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Pericardial DiseaseBy Dr. Muhammad Aftab ShahSenior Registrar Cardiology
KEMU/Mayo Hospital, Lahore.
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Pericardial Disease
• Acute Pericarditis
• Chronic Relapsing Pericarditis
• Constrictive Pericarditis
• Cardiac Tamponade
• Localized and Low Pressure Tamponade
• Restrictive Cardiomyopathy
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Pericardial Anatomy• Two major components– serosa (viceral pericardium)
mesothelial monolayerfacilitate fluid and ion exchange
– fibroa (parietal pericardium)fibrocollagenous tissue
• Pericardial Fluid– 15 - 50 ml of clear plasma ultrafiltrate
• Ligamentous attachments– to the sternum, vertebral column, diaphragm
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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
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Pericardial Inflammationpathogenesis
• Contiguous spread– lungs, pleura, mediastinal lymph nodes,
myocardium, aorta, esophagus, liver
• Hematogenous spread– septicemia, toxins, neoplasm, metabolic
• Lymphangetic spread
• Traumatic or irradiation
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Pericardial Inflammationpathology
• inflammation provokes a fibrinous exudate with or without serous effusion
• the normal transparent and glistening pericardium is turned into a dull, opaque, and “sandy” sac
• can cause pericardial scarring with adhesions and fibrosis
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PERICARDITIS
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Acute Pericarditiscommon 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
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Acute Pericarditiscommon causes
• Inpatient 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 Clues
• Historysudden onset of anterior chest pain that
is pleuritic and substernal
• Physical exampresence of two- or three-component rub
• ECGmost important laboratory clue
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Chest Pain Historypericarditis vs infarction
• Common characteristics– retrosternl or precordial with raditaion
to the neck, back, left shoulder or arm
• Special characteristics (pericarditis)–more likely to be sharp and pleuritic with coughing, inspiration, swallowing– worse by lying supine, relieved by
sitting and leaning forward
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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)
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Acute PericarditisECG 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
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Acute PericarditisManagement
• Treat underlying cause
• Analgesic agents– codeine 15-30 mg q 4-6 hr
• Anti-inflmmatory agents– ASA 648 mg q 3-4 hrs– NSAID (indomethacin 25-50 mg qid)– Corticosteroids are symptomatically
effective , but preferably avoided
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Types of Effusive Fluid
• serous– transudative - heart failure
• suppurative– pyogenic infection with cellular debris and
large number of leukocytes
• hemorrhagic– occurs with any type of pericarditis– especially with infections and malignancies
• serosanguinous
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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
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Noncompressing Effusion
• asymptomatic unless they are large enough to compress adjacent organs– dysphagia– cough– dyspnea– hoarseness– hiccups– abdminal fullness– nausea
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Cardiac Tamponade
• Decompensated cardiac compression from increased intracardaic press
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Cardiac Tamponade
• Early stage–mild 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 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
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Cardiac TamponadeBedside Diagnosis
• Elevated jugular venous pressure
• Paradoxical pulse
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Pulsus Paradoxus
• an exaggerated drop in blood pressure with inspiration (>10mmHg)
• tamponade without pulsus– atrial septal defect– aortic insufficiency– LVH with LVEDP
• pulsus without tamponade– COPD, RV infarct, pulmonary embolism
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Echocardiography
• 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
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Pericardiocentesis
• Diagnostic tap– usually not indicated– rarely have positive cytology or
infection that can be diagnosed
• Therapeutic drainage– indicated for significant elevation of the
central venous pressure