Pharm- Antidysrhythmics

Front 1

In Vaughan-Williams classification (antidysrhythmic drugs), what is each class ' general mechanism?
A. Class I
B. Class II
C. Class III
D. Class IV

Back 1

A. Class I : Na channel blockers (Subclasses IA, IB, IC for moderate, minimal and marked Phase 0 blockage)
B. Class II: beta blockers
C. Class III: K channel blockers
D. Class IV: Ca channel blockers

Front 2

Quinidine
A. what class of antidysrhythmic drug?
B. what are other drugs in its group?

Back 2

B. procainamide

Front 3

Procainamide
A. what class of antidysrhythmic drug?
B. what are other drugs in its group?

Back 3

B. Quinidine

Front 4

Lidocaine
A. what class of antidysrhythmic drug?
B. what are other drugs in its group?

Back 4

B. Phenytoin

Front 5

Phenytoin
A. what class of antidysrhythmic drug?
B. what are other drugs in its group?

Back 5

B. Lidocaine

Front 6

Flecainide
A. what class of antidysrhythmic drug?
B. what are other drugs in its group?

Back 6

B. Ecainide

Front 7

Encainide
A. what class of antidysrhythmic drug?
B. what are other drugs in its group?

Back 7

B. Flecainide

Front 8

Propranol
A. what class of antidysrhythmic drug?
B. what are other drugs in its group?

Back 8

B. Metoprolol, Sotalol, Esmolol

Front 9

Amiodarone
A. what class of antidysrhythmic drug?
B. what are other drugs in its group?

Back 9

B. Sotalol, Ibutilide, Bretylium

Front 10

Verapamil
A. what class of antidysrhythmic drug?
B. what are other drugs in its group?

Back 10

B. Diltiazem, Nifedipine

Front 11

Nifedipine
A. what class of antidysrhythmic drug?
B. what are other drugs in its group?

Back 11

B. Verapamil, Diltiazem

Front 12

Conduction in damaged/abnormal heart tissue is usually [ decreased / increased]. Antidysrhythmics work [ better /worse ] on Na channels in depolarized cells and decrease recovery.

Back 12

Conduction in damaged/abnormal heart tissue is usually DECREASED. Antidysrhythmics work BETTER on Na channels in depolarized cells and decrease recovery.

Front 13

What channels are open, closed or leaky in each phase?
A. phase 0: Fast upstroke
B. phase 1: partial repolarization
C. phase 2: plateau
D. phase 3: repolarization
E. phase 4: forward current

Back 13

A. phase 0 : Na channels open resulting in fast inward current, accounting for upstroke. Those are rapidly inactivated (upstroke ends).
B. phase 1: Initial rapid phase of repolarization is due to inactivationof sodium channels AND K channels rapidly open and close causing a transient outward current. So, Na channels closed, K+ channels transiently open/close.
C. phase 2: plateau. Voltage sensitive Ca++ channels open, resulting in slow inward (depolarizaing) current that balances the slow (polarizing) outward leak of K+. So, Ca channels open; K channels leaky.
D. phase 3: repolarization: Ca++ channels close. K+ further open resulting in an outward current leading to membrane repolarization. So, Ca channels close; K open.
E. phase 4: forward current. Potassium channel closes.

Front 14

The general strategy for antidysrhythmic drugs is suppression of dysrhythmias by altering three of the following. Which is NOT a strategy by which antidysrhythmics work?
A. alter automaticity
B. alter conduction velocity
C. alter contractility
D. alter refractory period

Back 14

C. alter contractility

note:
A. alter automaticity: by decreasing slope of Phase 4 depolarizations, increase the threshold potential, or decrease resting potential
B. alter conduction velocity: by decrease of phase 0 upstroke, decrease rate of rise of Phase 4 depol, decrease membrane resting potential
D. alter refractory period: increase phase 2 plateau, increase phase 3 repolarization, increase action potential duration

Front 15

The general strategy for antidysrhythmic drugs is suppression of dysrhythmias by altering automaticity, conduction velocity or refractory period. Name three specifics with regards to the phases of ion permeability for each strategy.

