1.

B
Betablocker increase CO, decrease stroke volume
2. B
Digoxin- causes increased availability of intracellular calcium in the
myocardium and conduction system, with consequent increased inotropy,
increased automaticity, and reduced conduction velocity
3. A
Discontinue ACE common reason:
A nonproductive and persistent cough may occur in 5%-25%
of individuals. It may take up to 2 weeks or longer for
coughing to subside after the ACE inhibitor is discontinued.
-Causes Hyperkalemia, sexual dysfunction, metallic taste
4. B
Adverse effect of Heparin
Heparin-induced thrombocytopenia (HIT) is the development
of thrombocytopenia (a low platelet count), due to the
administration of various forms of heparin, an anticoagulant.
5. A
Angiotensin II
Angiotensin stimulates the release of aldosterone
6. C
CHF will show s/sx of:
*increased sympathetic tone- produce vasoconstriction,
moist skin, pale complexion
7. A
Weight gain and edema in CHF
Decreased perfusion of the kidneys activates the renin-
angiotensin-aldosterone system, thus increasing Na and water
retention and renal and peripheral vascular tone.
8. C
Digoxin as positive intropic drug:
Digoxin acts by increasing sodium/calcium exchange. This
has the effect of increasing intracellular calcium levels which,
in myocardial muscle, has the effect of enhancing the
strength of contraction (positive inotropism). It also affects
the electrical physiology of the heart, blocking atrioventricular
(AV) conduction and reducing the heart rate by enhancing
vagal nerve activity (negative chronotropy).
It also produces a positive inotropic effect by inhibiting the Na/K
pump.
9. E
Chronic AF- Best drug for controlling ventricular rate: Digoxin
10. B
Digoxin- 2nd or 3rd degree AV conduction block, Bradycardia
(caused by increased vagal tone)
11. D
Beta-blockers and nondihydropyridine calcium channel blockers
(eg, verapamil, diltiazem) can be used to treat symptomatic
patients.
12. D
Furosemide cause hypokalemia

Quinidine slows the elimination of digoxin and simultaneously
reduces digoxin's apparent volume of distribution, As a result,
serum digoxin levels may be as much as doubled. Your blood
levels of digoxin may increase causing loss of appetite, nausea,
vomiting, diarrhea, headache, weakness, blurred vision, confusion, and
a fast or slow or irregular heartbeat. Quinidine prolonged the PR
intervals, while the increased digoxin's effect on atrioventricular
conduction, and produces more adverse gastrointestinal effects

Quinidine toxicity- Mild cinchonism includes symptoms of
blurred vision, transient deafness, anorexia, nausea,
weakness, vertigo, tinnitus, diarrhea, and headache. Mild
cinchonism does not always occur with higher dosages, nor
does it preclude further quinidine therapy. Moderate
cinchonism includes vomiting, hypotension, a 25% to 50%
increase in QRS duration, and rare premature ventricular
contractions. Severe cinchonism is characterized by
myocardial toxicity such as malignant arrhythmias, QRS
duration greater than 50%, high degree AV heart block, or
cardiac arrest.
13. D
Drug interaction cause digoxin toxicity
Furosemide - the amount of potassium in your blood may decrease.
Thus may cause digitalis toxicity
Verapamil - 50-75% increase
Amniodarone - 70% increase
Propanolol - increases effects of digoxin oral by
pharmacodynamic synergism. Enhanced bradycardia
Quinidine - 100% increase
14. D
Reentry in ventricular muscle may also cause some of the
arrhythmias that occur after myocardial infarction.
15. A
Digoxin has a positive inotropic effect and negative
chronotropic effect.