Anesthesia Pharmacology Chapter 
9:  Pharmacology of Antiarrhythmic Drugs
 Practice Questions
	Click on the correct answer.
 
 
 
- Factors that reduce membrane resting potential: -   ischemic cells damage
-   hyperkalemia
-   sodium pump blockade
-   B & C
-   A, B & C
 
- Activation status sodium channels that -55 mV: -   inactivated
-   activated
 
- Principal ion responsible for action potentials in specialized conducting SA nodal and AV nodal tissues: -   sodium
-   calcium
-   potassium
 
- Mechanism(s) of arrhythmia development: -   disturbances of impulse formation
-   abnormal impulse propagation
-   both
-   neither
 
- Mechanism(s) associated with many tachyarrhythmias: -   reduced automaticity
-   triggered automaticity
-   reentry
-   B & C
-   A & B
 
- Factor(s) predisposing to delayed afterdepolarizations (DAD): -   excessive adrenergic activity
-   low intracellular potassium
-   bradycardia
-   certain drugs -- including some antiarrhythmics
-   all of the above
 
- Triggered automaticity: associated with significant action potential duration prolongation -   delayed afterdepolarization
-   early afterdepolarization
-   both
-   neither
 
- Torsades de Pointes: -   supraventricular arrhythmia
-   associated with shortened QT intervals
-   possibly induced by early afterdepolarizations
-   A & B
-   B & C
 
- Most common cardiac conduction abnormality leading to arrhythmias: -   delayed afterdepolarization
-   early afterdepolarization
-   reentry
-   each mechanism equally likely
 
- Electrophysiological basis for increasing heart rate: -   increased slope of phase 4 depolarization
-   decreased slope of phase 4 depolarization
 
- Factors that increase slope of phase 4 depolarization: -   injury currents
-   acidosis
-   beta adrenergic receptor blockade
-   A & B
-   A, B & C
 
- More likely to decrease the slope of phase 4 depolarization: -   edrophonium (Tensilon)
-   atropine
-   isoproterenol (Isuprel)
 
- All cardiac cells may show pacemaker activity: -   true
-   false
 
- Mechanism(s) of antiarrhythmic drug action: -   disrupting re-entrant pathways
-   preventing delayed afterdepolarizations
-   suppressing automaticity
-   A & B
-   A, B & C