Back 15

1. alter automaticity by
- decreasing slope of Phase 4 depolarizations
- increase the threshold potential
- decrease resting potential

2. alter conduction velocity by:
- decrease of phase 0 upstroke
- decrease rate of rise of Phase 4 depol
- decrease membrane resting potential

3. alter refractory period by:
- increase phase 2 plateau
- increase phase 3 repolarization
- increase action potential duration

Front 16

According to the Vaughan-Williams classification for antidysrhythmic drugs, which class/subclass is described? Give at least two examples of drugs from that class.

Moderate block Phase 0. slow conduction, increase APD and increase QT interval.

Back 16

Class Ia: Sodium channel blockers.

Ex. Quinidine, Procainamide

Front 17

According to the Vaughan-Williams classification for antidysrhythmic drugs, which class/subclass is described? Give at least two examples of drugs from that class.

Minimal phase 0 block; slow conduction; shorten phase 3 repolarization, decreases APD

Back 17

Class IB Na channel blocker.

Ex. Lidocaine, Phenytoin.

Front 18

According to the Vaughan-Williams classification for antidysrhythmic drugs, which class/subclass is described? Give an example of a drug from that class.

Marked Phase 0 block. Slow conduction. No change in APD or repolarization. Increased suppression of Na channels.

Back 18

Class IC Na channel blocker.

Ex. Flecainide

Front 19

According to the Vaughan-Williams classification for antidysrhythmic drugs, which class/subclass is described? Give at least two examples of drugs from that class.

decrease adrenergic input. No effect APD, suppress phase 4 depolarization, slow conduction. Can affect phase 0 too to some extent but for our purposes, just focus on this drug class as affecting phase 4.

Back 19

Class II , Beta blockers! "-olols" .

Ex. propranolol, metoprolol, sotalol, esmolol

Front 20

According to the Vaughan-Williams classification for antidysrhythmic drugs, which class/subclass is described? Give at least two examples of drugs from that class.

Prolongs repolarization/ refractory period other means than exclusively INa block (mainly K channel blockade), increases QT interval.

Back 20

Class III, K channel blockade.

Ex. Amiodarone, Sotalol, Ibutilide, Bretylium.

Front 21

According to the Vaughan-Williams classification for antidysrhythmic drugs, which class/subclass is described? Give at least two examples of drugs from that class.

Slow conduction and increase effective refractory period in normal tisue (AV node) and Calcium dependent slow responses of depolarized tissue (atria, ventricle, Purkinjie).

Back 21

Class IV . Calcium channel blockers.

Ex. Verapamil, diltiazem, Nifedipine

Front 22

Which two groups of antidysrhythmic drugs increase the QT interval?

Back 22

Class IA sodium channel blockers like Quinidine and Procainamide; Class III potassium channel blockers like Amiodarone, Sotalol, Ibutilide, Bretylium.

Front 23

With regards to sodium channel blockers in antidysrhythmic drugs, describe the degree of phase 0 blocking (minimal, moderate, marked) and the effect on APD for Class Ia, Class Ib, Class Ic.

Back 23

Class IA : moderate phase 0 block, increase in APD (due to increase QT interval)
Class IB: minimal phase 0 block, decrease in APD (due to shortened phase 3 repol)
Class IC: marked phase 0 block, no affect on APD

Front 24

For the arrhythmia drugs, what are the shortcomings of the Vaughan-Williams system (V-W system)? (3-5)

Back 24

- based on drugs that modify the electrophysiological characteristics of NORMAL CARDIAC TISSUE. (Instead of diseased tissue which is what we actually use em for!)
- the system is incomplete and does not include adenosine, digitalis, cholinergic agonists, alpha adrenergic blockers or agents that modulate gap junctions, ion pumps or exchangers. it also ignores actions of metabolites of the drugs.
- some drugs can be put into multiple classes (ex. Amiodarone, can be put in all classes!)
- Does not consider drugs that activate channels or recpetors
- does not incorporate varying modes of action like slowing tachys, terminating dysrhythmias or preventing them

Front 25

Which of the following statements about key aspects of antidysrhythmic drug action and therapy is FALSE?

A. Antidysrhythmic drug action is state-dependent; drug effects depend on the molecular states of the channel.
B. Can be prodysrhythmic under certain circumstances
C. Can have significant cardiac and extracadriac toxicity
D. Often affect the autonomic nervous system and have hemodynamic effects and effects on cardiovascular reflexes.
E. All of the above are true

Back 25

E. All of the above are true

Front 26

Antidyshrythmic drugs affect different parts of the heart.

