • Typically normal in Pericarditis

  • 200ml of pericardial fluid needed to accumulate before enlargement of the cardiac silhouette seen

  • Calcification in chronic cases may be appreciated

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Lateral CXR of a person with chronic calcified pericarditis due to TB

A – cystic mass

B – calcified pericardium

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Echocardiogram due to TB

  • Should be done in all cases

  • Often normal in patients with pericarditis, unless associated with pericardial effusion

  • Presence of pericardial effusion helps support diagnosis, while absence does not exclude it

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Diagnostic evaluation due to TB

  • Not needed in all patients- Viral and idiopathic usually follow a benign course after treatment

  • It is important to rule out significant effusion and tamponade in patients

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Management due to TB

  • Simple, uncomplicated pericarditis

    • No high risk features

    • Medical management

    • outpatient if proper F/U is established

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Subacute onset due to TB

Fever >100.4


Cardiac tamponade

Large pericardial effusion (>2cm) not decreased after NSAIDS


Hx of anticoagulation

Acute Trauma

Failure to respond to NSAIDS

High Risk Features

Treatments l.jpg

ASA-Class I (2-6g/day) or (800mg q6h tapered by 800mg /week for 3-4 weeks)

ASA resistance at 1 week should prompt further investigation

NSAIDS- ClassI (Ibuprofen 300-800mg q6h)

GI prophylaxis

Colchicine- Class IIa

Intrpericardial Steroids –Class IIa

Corticosteroids if refractory to NSAIDS


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Pericardiocentesis for 3-4 weeks)

  • If moderate to severe tamponade is present –Class IA recommendation

  • If purulent, TB, or neoplastic pericarditis is suspected- Class II a recommendation

  • Persistent symptomatic pericardial effusion

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Complications for 3-4 weeks)

  • Constriction

    • scarring and consequent loss of elasticity of the pericardial sac

  • Tamponade

    • accumulation of pericardial fluid under pressure

  • Effusive-constrictive pericarditis

  • Recurrent Pericarditis- seen in 15-30% of patients with idiopathic pericarditis. Immune autoreactivity thought to play a primary role.

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Pericardial Tamponade for 3-4 weeks)

  • Increased Pericardial Pressures leading to compression of all cardiac chambers

  • Pericardial elasticity maybe limited (Acute vs Chronic)

  • Cardiac chambers become small and chamber diastolic compliance is reduced

  • Decreased cardiac filling

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Physiologic significance for 3-4 weeks)

  • Early diastolic filling decreases, leading to the majority of venous return occuring during ventricular systole

  • When tamponade is severe, total venous return falls and cardiac chambers shrink

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Sinus Tachycardia for 3-4 weeks)

Elevated JVP

Pulsus Paradoxus

Rub possible

Kussmaul's sign

Less likely w/o constrictive component

Physical Exam of Tamponade

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Pulsus Paradoxus for 3-4 weeks)

  • An exaggerated fall in systemic blood pressure during inspiration

  • Inspiratory decline in thoracic pressure is transmitted through the pericardium to the right side of the heart

  • Systemic Venous return increases with inspiration

  • In tamponade, the rigid pericardium prevents the RV free wall from expanding during diastole causing the pressure transmission to the septal wall and decreased LV filling during inspiration

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Acute vs chronic accumulation for 3-4 weeks)

  • As little as 20-50 ml acutely can cause tamponade acutely

  • As much as 2 liters can accumulate chronically prior to causing tamponade

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Pericarditis has many causes for 3-4 weeks)

A good history and physical will often lead to diagnosis

ECHO, EKG, HIV, CXR and PPD should be done

Outpatient management may be reasonable

Anti-inflammatories key for medical management