pericardial disease.ppt
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Pericardial Disease
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Pericardial DiseaseAcute PericarditisChronic Relapsing PericarditisConstrictive PericarditisCardiac TamponadeLocalized and Low Pressure TamponadeRestrictive Cardiomyopathy
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Pericardial AnatomyTwo major componentsserosa (viceral pericardium)mesothelial monolayerfacilitate fluid and ion exchangefibroa (parietal pericardium)fibrocollagenous tissuePericardial Fluid15 - 50 ml of clear plasma ultrafiltrateLigamentous attachmentsto the sternum, vertebral column, diaphragm
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Pericardial Physiologynot needed to sustain lifephysiologic functionslimit cardiac dilatationmaintain normal ventricular compliancereduce friction to cardiac movement barrier to inflammationlimit cardiac displacement
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Pericardial InflammationpathogenesisContiguous spreadlungs, pleura, mediastinal lymph nodes, myocardium, aorta, esophagus, liverHematogenous spreadsepticemia, toxins, neoplasm, metabolicLymphangetic spreadTraumatic or irradiation
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Pericardial Inflammationpathologyinflammation provokes a fibrinous exudate with or without serous effusionthe normal transparent and glistening pericardium is turned into a dull, opaque, and sandy saccan cause pericardial scarring with adhesions and fibrosis
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Acute Pericarditiscommon causesOutpatient settingusually idiopathicprobably due to viral infectionsCoxsackie A and B (highly cardiotropic) are the most common viral cause of pericarditis and myocarditisOthers viruses: mumps, varicella-zoster, influenza, Epstein-Barr, HIV
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Acute Pericarditiscommon causesInpatient settingT = 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 CluesHistory
sudden onset of anterior chest pain thatis pleuritic and substernalPhysical exam
presence of two- or three-component rubECG
most important laboratory clue
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Chest Pain Historypericarditis vs infarctionCommon characteristicsretrosternl or precordial with raditaion to the neck, back, left shoulder or armSpecial characteristics (pericarditis)more likely to be sharp and pleuritic with coughing, inspiration, swallowingworse by lying supine, relieved by sitting and leaning forward
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Heart Murmurs of PericarditisPericardial friction rub is pathognomic for pericarditisscratching or grating soundClassically three components:presystolic rub during atrial fillingventricular systolic rub (loudest)ventricular diastolic rub (after A2P2)
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Heart Murmur Demo
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Acute PericarditisECG featuresST-segment elevationreflecting epicardial inflammationleads I, II, aVL, and V3-V6lead aVR usually shows ST depressionST concave upward ST in AMI concave downward like a domePR segment depression (early stage)T-wave inversionoccurs after the ST returns to baseline
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Acute PericarditisManagementTreat underlying causeAnalgesic agentscodeine 15-30 mg q 4-6 hrAnti-inflmmatory agentsASA 648 mg q 3-4 hrsNSAID (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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Dresslers SyndromeDescribed 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
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Case Study 1A 56-year-old man develops recurrent chest discomfort 5 days after an anterior myocardial infarction, which was managed initially with tissue plasminogen activator.
The pain is sharp and positional, radiating toward both clavicles. It is different from the pain associated with his infarction.
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Case Study 1Physical Exam:AfebrileNo pericardial friction rub
ECG: mild PR depression in lead 2no significant change in the evolution pattern of his Q-wave anteroseptal myocardial infarction
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Case Study 1The most appropriate therapy for this patient is:SalicylatesIndomethacinCorticosteroidsColchicine
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Case Study 2A 36-year old woman presents to the ER for the second time in a week with pleuritic chest and left shoulder discomfort and a low-grade fever. She had been in an argument with her boy friend 6 days earlier during which he grabbed her by both shoulders and shook her violently.
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Case Study 2HR 82, BP 94/70.Left iris is green, right is blueShe is slender, has a straight back, long fingers, high-arched palate, and slight pectus excavatum.A pericardial friction rub is present.
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Case Study 2A chest radiograph shows an increased cardiac silhouette and a small left pleural effusion.
ECG shows NSR with diffuse J-point elevation and PR-segment depression in lead 2.