A. Which is selective for AV and SA nodes?
B. Which is useful for treating premature ventricular contractions (PVCs) in the Purkinje fibers?
C. Which affects both atrial and ventricular dysrhythmias but is used moreso to treat atrial fibrilation?

Back 26

A. selective for AV and SA nodes = Calcium channel blockers (Class IV). B/c calcium action potentials predminate. Thus good for treating AV reentrant tachycardias.
B. for treating premature ventricular contractions (PVCs) in the Purkinje fibers = Lidocaine (Class IB) b/c longer APDs in purkinje yield more inactivated Na channels. Lidocaine selectively blocks inactivated state Na channels.
C. affects both atrial and ventricular dysrhythmias but is used moreso to treat atrial fibrilation = quinidine (Class IA)

Front 27

Of the antiarrhythmic drugs, which two are the only ones to possibly increase automaticity?

A. Amiodarone
B. Bretylium
C. Digitalis
D. Esmolol
E. Flecainide

Back 27

B. Bretylium, C. Digitalis

all others decrease automaticity

Front 28

Of all the antiarrhythmics, which groups are the ones to NOT have any effect on conduction velocity? What type of effect do all others have on conduction velocity?

Back 28

Groups that DO NOT affect conduction velocity are:
Class IB (Lidocaine, Phenytoin), and Bretylium (a drug in Class III).

All other antiarrythmics decrease conduction velocity.

Front 29

Of all the antiarrhythmic drugs, which decrease refractory period?

Back 29

Class IB (Licodaine, Phenytoin), Class II (beta blockers), and digitalis (can both increase or decrease) decrease refractory period. All other antiarrhythmics increase the refractory period.

Front 30

Of all the anntiarrythmic drugs, which decreases the action potential duration and which does not have any affect on APD?

Back 30

APD are decreased with Class IB, Class IIs, and again digitalis can swing either way. Class IC does not affect APD.

Front 31

What antiarrhythmic drugs:
A. can increase automaticity?
B. have no affect on conduction velocity?
C. decrease the refractory period?
D. decrease the action potential duration?
E. do not have an effect on the action potential duration?

Back 31

A. can increase automaticity? BRETYLIUM, DIGITALIS
B. have no affect on conduction velocity? Class IB, Bretylium
C. decrease the refractory period? Class IB, Class II, Digitalis
D. decrease the action potential duration? Class IB, Class II, Digitalis
E. do not have an effect on the action potential duration? Class IC

Front 32

The T1/2 are special for emolol, amidoarone, and adenosine. Match em.

1. 15 seconds
2. 9 minutes
3. 25 days

Back 32

1. 15 seconds : Adenosine is ultrashort!!
2. 9 minutes: Esmolol
3. 25 days: Amiodarone prettty long

Front 33

Which antidysrhythmic is the DOC for atrial fibrillation?

Back 33

Class II Beta blockers

Related use regarding dysrhythmias is also for supraventricular tachys. But NOT ventric tachys.

Front 34

What are the 3 acute-supravent, 2 chronic-supravent, 5 acute-vent, 3 chronic-vent drugs?

Back 34

Front 35

This antidysrhythmic drug greatly lengthens QT intervals and thus is associated with Torsades de Pointe! Other adverse effects include GI effects like diarrhea and vomiting, CNS effects like HA, nausea, dizziness and tinnitus. A drug intrxn to note is that this displaces digoxin from binding sites. This is useful for chronic dysrhythmias in general requiring outpatient treatment.

A. Esmolol
B. Lidocaine
C. Flecainide
D. Procainamide
E. Quinidine

Back 35

E. Quinidine

Front 36

What is the antidysrhythmic drug that can yield drug-induced SLE?

Back 36

Procainamide!

Other noteable thing about procainamide is that it has a metabolite, NAPA, that is a weak sodium channel blocker (Class III activity).

Other two drugs are: hydralazine, isoniazid

Front 37

This drug has a metabolite, NAPA, that is a weak sodium channel blocker (Class III activity).

A. Quinidine
B. Procainamide
C. Lidocaine
D. Phenytoin
E. FLecainide

Back 37

B. Procainamide

Front 38

This drug has very low toxicity and good therapeutic index. Used IV since there is extensive first pass hepatic metabolism. T1/2 = 0.5-4 hours. Effective in suppressing dysrhythmia associated with depolarized tissue (ischemia; digitalis toxicity). Is also used as a local anesthetic and works on nerves at higher doses.


