2 OF THE ABOVE CRITERIA ARE NECESSARY FOR THE DIAGNOSIS ABSENCE OF A PERICARDIAL EFFUSION DOES NOT EXCLUDE THE DX PERICARDITIS SHOULD BE SUSPECTED WITH PERSISTANT FEVER PERICARDIAL EFFUSION OR CADIOMEGALLY SINCE THE SAME VIRUSES CAN CAUSE BOTH PERICARDITIS/ AND MYOCARDITIS THERE ARE COMMON ELEMENTS TERM: PERIMYOCARDITIS SOMETIMES USED

CHEST PAIN: - FAIRLY SUDDEN - OVER ANT. CHEST WALL - PLEURITIC/SHARP - DEC. LEANING FORWARD PERICARDIAL FRICTION RUB:- VERY SPECIFIC (85% OF CASES) CARDIAC BIOMARKERS: ACUTE PERICARDITIS- INCR. TROPONIN I (MYOCARDITIS) SIGNS OF INFLAMMATION: WBC/ SED RATE/CRP/ EKG: STAGE1- SEEN HOURS/DAYS- ST ELEV. CONCAVE UP ATRIAL INJURY- PR CHANGE (ST:PR CHANGE IN OPPOSITE DIRECTION) STAGE2- NORMALIZATION ST AND PR STAGE3- DIFFUSE T WAVE INVERSION (CAN BE ABSENT) STAGE4- MAY NORMALIZE OR T WAVES MAY PERSIST INDEFINITELY) CXR: USUALLY NORMAL

INITIAL EVALUATION– STANDARD APPROACH PERICARDITIS IS USUALLY BRIEF AND BENIGN 1. INITIAL HISTORY AND PHYSICAL 2. ECHOCARDIOGRAPHY 3. EKG 4. CHEST X-RAY 5. TB TEST 6. ANA 7. HIV 8. BLOOD CULTURES IF TEMP.> VIRAL STUDIES-USUALLY NOT DONE SINCE COURSE IS NOT ALTERED

TREATMENT 1. IF IDENTIFIED CAUSE OTHER THAN VIRAL/ OR IDIOPATHIC- TX UNDERLYING CAUSE 2. VIRAL OR IDIOPATHIC: NO THERAPY HAS PROVEN TO PREVENT SERIOUS SEQUELLA 3. IF NO HIGH RISK FEATURES- CAN BE TREATED AS AN OUTPATIENT 4. NSAIDS- RELIEF OF PAIN AND DECREASE INFLAMMATION/ OR EFFUSION ESC 2004 A) IBUPROFEN MG/Q6-8HR. Days or wks. OR ASA 2-5 G/DAY—ALTHOUGH DOESN’T CHANGE NATURAL HX B) KETOROLAC- IV 5. IF NO RESPONSE X 1WK. – LOOK FOR OTHER CAUSES/ AUTOIMMUNE DISORDERS 6. IN AMI- USE ONLY ASA/ NOT NSAID---( INDOMETHICIN) 7. COLCHICINE: - MAY HELP PREVENT RECURRENCE OF ACUTE IDIOPATHIC OR VIRAL ? FOR 1ST EPISODE 0.5-1MG TWICE ON THE 1ST DAY, THEN 0.5 1OR 2 X DAY FOR THREE MONTHS 8. GLUCOCORTICOIDS: USE ONLY IF REFRACTORY TO NSAIDS OR COLCHICINE - ACUTE PERICARDITIS DUE TO CONNECTIVE TISSUE DISEASE - IMMUNE MEDIATED PERICARDITIS - UREMIC PERICARDITIS HIGH DOSES OF STEROIDS WITH RAPID TAPERING

9/98medslides.com7 Pericardial Disease Acute Pericarditis Chronic Relapsing Pericarditis Constrictive Pericarditis Cardiac Tamponade Localized and Low Pressure Tamponade Restrictive Cardiomyopathy

9/98medslides.com8 Pericardial Anatomy Two major components serosa (viceral pericardium) mesothelial monolayer facilitate fluid and ion exchange fibroa (parietal pericardium) fibrocollagenous tissue Pericardial Fluid ml of clear plasma ultrafiltrate Ligamentous attachments to the sternum, vertebral column, diaphragm

