The pericardium is made
up of two layers. The epicardium (visceral pericardium) is a serous membrane
which lies directly adherent to the heart and the outer layer is called the
fibrous (parietal) pericardium. The normal thickness of the parietal
pericardium is approximately 2 mm. there is approximately 10 to 50 mL of fluid
normally between the epicardium and the fibrous pericardium. This normal
pericardial fluid may be seen as an echo-free space during ventricular systole.
When the echo-free space persists throughout the cardiac cycle, a pericardial
effusion is considered present. When quantitating the amount of pericardial
fluid by echocardiography the fluid should be measure during ventricular
diastole. Intrapericardial stands or fibrin strands within pericardial effusion
most likely indicate inflammation or long-standing pericardial effusion.
The most common
presenting symptom of acute Pericarditis is Chest pain; other symptoms include
dyspnea, fever and cough. The chest pain associated with acute Pericarditis may
be relieved by the patient sitting up and leaning forward.
The expected
echocardiographic finding for Pericarditis is a pericardial effusion but
patients may have Pericarditis without pericardial effusion (dry Pericarditis).
Additionally pericardial effusion can occur in the absence of pericardial
inflammation such as in post-operative cardiac surgery, chronic renal disease, collagen
vascular disease, cardiac trauma, malignancy, AIDS and hypothyroidism.
The best guideline for
differentiating pericardial effusion from pleural effusion by two dimensional
echocardiography is: pericardial effusion is located anterior to the descending
aorta; pleural effusion is present posterior to the descending aorta; in
addition, a large pericardial effusion usually surrounds the heart.
Pulsus paradoxus is
present when there is an exaggerated inspiratory decline in arterial blood pressure
of more than 10 mmHg. Pulsus paradoxus is associated with cardiac tamponade for
two reasons: filling of both ventricles against a common stiffness and
respiratory changes in the venous pressure differential (systemic versus
pulmonary) alternately favoring right and left ventricular filling. Respiratory
variations of the cardiac Doppler signal of the atrioventricular valves suggest
pulsus paradoxus.
In cardiac tamponade
the right ventricular diastolic collapse occurs in early diastolic when the
right ventricular volume and pressure are at lowest levels. Right ventricular diastolic
collapse can be observed in the parasternal long axis view, parasternal short
axis view, apical four chambers and the subcostal four chamber view.
With a large anterior
and posterior pericardial effusion the heart may move freely within the
pericardial cavity. This type of motion called the swinging heart syndrome
tends to occur in large pericardial effusions. The swinging may cause the
phenomenon of electrical alternant.
Marked (more than 25%)
respiratory variation of tricuspid valve (increase in inspiration; decrease
with expiration) and mitral valve (decrease in inspiration; increase with
expiration) peak flow velocities and/or velocity time integrals is a strong
indicator for the presence of cardiac tamponade. The orders in which changes
occur are fairly predictable. Changes in the tricuspid occur first, followed by
changes in the mitral valve with right atrial collapse being the next change
and right ventricular diastolic collapse occurring last. Hepatic vein flow in
cardiac tamponade mimics the flow changes of the tricuspid valve. The hepatic
vein will have a reduction or reversal of diastolic flow expiration.
Constrictive Pericarditis
results in the impairment of diastolic filling of the heart which may result in
diastolic heart failure. Diastolic filling is impaired because of the
constraint the pericardium places on the heart. Intracardiac filling pressures
are usually increased in patients with constrictive Pericarditis. Constrictive Pericarditis
should be a differential diagnosis in patients who present with congestive
heart failure and normal global ventricular systolic function. Virtually all
filling of the ventricle occurs in very early diastole. This abnormal pattern
of diastolic filling is reflected in the characteristic dip-and-plateau (square
root sign) waveforms in both the right and the left ventricles. The rapid rise
in pressure after the early diastolic correspond to the period of rapid
diastolic filling while the plateau phase correspond to the period of mid and
late diastole when there is little additional expansion of ventricular volume. This
can be expressed by the inflow patterns of the mitral valve and tricuspid valve
with increased E/A ratio (more than 1.5) and shortened deceleration time ( less
than 140 msec).
Causes of Constrictive Pericarditis
include prior pericardiotomy, idiopathic, Pericarditis, radiation, infection
and collagen vascular disease. Tuberculosis was at one time considered the
leading cause of constrictive Pericarditis but idiopathic and prior
pericardiotomy are the most common reason for Constrictive Pericarditis currently.
A thickened pericardium
more than 2 mm, interventricular/inter-Atrial septal bounce (shudder),
bound-down appearance of the ventricular walls with lack of pericardial slide,
inferior vena cava plethora, normal Atrial dimensions, normal ventricular dimensions
and normal global ventricular systolic function
are the echocardiographic findings associated with constrictive Pericarditis.
Pulsed wave Doppler in
Constrictive Pericarditis:
Ø Mitral
flow: restrictive pattern (increase E/A ratio, shortened DT)
Ø Increased
peak velocity across the mitral valve with expiration
Ø Hepatic
flow vein: expiratory flow decrease or reversal
Ø Tissue
Doppler in mitral valve annulus is Normal E’ wave peak velocity (more or equal to
8 cm/s) and the E/E’ ratio is normal (more than 8), it is called annulus
paradoxus
