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CPR Week 2 > 3.2.2. Antiarrythmic Drugs I and II > Flashcards

3.2.2. Antiarrythmic Drugs I and II Flashcards

1
Q

What are Class I drugs?

A

Na+ channel blockers

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2
Q

What are class II drugs?

A

Beta Blockers

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3
Q

What are class III drugs?

A

K+ channel blockers

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4
Q

What are class IV drugs?

A

Ca2+ channel blockers

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5
Q

What do the subtypes of Class I do?

A

IA - ↓ ventricular conduction (↑ QRS interval); prolong ventricular AP (↑ QT interval)

IB - slow conduction and ↑ threshold for firing of abnormal cells

IC - ↓ ventricular conduction (↑ QRS interval)

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6
Q

When do we use each of the subtypes of class I drugs?

A

IA - Atrial and ventricular arrhythmias IB - Acute ventricular arrhythmias IC - Ventricular arrhythmias

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7
Q

Examples of Class IA drugs

A

Quinidine, procainamide, disopyramide

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8
Q

Example of Class IB drugs

A

Lidocaine

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9
Q

Examples of Class IC drugs

A

Flecainide, propafenone

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10
Q

Side effects of Class IA drugs

A

Quinidine: cinchonism (headache, tinnitus) and torsades de pointes (polymorphic ventricular tachycardia due to ↑ QT interval);

procainamide: drug-induced lupus like symptoms

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11
Q

Side effects of Class IB drugs

A

CV and CNS depression w/ overdose

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12
Q

Side effects of Class IC drugs

A

Can cause arrhythmias (especially in post-MI patients)

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13
Q

How do Beta blockers work?

A

↓ AV nodal conduction (↑ PR interval)

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14
Q

When do we use beta blockers?

A

Ventricular and supraventricular arrhythmias

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15
Q

Side effects of Beta Blockers?

A

Bradycardia, AV block

Propanolol - Can cause bronchoconstriction

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16
Q

Examples of Beta Blockers

A

Esmolol (IV, rapid acting), metroprolol, propranolol

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17
Q

How do class III drugs work?

A

Prolong ventricular AP (↑ QT interval)

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18
Q

When do we use Class III drugs?

A

Treatment and prevention of ventricular arrhythmias

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19
Q

Examples of Class III drugs?

A

Amiodarone, sotalol, Ibutilide, Dofetilide (AIDS)

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20
Q

Side effects of class III drugs?

A

Amiodarone: pulmonary fibrosis, hepatotoxicity, thyroid disease

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21
Q

How do class IV drugs work?

A

↓ AV nodal conduction

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22
Q

When do we use class IV drugs?

A

Supraventricular arrhythmias

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23
Q

Examples of Class IV drugs?

A

Verapamil, diltiazem

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24
Q

Side effects of class IV drugs

A

Constipation, bradycardia, AV block

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25
Q

How does Adenosine work and when do we use it?

A

↓ AV nodal conduction Supraventricular arrhythmias

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26
Q

Side effects of Adenosine

A

Flushing, hypotension, chest pain

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27
Q

How does Magnesium work and when do we use it?

A

We don’t know how it works… Use it for Torsades de pointes

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28
Q

Side effects of using Mg2+

A

Respiratory depression

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29
Q

What is our “superstar” drug?

A

Amiodarone!

30
Q

What liver functions can Amioderone afffect and what results from it?

A

Potent inhibitor of hepatic CYP3A4, CYP2C9; p-glycoprotein (inhibits renal flow)

31
Q

What is automaticity?

A

In heart physiology, autorhythmicity (also called automacity) is the ability of cardiac cells to depolarize spontaneously, i.e. without external electrical stimulation from the nervous system.

32
Q

What are 3 mechanisms that can cause a Sinus Rhythm to speed up?

A

Beta-1 stimulation, Hypokalemia, or mechanical stretch

33
Q

What are 3 mechanisms that can cause a Sinus Rhythm to slow down?

A

ACh, INa blockers (Inward Sodium current), or Adenosine (Ca 2+ blocker)

34
Q

What does Digoxin do and what do we use it for?

