466
U N I T 5
Circulatory Function
mycobacterial infections, connective tissue diseases (e.g.,
systemic lupus erythematosus, rheumatoid arthritis), ure-
mia, postcardiac surgery, neoplastic invasion of the peri-
cardium, radiation, trauma, drug toxicity, and contiguous
inflammatory processes of the myocardium or lung.
42,43
Similar to other inflammatory processes, acute peri-
carditis is associated with local vasodilation, increased
capillary permeability, and accumulation of white blood
cells. The capillaries that supply the serous pericardium
become permeable, allowing plasma proteins, including
fibrinogen, to exit the capillaries and enter the pericar-
dial space. This results in an exudate that varies in com-
position and amount according to the causative agent.
Acute pericarditis frequently is associated with an exu-
date containing protein and fibrin and heals by reso-
lution or progresses to form scar tissue and adhesions
between the layers of the serous pericardium.
The manifestations of acute pericarditis include a triad
of chest pain, an auscultatory pericardial friction rub, and
electrocardiographic (ECG) changes. The clinical find-
ings may vary according to the causative agent. Nearly all
persons with acute pericarditis have chest pain and fever.
The pain usually is sharp and abrupt in onset, occurring
in the precordial area, and may radiate to the neck, back,
abdomen, or side. Pain in the scapular area may result
from irritation of the phrenic nerve. The pain typically
is pleuritic (aggravated by inspiration and coughing) and
positional (decreases with sitting and leaning forward)
because of changes in venous return and cardiac filling.
These pain characteristics differentiate pericarditis from
acute myocardial infarction or pulmonary embolism.
A pericardial friction rub (auscultated through the dia-
phragm of a stethoscope), often described as “leathery”
or “close to the ear,” results from the rubbing and fric-
tion between the inflamed pericardial surfaces.
43
Diagnosis of acute pericarditis is based on clinical
manifestations, ECG, chest radiography, and echocar-
diography, with laboratory tests being used to confirm
the diagnosis. Treatment depends on the cause. When an
infection is present, antibiotics specific for the causative
agent are prescribed. Aspirin and other non-steroidal
anti-inflammatory drugs (NSAIDs) may be given to min-
imize the inflammatory response and the accompanying
undesirable effects.
Recurrent pericarditis can occur in up to 30% of
persons with acute pericarditis who responded satisfac-
torily to treatment.
42
A minority of these develop recur-
rent bouts of pericardial pain, which can sometimes
be chronic and debilitating. The process commonly is
associated with autoimmune disorders, such as lupus
erythematosus, rheumatoid arthritis, scleroderma, and
myxedema, but may also occur following viral pericardi-
tis. Treatment includes the use of anti-inflammatory med-
ications such as NSAIDs, corticosteroids, or colchicine.
Pericardial Effusion
Pericardial effusion is the accumulation of fluid in the
pericardial cavity, usually as a result of an inflammatory
or infectious process that includes pericarditis. It may
also develop with neoplasms, cardiac surgery, or trauma.
Pericardial effusion exerts its effects through compres-
sion of the heart chambers. The normal pericardial
space contains about 15 to 50 mL of fluid. Increases
in the volume of this fluid, the rapidity with which it
accumulates, and the elasticity of the pericardium deter-
mine the effect that the effusion has on cardiac function.
Small pericardial effusions may produce no symptoms
or abnormal clinical findings. Even a large effusion
that develops slowly may cause few or no symptoms,
provided the pericardium is able to stretch and avoid
compressing the heart. However, a sudden accumula-
tion of even 200 mL may raise intracardiac pressure to
levels that significantly limit venous return of blood to
the heart. Symptoms of cardiac compression also may
occur with relatively small accumulations of fluid if the
pericardium has become thickened by scar tissue or neo-
plastic infiltrations and loses its elasticity.
The echocardiogram is a rapid, accurate, and widely
used noninvasive method of evaluating pericardial effu-
sion. Treatment depends on the extent of the effusion. In
small pericardial effusions, diuretics are given to remove
the fluid, and NSAIDs, colchicine, or corticosteroids
may minimize fluid accumulation. Pericardiocentesis,
or removal of fluid from the pericardial sac, often with
the aid of echocardiography, is the initial treatment of
choice for larger effusions. Aspiration of fluid with labo-
ratory evaluation of the pericardial fluid may be used to
identify the causative agent.
CardiacTamponade
Pericardial effusion can lead to or may initially pres-
ent as a condition called cardiac tamponade, in which
there is compression of the heart due to the accumula-
tion of fluid or blood in the pericardial sac. This life-
threatening condition can be caused by bleeding into
the pericardial sac after blunt or penetrating trauma,
rupture of the heart following myocardial infarction,
complications during percutaneous cardiac procedures
or device placement, or retrograde bleeding during aor-
tic dissection.
42,43
Cardiac tamponade results in increased intracardiac
pressure, progressive limitation of ventricular diastolic
filling, and reductions in stroke volume and cardiac out-
put. In other words, the heart cannot fill properly with
blood. The severity of the condition depends on the vol-
ume of fluid present and the rate at which it accumu-
lates. Rapid accumulation results in an elevated central
venous pressure, jugular vein distention, a fall in systolic
blood pressure, narrowed pulse pressure, and signs of
circulatory shock. The heart sounds may become muf-
fled because of the insulating effects of the pericardial
fluid and reduced cardiac function. Persons with slowly
developing cardiac tamponade usually appear acutely ill,
but not to the extreme seen in those with rapidly devel-
oping tamponade.
A significant accumulation of fluid in the pericar-
dium results in increased sympathetic nervous system
stimulation, which leads to tachycardia and increased
cardiac contractility. A key diagnostic finding in cardiac
