Anti-Arrythmics

Question 1

Unlike other regions of the heart, where phase 0 is driven by Na+ channels, the SA node and AV node have slower action potentials driven by

Answer 1

Ca2+ channels

Question 2

Antiarrhythmic drug actions generally fall into 4 classes. Class 1 action is

Answer 2

Na+ channel blocker

Question 3

Pronlong the PD and dissociate from the channel w/ intermediate kinetics and exhibit moderate blockade

Answer 3

Class 1A

Question 4

The prototype class 1A drug is

Answer 4

Procainamide

Question 5

Shorten the APD in some tissues of the heart and dissociate from the channel w/ rapid kinetics

Answer 5

Class 1B

Question 6

The prototype class 1B drug is

Answer 6

Lidocaine

Question 7

Have minimal effects on the APD and dissociate from the channel w/ slow kinetics

Answer 7

Class 1C

Question 8

The prototype class 1C drug is

Answer 8

Flecainide

Question 9

Class 2 action is sympatholytic and the prototypes are

Answer 9

Propranolol and esmolol

Question 10

Prolongs the APD by blocking phase 2 K+ current

Answer 10

Class 3

Question 11

What are the prototype class 3 drugs?

Answer 11

Sotalol, ibutilide, and amiodarone

Question 12

Class 4 action is blockade of the cardiac

Answer 12

Ca2+ current

Question 13

The prototype class 4 drugs are?

Answer 13

Verapamil and diltiazem

Question 14

The prototype is procainamide but others are quinidine and disopyramide

Answer 14

Class 1A

Question 15

Causes a slow upstroke of AP and prolongs the action potential duration

Answer 15

Class 1A drugs

Question 16

Class 1A drugs can be used for

Answer 16

Atrial fibrillation or stable V-tach

Question 17

Reduces peripheral vascular resistance

Answer 17

Procainamide

Question 18

Slowing of conduction and AP prolongation increases the risk of

Answer 18

Torsade de pointes, syncope, and arrhythmias

Question 19

Can cause a syndrome resembling lupus in 1/3 of patients receiving long-term therapy

Answer 19

Procainamide

Question 20

Can cause atropine-like adverse effects such as urinary retention and dry mouth, as well as worsening of preexisting glaucoma

Answer 20

Class 1A drugs

Question 21

Eliminated by hepatic metabolism to a metabolite which has class 3 activity

-accumulation of this metabolite can cause torsade de pointes

Answer 21

Procainamide

Question 22

Class 1A prolongs the

Answer 22

Refractory period

Question 23

Blocks activated and inactivated Na+ channels w/ rapid kinetics

Answer 23

Lidocaine

Question 24

SHORTEN AP duration and the refractory period

Answer 24

Class IB drugs

Question 25

Increased inactivation and slow unwinding kinetics results in the selective depression of conduction in depolarized cells. This is called

Answer 25

State Dependent Block

Question 26

Toxicity causes parethesia, tremor, nausea, lightheaded ness, and hearing disturbances

Answer 26

Class 1B toxicity

Question 27

Has extensive first pass metabolism -Only 3% of orally administered lidocaine appears in the plasma

Answer 27

Class 1B

Question 28

Used for arrhythmias associated w/ MI and used for termination of V-tach/prevention of V-fib

Answer 28

Class 1B

Question 29

Ineffective for supraventricular tachycardias, atrial fibrillation, and atrial flutter

Answer 29

Class 1B drugs

Question 30

An orally active congener of lidocaine used in the treatment of ventricular arrhythmias -Also used for chronic pain from diabetic neuropathy and nerve injury

Answer 30

Mexiletine

Question 31

Bind readily to activated channels (phase 0) or inactivated channels (phase 2) but bind poorly to rested channels

Answer 31

Use-dependent or State-dependent Drugs

Question 32

Block electrical activity when there is fast tachycardia or when there is a significant loss of the resting potential

Answer 32

Use-dependent or State-dependent drugs

Question 33

Selectively targets channels in depolarized tissue

Answer 33

Lidocaine

Question 34

Have slow unblocking kinetics

Answer 34

Class 1C drugs

Question 35

Have little effect on the action potential duration except for in the AV node and bypass tracts

Answer 35

Class 1C drugs

Question 36

Toxicity cause provocation or exacerbation of potentially lethal arrhythmias including the acceleration of ventricular rate in patients w/ atrial flutter

Answer 36

Class 1C

Question 37

Used for supraventricular arrhythmias and pharmacologic conversion of AF

Answer 37

Class 1C drugs

Question 38

Shown in a study to increase mortality in patients convalescing from MI

Answer 38

Flecainide and propafenone (Class 1C drugs)

Question 39

Can cause heart failure in patients with heart abnormalities

Answer 39

Class 1C Drugs

Question 40

Decrease pacemaker activity and slow conduction through the AV node to increase the effective refractory period

Answer 40

Beta-blockers

Question 41

A non selective beta-blocking drug that prolongs the action potential and is usually categorized as a class 3 drug

