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 FEVERPERICARDIAL EFFUSIONOR CADIOMEGALLY
SINCE THE SAME VIRUSES CAN CAUSE BOTH PERICARDITIS/ AND MYOCARDITIS THEREARE 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 UPATRIAL INJURY‐ PR CHANGE (ST:PR CHANGE IN OPPOSITE DIRECTION)
STAGE2‐ NORMALIZATION ST AND PRSTAGE3‐ 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 PHYSICAL2. ECHOCARDIOGRAPHY3. EKG4. CHEST X‐RAY5. TB TEST6. ANA7. HIV8. BLOOD CULTURES IF TEMP.> 100.49. VIRAL STUDIES‐USUALLY NOT DONE SINCE COURSE IS NOT ALTERED
TREATMENT
1. IF IDENTIFIED CAUSE OTHER THAN VIRAL/ OR IDIOPATHIC‐ TX UNDERLYING CAUSE2. VIRAL OR IDIOPATHIC: NO THERAPY HAS PROVEN TO PREVENT SERIOUS SEQUELLA3. IF NO HIGH RISK FEATURES‐ CAN BE TREATED AS AN OUTPATIENT4. NSAIDS‐ RELIEF OF PAIN AND DECREASE INFLAMMATION/ OR EFFUSION ESC 2004
A) IBUPROFEN 300‐800 MG/Q6‐8HR. Days or wks. OR ASA 2‐5 G/DAY—ALTHOUGH DOESN’T CHANGE NATURAL HXB) KETOROLAC‐ IV
5. IF NO RESPONSE X 1WK. – LOOK FOR OTHER CAUSES/ AUTOIMMUNE DISORDERS6. 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 MONTHS8. GLUCOCORTICOIDS: USE ONLY IF REFRACTORY TO NSAIDS OR COLCHICINE
‐ ACUTE PERICARDITIS DUE TO CONNECTIVE TISSUE DISEASE‐ IMMUNE MEDIATED PERICARDITIS‐ UREMIC PERICARDITISHIGH DOSES OF STEROIDS WITH RAPID TAPERING
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Pericardial DiseaseAcute PericarditisChronic Relapsing PericarditisConstrictive PericarditisCardiac TamponadeLocalized and Low Pressure TamponadeRestrictive Cardiomyopathy
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Pericardial Anatomy
Two major componentsserosa (viceral pericardium)mesothelial monolayerfacilitate fluid and ion exchange
fibroa (parietal pericardium)fibrocollagenous tissue
Pericardial Fluid15 ‐ 50 ml of clear plasma ultrafiltrate
Ligamentous attachmentsto the sternum, vertebral column, diaphragm
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Pericardial Physiologynot needed to sustain lifephysiologic functionslimit cardiac dilatation
maintain normal ventricular compliance
reduce friction to cardiac movement
barrier to inflammation
limit cardiac displacement
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Acute Pericarditiscommon causes
Outpatient settingusually 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 PericarditisNon‐infectiousPost‐myocardial infarction
Uremia
Neoplastic disease
Radiation induced
Connective tissue diseases
Drug induced
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Acute Pericarditiscommon causes
Inpatient setting
T = Trauma, TUMORU = UremiaM = Myocardial infarction (acute, post) Medications (hydralazine, procain)O = Other infections (bacterial, fungal, TB)R = Rheumatoid, autoimmune disorder Radiation
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Acute PericarditisDiagnostic Clues
Historysudden onset of anterior chest pain that
is pleuritic and substernal
Physical exampresence of two‐ or three‐component rub
ECGmost important laboratory clue
Acute pericarditis: clinical findings
Chest painPleuritic, positional, may mimic MI
Fever, tachycardia, dyspneaPericardial friction rub3 component “scratchy” sound
Abnormal ECG Diffuse ST elevation
PR depression *
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Heart Murmurs of PericarditisPericardial friction rub is pathognomic for pericarditisscratching or grating soundClassically three components:presystolic rub during atrial filling
ventricular systolic rub (loudest)
ventricular diastolic rub (after A2P2)
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Acute PericarditisECG features
ST‐segment elevationreflecting epicardial inflammation
leads I, II, aVL, and V3‐V6
lead aVR usually shows ST depression
ST concave upwardST in AMI concave downward like a “dome”
PR segment depression (early stage)T‐wave inversionoccurs after the ST returns to baseline
Acute Pericarditis: Electrocardiogram
Viral PericarditisCoxsackievirus and EchovirusOften diagnosed as idiopathic
Seasonal variation
Can occur with AIDS as a result of CMVHistoryUsually self‐limited
Complications: myocarditis, recurrence, tamponade, constriction
Treat underlying disorder
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Acute PericarditisManagement
Treat underlying causeAnalgesic agentscodeine 15‐30 mg q 4‐6 hr
Anti‐inflmmatory agentsASA 648 mg q 3‐4 hrs
NSAID (indomethacin 25‐50 mg qid)
Corticosteroids are symptomatically effective , but preferably avoided
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Chronic Relapsing Pericarditisoccurs in a small % of patients with acute idiopathic pericarditissteroid dependency requiring gradual tapering over 3‐12 months; NSAIDs, analgesics, and colchicine may be beneficialpericardiectomy for relief of symptoms is not always effective