A. Quinidine
B. Procainamide
C. Lidocaine
D. Phenytoin
E. Flecainide

Back 38

C. Lidocaine

Front 39

This drug is a second-line antiarrhythmic. Effective for supraventric AND ventirc tachys as well as digitalis-induced dysrhythmias. Other notables about the drug: Non-sedative anticonvulsant used in treating epilepsy; One of three drugs whose use is associated with gingival hyperplasia.

A. Quinidine
B. Procainamide
C. Lidocaine
D. Phenytoin
E. Flecainide

Back 39

D. Phenytoin

Gingival hyperplasia can be seen also with
other two are cycolosporin and nifedipine.

Front 40

Used primarily for ventricular dysrhythmias but effective for atrial and supraventricular arrhythmias and prevention of atrial fib /flutter. BUT, that said, Associated with signif mortality; marked tendency to exacerbate or precipitate dysrhythmias, thus used as last resort!

A. Quinidine
B. Procainamide
C. Lidocaine
D. Phenytoin
E. Flecainide

Back 40

E. Flecainide

Front 41

This is a non-selective beta blocker. Is CI in patients with ventricular failure (can lead to AV block) but others in its same class are sometimes recommended for HF.

Back 41

Propranolol.

Front 42

This drug prolongs refractory period by blocking potassium channels; is a structural analog of thyroid hormone, contains iodine, very lipophilic.

Back 42

Amiodarone, Class III K channel blocker (also belongs to IA, II, IV) .

Other notable: has very long half life of 13 days -15 weeks! Is a CYP3A4 substrate and inhibitor and thus may enhance the effect of other CYP3A4 substrates like Warfarin, Simvastatin, Verapamil. Also, increases QT interval so risk of TdP.

Front 43

Amiodarone, Class III K channel blocker (also belongs to IA, II, IV) .

This antiaarythmic drug has a very long half life of 13 days -15 weeks! Is a CYP3A4 substrate and inhibitor and thus may enhance the effect of other CYP3A4 substrates like Warfarin, Simvastatin, Verapamil.

Back 43

Amiodarone

Front 44

This drug originally was used as an antiHTN but its availability is now limited. Now is used in emergencies only as it can cause ventricular fibrillation due to QT lengthening.

A. Bretylium
B. Ibutilide
C. Sotalol
D. Verapamil

Back 44

A. Bretylium

Front 45

This is a class III drug that is generally well tolerated and actually has a low incidence of TdP despite being a Class III drug! Most effective current agent to convert atrial fibrillation and flutter of recent onset to normal rhythm.

A. Bretylium
B. Ibutilide
C. Sotalol
D. Verapamil

Back 45

B. Ibutilide

Front 46

This is a drug that is a nonselective beta blocker but also has the characteristic of increasing APD by incresing QT intervals.

A. Ibutilide
B. Bretylium
C. Sotalol
D. Verapamil

Back 46

Those characteristics indicate both Class II and Class III characteristics. The only drug that is both of those is Sotalol.

Front 47

Note that dihydropyridine types of this drug are poor antiarrythmics!!

Back 47

Calcium channel blockers. The calcium blockers used in treating dysrhythmias MUST be non-dihydropiyridines! (Verapamil, Diiltiazem, Nifedipine. Amlodipine IS a DHP.)

Front 48

This drug for dysrhythmia has side effects of flushing due to vasodilation, hypotension, shortness of breath or burning sensation in chest. It is administered as an IV bolus and has a super short half life of 15 SECONDS!

Back 48

Adenosine

Front 49

True or False:
Digoxin is used to treat atrial flutter and fibrillation, since slows ventric responses by slowing AV node conduction.

Back 49

True

Front 50

This is used to treat Torsades de Pointe.
A. Adenosine
B. Potassium K+ ions
C. Digoxin
D. Mg

Back 50

D. Mg

Front 51

Which of the following are used for acute supraventricular tachycardias?

A. Adenosine, digoxin, Ca2+ channel blocker
B. Beta-blocker, Ca2+ channel blocker
C. Sotalol, amiodarone, procainamide, lidocaine, bretylium
D. Amiodarone, Sotalol, Flecainide

Back 51

A. Adenosine, digoxin, Ca2+ channel blocker

Front 52

Which of the following are used for chronic supraventricular tachycardias?

