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Pharm 5 > Last Exam > Flashcards

Last Exam Flashcards

1
Q

Causes of arrhythmias

A

coronary ischemia, tissue hypoxia, electrolyte disturbances, drugs, scarring or overstretching of heart fibers, overstimulation of sympathetic nervous system

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2
Q

Problems when conduction system goes wrong

A
  1. abnormal impulse conduction (SA stops firing, AV picks up and fires at slower rate)
  2. Abnormal impulse formation (early firing, leak of ions, causing everything to depolarize - speeds SA node up)
  3. Combo of both
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3
Q

Downside of anti-arrhythmias

A

All drugs that are used to treat arrhythmias can cause lethal arrhythmias

When you have normal tissues as well as abnormal tissue drugs can induce abnormal arrhythmias

A drug that was helpful when the heart was beating slowly becomes harmful when heart starts to beat fast.

Development of a myocardial infarction due to O2 depletion from suppressing abnormal rhythm

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4
Q

When to treat?

A

too fast, too slow, asynchronous beating

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5
Q

Class 1

A

Sodium Channel Blockade
Sodium channel-blocking drugs
subgroups 1A, 1B, 1C

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6
Q

Class 2

A

Blockade of Sympathetic Autonomic affects in heart-Beta Blockers

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7
Q

Class 3

A

Prolongation of the effective refractory period-Potassium channel blockers

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8
Q

Class 4

A

Calcium Channel Blockade

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9
Q

1A

A

prolong action potential and interact with sodium channel a medium length of time

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10
Q

1B

A

shorten action potential and interact with channel rapidly

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11
Q

1C

A

least effect on sodium channel and dissociate from sodium channel slowly

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12
Q

When do Class 1 work best?

A

Sodium channel blockers work better on cardiac tissue that is rapidly firing (tachycardia) because sodium channels spend more time in an open state

they suppress cardiac conduction more in a person with tachycardia versus a person with normal heart rate.

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13
Q

1A drugs

A

isopyramide (Norpace)
Quinidine (Quinidex)
Procainamide (Procan)

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14
Q

1B drugs

A

Lidocaine (Xylocaine)

Mexiletine (Mexitil)

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15
Q

1C drugs

A

Flecainide (Tambocor)

Propafenone (Rythmol)

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16
Q

MOA of 1A

A

Blocks sodium channel slowing upstroke of action potential, slowing conduction of electrical impulse

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17
Q

S/E of 1A procainamide

A

arrhythmias (torsade de pointes), SLE like syndrome, nausea, diarrhea, hypotension

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18
Q

Is 1A a first line option?

A

procainamide - no, short half life (q6) & bad side affects

quinidine - no, maintains normal sinus rhythm nicely, but increases mortality 2-fold

disopyramide - no, anticholinergic (occasionally used for ventricular arrhythmias)

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19
Q

S/E of quinidine (1A)

A

GI ( N,V,D) 33-50%, cinchonism (HA, dizziness and tinnitus), thrombocytopenia, prolongation of QT interval

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20
Q

drug interactions of quinidine?

A

warfarin & digoxin

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21
Q

S/E of disopyramide

A

Cause heart failure because it has negative inotropic actions (caution in elderly and those with HF), anticholinergic effects

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22
Q

Indications for 1A

A

Conversion/prevention of atrial fibrillation
Atrial flutter
Ventricular tachycardia
Prevention of ventricular fibrillation

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23
Q

1B MOA

A

blocks Na channels, more effect on cells with longer action potential like conduction and ventricular cells less effect on atrial cells

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24
Q

S/E of 1B lidocaine

A

hypotension, CNS (paresthesias, tremor, nervousness), nausea, light headed, slurred speech, seizures, drowsiness

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25
Q

drug interactions of lidocaine (1B)

A

amiodarone (increased lidocaine levels)

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26
Q

How is 1B lidocaine given?

A

IV

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27
Q

when to use lidocaine (1B)?

A

Often first line to stop ventricular arrhythmias (ventricular tachycardia & prevent ventricular fibrillation) after cardio version or with an MI

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28
Q

when don’t you use lidocaine 1B?

A

Should not be used as prophylaxis (to prevent) arrhythmias b/c that increases mortality

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29
Q

how is mexiletine given (1B)?

A

oral

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30
Q

S/E of mexiletine (1B)

A

tremor, gait disturbances blurred vision, lethargy and nausea

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31
Q

When is mexiletine used?

A

Used for long term suppression of ventricular arrhythmias

also helps chronic pain

32
Q

1C MOA

A

Blocks sodium and potassium channels to a lesser extent and may cause more death than helps

33
Q

Uses for 1C?

A

Conversion/prevention fo atrial fibrillation, atrial flutter, ventricular tachycardia, prevention of ventricular fibrillation

34
Q

drug interactions for 1C?

A

digoxin (increases levels) warfarin (increases INR levels)

35
Q

S/E of 1C?

A

ventricular arrhythmias, agranulocytosis, anemia, thrombocytopenia

36
Q

class 2 uses?

A

Rate control for atrial fibrillation, atrial flutter, prevention of supraventricular tachycardia, with adjunctive ventricular antiarrhythmic therapy

Beta blockers can prevent re-infarction and sudden death after an MI & Class 1s don’t. So they save lives.

