Transcript Acute Pericarditis

Acute Pericarditis
 Incidence – Post mortem 1-6%, diagnosed
in only 0.1% of hospitalized patients. 5% of
patients seen in emergency rooms with CP
and no MI.
 Sequelae – Cardiac tamponade
Recurrent pericarditis
Pericardial constriction
Etiology
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Viral or idiopathic
After MI
Infectious diseases
With dissecting aortic aneurysms
Trauma
Metastasis
XRT
Uremia
After cardiac or other thoracic surgery
Autoimmune diseases
Medications
Clinical Presentation
 History
 Physical Exam- 85% have audible friction rub
during the course of their disease ( the rub is high
pitched scratchy or squeaky sound best heard at
the left sternal border at end of expiration with the
patient leaning forward)
 The rub has three components- atrial systole,
ventricular systole and rapid ventricular filling
during early diastole.
Evaluation
 A diagnosis of acute pericarditis should be
reserved for patients with an audible
pericardial friction rub or CP with typical
EKG findings, most notably ST- segment
elevation.
EKG
 Stages of pericarditis:
I- Diffuse ST elevation and PR segment depression
(seen in more than 80%)
II- Normalization of the ST and PR
III- Widespread T- wave inversions
IV- Normalization of the T waves
 The most reliable distinguishing feature may be
the ratio of ST segment elevation (in millimeters)
to T-wave amplitude in lead V6; ratio > 0.24
Cardiac Tamponade
Clinical Findings
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Systemic arterial hypotension
Tachycardia
Elevated JVP
Pulsus paradoxus (most sensitive but not
specific)
 15% of patients with idiopathic pericarditis or
as many as 60% of those with neoplastic,
tuberculous, or purulent pericarditis can
present with Cardiac Tamponade.
Echo Findings in Pre-Tamponade
Physiology
 Diastolic right ventricular collapse
 Right atrial collapse/inversion
 Exagerated respiratory variation in inflow
velocity
 Exagerated respiratory variation in inferior
vena cava flow
 Dilated IVC in the right setting
Echo-Guided Pericardiocentesis
 Multiple Echo windows should be used to
determine the distribution of the fluid. Specifically,
the distribution and depth from the surface of the
chest at which contact with the fluid is anticipated
by the pericardiocentesis needle should be
determined. If the location of a pericardiocentesis
needle is in question, agitated saline can be
injected to further define the location of the tip.
Differential Diagnosis
Pericarditis
 Clinical presentation should guide the ordering of
additional tests. Routine serologic testing,
including testing for ANA and RF, reveals a source
for the pericarditis for only 10-15% of patients.
 Plasma troponin concentrations are elevated in
35-50% of patients with pericarditis. The
magnitude of the ST elevation appears to correlate
with magnitude of troponin elevation. A troponin
elevation lasting more than 2 weeks, suggests
associated myocarditis.
Pericardiocentesis and Biopsy
 In those with pericardial tamponade and in
those with known or suspected purulent or
neoplastic pericarditis.
 In a study involving 230 patients with acute
pericarditis in whom the cause was
unknown, pericardiocentesis and pericardial
biopsy provided a diagnosis in only 6% and
5% respectively.
Laboratory Evaluation
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Red and white cell count.
Cytology
TG
CTX
No evidence for PH, glucose, LDH and
protein measurement.
 PCR > 30 U/L for adenosine deaminase
activity may help in identifying MTB
Treatment
 In observational studies, NSAIDS relieved CP in
85-90% of patients: ASA, Indomethacin or
Ibuprofen.
 Indomethacin may impair coronary blood flow in
CAD.
 In a multicenter trial of 51 patients who had
recurrent pericarditis despite tx with NSAIDS,
glucocorticoids, pericardiocentesis or some
combination. Only 7 of those treated with
colchicine had a recurrence during 1004 patientmonths of follow up.
Sauleda
Treatment
 Typically CP improves within days of initiating
antinflammatory tx.
• If CP persists after two weeks of tx with an NSAID,
a different NSAID should be given or colchicine
should be added to provide combination therapy.
• Glucocorticoids should be considered if CP
persists after combination tx.
• Lack of response to steroids often reflects the use
of an inadequate dose or too rapid tapering.
Treatment
Several indicators of poor prognosis:
 >38*C
 Subacute onset
 Immunosuppressed
 After trauma
 Anticoagulation use
 Myopericarditis
 Large effusion or tamponade
Treatment
 Use of steroids should be reserved for patients
with CTD, recurrent severe pericarditis that is
unresponsive to combination of NSAIDS and
colchicine.
 Some studies suggest that the early use of these
drugs may increase the risk of recurrence
(exception colchicine).
 Observational data suggest that physical invasion
of the pericardium (pericardiotomy or a window)
promotes recurrences.
Effusive Constrictive Pericarditis
 Is a clinical hemodynamic syndrome in
which constriction of the heart by the
visceral pericardium occurs in the
presence of tense effusion in a free
pericardial space.
 The hallmark is the persistence of elevated
right atrial pressure after intrapericardial
pressure has been reduced to normal levels
by removal of pericardial fluid.