Pericardial DiseaseBy:Dawit Ayele
MD,Internist
Acute Pericarditis Chronic Relapsing Pericarditis Constrictive Pericarditis Cardiac Tamponade
Pericardial Disease
Two major components◦ serosa (viceral pericardium)
mesothelial monolayerfacilitate fluid and ion exchange
◦ fibrosa (parietal pericardium)fibrocollagenous tissue
Pericardial Fluid◦ 15 - 50 ml of clear plasma ultrafiltrate
Ligamentous attachments◦ to the sternum, vertebral column, diaphragm
Pericardial Anatomy
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
Pericardial Physiology
Contiguous spread◦ lungs, pleura, mediastinal lymph nodes,
myocardium, aorta, esophagus, liver Hematogenous spread
◦ septicemia, toxins, neoplasm, metabolic Lymphangetic spread Traumatic or irradiation
Pericardial Inflammationpathogenesis
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
Pericardial Inflammationpathology
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 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
Acute Pericarditiscommon causes
Historysudden onset of anterior chest pain thatis pleuritic and substernal
Physical exampresence of two- or three-component rub
ECGmost important laboratory clue
Acute PericarditisDiagnostic Clues
Common characteristics◦ retrosternal 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
Chest Pain Historypericarditis vs infarction
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)
Heart Murmurs of Pericarditis
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 PericarditisECG features
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
Acute PericarditisManagement
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
Chronic Relapsing Pericarditis
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
Dressler’s Syndrome
Acute myocardial infarction Pulmonary embolism Pneumonia Aortic dissection
Acute PericarditisDifferential Diagnosis
rarely develop after an episode of acute idiopathic pericarditis
more likely to develop after subacute pericarditis with effusion that evolve over several weeks
more frequent after purulent bacterial or tuberculous pericarditis
Constrictive Pericarditis
Idiopathic radiotherapy cardiac surgery connective tissue disorders dialysis bacterial infection
Constrictive Pericarditiscauses
Incidence of pericarditis in patients with pulmonary TB ranged from 1-8%
Physical findings: fever, pericardial friction rub, hepatomegaly
TB skin test usually positive Fluid smear for TB often negative Pericardial biopsy more definitive
Tuberculous Pericarditis
Jugular veins◦ prominent X and Y descent◦ with inspiration (Kussmaul’s sign)
Lungs - possible pleural effusion Heart - diastolic pericardial knock Abdomen: ascites, pulsatile liver Extremities: peripheral edema
Constrictive Pericarditis Physical Findings
often not recognized in its early phases by exam, x-ray, ECG, echo
tendency to overlook elevated JVPsubacute chronic
diastolic knock + ++Kussmaul’s + ++paradoxical pulse ++ ++
Constrictive PericarditisDiagnosis
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
Types of Effusive Fluid
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
Dignostic Evaluation
asymptomatic unless they are large enough to compress adjacent organs◦ dysphagia◦ cough◦ dyspnea◦ hoarseness◦ hiccups◦ abdminal fullness◦ nausea
Noncompressing 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
ECG in Pericardial Effusion
Decompensated cardiac compression from increased intracardaic press
Cardiac Tamponade
Early stage◦ mild to moderate elevation of central venous
pressure Advanced stage
◦ intrapericardial pressure ventricular filling, stroke volume
◦ hypotension ◦ impaired organ perfusion
Cardiac Tamponade
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
Beck’s Triad
Elevated jugular venous pressure Paradoxical pulse
Cardiac TamponadeBedside Diagnosis
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
Pulsus Paradoxus
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
Echocardiography
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
Pericardiocentesis
Balloon dilatation of a needle pericardiostomy
subxyphoid surgical pericardiostomy video-assisted thoracoscopy with localized
pericardial resection anterolateral thoracotomy with parietal
pericardial resection
Pericardial Window