Transcript Document

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Anatomy of pericardium
Overview of pericardial disease
Etiology
Clinical presentation
Treatment
 Normal
amount of
pericardial fluid: 15-50
cc
 Two layers:
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
Outer layer is the
parietal pericardium and
consists of layers of
fibrous and serous tissue
Inner layer is visceral
pericardium and consists
of serous tissue only
Fibroelastic sac
consisting of 2 layers
 Visceral at
epicardial side
 Parietal at
mediastinal side
 Pericardial fluid
formed from
ultrafiltrate of
plasma

 Acute
Fibrinous Pericarditis
 Pericardial Effusion
 Cardiac
 Recurrent
tamponade
Pericarditis
 Constrictive Pericarditis
 0.1%
 5%
of hospitalized patients
of patients admitted to Emergency
Department for non-acute myocardial
infarction chest pain
 Exact
incidence and prevalence are unknown
 Diagnosed in 0.1% of hospitalized patients
and 5% of patients admitted for non-acute MI
chest pain
 Observational study: 27.7 cases/100,000
population/year
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Chest pain: anterior chest, sudden onset, pleuritic;
may decrease in intensity when leans forward, may
radiate to one or both trapezius ridges
Pericardial friction rub: most specific, heard best at
LSB
EKG changes: new widespread ST elevation or PR
depression
Pericardial effusion: absence of does not exclude
diagnosis of pericarditis
Supporting signs/symptoms:
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Elevated ESR, CRP
Fever
leukocytosis
1) Chest pain
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Sudden onset
localized to anterior chest wall
pleuritic
sharp
Positional: may improve if pt leans forward, worse with lying
flat
2) Cardiac auscultation: Pericardial friction rub
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
Present in up to 85% of pts with pericarditis without effusion
friction of the two inflamed layers of pericardium, typically
triphasic rub, heard with diaphragm of stethoscope at left
sternal border
3) Characteristic ECG changes
4) Pericardial effusion
 Stage
days


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Diffuse ST elevation
-sensitive v5-v6, I,
II
ST depression I/aVR
PR elevation aVR
PR depression diffuse
-especially v5-v6
PR change is marker
of atrial injury
 Stage

1: hours to
2:
Normalization
 Stage
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3:
Diffuse T wave
inversions
ST segments
isoelectric
 Stage
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4:
EKG may normalize
T wave inversions
may persist
indefinitely
 ST
elevation in
pericarditis
Starts at J point
 Rarely exceeds 5mm
 Retains normal concavity
 Non-localizing

 Arrhythmias
very
unlikely in pericarditis
(suggest myocarditis or
MI)
 51yo
man with acute onset sharp substernal
chest pain two days prior
Electrocardiogram in acute pericarditis showing diffuse upsloping ST segment elevations seen best here in
leads II, III, aVF, and V2 to V6. There is also subtle PR segment deviation (positive in aVR, negative
in most other leads). ST segment elevation is due to a ventricular current of injury associated with epicardial
inflammation; similarly, the PR segment changes are due to an atrial current of injury which, in pericarditis,
typically displaces the PR segment upward in lead aVR and downward in most other leads.
Small
Moderate
Large
Location
Posterior
Inferior to LV
Extends to
apex
Circumscribes
heart
*Meas. @
Diastole
<10 mm
10-15 mm
>15 mm
*maximal width of pericardial stripe
 Low
voltage and Electric Alternans
Cardiomegaly due to a massive pericardial effusion. At least 200 mL of
pericardial fluid must accumulate before the cardiac silhouette enlarges.
 M-Mode
 M-mode
Cannot determine volume of
accumulated fluid accurately
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Aspirin
NSAIDs
Colchicine: can reduce or eliminate need for glucocorticoids
Glucocorticoids: should be avoided unless required to treat patients who
fail NSAID and colchicine therapy
Many believe that prednisone may perpetuate recurrences
 Intrapericardial glucocorticoid therapy: sx improvement and prevention of
recurrence in 90% of patients at 3 months and 84% at one year
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Other immunosuppression
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Azothoprine (75-100 mg/day)
Cyclophosphamide
Mycophenolate: anecdotal evidence only
Methotrexate: limited data
IVIG: limited data
Pericardiectomy: To avoid poor wound healing, recommended to be off
prednisone for one year. Reserved for the following cases:
If >1 recurrence is accompanied by tamponade
 If recurrence is principally manifested by persistent pain despite an intensive
medical trial and evidence of serious glucocorticoid toxicity