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9/98medslides.com10 Pericardial Physiology not needed to sustain life physiologic functions limit cardiac dilatation maintain normal ventricular compliance reduce friction to cardiac movement barrier to inflammation limit cardiac displacement

9/98medslides.com11 Acute Pericarditis common causes Outpatient setting usually idiopathic probably due to viral infections Coxsackie A and B (highly cardiotropic) are the most common viral cause of pericarditis and myocarditis Others viruses: mumps, varicella-zoster, influenza, Epstein-Barr, HIV

Acute Pericarditis Non-infectious Post-myocardial infarction Uremia Neoplastic disease Radiation induced Connective tissue diseases Drug induced

9/98medslides.com13 Acute Pericarditis common causes Inpatient setting T = Trauma, TUMOR U = Uremia M = Myocardial infarction (acute, post) Medications (hydralazine, procain) O = Other infections (bacterial, fungal, TB) R = Rheumatoid, autoimmune disorder Radiation

9/98medslides.com14 Acute Pericarditis Diagnostic Clues History sudden onset of anterior chest pain that is pleuritic and substernal Physical exam presence of two- or three-component rub ECG most important laboratory clue

Acute pericarditis: clinical findings Chest pain Pleuritic, positional, may mimic MI Fever, tachycardia, dyspnea Pericardial friction rub 3 component “scratchy” sound Abnormal ECG Diffuse ST elevation PR depression *

9/98medslides.com16 Heart Murmurs of Pericarditis Pericardial friction rub is pathognomic for pericarditis scratching or grating sound Classically three components: presystolic rub during atrial filling ventricular systolic rub (loudest) ventricular diastolic rub (after A2P2)

9/98medslides.com17 Acute Pericarditis ECG features ST-segment elevation reflecting epicardial inflammation leads I, II, aVL, and V3-V6 lead aVR usually shows ST depression ST concave upward ST in AMI concave downward like a “dome” PR segment depression (early stage) T-wave inversion occurs after the ST returns to baseline

Acute Pericarditis: Electrocardiogram

Viral Pericarditis Coxsackievirus and Echovirus Often diagnosed as idiopathic Seasonal variation Can occur with AIDS as a result of CMV History Usually self-limited Complications: myocarditis, recurrence, tamponade, constriction Treat underlying disorder

9/98medslides.com20 Acute Pericarditis Management Treat underlying cause Analgesic agents codeine mg q 4-6 hr Anti-inflmmatory agents ASA 648 mg q 3-4 hrs NSAID (indomethacin mg qid) Corticosteroids are symptomatically effective, but preferably avoided

9/98medslides.com21 Chronic Relapsing Pericarditis occurs in a small % of patients with acute idiopathic pericarditis steroid dependency requiring gradual tapering over 3-12 months; NSAIDs, analgesics, and colchicine may be beneficial pericardiectomy for relief of symptoms is not always effective

9/98medslides.com22 Dressler’s Syndrome Described by Dressler in 1956 fever, pericarditis, pleuritis (typically with a low grade fever and a pericardial friction rub) occurs in the first few days to several weeks following MI or heart surgery incidence of 6-25% treat with high-dose aspirin

9/98medslides.com23 Acute Pericarditis Differential Diagnosis Acute myocardial infarction Pulmonary embolism Pneumonia Aortic dissection

Recurrent Pericarditis Incidence ~25% Treatment NSAID’s initially Steroids Rarely Colchicine Well Tolerated 60% effective long-term, more effective if taken chronically Fewer side effects than long-term steroids

Large pericardial effusion: signs Soft heart sounds Reduced intensity of friction rub Ewart’s sign: Dullness, decreased breath sounds, and egophony over posterior L lung due to compression by large pericardial sac Electrical alternans on ECG

9/98medslides.com26 ECG in Pericardial Effusion Diffuse low voltage amount of fluid electrical conductivity of the fluid Electrical alternans alternating amplitude of the QRS produced by heart swinging motion also seen in PSVT, HTN, ischemia

9/98medslides.com27 Dignostic Evaluation Chest x-ray usually requires > 200 ml of fluid cannot distinguish between pericardial effusion and cardiomegly Echocardiography standard for diagnosing pericardial effusion convenient, highly reliable, cost effective false positives (M-mode)- left pleural effusion, epicardial fat, tumor tissue, pericardial cysts

