cardio end of chapter questions Flashcards
Digoxin has a profound effect on myocyte intracellular concentrations of Na+, K+, and Ca2+. These effects are caused by digoxin inhibiting:
a. Ca2+/ATPase of the SR
b. Na+/K+/ATPase of the myocyte membrane
c. Cardiac phosphodiesterase
d. Cardiac B1 receptors
e. Juxtaglomerular renin release
B.
Digoxin binds to and blocks the action of the Na+/K+/ATPase, leading to increased intracellular sodium. The diminished sodium gradient results in less Ca2+ leaving the cell via the Na+/Ca2_ exchagner. Digoxin does not bind to the Ca2+/APase. It has no direct effect on phosphodiesterase, B1 receptors, or renin release.
Compensatory increases in heart rate and renin release that occur in heart failure may be alleviated by which of the following drugs?
a) Milrinone
b) Digoxin
c) Dobutamine
d) Enalapril
e) Metoprolol
E.
Metroprolol, a B1 selective antagonist, prevents the increased heart rate and renin release that results from sympathetic stimulation, which occurs as compensation for reduced cardiac output of heart failure.
- Enalapril is an ACE inhibitor that actually increases renin release.
- Dobutamine increases cardiac contractility but does not slow HR or interfere with renin release.
- Digoxin decreases HR but does not decreases renin release.
A 58 year old man is admitted to the hospital with acute heart failure and pulmonary edema. Which of the following drugs would be most useful in treating the pulmonary edema?
a) Dogoxin
b) Dobutamine
c) Furosemide
d) Minoxidil
e) spironolactone
C.
Furosemide has the ability to dilate vessels in the context of acute heart failure. It also mobilizes the edematous fluid and promotes its excretion.
- Dobutamine increases contractility but does not improve pulmonary edema.
- Digoxin acts too slowly and has no vasodilating effects.
- Minoxidil decreases arterial pressure and causes reflex tachycardia.
- Spironolactone does not relieve pulmonary edema.
A 46 year old man is admitted to the ED. He has taken more than 90 digoxin tablets (.25mg each), ingesting them about 3 hours before admission. His pulse is 50-60bpm, and the EKG shows third degree heart block. His serum K+ is normal. Which of the following is the most important therapy to initiate in this patient?
a) Digoxin immune Fab
b) Potassium salts
c) Lidocaine
d) Verapamil
e) Amiodarone
A.
In the severely poisoned patient, reduction of digoxin plasma concentrations is paramount and can be accomplished with administration of antidigoxin antibodies. DIGOXIN CAN BE TOXIC, MONITOR CLOSELY.
- Potassium concentrations, if low, can be increased.
- Antiarrhythmics are useful if there is need, but this is not the case here.
- Amiodarone would enhance digoxin intoxication by displacing digoxin from tissue protein binding sites and by competing with digoxin for renal excretion. DO NOT ADMINISTER TOGETHER.
- Verapamil would increase heart rate.
A 66 year old man had a myocardial infarction. Which of the following would be appropriate prophylactic antiarrhythmic therapy?
a) lidocaine
b) metroprolol
c) procainamide
d) quinidine
e) verapamil
B.
Beta blockers like metoprolol prevent cardiac arrhythmias that occur subsequent to an MI. None of the other drugs have been shown to be particularly effective in preventing post infarct arrhythmias.
Suppression of arrhythmias resulting from a reentry focus is more likely to occur if the drug:
a) has vagomimetic effects on the AV node
b) is a beta blocker
c) converts a unidirectional block to a bidirectional block
d) slows conduction through the atria
e) has atropine-like effects on the AV node
C. A reentrant arrhythmia is caused by damaged heart muscle so that conduction is slowed through the damaged area in only one direction. A drug that prevents conduction in either direction through the damaged area interrups the reentrant arrhythmia. Class I antiarrhythmitics, like lidocaine, are capable of producing a bidirectional block.
The other choices do not have any effects on the direction of blocade of conduction through the damaged cardiac muscle.
A 57 year old man is being treated for an atrial arrhythmia. He complains of headache, dizziness, and tinnitus. Which one of the following is most likely the cause?
A) Amiodarone B) Procainamide C) Propanalol D) Quinidine E) Verapamil
D. Quinidine
The clustered sx of HA, dizziness, and tinnitus are characteristic of cinchonism, which is caused by quinidine. The other drugs have adverse effects, but not in this particular grouping.
A 58 year old woman is being treated for chronic suppression of a ventricular arrhythmia. After two months of therapy, she complains about feeling tired all the time. Exam reveals a resting heart rate of 10bpm lower than her previous rate. Her skin is cool and clammy. Laboratory test results indicate low thyroxin and elevated TSH. Which is the most likely cause?
a) Amiodarone
b) Procainamide
c) Propranalol
d) Quinidine
e) Verapamil
A.
The patient is showing signs of hypothyroidism, often associated with amiodarone therapy.
Propanalol would slow the heart but would not produce thyroid changes. None of the other antiarrhythmics is likely to cause hypothyroidism.
