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CRRAB FINAL REVIEW > Antiarrhythmic Drugs- Nordgren > Flashcards

Antiarrhythmic Drugs- Nordgren Flashcards

1
Q

What ion causes depolarization (phase 0 of AP) in atrial, purkinje, and ventricular cells?

A

Na+ current

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2
Q

What ion causes depolarization (phase 0 of AP) in SA and AV nodal cells?

A

Ca2+ current

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3
Q

Describe the different phases of Na channel positions

A

Resting = activation gate closed, inactivation gate open

Activated = both gates open

Inactivated= activation gate still open, but inactivation gate closes

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4
Q

What causes repolarization in all cell types?

A

Efflux of K+

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5
Q

Define refractory period

A

the time between phase 0 and sufficient recovery of Na+ channels in phase 3 to allow another action potential to occur

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6
Q

What happens to Na channel recovery time at more positive (depolarized) membrane potential?

A

Recovery time will increase (it will be slower at more depolarized potentials)
Increases refractory period of cell

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7
Q

What are the two mechanisms that can produce an arrhythmia?

A

Disturbances in impulse formation or impulse conduction

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8
Q

Define State-Dependent Drugs

A

Bind readily to activated or inactivated channels
Phase 0 = activated
Phase 2 = inactivated
Bind poorly or not at all to rested channels

**Prevents drug binding in this state and/or promotes drug dissociation from receptors when channels become rested

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9
Q

What are the three drugs in Class IA?

A

Quinidine
Procainamide
Disopyramide

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10
Q

How does the action potential curve shift in response to drugs in Class IA?

A

Moderate decrease in slope of phase 0

Takes longer for repolarization (some effect on K+ channels)

Increase AP duration
Increase EFP
Increase QT interval

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11
Q

What is a noted side effect of the drugs in class IA?

A

Increasing the QT interval can lead to torsades de point

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12
Q

Specific side effect of procainamide?

A

Reversible SLE-like syndrome

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13
Q

List the three drugs in Class IB

A

Mexiletine
Tocainide
Lidocaine

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14
Q

How does the action potential curve shift in response to drugs in class IB?

A 
Slightly decrease slope of phase 0
Quickens repolarization (opens K+ channels)

Decreases AP duration
Decrease ERP
Shortens QT interval

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15
Q

Which of the class I subytpes is best for ventricular arrythmias post MI?

A

Class IB

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16
Q

List the three drugs in Class IC

A

Flecainide
Propafenone
Moricizine

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17
Q

How does the action potential curve shift in class IC?

A

Drastically decreases slope of phase 0

No effect on refractory period or duration of action potential

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18
Q

What are the three components of rhythm?

A

Rate of impulse
Site of origin
Conduction (transport) of impulse

19
Q

What can cause an early afterdepolarization?

A

Early afterpolarization occurs DURING the action potential and interrupts orderly repolarization of myocytes.

Caused by

  • opening of more Ca2+ channels in late phase 2
  • Opening of Na+ channels in early phase 3
  • Inhibition of K+ channels
20
Q

What can cause delayed afterdepolarization?

A

Occurs AFTER action potential, when nearly or fully repolarized but before another action potential would normally occur. Can be caused by:

Elevated cytoslic Ca2+ levels -> overload of SR causes spontaneous release of Ca2+ and leads to depolarizing current

21
Q

Are early afterdepolarizations exacerbated at fast or slow HRs?

A

Slow HRs

22
Q

Are delayed afterdepolarization exacerbated at fast or slow HRs?

A

Fast HRs

Increased HR -> increased intracellular Ca2+ -> overload of SR causes spontaneous release of Ca2+ and leads to a depolarizing current

23
Q

Procainamide

A

Class IA
Induction of torsades de points
Long term use can cause SLE-like syndrome

24
Q

Quinidine

A

Class IA

Torsade de pointes

25
Q

Disopyramide

A

Class IA

Loading dose NOT reccommended because of risk of percipitating heart failure

26
Q

Lidocaine

A

Class 1BUsed for prevention of ventricular fibrillation AFTER cardioversion in the setting of acute ischemia. Prophylactic use may actually increase totally mortality → DO NOT DO IT!

27
Q

Mexiletine

A

Class IBSignificant efficacy in relieving chronic pain, especially due to diabetic neuropathy and nerve injury (off-label use)

28
Q

Flecainide

A

Class IC
Drastically decreases slope of phase 0, Potent blocker of Na+ and K+ channels with SLOW UNBLOCKING KINETICS (but does not prolong the AP or QT-interval)

29
Q

Propafenone

A

Class IC

Weak B-blocking activity

30
Q

Amiodarone

A

Class III K+ blockerToxicity = bradycardia and heart block in patients w/ pre-existing SA or AV node disease
• Drug accumulates in tissues → DOSE RELATED PULMONRY TOXICITY!!!!

31
Q

Dofetilide

A

Class III K+ blocker

Contraindicated in long QT, bradycardia, hypokalemia

32
Q

Ibutilide

A

Class III K+ channel blocker but also slow inward Na+ activator - delays repolarization

33
Q

Verapail

A

Class IV Ca+ channel blocker

Blocks both activated and inactivated L-type Ca2+ channels, so greater affect in tissue that fires frequently, those less polarized, or nodal tissue. Contraindicated in WPW

34
Q

Nitroglycerine

A

synergistic hypotension with phsophodiesterase type 5 inhibitors such a Vardenafil (Viagra, Cialis, Levitra)

35
Q

What are the three drug classes used for angina?

A

Nitrates- venodilation

Ca2+ Channel blockers - decrease HR and contractility

B-Blockers- decrease HR, BP and contractility

36
Q

How do Class IA drugs effect an EKG?

A

Increase QT interval, Increase QRS duration

37
Q

How do class IB drugs effect an EKG?

A

Decrease QT in Purkinje Cells

38
Q

How do class IC drugs effect an EKG?

A

Slight increase in PR interval (effect on AV nodal cells)

Increase QRS duration

39
Q

What do Propranolol and Esmolol do to EKG?

A

Increase PR interval (because they block calcium currents to increase length of phase 4 in Pacemaker cells)

40
Q

What does Amiodarone do to EKG?

A

Increases PR, Increases QRS, Increases QT

Note: Amiodarone is also a sodium channel blocker, calcium channel blocker, and weak beta blocker!

41
Q

Ibutilide and Dofetilide effect on EKG?

A

Increase QT interval (only block K+)!

42
Q

Sotalol effect on EKG?

A

Increase PR and Increase QT

43
Q

Adenosine effect on EKG?

A

Increases PR (adenosine suppress L type calcium channels in nodal tissue).

CRRAB FINAL REVIEW (12 decks)

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