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Dressler’s Syndrome
Described by Dressler in 1956fever, 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 surgeryincidence of 6‐25% treat with high‐dose aspirin
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Acute PericarditisDifferential Diagnosis
Acute myocardial infarctionPulmonary embolismPneumoniaAortic dissection
Recurrent PericarditisIncidence ~25%TreatmentNSAID’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 soundsReduced intensity of friction rubEwart’s sign: Dullness, decreased breath sounds, and egophony over posterior L lung due to compression by large pericardial sacElectrical alternans on ECG
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ECG in Pericardial EffusionDiffuse low voltageamount of fluid
electrical conductivity of the fluid
Electrical alternansalternating amplitude of the QRS
produced by heart swinging motion
also seen in PSVT, HTN, ischemia
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Dignostic Evaluation
Chest x‐rayusually requires > 200 ml of fluid
cannot distinguish between pericardial effusion and cardiomegly
Echocardiographystandard 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 pressureExceeds ventricular diastolic pressure
Causing impaired diastolic fillingElevated venous pressureIncreased JVP, hepatomegaly, edema
Dyspnea
Decreased filling � decreased stroke volumeReflex tachycardia, hypotension
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Cardiac TamponadeEarly stagemild to moderate elevation of central venous pressure
Advanced stage� intrapericardial pressure� ventricular filling, � stroke volume
hypotension
impaired organ perfusion
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Beck’s TriadDescribed in 1935 by thoracic surgeon Claude S. Beck3 features of acute tamponade Decline in systemic arterial pressure
Elevation in systemic venous pressure (e.g. distended neck vein)
A small, quiet heart
Pulsus paradoxusExaggerated (>10mmHg) cyclic decrease in systolic BP during normal inspirationInspiration: 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 Tamponadeclinical features
Symptomsdyspnea, fatigue, cough, agitation and restlessness, syncope, shock, anuria
Physical examination pulsus paradoxus
tachycardia
increased jugular venous pressure
hypotension
Echocardiographic Diagnosis
Pericardial effusionhighly reliable
Cardiac tamponadeRA 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 collapseRA and RV walls are thin with relatively low intracavitary pressuresAbsence of compression virtually excludes tamponadePresence of compression is suggestive but not diagnostic
When to treat pericardial effusion ?
Tamponade is not an all‐or‐non‐phenomenaEcho more sensitive than clinical criteriaLimited data exist with respect to the optimal timing of intervention for pericardial effusionCardiogenic shock must be aggressively addressedInfusion of large volume of IV fluids may temporarily stabilize the patient
Echo‐guided PericardiocentesisSAFE and EFFECTIVElocating the optimal site of puncturedetermining the depth of the pericardial effusion and the distance form the puncture site to the effusionmonitoring the results of the pericardiocentesis
PericardiocentesisDiagnostic tapnot always indicated
Pericardial biopsy may be more definitive
Therapeutic drainageindicated for tamponade
Clearance for percutaneous pericardiocentesis
Subcostal viewAt least 1 cm fluid between visceral and parietal pericardiumNo significant adhesionsEffusion not consolidatedPath 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
ConstrictionThickening of the pericardium that limits diastolic volumeResultant syndrome mimicking right heart failureDifficult to separate from Restriction
ConstrictionEtiologyIdiopathic 33%
Post‐pericarditis 18%
Post‐surgical 16%
Radiation 14%
Rheumatic 6%
Infection 3%
Constrictive pericarditis: clinical findings
Fatigue, hypotension, tachycardiaElevated JVPKussmaul’s signPericardial “knock”Ascites, edema
Constrictive pericarditis: Diagnosis
Calcified pericardium on XrayImage thickened pericardium: CT scan, MRICardiac 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 pericardiumRespiratory “bounce” of septumDiastolic mitral regurgitationDilated IVC without respiratory variationNormal E’ and loss of A’ on tissue Doppler
Constriction Treatment
Medical management‐palliativeDiuretics to minimize edema
Anti TB drugs x 4 weeks before surgery
Surgical management‐PericardiectomyMortality ~10%
Symptomatic improvement 90%
Poor Prognostic Indicators:
NYHA class III or IV
Incomplete resection
Radiation induced