Antidysrhythmic Drugs Flashcards

1
Q

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

A

Available Na channels

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2
Q

What is the normal sinus rhythm?

A

60-90bpm

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3
Q

How do flutter and fibrillation differ?

A

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

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4
Q

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

A

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

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5
Q

Two general mechanisms of arrhythmias? Which is more common?

A
  1. Abnormal impulse generation 2. Abnormal impulse conduction (more common)
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6
Q

Two ways to get abnormal impulse generation?

A
  1. Abnormal automaticity of normally automatic cells (SA, AV, His) 2. Generation of impulses in normally non-automatic cells
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7
Q

Two ways to get abnormal impulse conduction? More common?

A
  1. AV block: ventricle free to start own pacemaker rhythm 2. Re-entry: re-excitation around a conducting loop, producing tachycardia (more common)
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8
Q

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

A

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

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9
Q

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

A

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

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10
Q

How do antiarrhythmic drugs generally function?

A

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

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11
Q

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

A

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)

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12
Q

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

A

SA then AV node; spontaneous repolarization

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13
Q

What are three general strategies of antidysrhythmic drugs?

A
  1. Decrease automaticity 2. Decrease conduction velocity 3. Increase refractory period
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14
Q

Which two drugs increase the QT?

A

Classes IA and III

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15
Q

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

A

T.

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16
Q

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

A

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

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17
Q

How are quinidine and procainamide similar?

A

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

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18
Q

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

A

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

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19
Q

What is NAPA?

A

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

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20
Q

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

A

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

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21
Q

What does lidocaine do, where effect, how administered?

A

Class IB, VT/VF, IV/IM

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22
Q

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

A

Phenytoin; gingival hyperplasia; pregnancy

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23
Q

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

A

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

24
Q

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

A

Flecainide

25
Q

Why is flecainide not used as often?

A

Inc mortality, so last resort agent

26
Q

Side effects: what drug has tinnutis? Lupus?

A

Quinidine; procainamide,

27
Q

What drug has Class II and III qualities?

A

Sotalol

28
Q

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

A

Esmolol and metoprolol

29
Q

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

A

Metaprolol and propranolol

30
Q

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

A

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

31
Q

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

A

Beta blockers; can lead to A-V block

32
Q

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

A

Partial agonist

33
Q

What is the new drug of choice for VT?

A

Amiodarone (dronedarone is close second)

34
Q

What drug has Toursades de pointes?

A

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

35
Q

What drugs should not be taken with amoidarone?

A

CG (like Class IA) or warfarin

36
Q

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

A

9min, 15sec, and 25 days

37
Q

What drug is preferred of amiodarone? Why?

A

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

38
Q

What are three bad side effects of amiodarone?

A

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

39
Q

What two drugs increase the plateau phase?

A

Verapamil and diltiazem (NOT Nifedipine)

40
Q

VT or SVT: which one is verapamil used for?

A

SVT (acute and chronic)

41
Q

What is a CI for verapamil?

A

Heart Failure

42
Q

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

A

Acute SVT; not in a class

43
Q

How does adenosine work?

A

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

44
Q

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

A

Digoxin

45
Q

What drug can both treat and cause ventricular tachycardia?

A

Digoxin

46
Q

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

A

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

47
Q

What drugs treat VT (acute v. chronic)?

A

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

48
Q

What drug treats both VT and SVT?

A

Phenytoin, satolol, quinidine (chronic), ibutilide

49
Q

What drug is used during surgery if an arrhythmia occurs?

A

Esmolol

50
Q

What drug moderate blocks Ph 0 and increases APD?

A

Quinidine (IA)- also increases QT

51
Q

What drug shortens Phase 3 and decreases APD?

A

Lidocaine/phenytoin (IB)

52
Q

What drug doesn’t change APD and slows conduction?

A

Flecainide (IC) or Beta blockers (II)

53
Q

Drug that suppresses Phase 4 depolarization?

A

Beta blocker

54
Q

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

A

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

55
Q

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

A

Verapamil/diltiazem (IV)

56
Q

What are three shortcomings of V-W system?

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