A

Digoxin - used to lower resting potential used to treat arrhythmias complicated by Heart Failure

35
Q

Describe what is meant by slow response cells

A

Sino-Atrial Node cells (slow response cells) - Phase 0 (upswing/depolarization) is driven by Ca channels - Phase 3 is K channel these cells are ONLY time dependent

36
Q

Describe what is meant by fast response cells

A

Atrial & Ventricular Muscle Cells (fast response cells)

  • Phase 0 is driven by INa
  • Phase 1& 2 (plateau) (2 = absolute refractory period) is driven by Ca channels (ICaL (long), ICaT (transient))
  • Phase 3 (relative refractory) is K channel (IK, IK1)

These cells are time AND voltage dependent

37
Q

Effect of INa blockers on fast response cells

A

with INa blockers (Class I), these cells become ONLY time dependent

38
Q

Effect of IK blockers on fast response cells

A

with IK blockers (Class III), these cells become ONLY voltage dependent

39
Q

What is happening during the p wave?

A

P wave = SA depolarization

40
Q

What is occurring between P and S

A

P through QRS = atrial (SA node) depolarization and complete repolarization

41
Q

What is the QRS wave?

A

QRS = depolarization of the ventricles

42
Q

What is happening with the T wave?

A

T wave = repolarization of the ventricles

43
Q

What is happening with the QT interval?

A

QT Interval = complete ventricular depolarization and repolarization

44
Q

many drugs can prolong the time in the QT interval and predispose people to _____.

A

many drugs can prolong the time in this interval and predispose people to arrhythmias

45
Q

How does the Na channel work?

A

Opens for a VERY short amount of time and gets inactivated via the “ball and chain” mechanism Goes from closed → Open → inactivated → Closed (and repeat)

46
Q

What activates and deactivates the Na Channel?

A

phosphorylation = inactivation dephosphorylation = activation

47
Q

In the process of the Na channel Goes from closed → Open → inactivated → Closed (and repeat) What portion is slow? Fast?

A

Closed → Open = fast Inactivated → Closed = slow

48
Q

What part of the Na channel pathway do Na channel blockers act?

A

Inactivated → Closed = slow this is when Na channel blockers act.

49
Q

What type of channel positions do Na Channel blockers act?

A

some bind to open some bind to inactivated does not bind to closed state

50
Q

How do Na Channel blockers work?

A

Na channel blockers decrease the potential at which Na channels can recover

51
Q

What does this show? How do you know?

A

Sinus tachycardia (A); arrows = P waves

52
Q

What does this show? How do you know?

A

Sinus bradycardia (B); arrows = QRS complex (P wave = tiny)

53
Q

What does this show?

A

Irregular Arrhythmia

54
Q

Arrhythmias due to conduction issues are treated how? What is happening in these cases?

A

If Vagal input becomes too high, you can get P waves without associated QRS complexes, because the AP cannot get passed the AV node

No drugs to treat this, we just use pacemakers

55
Q

Effect of Class Ia, b, and c drugs on the ventricular action potential:

A
56
Q

Clinically, what do we use for supraventricular tachycardia?

A

IV adenosine and Verapamil

57
Q

Clinically what do we use for Atrial Fibrillation with heart failure?

A

Digoxin

58
Q

Clinically, what do we use for non-life threatening tachycardia?

A

Beta blockers

59
Q

Clinically, what do we use for Ventricular tachcardia?

A

IV Amiodarone, Lidocaine, Sotalol, Procainamide

60
Q

What is the first and most important therapeutic principle of antiarrhythmic drugs?

A

Identify and remove the precipitating factors

(Hypoxia, ischemia, electrolyte disturbances, diseases, etc)

61
Q

There are two main mechanisms that generate arrhythmias, what are they?

A
  1. reduce automaticity
  2. increase refractoriness
62
Q

How can we reduce automaticity?

A

decrease phase 4 slope

increase threshold

increase maximum diastolic potential

increase AP duration

63
Q

How can we increase refractoriness?

A

blockade of Na channels

prolong action potential (K channels)

64
Q

Where does Atropine do its thing?

A

M2 neurotransmitter receptor

65
Q

Where does Digoxin do its thing?

A

Na/K ATPase pump

66
Q

Compare the Cardiac EKG phases of a pacemaker vs. standard ventricular contraction

A
67
Q

What type of pattern is this?

A

Paroxysmal Super Ventricular Tachy

68
Q

What is PSVT? How do we treat it?

A
69
Q

Describe Torsades de Pointes and what it looks like on an ECG

A
70
Q

Explain triggered arrhythmias and the two types

A

CPR Week 2 (19 decks)

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