Molecular Mechanisms of Arrhythmias & Antiarrhythmic Drugs Flashcards Preview

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Flashcards in Molecular Mechanisms of Arrhythmias & Antiarrhythmic Drugs Deck (36):
1

Almost all arrhythmias are:

acquired: (MI), ischemia,
acidosis, alkalosis, electrolyte abnormalities.

Drug toxicity is a common cause of arrhythmia

2

cardiac Na+ channels
cardiac Ca2+ channels
cardiac K+ channels
β-adrenergic receptors (βAR)

primary targets of antiarrhythmic drugs

3

To date, only β-blockers have been demonstrated to reduce the incidence of_______

sudden cardiac death

4

Usually, catheter ablation of ectopic foci and implantable __________ are very often used in place of drugs

cardioverterdebrillator devices (ICDs)

5

primary targets of antiarrhythmic drugs

cardiac Na+ channels
cardiac Ca2+ channels
cardiac K+ channels
β-adrenergic receptors (βAR)

6

If, ICa-L, and IKs are indirect targets of antiarrhythmic drug action via

Via the β-adrenergic receptor pathway:

7

Prolonged QT is caused by

taking too long to repolarize, increased AP duration

8

Mutations in some _____ can cause a prolonged QT interval

sodium and potassium channels.

9

ventricular fibrillation results in a survival rate of only 40% by 5 years of
age
> 30 mutations in the cardiac Na+ channel reduce peak inward Na+ current in ventricular myocytes

Brugada syndrome

10

Two major sources of inappropriate impulse initiation:

a.) ectopic foci
b.) triggered afterdepolarizations: triggered by action potentials

11

an excitable group of cells that causes a premature heart beat outside the normally functioning SA node of the human heart

ectopic focus

12

abnormal depolarizations of cardiac myocytes that interrupt phase 2/phase 3 of the cardiac action potential in the electrical conduction system of the heart.

triggered afterdepolarizations: triggered by action potentials

13

Prolonged phase 2 causes excess:

Ca entry

14

Disturbed impulse conduction

-Reentry

15

Reentry factors that can be combated

-unidirectional conduction block in fx circuit

-conduction time around the circuit > refractory

16

Class I: blockers of voltage-gated cardiac Na+ channels

Class II: β-adrenergic receptor blockers (“β blockers”)

Class III: drugs that prolong fast response phase 2 by delaying repolarization

Class IV: blockers of voltage-gated cardiac Ca2+ channels

Vaughan Williams classification of antiarrhythmic drugs

17

blockers of voltage-gated cardiac Na+ channels

Vaughan Williams classification of antiarrhythmic drugs

Class I

18

β-adrenergic receptor blockers (“β blockers”)

Vaughan Williams classification of antiarrhythmic drugs

Class II

19

drugs that prolong fast response phase 2 by delaying repolarization

Vaughan Williams classification of antiarrhythmic drugs

Class III

20

blockers of voltage-gated cardiac Ca2+ channels

Vaughan Williams classification of antiarrhythmic drugs

Class IV

21

adenosine is class?

trick question, unclassified

22

Class Ia drugs: Na+ channel blockers

Class IA quinidine, procainamide, disopyramide

23

Class Ib drugs: Na+ channel blockers

Class IB lidocaine, mexiletine, phenytoin

24

Class Ic drugs: Na+ channel blockers

Class IC propafenone, flecainide, encainide

25

All class I drugs show

↑refractory period
↓ conduction velocity
↓re-entry

26

Re-entry can be defeated by either:

slowed conduction velocity or longer refractory period

27

Class Ib drugs show pure class I action:

slow upstroke, decreased AP duration

28

Class Ia & Class Ic drugs delay phase 3 onset via________

K+ channel block

29

Class 1a has a prolonged

repolarization

30

Two conditions are required for re-entry:

(1) have unidirectional conduction block in any kind of functional circuit

(2) the conduction time around the circuit > refractory period

31

Re-entry could be terminated by:

(1) converting uni- to bi-directional block

(2) or by prolonging refractory time

32

Prolonged refractoriness can suppress re-entrant arrhythmias because:

• refractory tissue will not generate an action potential

• and so the re-entrant wave of excitation is extinguished

33

Class II drugs (β-adrenergic receptor blockers) CURRENT

↓ If current
↓ L-type Ca2+ current
↓ K+ current

34

β-blockers are consequently used to terminate arrhythmias that involve AV
nodal re-entry, and in controlling ventricular rate during _______

atrial fibrillation.

35

Class II drugs (β-adrenergic receptor blockers) RESULTS

↓ rate of diastolic depolarization in pacing cells
↓ upstroke rate, and slows repolarization, particularly in AV nodal myocytes

36

Adenosine-induced changes in membrane currents:

↓ SA node and AV node firing rate
↓ conduction rate in the AV node