Pericardial effusion L

Pericardial tamponade: pathophysiology Increased intra-pericardial pressure Exceeds ventricular diastolic pressure Causing impaired diastolic filling Elevated venous pressure Increased JVP, hepatomegaly, edema Dyspnea Decreased filling  decreased stroke volume Reflex tachycardia, hypotension

9/98medslides.com30 Cardiac Tamponade Early stage mild to moderate elevation of central venous pressure Advanced stage  intrapericardial pressure  ventricular filling,  stroke volume hypotension impaired organ perfusion

9/98medslides.com31 Beck’s Triad Described in 1935 by thoracic surgeon Claude S. Beck 3 features of acute tamponade Decline in systemic arterial pressure Elevation in systemic venous pressure (e.g. distended neck vein) A small, quiet heart

Pulsus paradoxus Exaggerated (>10mmHg) cyclic decrease in systolic BP during normal inspiration Inspiration: increased venous return increased RV volume. Interventricular septum shifts left, decreased LV volume decreased stroke volume systolic pressure falls.

Pulsus Paradoxus an exaggerated drop in SBP with inspiration (>10mmHg) Berliner Klinische Wochenschrift 1878; 10:461

Cardiac Tamponade clinical features Symptoms dyspnea, fatigue, cough, agitation and restlessness, syncope, shock, anuria Physical examination pulsus paradoxus tachycardia increased jugular venous pressure hypotension

Echocardiographic Diagnosis Pericardial effusion highly reliable Cardiac tamponade RA and RV diastolic collapse reduced chamber size distension of the inferior vena cava exaggerated respiratory variation of the mitral and tricuspid valve flow velocities

RA and RV diastolic collapse RA and RV walls are thin with relatively low intracavitary pressures Absence of compression virtually excludes tamponade Presence of compression is suggestive but not diagnostic

When to treat pericardial effusion ? Tamponade is not an all-or-non-phenomena Echo more sensitive than clinical criteria Limited data exist with respect to the optimal timing of intervention for pericardial effusion Cardiogenic shock must be aggressively addressed Infusion of large volume of IV fluids may temporarily stabilize the patient

Echo-guided Pericardiocentesis SAFE and EFFECTIVE locating the optimal site of puncture determining the depth of the pericardial effusion and the distance form the puncture site to the effusion monitoring the results of the pericardiocentesis

Pericardiocentesis Diagnostic tap not always indicated Pericardial biopsy may be more definitive Therapeutic drainage indicated for tamponade

Clearance for percutaneous pericardiocentesis Subcostal view At least 1 cm fluid between visceral and parietal pericardium No significant adhesions Effusion not consolidated Path to pericardium not THROUGH the liver

Constrictive pericarditis Fibrous thickening, adhesion, calcification of the pericardium. Most common etiologies: TB Idiopathic Post pericarditis of any etiology

Constriction Thickening of the pericardium that limits diastolic volume Resultant syndrome mimicking right heart failure Difficult to separate from Restriction

Constriction Etiology Idiopathic 33% Post-pericarditis 18% Post-surgical 16% Radiation 14% Rheumatic 6% Infection 3%

Constrictive pericarditis: clinical findings Fatigue, hypotension, tachycardia Elevated JVP Kussmaul’s sign Pericardial “knock” Ascites, edema

Constrictive pericarditis: Diagnosis Calcified pericardium on Xray Image thickened pericardium: CT scan, MRI Cardiac cath: Elevated, equalized diastolic pressures Restricted filling pattern in RV (“dip and plateau”) Prominent “y” descent on RA pressure tracing

MRI- Constriction LV RV

Echocardiographic signs of constriction Thickened and adherent pericardium Respiratory “bounce” of septum Diastolic mitral regurgitation Dilated IVC without respiratory variation Normal E’ and loss of A’ on tissue Doppler

Constriction Treatment Medical management-palliative Diuretics to minimize edema Anti TB drugs x 4 weeks before surgery Surgical management-Pericardiectomy Mortality ~10% Symptomatic improvement 90% Poor Prognostic Indicators: NYHA class III or IV Incomplete resection Radiation induced