radiographs are usually normal. Twenty-four to seventy-two hours after a
PE, atelectasis or a focal infiltrate may be seen. Radiographic findings clas-
sically associated with PE are Hampton hump (triangular pleural-based
infiltrate) and Westermark sign (dilation of pulmonary vessels proximal to
PE with collapse of distal vessels).
20.The answer is d.(Tintinalli, p 347.)Serum cardiac markers are used
to confirm or exclude myocardial cell death, and are considered the gold
standard for the diagnosis of MI. While there are many markers currently
used; the most sensitive and specific markers are troponin I and T.A rise
in these levels, as seen in the figure, is diagnostic for an acute MI. Troponin
levelsrise within 3 to 6 hours of chest pain onset, peak at 12 to 24 hours,
andremain elevated for 7 to 10 days.
(a)Myoglobin is found in both skeletal and cardiac muscle and
released into the bloodstream when there is muscle cell death. It tends to
rise within 1 to 2 hours of injury, peaks in 4 to 6 hours, and returns to base-
line in 24 hours. (b)CK is an enzyme found in skeletal and cardiac muscle.
Following acute MI, increases in serum CK are detectable within 3 to 8 hours
with a peak at 12 to 24 hours after injury, and normalizes within 3 to 4 days.
(c)CK-MB is an isoenzyme found in cardiac muscle and released into the
bloodstream upon cell death. It rises 4 to 6 hours after acute MI, peaks in 12 to
36 hours, and returns to normal within 3 to 4 days. (e)Lactic dehydrogenase
is an enzyme found in muscle and rises 12 hours after acute MI, peaks at
24 to 48 hours, and returns to normal at 10 to 14 days.
21.The answer is d.(Tintinalli, p 1079.)Narrow-complex tachycardias
are defined as rhythms with a QRS complex duration less than 100 ms and
a ventricular rate greater than 100 beats per min. Although virtually all
narrow-complex tachydysrhythmias originate from a focus above the ventri-
cles, the term supraventricular tachycardia (SVT)is conventionally used
to denote those rhythms aside from sinus tachycardia, atrial tachycardia,
atrial fibrillation, and atrial flutter (eg, atrioventricular nodal reentry tachy-
cardia and atrioventricular reentry tachycardia).Adenosine,an ultrashort-
acting AV-nodal blocking agent, is typically used to treat SVTs. Because it is
so fast-acting, it must be delivered through a large vein (eg, the antecubital fossa)
with a rapid intravenous fluid bolus. In addition to adenosine, maneuvers that
increase vagal tonehave been shown to slow conduction through the AV node.
Some of these maneuvers include carotid sinus massage, Valsalva maneuver,
and facial immersion in cold water.
Chest Pain and Cardiac Dysrhythmias Answers 35