Internal-Medicine

26 1: Cardiology
and other bradyarrhythmias are very common.
Slow atrial fibrillation with very little variation
in the ventricular rate (regularization of the R-
R interval) may occur. This arrhythmia is likely
slow atrial fibrillation. Symptoms of digitalis
toxicity include anorexia, nausea, fatigue, dizziness,
and visual disturbances. The presence of
hypokalemia increases the likelihood of digitalis
toxicity. (Fuster, p. 795)
29. (A) Commonly, no cause is found for constrictive
pericarditis. Some patients do give a history
of previous acute pericarditis. TB is now an
uncommon cause. Cancer can cause constriction
but is uncommon. Rheumatic fever does
not cause pericarditis. (Fuster, pp. 1989–1991)
30. (E) The maneuvers listed increase the block and
are useful for diagnosis, but not for converting
the atrial flutter to a sinus rhythm. Electrical
cardioversion is the method of choice in patients
who are hemodynamically unstable. Often very
low amounts of energy during cardioversion
will convert atrial flutter. (Fuster, p. 844)
31. (C) Atrial flutter is characterized by regular
atrial activation with an atrial rate of >240 beats/
min. The ventricular response depends on the
conduction of the AV node, usually there is 2:1
or 3:1 conduction. It is now known that the predominant
mechanism for atrial flutter is right
atrial macroreentry with circular activation.
Atrial flutter typically originates from the right
atrium and most often involves a large circuit
that travels around the area of the tricuspid
valve. This type of atrial flutter is referred to as
typical atrial flutter. Less commonly, atrial flutter
can result from circuits in other areas of the
right or left atrium. (Fuster, pp. 841–842)
32. (B) Retention of fluid is complex and not due to
any one factor, however, hormones may contribute.
Growth hormone does not have fluidretaining
properties. The exact mechanisms
that initiate renal conservation of salt and water
are not precisely understood, but may include
arterial volume receptors sensing a decrease in
the effective arterial blood volume. Aldosterone,
renin, and vasopressin are generally increased
in heart failure. (Fuster, p. 713)
33. (A) ST elevation persisting 2 weeks after an
infarct, an abnormal pericardial impulse, and a
bulge on the left ventricular border on x-ray are
characteristic of an aneurysm. Ventricular
aneurysms are most often a result of a large
anterior infarct. The poor prognosis associated
with these aneurysms is due to the associated
left ventricular dysfunction, rather than to the
aneurysm itself. (Fuster, pp. 1321–1322)
34. (D) In aortic stenosis, there is normal overall
cardiac size, but dilatation of the proximal
ascending aorta and blunt rounding of the
lower left cardiac contour. Calcification of the
valve is often difficult to determine on plain
films. Although left atrial enlargement can
occur, its presence on the CXR should raise
other diagnostic possibilities, such as mitral
valve disease. (Fuster, p. 1647)
35. (D) This combination, although the total cholesterol
is borderline, has high HDL cholesterol,
which is protective. Nevertheless, a level this
high would likely require treatment. (Fuster,
pp. 1099–1100)
36. (B) Besides coarctation of the aorta, aortic
occlusive disease, dissection of the aorta, and
abdominal aneurysm may lead to differential
blood pressure in arms and legs. Coarctation is
the third most common form of congenital cardiac
disease. One-third of the patients will be
hypertensive. The femoral pulses are weak,
delayed, and even absent. (Fuster, p. 1809)
37. (D) He likely has LVH.
Signs include left axis deviation, highvoltage
QRS complexes in V5 and V6, deep S
in V1 and V2, and prolonged QRS in the left
precordial leads. Age, orientation of the heart
in the chest, and noncardiac factors make the
ECG an imperfect tool for diagnosing or
excluding LVH. The ECG is more accurate
and better for following progression or regression
of LVH. (Fuster, pp. 311–312)
38. (A) High urinary specific gravity, nocturia, and
daytime oliguria occur in addition to low urinary
sodium content in untreated CHF. These
changes are the result of the activation of the