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Pericardial Disease

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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 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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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, varicella-zoster,
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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Heart Murmur Demo

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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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Dresslers 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

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

Idiopathic
radiotherapy
cardiac surgery
connective tissue disorders
dialysis
bacterial infection
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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 (Kussmauls sign)

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
+
++
Kussmauls
+
++
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 (Kussmauls 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 Hodgkins 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

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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Becks 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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