Antidysrhythmic Drugs

Question 1

Response of cells to excitatory electrical stimuli is a function of what?

Answer 1

Available Na channels

Question 2

What is the normal sinus rhythm?

Answer 2

60-90bpm

Question 3

How do flutter and fibrillation differ?

Answer 3

Flutter: very rapid but regular contractions Fibrillation: disorganized contractile activity

Question 4

How many phases are in a heart contraction and what generally happens in each?

Answer 4

Phase 0: Fast upstroke (Na channels open) Phase 1: Partial repolarization Phase 2: Plateau Phase 3: Repolarization Phase 4: Forward current

Question 5

Two general mechanisms of arrhythmias? Which is more common?

Answer 5

1. Abnormal impulse generation 2. Abnormal impulse conduction (more common)

Question 6

Two ways to get abnormal impulse generation?

Answer 6

1. Abnormal automaticity of normally automatic cells (SA, AV, His) 2. Generation of impulses in normally non-automatic cells

Question 7

Two ways to get abnormal impulse conduction? More common?

Answer 7

1. AV block: ventricle free to start own pacemaker rhythm 2. Re-entry: re-excitation around a conducting loop, producing tachycardia (more common)

Question 8

What type of drug and how do quinines work (3)?

Answer 8

Class IA: 1. Moderate block of Na+ channels 2. Decrease automaticity of pacemaker cells 3. Increase effective refractory period/AP duration

Question 9

In what state is abnormal heart tissue typically found and what three things does this cause?

Answer 9

Usually depolarized, reducing Na current, decrease dV/Dt and and decreases conduction velocity

Question 10

How do antiarrhythmic drugs generally function?

Answer 10

Decrease # of functional Na channels, and recovery time of Na channels determines refractory period (thus RP is increased)

Question 11

How do specific ion channels open/close in each phase? Which class affects which phase?

Answer 11

Phase 0: Na+ channels Open (I) Phase 1: Na+ closed, K+ open Phase 2: Ca2+ open, K+ open (leaky) (IV) Phase 3: Ca2+ close, K+ open, Na/K ATPase (III) Phase 4: Inc in Na+ permeability (IV)

Question 12

What part of the heart has the steepest Phase 4? What does this infer?

Answer 12

SA then AV node; spontaneous repolarization

Question 13

What are three general strategies of antidysrhythmic drugs?

Answer 13

1. Decrease automaticity 2. Decrease conduction velocity 3. Increase refractory period

Question 14

Which two drugs increase the QT?

Answer 14

Classes IA and III

Question 15

T/F. All drug classes discussed will slow conduction.

Answer 15

T.

Question 16

How do the subtypes of Class I differ with regards to the Action Potential Duration (APD)?

Answer 16

IA: Inc APD, IB: Dec APD, IC: No change in APD

Question 17

How are quinidine and procainamide similar?

Answer 17

Class IA, Dec CV and Inc Qt/APD; S: blocks M- and alpha-adrenocreceptors (dec TPR), diarrhea, nausea, cardiac dep.

Question 18

How do quinidine and procainamide differ (including side effects)?

Answer 18

Tx: Q=Atrial arrhythmias, SVT (chronic) and P=Ventric arrhyth and NAPA (acute) S: Q=tinnitus w/ CG and P=Lupus

Question 19

What is NAPA?

Answer 19

N-acetylprocainamide and is procainamide’s metabolite with Class III Activity

Question 20

What are the classes of drugs and what do they each generally do?

Answer 20

I: Na-Channel blocker II: Beta blockers (suppress phase 4 depol) III: K+ channel blocker (prolong repolar/RP) IV: CCB: slow conduction and inc RP and Ca-dependent slow responses

Question 21

What does lidocaine do, where effect, how administered?

Answer 21

Class IB, VT/VF, IV/IM

Question 22

What drug is an arrhythmia and oral anticonvulsant? What is its main side effect? CI?

Answer 22

Phenytoin; gingival hyperplasia; pregnancy

Question 23

What class increase phase III? Dec Phase III? Suppresses Phase 4?

Answer 23

Class III (amiodarone); Class IB (Lido/phenytoin); Class II (Esmolol or sotalol)

Question 24

What drug has a marked block on phase 0, dec CV, no change in APD?

