T

tachycardia See ARRHYTHMIA.

tamponade, cardiac A life-threatening compres-
sion of the HEARTthat prevents it from expanding
to fill with BLOOD. Cardiac tamponade is most
often a complication of PERICARDITISand develops
when fluid rapidly accumulates within the layers
of the PERCARDIUM. The pericardium’s fibrous outer
layer does not readily expand, which forces the
fluid to press inward against the heart. Without
immediate action to drain the fluid, the heart will
stop beating. ELECTROCARDIOGRAM (ECG) demon-
strates the characteristic patterns of electrical
changes in the heart’s rhythm that strongly indi-
cate cardiac tamponade. COMPUTED TOMOGRAPHY
(CT) SCANor MAGNETIC RESONANCE IMAGING(MRI) can
confirm the diagnosis. Generally the doctor can
aspirate (withdraw) the fluid using a needle and
syringe (pericardiocentesis), which relieves the
pressure and allows the heart to resume normal
function. Surgery to create an opening in
the pericardium may be necessary to manage car-
diac tamponade that occurs with chronic peri-
carditis. Penetrating trauma that causes bleeding
into the pericardium may also cause cardiac tam-
ponade.
See also MYOCARDIAL INFARCTION.

thrombolytic therapy Emergency treatment
with medications to dissolve BLOODclots that are
in the process of forming. When initiated
promptly, thrombolytic therapy can avertMYOCAR-
DIAL INFARCTION or ischemic (nonhemorrhagic)
STROKE, mitigating damage to the HEARTor BRAIN
respectively. Doctors also may use thrombolytic
therapy to treat blood clots that form elsewhere in
the body, such as in the leg (DEEP VEIN THROMBOSIS
[DVT]) or the LUNGS(PULMONARY EMBOLISM).

Thrombolytic agents act by converting plas-

minogen, an inactive protein in the blood circula-

tion, to plasmin, an active protein that breaks

down the key proteins that form blood clots (fib-

rinogen and fibrin). These agents can only act

before the clot fully forms and hardens, which

establishes a therapeutic window of about four

hours from the onset of clot formation. Early diag-

nosis is therefore essential.

COMMON THROMBOLYTIC AGENTS

alteplase (aPA) anisoylated purified streptokinase

anistreplase activator complex (APSAC)

tissue plasminogen streptokinase

activator (tPA) urokinase

The oldest of the thrombolytic agents is strep-

tokinase, which doctors began using in the 1940s.

Streptokinase and anistreplase derive from strep-

tococcal BACTERIA. When administered, these

agents initiate ANTIBODYproduction. The antibodies

become active after five days and remain active

for about six months. During that timeframe, doc-

tors cannot re-administer streptokinase or anistre-

plase. Some people also have adverse responses to

these agents, especially streptokinase. Laboratories

manufacture most of the newer thrombolytic

agents using recombinant technology, which

nearly eliminates these immune responses.

The most significant risk of thrombolytic ther-

apy is uncontrolled bleeding (HEMORRHAGE). For

this reason, it is crucial for doctors to determine

whether a stroke is ischemic (caused by a clot) or

hemorrhagic (caused by bleeding) before adminis-

tering a thrombolytic agent. For venous clots, such

as with deep vein thrombosis, the doctor may

directly inject the agent into the clot. For arterial

110