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Acute Pericarditis and
Pericardial Effusion
Meghan York
September 9, 2009
Outline
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Anatomy of pericardium
Overview of pericardial disease
Etiology
Clinical presentation
Ancillary diagnostics
Echocardiography in evaluation
Anatomy


Normal amount of
pericardial fluid: 15-50 cc
Two layers:


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
Pericardium


Fibroelastic sac
consisting of 2 layers
 Visceral at
epicardial side
 Parietal at
mediastinal side
Pericardial fluid
formed from
ultrafiltrate of plasma
Diseases of the Pericardium


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Acute Fibrinous Pericarditis
Pericardial Effusion
 Cardiac tamponade
Recurrent Pericarditis
Constrictive Pericarditis
Epidemiology of Acute Pericarditis

0.1% of hospitalized patients

5% of patients admitted to Emergency
Department for non-acute myocardial infarction
chest pain
Findings on Echo

Pericardial effusion


If present, possibility of tamponade physiology
needs to be considered
Pericardial thickening
Increased echogenicity of pericardial reflection and
as multiple parallel reflections posterior to the LV on
M-mode
 If present, evidence of constrictive physiology
should be considered

Tamponade: 2D
Pericardial thickening on Echo
Findings on CT
Chest X ray



Normal in patients
with acute
pericarditis unless
pericardial effusion
is present
Enlarged cardiac
silhouette
Requires 200cc of
fluid
Chest X Ray
Major Causes of Pericardial Disease
1)Infection
2)Radiation
3)Neoplasm
4)Myocardial intrinisic disease
5)Trauma
6)Autoimmune
7)Drugs
8)Metabolic
*viral, autoreactive/autoimmune, and neoplastic most
common diagnosis
Etiology of Acute Pericarditis:
Infectious
Viral
-adenovirus
-enterovirus
-cytomegalovirus
-influenza
-hepatitis B
-herpes simplex
-echovirus
-mumps
Mycoplasma
Fungal
Parasitic
Bacterial
-staphylococcus
-streptococcus
-pneumococcus
-haemophilus
-neisseria
-chlamydia
-legionella
-tuberculous
-lyme disease
Etiology: continued
Radiation
Neoplasm
-metastatic
-primary cardiac
-paraneoplastic
Cardiac
-early infarction
-Dressler’s
-myocarditis
-aortic dissection
Trauma
-blunt
-iatrogenic (perforations, post-surg)
Autoimmune
-rheumatic disease
-non-rheumatic
-Wegners, sarcoid, IBD
Etiology: continued
Drugs
-drug induced lupus
hydralazine
isoniazid
procainamide
-doxorubicin
-phenytoin
Metabolic
-hypothyroid
-uremia
-ovarian hyperstimulation
Lab Testing

the historic yield of diagnostic evaluation is low,
typically only in 16% of patients is etiology
determined.

evaluation of pericardial fluid and tissue with
tumor markers, PCR, immunohistochemistry,
flourescence-activated cell sorting has shown a
trend toward higher yield of diagnosis
Diagnosis of Pericarditis:
Presence of two of the following necessary
1) Chest pain
 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
 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
Pertinent Lab Results

Elevated C reactive protein level
 strong correlation - normal CRP makes acute
pericarditis diagnosis less likely

Elevated CK, CK-MB, and Troponin
 Often elevated Troponin alone
 Indicates inflammation of myocardium just
beneath the visceral pericardium
 Not associated with worse outcomes

Leukocytosis
ECG Findings: 60% of patients


Stage 1: hours to days
 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 2:
 Normalization
ECG changes over weeks

Stage 3:


Diffuse T wave
inversions
ST segments isoelectric

Stage 4:


EKG may normalize
T wave inversions may
persist indefinitely
STEMI or Pericarditis by ECG

ST elevation in pericarditis



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Starts at J point
Rarely exceeds 5mm
Retains normal concavity
Non-localizing
Arrhythmias very unlikely
in pericarditis (suggest
myocarditis or MI)
Acute Pericarditis

51yo man with acute onset sharp substernal chest pain
two days prior
Pericardial Effusion

Low voltage and Electric Alternans
ACC/AHA/ASE 2003 guideline
update for the clinical application of
echocardiography: summary article

Recommended specific circumstances for
use of echocardiography in pericardial
disease
Class I Recommendations
1. Patients with suspected pericardial disease,
including effusion, constriction, or effusiveconstrictive process.
2. Patients with suspected bleeding into the
pericardial space (trauma, perforation,
dissection)
Class I (continued)
3. Follow-up study to evaluate recurrence of
effusion or to diagnose early constriction;
repeat studies may be goal directed to
answer a specific clinical question
4. Pericardial friction rub developing in acute
myocardial infarction accompanied by
symptoms such as persistent pain,
hypotension, and nausea.
Class IIa
1)Follow-up studies to detect early signs of
tamponade in the presence of large or
rapidly accumulating effusions. A goaldirected study may be appropriate.
2)Echocardiographic guidance and
monitoring of pericardiocentesis.
Class IIb
1) Postsurgical pericardial disease, including
postpericardiotomy syndrome, with
potential for hemodynamic impairment.
2) In the presence of a strong clinical
suspicion and nondiagnostic TTE, TEE
assessment of pericardial thickness to
support a diagnosis of constrictive
pericarditis.
Effusion: 2D Parasternal Long
Pericardial Fat Pad


Often pericardial fat pads can be seen in this
view anterior to the RVOT
Fat pads usually not seen elsewhere
Effusion: Parasternal Short Axis
Posterior Effusions


Pericardial effusions can track posteriorly toward
sinus
In this case, may only be seen in axial 4 chamber
view
Effusion: 2D Apical
Tamponade



Pressure in pericardium exceeds pressure in the cardiac
chambers, lower chamber atria affected before higher
pressure ventricles
Compressive effect is seen best in the phase when the
intrachamber pressure is lowest – systole for atria and
diastole for ventricles
Diagnostic techniques



2D looking for RA/RV collapse during diastole
M-mode for RA/RV collapse during diastole
Doppler of Mitral and Tricuspid inflow



Mitral inflow to decrease by 25% with inspiration
Tricuspid inflow increased by 40% with inspiration
IVC diameter fails to increase with inspiration
Tamponade: 2D
Tamponade: M-Mode
Tamponade: Doppler
Mitral Inflow
Fibrinous Pericarditis