A. Adenosine, digoxin, Ca2+ channel blocker
B. Beta-blocker, Ca2+ channel blocker
C. Sotalol, amiodarone, procainamide, lidocaine, bretylium
D. Amiodarone, Sotalol, Flecainide

Back 52

B. Beta-blocker, Ca2+ channel blocker

Front 53

Which of the following groups is use to treat acute, ventricular tachycardias?

A. Adenosine, digoxin, Ca2+ channel blocker
B. Beta-blocker, Ca2+ channel blocker
C. Sotalol, amiodarone, procainamide, lidocaine, bretylium
D. Amiodarone, Sotalol, Flecainide

Back 53

C. Sotalol, amiodarone, procainamide, lidocaine, bretylium

Front 54

Which of the following are used to treat chronic ventricular tachycardias?

A. Adenosine, digoxin, Ca2+ channel blocker
B. Beta-blocker, Ca2+ channel blocker
C. Sotalol, amiodarone, procainamide, lidocaine, bretylium
D. Amiodarone, Sotalol, Flecainide

Back 54

D. Amiodarone, Sotalol, Flecainide

Front 55

What drug has the following adverse effects/ toxicity:
- syncope/ fainting (due to disorganized ventricular tachy)
- associated with prolonged QT interval
- negative ionotropic action (decreases contractility)
- GI: diarrhea, vomiting
- CNS: headaches, nausea, dizziness, tinnitus

A. Amiodarone
B. Bretylium
C. Flecainide
D. Ibutilide
E. Lidocaine
F. Phenytoin
G. Procainamide
H. Quinidine

Back 55

H. Quinidine

Note: Procainamide, also a Class IA antidysrhythmic, has similar SE but no GI or CNS effects.

Front 56

What three drugs can yield drug-induced SLE?

Back 56

Procainamide, hydrasalazine, isoniazid

Front 57

Which three drugs yields drug-induced gingival hyperplasia?

Back 57

Phenytoin, Caclium channel blocker nifedipine, cyclosporin

Front 58

New drug of choice for ventricular dysryhtymias is
A. Amiodarone
B. Bretylium
C. Lidocaine
D. Phenytoin

Back 58

A. Amiodarone

Front 59

What are important side effects / toxicities of Amiodarone? (Cardiac = 3 ; Non-cardiac = 9)

Back 59

Amiodarone SE and toxicities

Cardiac: prolonged QT interval, sinus bradycardia, negative ionotropic action due to block of Ca channels and beta receptors (but can improve heart vailure via vasodilation)

Non-cardiac:
- reduces clearance of drugs like procainamide, flexainide, digitalis, quinidine, diltiazem
- THYROID DYSFUNCTION (hypo or hyper) since contains iodine
- PULMONARY FIBROSIS (most serious adverse effect)
- paresthesias
- photosensitivity
- blurred vision
- ataxia, dizziness, tremor
- anorexia, nausea

Front 60

Though this class III antidysrhythmic drug increases APD, it has a low incidence of Torsades de Pointe compared to other drugs. Also, this drug is more effective for atrial flutter than fibrillation and is generally well tolerated.
A. Amiodarone
B. Bretylium
C. Ibutilide
D. Sotalol

Back 60

C. Ibutilide

Front 61

True or False:
Dihydropyridine (DHPs) Ca channel blockers (ie. Nifedipine) are poor antiarrythmics.

Back 61

TRUE

Front 62

What drug has the following side effects?
- flushing (due to vasodilation)
- hypotension
- shortness of breath or burning sensation in chest

A. Adenosine
B. Amiodarone
C. Bretylium
D. Phenytoin

Back 62

A. Adenosine

Note: Amiodarone has a LOT.
Cardiac: prolonged QT interval, sinus bradycardia, negative ionotropic action due to block of Ca channels and beta receptors (but can improve heart vailure via vasodilation)

Non-cardiac:
- reduces clearance of drugs like procainamide, flexainide, digitalis, quinidine, diltiazem
- THYROID DYSFUNCTION (hypo or hyper) since contains iodine
- PULMONARY FIBROSIS (most serious adverse effect)
- paresthesias
- photosensitivity
- blurred vision
- ataxia, dizziness, tremor
- anorexia, nausea