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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

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Morning report l.jpg

Morning Report

Steven Hart, MD


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History

  • 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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History

  • Any thing else you like to know?


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History

  • 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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History

  • 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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Labs

  • Cardiac enzymes slightly elevated

  • WBC 12


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EKG

Note diffuse ST seg elevations


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Imaging

  • CXR – any guesses

  • ECHO – any guesses


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Introduction

  • 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

TB

Mediastinal radiation

MI

Cardiac surgery

Trauma

Cardiac procedures

Drugs and Toxins

Metabolic disorders

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

Collagen Vascular Disease

Idiopathic

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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Drugs

  • Lupus like sydromes

    • Procainamide

    • Hydralazine

    • Phenytoin

    • INH

  • Penicillins- Hypersensitivity Pericarditis

  • Chemotherapy

    • Doxorubicin/Daunorubicin-cardiomyopathy/pericardiopathy

  • Bleomycin - sclerosing agent


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Toxins

  • 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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Malignancy

  • 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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Idiopathic

  • 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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History

Physical

Search for systemic disorders

ECG

CXR

ANA in selected cases

PPD

HIV

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

  • 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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Pericardial Effusion


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Diagnostic evaluation

  • 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

  • Simple, uncomplicated pericarditis

    • No high risk features

    • Medical management

    • outpatient if proper F/U is established


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Subacute onset

Fever >100.4

Leukocytosis

Cardiac tamponade

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

Immunosuppressed

Hx of anticoagulation

Acute Trauma

Failure to respond to NSAIDS

High Risk Features


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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

Treatments


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Pericardiocentesis

  • 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

  • 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

  • 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

  • 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

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

  • 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

  • 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

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

Conclusion


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