Answer 41

Sotalol

Question 42

Lowers cAMP which results in reduction of both Na+ and Ca2+ currents and the suppression of abnormal pacemakers

Answer 42

Beta-blockers like propranolol

Question 43

Particularly sensitive to beta-blockers

Answer 43

AV node

Question 44

Decreases phase 4 slope and decreases myocardial oxygen demand

Answer 44

Beta-blockers

Question 45

A non-selective beta antagonist that also exhibits Na+ channel blocking in vitro

Answer 45

Propranolol

Question 46

An IV cardioselective beta-blocker that is effective in controlling the ventricular response in atrial flutter or fibrillation

Answer 46

Esmolol

Question 47

Control the ventricular rate in atrial fibrillation or flutter, suppress PVCs, and terminate and prevent recurrences of paroxysmal supraventricular tachycardias

Answer 47

Beta-blockers

Question 48

Beta-blockers are contraindicated in patients with

Answer 48

WPW syndrome

Question 49

A use-dependent drug that blocks the “funny” current in the SA node and reduces heart rate w/out affecting myocardial contractility

Answer 49

Ivabradine

Question 50

Made up of the pneumonic ISBAD which comprises ibutilide, sotalol, bretylium, amiodarone, and dofetilide

Answer 50

Class III antiarrhythmics

Question 51

Usually classified as a class III because it markedly prolongs AP duration as well as blocks sodium channels

Answer 51

Amiodarone

Question 52

Prolongs the AP duration by blockade of IK+ channels or by enhancing inward current

Answer 52

Class III drugs

Question 53

AP prolongation increases the effective refractory period and reduces the ability of the heart to respond to rapid

Answer 53

Tachycardias

Question 54

AP prolongation by many class III drugs are reverse-dependent, such that the AP prolongation is least marked at fast rates and most marked at slow rates where it can contribute to the risk of torsade de pointes. One exception to this is

Answer 54

Amiodarone

Question 55

Prolonging AP can sometimes precipitate

Answer 55

Arrhythmias

Question 56

Are more likely to develop in conditions that prolong AP duration

Answer 56

Early After Depolarizations (EADs)

Question 57

A non selective beta-blcoking drug that is more effective for many arrhythmias than other beta-blockers because of its IK+ blocking activities

Answer 57

Sotalol

Question 58

Can cause dose-related incidence of excessive QT-interval prolongation w/

Answer 58

Sotalol

Question 59

Used to treat life-threatening ventricular arrhythmias and maintenance of sinus rhythm in patients w/ A-fib

Answer 59

Sotalol

Question 60

Used therapeutically for the conversion of atrial flutter and fibrillation to normal sinus rhythm

Answer 60

Ibutilide and Dofetilide

Question 61

Effective in most types of arrhythmias and is considered the most efficacious of all antiarrhythmic drugs likely due to its ability to block Na+, Ca2+, and Beta activity

Answer 61

Amiodarone

Question 62

Is not reverse-use dependent and prolongs the AP duration over a wide range of HRs and prolongs the QT interval on the ECG by blockade of IKr

Answer 62

Amiodarone

Question 63

Causes pulmonary fibrosis, microcrystalline deposits in the cornea and skin, and thyroid dysfunction

Answer 63

Amiodarone

Question 64

Structural analogue of amiodarone, lacking iodine -lacks major side effects of amiodarone

Answer 64

Dronedarone

Question 65

Blocks IKur, IAch, and Ito in atria and is a less potent blocker of IKr

Answer 65

Vernakalant

Question 66

Anti-ischemic drug for chronic angina -Lessens incidences of supraventricular arrhythmias including AF

Answer 66

Ranolazine

Question 67

Ca2+ channel blockers that are not useful as antiarrhythmics

Answer 67

Nifedipine and other dihydropyridines

Question 68

Block both activated and inactivated Ca2+ channels which decreases conduction velocity and increases refractory period

Answer 68

Ca2+ channel blockers verapamil and diltiazem

Question 69

Both verapamil and diltiazem also cause

Answer 69

Peripheral vasodilation

Question 70

Major use is to prevent reentrant atrioventricular nodal re-entrant tachycardia (AVNRT) PSVT -Contraindicated in WPW Syndrome

Answer 70

Diltiazem and Verapamil

Question 71

Ca2+ channel blockers reduce automaticity by decreasing the

Answer 71

Phase 4 slope

Question 72

Activated inward rectifier K+ current, inhibits Ca2+ and If current, and causes hyperpolarization and suppression of Ca2+-dependent APs

Answer 72

Adenosine

Question 73

Drug of choice for prompt conversion of paroxysmal supraventricular tachycardia to sinus rhythm because of its high efficacy (90-95%)

Answer 73

Adenosine

Question 74

Cofactor for Na+/K+ ATPase and antagonist of Ca2+ channels -Deficit is known to contribute to several arrhythmias

Answer 74

Magnesium

Question 75

Used as an adjunctive agent and can help control ventricular response in A-fib and flutter and may terminate some paroxysmal (reentrant) supraventricular arrhythmias

Answer 75

Digoxin