One of the applications that first brought echocardiography to
the general attention of clinicians was its unique ability to
detect pericardial effusion. It remains the most sensitive technique
for the detection of this disorder.
Around the heart there exists a potential cavity between the
visceral and parietal layers of the serous pericardium, into which
the heart is invaginated during its development. There is normally
a little fluid in this cavity that acts as a lubricant for heart
movement, but the two layers of the serous pericardium essentially
remain in contact. However, if the amount of fluid increases as
a result of exudate from the pericardium, hemorrhage or the inadvertent
infusion of fluid, the two layers become more widely separated.
 |
| Fig. 35 |
(Fig.
35) shows a slow sweeping M-mode from a patient with a small
posterior pericardial effusion. Behind the region of the left
ventricle a strong echo arises from the fibrous pericardium, which
is stationary and separated by a relatively anechoic space from
the moving myocardium. At the level of the atrioventricular groove,
the pericardial echo joins the posterior heart wall again. This
is because this region of the pericardial cavity, a cul-de-sac
termed the oblique sinus, has little ability to expand due to
its attachments to the pulmonary veins and so, although it forms
a potential cavity, ir rarely fills with fluid. This frequently
is a helpful sign for detection of pericardial effusion, and the
differential diagnosis of pericardial from pleural effusion, or
other anechoic spaces behind the heart.
Small effusions are generally confined to the region behind the
left ventricle when the patient is supine, and may appear to vanish
when the patient sits up, as they drain to the apical region.
For these positional reasons, the echocardiogram first detects
small effusions posteriorly while the chest X-ray first manifests
effusions anteriorly. The echo is performed with the patient recumbent
while the lateral chest X-ray is performed with the patient upright.
 |
| Fig. 36 |
Larger effusions, on the other hand, can be detected both anterior
and posterior to the heart. In the case of very large effusions
(Fig.
36), the heart may take on a swinging motion within the bag
of fluid, resulting in a characteristic echocardiographic appearance.
The ECG in such cases shows alternation of QRS complex amplitude,
a finding virtually diagnostic of pericardial effusion. With such
unusual motion of the entire heart, analysis of the relative motions
of cardiac structures becomes impossible. Thus, the apparent presence
of such echocardiographic features as mitral prolapse or reversed
septal motion is liable to be artifactual, and must be reassessed
after removal of the pericardial fluid.
M-mode studies permit some broad classification of the size of
pericardial effusion, yet the extend and distribution of fluid
surrounding the hear are better assessed by two-dimensional echocardiography,
particularly in the case of postsurgical patients whose adhesions
may confine an effusion to a localized region (sometimes causing
it to remain undetected by a conventional M- mode examination),
or when the effusion comprises blood following post-infarction
myocardial rupture ("pseudoaneurysm").
 |
| Fig. 37 |
A complete two-dimensional echocardiogram from all transducer
positions provides the most sensitive method available for detection
of pericardial effusion. (Fig.
37) demonstrates a parasternal long axis in a patient with
a small pericardial effusion.
 |
| Fig. 38 |
(Fig.
38) shows the heart suspended in a large pericardial effusion,
seen both anteriorly and posteriorly.
 |
| Fig. 39 |
The short axis view usually shows a symmetric distribution of
the fluid around the circumference of the heart in effusions that
are not loculated (Fig.
39).
 |
| Fig. 40 |
When effusions are smaller, or loculated, this symmetric distribution
is no longer seen
(Fig.
40).
 |
| Fig. 41 |
Loculated effusions may be found anywhere in the pericardial
space. (Fig.
41) shows an effusion confined to the oblique sinus of the
pericardium, just posterior to the left atrium.
 |
| Fig. 42 |
(Fig.
42) demonstrates an effusion loculated behind the right atrium.
A small bit of separation may be seen inferiorly (as in the subcostal
views) with a normal amount of pericardial fluid.
 |
| Fig. 43 |
Certain effusions may be seen to contain fibrinous material (Fig.
43). Such material is rarely encountered in effusions of viral,
uremic or post-infarction origin. In the absence of a history
of trauma (where blood may clot in the pericardium) or bacterial
infection (where the purulent fluid may contain fibrin) such material
is invariably found with effusions of malignant origin.
An echocardiogram is of inestimable value for patients with an
enlarged cardiac silhouette on chest X-ray. It can readily differentiate
between enlargement due to chamber dilatation, ventricular hypertrophy
or effusion.
When a pericardiocentesis is contemplated, it is now prudent
to perform such a procedure with echocardiographic guidance. The
most practical method to approach such a procedure is to cover
the transducer in a sterile sheath and direct the beam parallel
to the needle. By visually interacting with the ultrasound image
the pericardial space may be rapidly and safely entered, reducing
risk of perforation of myocardium.
 |
| Fig. 44 |
Large pleural effusions may mimic pericardial effusions. In such
cases, it is necessary to identify the bright target of the pericardium.
While this may be done by M-mode (Fig.
44), it is more easily accomplished by the two-dimensional
approach because of the spatial target information available (Fig.
45).
 |
| Fig. 45 |
Particular care is needed in the case of an effusion that has
been present for some time, or one that has otherwise become organized.
Its ultrasound characteristics then closely resemble those of
the myocardium and so it will no longer appear to be echo-free.
Moreover, the pericardium will no longer be stationary, but will
move more or less parallel to the myocardium. Careful adjustment
of amplifier gain and correct identification of all structures
involved (the mitral chordae, epicardium, endocardium, and pericardium),
plus confirmation of epicardial/pericardial apposition at the
level of the atrioventricular groove are necessary to avoid misdiagnosis.
 |
| Fig. 46 |
(Fig.
46) demonstrates an area around the heart filled with multiple
echo dense targets. In this case, the patient had pericardial edema
due to metastatic lung cancer.
Chronic inflammation of the pericardium leading to calcification
and adhesions to the myocardium can so restrict cardiac function
that surgical removal of the pericardium becomes necessary. Unfortunately,
direct detection of pericardial calcification by echocardiography
is not normally possible. At first sight this is surprising, since
calcium in valves is easily visualized. However, when such calcification
is encountered between the transducer and the heart, little ultrasound
penetrates to create images of adequate quality for interpretation.
 |
| Fig. 47 |
One of the clinical features of constrictive pericarditis, namely
paradoxical arterial pulse, can sometimes be demonstrated by echocardiography.
As shown in (Fig.
47), inspiratory increase of right ventricular stroke volume
causes the septum to be pushed back, thus lowering left-sided
stroke volume. While the echocardiogram may be helpful in the
diagnosis of constrictive pericarditis, the findings may be very
subtle. An otherwise normal echocardiographic appearance doe not
routinely exclude pericardial constriction, and further hemodynamic
study may be necessary to establish this diagnosis.
In the setting of pericardial tamponade, the fluid may compress
the right atrium and/or the right ventricle from within the pericardium,
impeding filling of the right heart. While such right atrial or
ventricular "collapse" may be found in patients in clinical tamponade
it is not always present. It is best to make all observations
possible from the echocardiogram, but to restrict the absolute
diagnosis of tamponade to the physical examination, and/or other
available hemodynamic data.
2004