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class I
.1In 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
(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

.2In 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
b
(C) Procainamide cannot be used if the patient has
asthma because it has a ~-blocking effect

(D) Procainamide has a duration of action of


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( E) Procainamide is not active by the oral route

.3If this patient should manifest severe acute


procainamide toxicity from an overdose, rational
therapy would entail the immediate administration of

(A) A calcium chelator such as EDTA

(B) Digitalis NOT included


e

(C) KCI

(D) Nitroprusside

(E) Sodium lactate

.4When used as an antiarrhythmic drug, lidocaine


typically

(A) Increases action potential duration


low cvs toxicity>> so MI
(B) Increases contractility high cnz toxicty :)

(C) Increases PR interval

(D) Reduces abnormal automaticity d

(E) Reduces resting potential

.5Which of the following drugs is NOT suitable for


chronic oral therapy of arrhythmias?

(A) Amiodarone

(B) Disopyramide

(C) Esmolol
c
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(D) Quinidine

(E) Verapamil

.6A 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
a

(C) Flecainide

(D) Propranolol

(E) Quinidine

7. A patient is admitted to the emergency department


for evaluation ofan abnormal ECG. Overdose
ofanantiarrhythmic 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 c

(D) Lidocaine: decreased QRS and PR interval

(E) Metoprolol: increased QRS duration


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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 c

(D) Quinidine

(E) Sotalol

9. Recognized adverse effects of quinidine include


which one of the following?

(A) Cinchonism

(B) Constipation

(C) Lupus erythematosus a

(D) Increase in digoxin clearance

(E) Pulmonary fibrosis

10. A drug that hyperpolarizes and prevents conduction


of impulses in the AV node is

(A) Adenosine

(B) Digoxin

(C) Lidocaine a

(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 action
potential duration in ischemic tissue?

(A) Adenosine

(B) Amiodarone

(C) Disopyramide

(D) Esmolol
g

(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 action
directly on L-type calcium channels?

(A) Adenosine

(B) Amiodarone

(C) Disopyramide

(0) Esmolol
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(E) Flecainide

(F) Lidocaine

(G) Mexiletine
j

(H) Procainamide

(I) Quinidine

(J) Verapamil

13. Which of the following has the longest half-life of


all antiarrhythmic drugs?

(A) Adenosine

(B) Amiodarone

(C) Disopyramide

(0) Esmolol

(E) Flecainide b

(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 d
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


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.


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.
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.
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


drugs. The answer is D, procainamide.