Answer 24

Flecainide

Question 25

Why is flecainide not used as often?

Answer 25

Inc mortality, so last resort agent

Question 26

Side effects: what drug has tinnutis? Lupus?

Answer 26

Quinidine; procainamide,

Question 27

What drug has Class II and III qualities?

Answer 27

Sotalol

Question 28

What other beta-blockers are used to help with antiarrhytmias?

Answer 28

Esmolol and metoprolol

Question 29

What two beta blockers also have the added benefit of blocking Na+ channels at high doses?

Answer 29

Metaprolol and propranolol

Question 30

What class of drugs can also help those with Pheochromocytoma? Thyroid disorders?

Answer 30

Beta-blockers (II); amiodarone (III) and beta-blockers (II)

Question 31

What drug is CI in patients with ventricular failure? Why?

Answer 31

Beta blockers; can lead to A-V block

Question 32

What type of beta blocker would a dysrhythmic patient never take?

Answer 32

Partial agonist

Question 33

What is the new drug of choice for VT?

Answer 33

Amiodarone (dronedarone is close second)

Question 34

What drug has Toursades de pointes?

Answer 34

Quinidine and Amiodarone (also both have negative inotropic action aka dec contractility)

Question 35

What drugs should not be taken with amoidarone?

Answer 35

CG (like Class IA) or warfarin

Question 36

What is the half life of esmolol, adenosine and amiodarone?

Answer 36

9min, 15sec, and 25 days

Question 37

What drug is preferred of amiodarone? Why?

Answer 37

Dronedarone has almost exact same properties but less bad effects and smaller half life

Question 38

What are three bad side effects of amiodarone?

Answer 38

Deposits in almost every organ (corneal), thyroid dysfunction (hypo more common), and pulmonary fibrosis

Question 39

What two drugs increase the plateau phase?

Answer 39

Verapamil and diltiazem (NOT Nifedipine)

Question 40

VT or SVT: which one is verapamil used for?

Answer 40

SVT (acute and chronic)

Question 41

What is a CI for verapamil?

Answer 41

Heart Failure

Question 42

What heart condition is adenosine used for? What class is it?

Answer 42

Acute SVT; not in a class

Question 43

How does adenosine work?

Answer 43

Activates adenosine receptors which open K+ channels; this increases RP and dec CV

Question 44

What drug triggers the vagal nerve to depress RP and AV?

Answer 44

Digoxin

Question 45

What drug can both treat and cause ventricular tachycardia?

Answer 45

Digoxin

Question 46

What drugs treat SVT arrhythmias (Acute v. Chronic)?

Answer 46

Acute: Adenosine/digoxin, verapamil Chronic: Beta-blocker, CCRB, Quinidine, Phenytoin, verapamil

Question 47

What drugs treat VT (acute v. chronic)?

Answer 47

Acute: amiodarone, procainamide, sotalol, bretylium, lidocaine Chronic: Amiodarone, sotalol, flecainide, quinidine

Question 48

What drug treats both VT and SVT?

Answer 48

Phenytoin, satolol, quinidine (chronic), ibutilide

Question 49

What drug is used during surgery if an arrhythmia occurs?

Answer 49

Esmolol

Question 50

What drug moderate blocks Ph 0 and increases APD?

Answer 50

Quinidine (IA)- also increases QT

Question 51

What drug shortens Phase 3 and decreases APD?

Answer 51

Lidocaine/phenytoin (IB)

Question 52

What drug doesn't change APD and slows conduction?

Answer 52

Flecainide (IC) or Beta blockers (II)

Question 53

Drug that suppresses Phase 4 depolarization?

Answer 53

Beta blocker

Question 54

What drug's main function is prolonging phase III and increasing QT?

Answer 54

Amiodarone (III) (and sotalol (II) to an extent)

Question 55

Drug that increases effective refractory period and Ca-dependent slow responses of depolarized tissue?

Answer 55

Verapamil/diltiazem (IV)

Question 56

What are three shortcomings of V-W system?

Answer 56

1. Classification based on normal tissue effects 2. It's incomplete (doesn't contain many drugs) 3. Some drugs have properties of several classes.