 Normal
amt of pericardial fluid = 20-50 mL
 Tamponade
occurs when lg or rapidly formed
effusions  inc’d pressure in the pericardial
space throughout the cardiac cycle
 During
inspiration, RV volume inc’s & in
tamponade, the RV is unable to expand into
the maximally stretched pericardium  Lward bulging of the interventricular septum
 dec’d LVEDV  dec’d cardiac output &
dec’d SBP during inspiration
 Pressure
in pericardium exceeds s
 Compressive effect in intrachamber
 Diagnostic techniques
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2D looking for RA/RV collapse during diastole
M-mode for RA/RV collapse during diastole
Doppler of Mitral and Tricuspid inflow
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Mitral inflow to decrease by 25% with inspiration
Tricuspid inflow increased by 40% with inspiration
IVC diameter fails to increase with inspiration

HIV, bacterial (incl mycobacterial), viral, fungal
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CA - Esp lung, breast, Hodgkin’s, mesothelioma
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Radiation tx
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Meds - Hydralazine, Procainamide, INH, Minoxidil
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Post-MI (free wall ventricular rupture, Dressler’s syndrome)
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Connective tissue dzs – SLE, RA, Dermatomyositis
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Uremia
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Trauma
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Iatrogenic – (eg, from TLC / PA Cath / TV pacemaker insertion, coronary
dissection & perforation, sternal bx, pericardiocentesis, GE jnx surgeries)
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Other - Pneumopericardium (d/t mech ventilation or gastropericardial
fistula), Pleural effusions

Idiopathic
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Sxs
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Chest Pain, dyspnea, near-syncope
Generally more comfortable sitting forward
Sxs c/w the underlying cause of tamponade
Physical Exam
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Beck’s Triad - Elev’d JVP, hypotension, dec’d heart
sounds
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JVP w/ preserved x descent and dampened or absent y
descent
Generally w/ narrow pulse pressure
Tachycardia, other signs of HF (tachypnea, diaphoresis,
cool extremities, cyanosis, etc)
Pulsus paradoxus
Dec’d or absent cardiac impulse
+/- Friction rub
 Dec
in SBP > 10-12 mmHg
w/ inspiration
 Can
also occur in pts w/
COPD, pulm dz, PTX,
severe asthma
 Can
have tamponade
w/o pulsus paradoxus
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In pts w/ pre-existing
elev’s in diastolic pressures
and/or volume (eg, LV
dysfnx, AI and ASD)
 Tamponade
 Other
is a Clinical Diagnosis
Detection Methods
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EKG
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CXR
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TTE
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R Heart Cath
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CT, MRI
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Common Findings
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Sinus tachycardia
Non-specific ST segment and T wave changes
Changes assoc’d w/ acute pericarditis (incl diffuse STE & PR
depression)
Other Findings
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Dec’d voltage (non-specific and can also be d/t emphysema,
infiltrative myocardial dz, PTX, etc)
Electrical alternans (specific but relatively insensitive for lg
effusions)
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2/2 anterior-posterior swinging of the heart w/ each beat
Best seen in leads V2 to V4
Combined P wave and QRS complex alternation (specific for
cardiac tamponade)
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Sudden inc in size of
cardiac silhouette w/o
specific chamber
enlargement
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Effacement of the normal
cardiac borders
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Development of a “flask”
or “H2O-bottle” shaped
heart
 May
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have (+) fat pad sign
Separation of mediastinal /
retrosternal fat and
epicardial fat by > 2 mm
 Normal
in patients
with acute
pericarditis unless
pericardial
effusion is present
 Enlarged cardiac
silhouette
 Requires 200cc of
fluid
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If mild, can sometimes tx w/ medical mgmt
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Including 1 or more of the following: NSAIDs,
Colchcine, and/or steroids, depending on the
suspected cause.
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Require very close monitoring, including w/
serial TTEs and/or RHC
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Most require urgent/emergent
pericardiocentesis
Closed pericardiocentesis
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Open Pericardiocentesis in the OR
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Generally in cath lab but can be at bedside
Subxiphoid approach under echo guidance is most
common - minimizes risk & can assess completeness of
fluid removal
Can alternatively use Fluoroscopic guidance
Pigtail catheter often left in place
May be best for loculated effusions, effusions
containing clots or fibrinous material, and/or effusions
that are borderline in size
Allow for bx and creation of a pericardial window for
recurrent effusions
Bedside pericardiocentesis if pt is in extremis
 16-
or 18-gauge needle
inserted at angle of
30-45° to the skin,
near the left
xiphocostal angle,
aiming toward the L
shoulder