Pericardial Disease
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Pericardial Disease
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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 monolayer
facilitate 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 Inflammation
pathogenesis
• 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 Inflammation
pathology
• 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 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, varicellazoster, influenza, Epstein-Barr, HIV
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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
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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
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Chest Pain History
pericarditis 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 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
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Acute Pericarditis
Management
• 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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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
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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
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Acute Pericarditis
Differential Diagnosis
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Acute myocardial infarction
Pulmonary embolism
Pneumonia
Aortic dissection
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Case Study 1
A 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 1
Physical Exam:
Afebrile
No pericardial friction rub
ECG:
mild PR depression in lead 2
no significant change in the evolution
pattern of his Q-wave anteroseptal
myocardial infarction
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Case Study 1
The most appropriate therapy for this
patient is:
– Salicylates
– Indomethacin
– Corticosteroids
– Colchicine
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Case Study 2
A 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 2
HR 82, BP 94/70.
Left iris is green, right is blue
She 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 2
A 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 2
Which one of the following tests
should you order?
– An erythrocyte sedimentation rate
– A creatine kinase determination
– An echocardiogram
– An antinuclear antibody
– A D-dimer
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Constrictive Pericarditis
• 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
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Constrictive Pericarditis
in the United States
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Idiopathic
radiotherapy
cardiac surgery
connective tissue disorders
dialysis
bacterial infection
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CONSTRICTIVE PERICARDITIS
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Tuberculous Pericarditis
• 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
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Constrictive Pericarditis
Physical Findings
• Jugular veins
– prominent X and Y descent
–  with inspiration (Kussmaul’s sign)
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Lungs - possible pleural effusion
Heart - diastolic pericardial knock
Abdomen: ascites, pulsatile liver
Extremities: peripheral edema
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Constrictive Pericarditis
Diagnosis
• often not recognized in its early
phases by exam, x-ray, ECG, echo
• tendency to overlook elevated JVP
subacute chronic
diastolic knock
+
++
Kussmaul’s
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paradoxical pulse
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Constrictive Pericarditis
catheterization findings
• Right and left heart pressure are
measured simultaneously
– right and left ventricular diastolic
pressure are elevated and nearly equal;
may show classic “square root sign”
– RA pressure has steep X and Y
descents and may rise during
inspiration (Kussmaul’s sign)
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Case Study 3
A 42-year old man presented
because of increasing abdominal
girth and lower extremity edema. A
decade ago he underwent treatment
for Hodgkin’s disease that included
mantle field radiation therapy and
MOPP chemotherapy.
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Case Study 3
HR 84, BP 100/70
JVD not observed at 45 degrees
Absent vocal fremitus at right base
Heart sound is distant
An early-mid diastolic sound
3+ pitting edema bilaterally
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Case Study 3
What is the most likely diagnosis?
– Effusive pericarditis
– Occult constrictive pericarditis
– Constrictive pericarditis
– Idiopathic dilated cardiomyopathy
– Restrictive cardiomyopathy
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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
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dysphagia
cough
dyspnea
hoarseness
hiccups
abdminal fullness
nausea
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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
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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 Tamponade
Bedside 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
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Pericardial Window
• Balloon dilatation of a needle
pericardiostomy
• subxyphoid surgical pericardiostomy
• video-assisted thoracoscopy with
localized pericardial resection
• anterolateral thoracotomy with
parietal pericardial resection
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Localized and Low Pressure
Cardiac Tamponade
• Localized tamponade
due to loculated pericardial effusion
• Low pressure tamponade
due to relative intravascular volume
depletion
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Restrictive Cardiomyopathy
• Differentiation from constrictive
pericarditis may be difficult from
intracardiac pressure tracings
• clues from history, physical exam,
ECG, echo, CT and MR scan
• amyloidosis is most likely to
simulate constrictive pericarditis
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