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1. In making your decision to treat with procainamide,
which of the following statements
would be most relevant?
(A) Procainamide may worsen or precipitate
hyperthyroidism
(B) Procainamide is not effective for atrial arrhythmias
(C) Procainamide prolongs the action potential and may
precipitate torsade de pointes arrhythmia
(D) Procainamide commonly induces thrombocytopenia
(E) Procainamide commonly induces headache and
tinnitus
2.In deciding on a treatment regimen with
procainamide for this patient, which of the following
statements is MOST correct?
(A) A possible drug interaction with digoxin suggests
that digoxin blood levels should be
obtained before and after starting procainamide
(B) Hyperkalemia should be avoided to reduce the
likelihood of procainamide toxicity
(C) Procainamide cannot be used if the patient has
asthma because it has a ~-blocking effect
(D) Procainamide has a duration of action of
class I
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( E) Procainamide is not active by the oral route
3. If this patient should manifest severe acute
procainamide toxicity from an overdose, rationaltherapy would entail the immediate administration of
(A) A calcium chelator such as EDTA
(B) Digitalis
(C) KCI
(D) Nitroprusside
(E) Sodium lactate
4. When used as an antiarrhythmic drug, lidocaine
typically
(A) Increases action potential duration
(B) Increases contractility
(C) Increases PR interval
(D) Reduces abnormal automaticity
(E) Reduces resting potential
5. Which of the following drugs is NOT suitable for
chronic oral therapy of arrhythmias?
(A) Amiodarone
(B) Disopyramide
(C) Esmolol
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NOT included
low cvs toxicity>> so MIhigh cnz toxicty :)
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(D) Quinidine
(E) Verapamil
6. A 16-year-old girl is found to have paroxysmal
attacks of rapid heart rate. The antiarrhythmic of
choice in most casesof acute AVnodal tachycardia is
(A) Adenosine
(B) Amiodarone
(C) Flecainide
(D) Propranolol
(E) Quinidine
7. A patient is admitted to the emergency department
for evaluation ofan abnormal ECG. Overdoseofanantiarrhythmic drug is considered. Which of the
following drugs is correctly paired with its ECG
effects?
(A) Quinidine: increased PR and decreased QT intervals
(B) Flecainide: increasedPR, QRS, and QT intervals
(C) Verapamil: increased PR interval
(D) Lidocaine: decreased QRS and PR interval
(E) Metoprolol: increased QRS duration
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a
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8. Which of the following drugs does NOT consistently
reduce the potassium (IK) repolarizing current and
thereby prolong the action potential duration?
(A) Amiodarone
(B) Iburilide
(C) Lidocaine
(D) Quinidine
(E) Sotalol
9. Recognized adverse effects of quinidine include
which one of the following?
(A) Cinchonism
(B) Constipation
(C) Lupus erythematosus
(D) Increase in digoxin clearance
(E) Pulmonary fibrosis
10. A drug that hyperpolarizes and prevents conductionof impulses in the AV node is
(A) Adenosine
(B) Digoxin
(C) Lidocaine
(D) Quinidine
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(E) Verapamil
11. Which of the following drugs is used by the oral
route, blocks sodium channels, and decreases actionpotential duration in ischemic tissue?
(A) Adenosine
(B) Amiodarone
(C) Disopyramide
(D) Esmolol
(E) Flecainide
(F) Lidocaine
(G) Mexiletine
(H) Procainamide
(I) Quinidine
(J) Verapamil
12. Which of the following slows conduction through
the atrioventricular node and has its primary actiondirectly on L-type calcium channels?
(A) Adenosine
(B) Amiodarone
(C) Disopyramide
(0) Esmolol
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(E) Flecainide
(F) Lidocaine
(G) Mexiletine
(H) Procainamide
(I) Quinidine
(J) Verapamil
13. Which of the following has the longest half-life ofall antiarrhythmic drugs?
(A) Adenosine
(B) Amiodarone
(C) Disopyramide
(0) Esmolol
(E) Flecainide
(F) Lidocaine
(G) Mexiletine
(H) Procainamide
(I) Quinidine
(J) Verapamil
14. A drug was tested in the electrophysiology
laboratory to determine its effects on the cardiac
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action potential in ventricular cells. The results are
shown in the diagram. Which of the following drugs
does this agtent most resemble?
(A) Adenosine
(B) Flecainide
(C) Lidocaine
(0) Procainamide
(E) Verapamil
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1. Procainamide prolongs refractory period by block-
ing sodium channels and by prolonging the AP. All
of the other statements are false. The answer is C.
2. Hyperkalemia facilitates procainamide tOXICIty.
Procainamide is active by the oral route and has a
duration of action of 2-4 h (in the prompt-release
form). Procainamide has no documented interac-
tion with digoxin and little or no ~-blocking action.
The answer is B.
3. The most effective therapy for procainamide
toxicity
appears to be concentrated sodium lactate. This
drug may (1) increase sodium current by increasing
the ionic gradient and (2) reduce drug-receptor
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binding by alkalinizing the tissue. The answer is E.
4. Lidocaine reduces automaticity in the ventricles;
the drug does not alter resting potential or AP dura-
tion and does not increase contractility. The answer
isO.
5. Esrnolol is an ester that is rapidly metabolized even
when given intravenously; it is inactive by the oral
route. Therefore, esrnolol would not be suitable for
chronic therapy. The answer is C.
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6. Calcium channel blockers are effective in
supraventricular tachycardias. However, adenosine
is just as effective in most acute nodal tachycardias
and is less toxic because of its extremely short dura-
tion of action. The answer is A.
7. All the associations listed are incorrect except vera-
pamil. This class IV drug increases PR interval. The
answer is C.
8. All of the IA drugs and class III agents reduce
potassium current during phase 3 and prolong the
AP. Lidocaine, the prototype IB drug, actually
shortens the duration under some circumstances.
The answer is C.
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9. Quinidine, derived from the bark of the cinchona
tree, has a wide spectrum of adverse effectsbut
causes increased-not decreased-gastrointestinal
motility and often resulrs in diarrhea. Procainamide
causes lupus; quinidine causes thrombocytopenia; amio-
darone causes pulmonary fibrosis.The answer is A.
10. The only antiarrhythmic agent that consistently
alters the resting potential of the AV node is adeno-
sine. It apparently activates IKI potassium channels
in the AV node, thus forcing the membrane poten-
tial closer to the Nernst potassium potential; thus,
adenosine significantly hyperpolarizes this tissue,
preventing the conduction of action potentials. The
answer is A.
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11. Class IB drugs such as lidocaine and mexiletine typ-
ically block sodium channels and decrease the AP
duration. Mexiletine-but not lidocaine-is orally
active. The answer is G.
12. Verapamil is the calcium channel blocker in this list.
(Adenosine and ~-blockers also slowAV conduction but
do not act directly on calcium channels.) The
answer is J.
13. Amiodarone has the longest half-life of all the
antiarrhythrnics (Table 14-1). The answer is B.
14. The drug effect shown in the diagram includes
slowing of the upstroke of the AP and prolongation
of repolarization. This is most typical of class lA
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drugs. The answer is D, procainamide.