Download Echocardiography

Constrictive pericarditis
경희의료원 내과학교실 순환기내과
R3 우종신
Pericardium
Cardiac tamponade
Constrictive pericarditis
Effusive – constrictive pericarditis
Constrictive pericarditis
Etiology
Idiopathic or viral : 42 to 49 percent
Following cardiac surgery : 11 to 37 percent
Following radiation therapy : 9 to 31 percent
(mostly for Hodgkin's disease or breast cancer)
Connective tissue disorder : 3 to 7 percent
Postinfectious : 3 to 6 percent
(tuberculous or purulent pericarditis)
Miscellaneous causes : 1 to 10 percent
(malignancy, trauma, drug-induced, asbestosis, sarcoidosis, uremic
pericarditis)
Etiology
Circulation. 1999;100:1380-1386
History
Fluid overload
Peripheral edema
Generalized edema
Diminished cardiac output response to exertion
Fatiguability
Dyspnea on exertion
Symptoms of heart failure : 67 %
Chest pain : 8 %
Abdominal symptoms : 6 %
Atrial arrhythmia: 4 %
Symptoms of cardiac tamponade : 5 %
Unexplained elevation in jugular venous pressure,
particularly if there is a history of a predisposing condition.
Physical examination
Elevated jugular venous pressure
Peripheral edema
Ascites
Pulsatile hepatomegaly (part of the syndrome of congestive hepatopathy)
Pleural effusion
Pulsus paradoxus
Physical examination
Kussmaul’s sign
Place Pt. sitting up at 90°.
JVP becomes more distended during inspiration
(classically constrictive pericarditis, severe RHF, severe TR).
This is opposite of what happens in normal pt.
Usually negative in cardiac tamponade
Pericardial knock
Electrocardiography
Group 1 : normal thickness (< 2 mm)
Group 2 : thickened pericardium (>2 mm)
Circulation. 2003;108:1852-1857
Chest radiograph
Chest radiograph
A greater likelihood of having idiopathic pericardial disease (67 versus 21 %)
A longer duration of symptoms
A greater likelihood of pericardial knock, larger atria, and atrial arrhythmias
A higher perioperative mortality, but the same long-term survival
Ann Intern Med. 2000;132:444-450.
Echocardiography
Increased pericardial thickness, sometimes with calcification
J Am Coll Cardiol 1997;29:1317–23
TEE assessment of pericardial thickness to support a diagnosis of
constrictive pericarditis
Class IIb recommendation
Echocardiography
Abrupt posterior motion of the ventricular septum in early
diastole with inspiration (septal shudder and bounce)
Echocardiography
M-mode
Notching of the
ventricular septum in
early diastole or with
atrial systole
Rapid posterior motion
of the left ventricular
posterior wall in early
diastole followed by a
flattening
Rapid left atrial emptying
Premature opening of
the pulmonic valve
Echocardiography
Echocardiography
Doppler recording of transmitral inflow velocities
Echocardiography
Doppler of the hepatic vein
Plethora
(dilation and absent or diminished collapse of the inferior vena cava
and hepatic veins)
Computed tomographic (CT) scan
Increased pericardial thickness and calcification
Dilatation of the inferior vena cava
Deformed ventricular contours
Angulation of the ventricular septum
Magnetic resonance imaging
increased pericardial thickening
dilatation of the inferior vena cava
an indirect sign of impaired RV diastolic filling
Hemodynamic evaluation
Hemodynamic evaluation
Prominent x and y descents
Hemodynamic evaluation
True dip and plateau in constrictive pericarditis ("Square root" sign )
Plasma BNP
increased in patients with left ventricular dysfunction
Constrictive pericarditis
wall stretch is limited by the thickened stiff pericardium
Restrictive cardiomyopathy
released in response to left ventricular dysfunction and wall stretch
J Am Coll Cardiol. 2006 47:1489-91
Differential diagnosis
Suggested by history
Prior pericarditis
Tuberculosis
Connective tissue disease
Malignancy
Trauma
Cardiac surgery
Pericardial knock favors constriction
Thickened pericardium on TEE, CT or calcification on CXR
Doppler studies
Hepatic vein flow reversal is expiratory
RVEDP and LVEDP are equal
Endomyocardial, or less commonly, pericardial biopsy
Pro-BNP normal as myocardium not stretched
Restrictive Cardiomyopathy
nondilated rigid ventricle
severe diastolic dysfunction and restrictive filling
History of infiltrative disease
amyloidosis
Sarcoidosis
bundle branch block, ventricular hypertrophy, pathologic Q
waves, or impaired atrioventricular conduction strongly favors
restrictive cardiomyopathy
Decreased myocardial tissue velocity by Doppler
Pro-BNP elevated
Cardiac Tamponade
Pericardial fluid enlarging around the heart
Acute vs Subacute
Equalization of pressures measured by catheterization
RA = RVED = PCW = Pericardial
Blunting of y descent
As opposed to exaggerated y descent in constrictive pericarditis
Treatment and outcome
Transient constrictive pericarditis
The presence
of acute
inflammatory
pericarditis
with
constriction
J Am Coll Cardiol
2004;43:271–5
Treatment and outcome
Transient constrictive pericarditis
newly diagnosed
absence of evidence that the condition is chronic (eg, cachexia,
atrial fibrillation, hepatic dysfunction, or pericardial calcification)
indication for pericardiectomy
Worsening systemic congestion, as manifested by increased
symptoms
otherwise unexplained weight gain
a new or increased pleural effusion or ascites
Treatment and outcome
Pericardiectomy
standard of treatment for persistent and prominent symptoms
Mortality : 6 - 12 %
should be considered cautiously
with either mild or very advanced disease
(cachexia, atrial fibrillation,
a low cardiac output (cardiac index 1.2 L/m2 per min) at rest,
hypoalbuminemia due to protein losing enteropathy
impaired hepatic function due to chronic congestion or
cardiogenic cirrhosis)
radiation-induced constriction
myocardial dysfunction
significant renal dysfunction
Treatment and outcome
Pericardiectomy
J Am Coll Cardiol 1999;33:1182– 8