Morning ReportSteven 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• Improves by leaning forward• Worsened when laying down

Recent URI symptoms, low grade fevers, malaise

Recent orthopnea, now PND

History PMHx

HTN Hyperlipidemia

Social Non-smoker Works as secretary Social ETOH (1-2 times per month)

Physical Exam

What things might you look for?

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

Physical Exam Extremities - +1 edema Pulses

Exaggerated drop in pulses with inspiration

Labs Cardiac enzymes slightly elevated WBC 12

EKG

Note diffuse ST seg elevations

Imaging CXR – any guesses

ECHO – any guesses

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

Diseases of the Pericardium Acute Fibrinous Pericarditis Pericardial Effusion without major

hemodynamic compromise Cardiac Tamponade Constrictive Pericarditis

Etiology of Pericardial Diseases 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

Etiologies of Pericarditis Neoplastic-35% Immune Mediated- 23% Viral- 21% Bacterial-6% Uremia-6% TB- 4% Idiopathic-4%

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

Bacterial Pericarditis Staphylococcus Pneumococccus Streptococcus(rheumatic pancarditis) Haemophilus M.Tuberculosis Can occur as systemic spread or direct

extension Frequently purulent

Fungal Pericarditis Histoplasma- most common fungus

in immunocompetent patients Especially the Ohio River Valley

In immunocompromised Aspergillus Candida Coccidoides

Frequently purulent

Other Infectious Etiologies Rickettsia Ricketsii Chlamydia Psittaci Borrelia burgdorferi Treponema Pallidum Actinomycosis Mycoplasma Pneumonia Nocardia

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

Iatrogenic Causes

Mediastinal Radiation-wide spectrum of diseases seen

Cardiac Surgeries Cardiac Procedures Traumatic

Drugs Lupus like sydromes

Procainamide Hydralazine Phenytoin INH

Penicillins- Hypersensitivity Pericarditis Chemotherapy

Doxorubicin/Daunorubicin-cardiomyopathy/pericardiopathy

Bleomycin - sclerosing agent

Toxins Asbestosis can cause pericardial

lesions Scorpion fish venom can cause

pericarditis

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

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

Collagen Vascular Disease SLE- pericardial involvement in up to

50% Rheumatoid Arthritis Progressive Systemic Sclerosis MCTD Polyarteritis Giant Cell Arteritis Inflammatory Bowel Disease

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

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.

Diagnostic evaluation 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

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

EKG FindingsStage 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 IV Normalization vs persistent changes

*No changes in metabolic causes

EKG changes Arrhythmias uncommon.

Arryhthmias suggest myocarditis or ischemia

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

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

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

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

A – cystic mass

B – calcified pericardium

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

Pericardial Effusion

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

Management Simple, uncomplicated pericarditis

No high risk features Medical management outpatient if proper F/U is established

High Risk Features 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

Treatments 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

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

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.

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

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

Physical Exam of Tamponade Sinus Tachycardia Elevated JVP Pulsus Paradoxus Rub possible Kussmaul's sign

Less likely w/o constrictive component

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

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

Conclusion 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