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 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 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 Findings Stage I ST elevation in most leads Exceptions aVR and V1 Depression of PR segment Low voltage QRS – usually assoc with tampanode Stage II Transition or “pseudonormalization” or ST/PR segments Stage III T 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 mg 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 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