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Case Study 2Which one of the following tests should you order?An erythrocyte sedimentation rateA creatine kinase determinationAn echocardiogramAn antinuclear antibodyA D-dimer
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Constrictive Pericarditisrarely develop after an episode of acute idiopathic pericarditismore likely to develop after subacute pericarditis with effusion that evolve over several weeksmore frequent after purulent bacterial or tuberculous pericarditis
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Constrictive Pericarditisin the United StatesIdiopathicradiotherapycardiac surgeryconnective tissue disordersdialysisbacterial infection
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Tuberculous PericarditisIncidence of pericarditis in patients with pulmonary TB ranged from 1-8%Physical findings: fever, pericardial friction rub, hepatomegalyTB skin test usually positiveFluid smear for TB often negativePericardial biopsy more definitive
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Constrictive Pericarditis Physical FindingsJugular veinsprominent X and Y descent with inspiration (Kussmauls sign)Lungs - possible pleural effusionHeart - diastolic pericardial knockAbdomen: ascites, pulsatile liverExtremities: peripheral edema
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Constrictive PericarditisDiagnosisoften not recognized in its early phases by exam, x-ray, ECG, echotendency to overlook elevated JVP
subacute chronicdiastolic knock+++Kussmauls+++paradoxical pulse++++
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Constrictive Pericarditiscatheterization findingsRight and left heart pressure are measured simultaneouslyright and left ventricular diastolic pressure are elevated and nearly equal; may show classic square root signRA pressure has steep X and Y descents and may rise during inspiration (Kussmauls sign)
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Case Study 3A 42-year old man presented because of increasing abdominal girth and lower extremity edema. A decade ago he underwent treatment for Hodgkins disease that included mantle field radiation therapy and MOPP chemotherapy.
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Case Study 3HR 84, BP 100/70JVD not observed at 45 degreesAbsent vocal fremitus at right base Heart sound is distantAn early-mid diastolic sound3+ pitting edema bilaterally
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Case Study 3What is the most likely diagnosis?Effusive pericarditisOccult constrictive pericarditisConstrictive pericarditisIdiopathic dilated cardiomyopathyRestrictive cardiomyopathy
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Types of Effusive Fluidseroustransudative - heart failuresuppurativepyogenic infection with cellular debris and large number of leukocyteshemorrhagicoccurs with any type of pericarditisespecially with infections and malignanciesserosanguinous
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Dignostic EvaluationChest x-rayusually requires > 200 ml of fluidcannot distinguish between pericardial effusion and cardiomeglyEchocardiographystandard for diagnosing pericardial effusionconvenient, highly reliable, cost effectivefalse positives (M-mode)- left pleural effusion, epicardial fat, tumor tissue, pericardial cysts
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Noncompressing Effusionasymptomatic unless they are large enough to compress adjacent organsdysphagiacoughdyspneahoarsenesshiccupsabdminal fullnessnausea
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ECG in Pericardial EffusionDiffuse low voltageamount of fluidelectrical conductivity of the fluidElectrical alternansalternating amplitude of the QRSproduced by heart swinging motionalso seen in PSVT, HTN, ischemia
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Cardiac TamponadeDecompensated cardiac compression from increased intracardaic press
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Cardiac TamponadeEarly stagemild to moderate elevation of central venous pressureAdvanced stage intrapericardial pressure ventricular filling, stroke volumehypotension impaired organ perfusion
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Becks TriadDescribed in 1935 by thoracic surgeon Claude S. Beck3 features of acute tamponade Decline in systemic arterial pressureElevation in systemic venous pressure (e.g. distended neck vein)A small, quiet heart
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Cardiac TamponadeBedside Diagnosis
Elevated jugular venous pressure Paradoxical pulse
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Pulsus Paradoxusan exaggerated drop in blood pressure with inspiration (>10mmHg)tamponade without pulsusatrial septal defectaortic insufficiencyLVH with LVEDPpulsus without tamponadeCOPD, RV infarct, pulmonary embolism
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EchocardiographyPericardial effusionhighly reliableCardiac tamponadeRA and RV diastolic collapsereduced chamber sizedistension of the inferior vena cavaexaggerated respiratory variation of the mitral and tricuspid valve flow velocities
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PericardiocentesisDiagnostic tap usually not indicatedrarely have positive cytology or infection that can be diagnosedTherapeutic drainageindicated for significant elevation of the central venous pressure
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Pericardial WindowBalloon dilatation of a needle pericardiostomysubxyphoid surgical pericardiostomyvideo-assisted thoracoscopy with localized pericardial resectionanterolateral thoracotomy with parietal pericardial resection
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Localized and Low PressureCardiac Tamponade
Localized tamponadedue to loculated pericardial effusionLow pressure tamponadedue to relative intravascular volume depletion
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Restrictive CardiomyopathyDifferentiation from constrictive pericarditis may be difficult from intracardiac pressure tracingsclues from history, physical exam, ECG, echo, CT and MR scanamyloidosis is most likely to simulate constrictive pericarditis
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