37
Q

class 2 agents?

A

Metoprolol, esmolol (IV), atenolol

38
Q

Class 2 MOA?

A

Are beta blockers and reduce beta adrenergic activity in the heart.

Elicit effect by:

  • Inhibit sympathetic activation of cardiac automaticity and conduction
  • Slowing heart rate, decreasing AV node conduction, and increasing AV node refractory period
39
Q

Class 3 MOA?

A

Prolong the ventricular action potential by blocking rapid component of K+ channel

40
Q

Uses for class 3?

A

These work best at slower heart rates, not at faster rates when needed most

41
Q

Risk of class 3?

A

target AP puts pt at risk

Slowing action potential at slower rates increases the risk of torsade de pointes

42
Q

Class 3 drugs

A 
Amiodarone (Cordarone)*
Dronedarone (Multaq)*
Sotalol (Betapace)+
Dofetilide (Tikosyn)
Ibutilide (Corvert)
*Amiodarone & dronedarone have Ib, II, and IV class activity in addition to class III actions
\+Sotalol has 50%/50% beta blocking properties and potassium blocking properties
43
Q

MOA of Amiodarone

A

Prolong the action potential by blocking rapid component of K+ channel (primary)
Also blocks sodium and calcium channels, & beta-adrenoceptors

long half life (months) can cause problems due to that

44
Q

Uses for Amiodarone?

A
  • Approved for serious ventricular arrhythmias.
  • It is a first line drug for prevention of ventricular tachycardia
  • It does not increase death (like other anti-arrhythmics)
  • The treatment of first choice for ventricular arrhythmias & sudden death is an implantable defibrillator NOT drugs
  • If have an defibrillator & it is going off a lot use amiodarone to prevent uncomfortable discharges
  • Also used for atrial fibrillation. In low doses can keep someone in NSR
45
Q

S/E of Amiodarone**

A

Cardiac: Bradycardia and heart block & can see prolonged QT on EKG
Lung: Fatal pulmonary fibrosis
Liver: Hepatitis
Skin: Gray-blue skin discoloration
Eye: Deposits pigment in retina- get halos; rarely optic neuritis & blindness
Thyroid: Has iodine molecules and blocks conversion of thyroid hormone
Can make hyperthyroid or hypothyroid*
Check thyroid function tests before start and when on it*

46
Q

**Drug interactions of Amiodarone?

A

warfarin, digoxin, statins

47
Q

How does dronedarone differ from amiodarone? (class 3)

A

Analog of amiodarone with a shorter ½ life (1 to 2 days vs. months) and the potential for less thyroid and pulmonary toxicity.

Less effective in maintaining NSR than amiodarone

48
Q

use of dronedarone? (class 3)

A

prevention of atrial fibrillation/flutter

49
Q

S/E of dronedarone (class 3)

A

nausea, vomiting, diarrhea, abdominal pain, liver toxicities

50
Q

MOA of sotalol? (class 3)

A

Beta blocker and action potential prolonging therapy by blocking potassium channels responsible for repolarization

51
Q

uses for sotalol? (class 3)

A

for life threatening ventricular arrhythmias and maintenance of normal sinus rhythm (NSR) in atrial fibrillation

52
Q

ADRs of sotalol? (class 3)

A

torsade de pointes, HF, bradycardia, AV block, wheezing, fatigue

53
Q

Uses of Dofetilide? (class 3)

A

Conversion/prevention of atrial fibrillation/flutter

54
Q

S/E of dofetilide? and special considerations? (class 3)

A

QT prolongation*, torsades de pointes, headache, dizziness

Initial administration done in hospital under careful monitoring due to ADR

55
Q

Uses for Ibutilide? (class 3)

A

IV, for rapid conversion fo recent onset of atrial fibrillation/flutter

56
Q

S/E of ibutilide? (class 3)

A

torsades de pointes, hypotension, nausea

57
Q

MOA of dofetilide and ibutilide? (Class 3)

A

target K channels

58
Q

Class 4 MOA?

A
  • Block the calcium channel
  • Do not work equally well in all cardiac cells.
  • These drugs work primarily in cardiac cells where the action potential upstroke is dependent on calcium i.e. SA and AV node
59
Q

Class 4 drugs?

A

Diltiazem & verapamil

60
Q

MOA of verpamil & diltiazem as antiarrhythmics?

A

Prolong conduction through the AV node & SA node

61
Q

Uses of verapamil & diltiazem?***

A
  • Supraventricular tachycardia (SVT; in other words non-ventricular tachycardia)
  • Reduce the rate in which the impulses go through the AV node.
  • Atria still beats fast but many of impulses get blocked at AV node so don’t send as many impulses to the ventricle which is the main pump
62
Q

S/E of verapamil and diltiazem?

A

If give to someone with a misdiagnosed rhythm (think SVT and really is ventricular arrhythmia) can kill

63
Q

Drugs that decrease conduction velocity?

A

1a, 1b, 1C**, class 4

64
Q

drugs that increase refractory period

A

1a, class 2, class 3***, a little of class 4

65
Q

drugs that decrease refractory period?

A

1b, some class 4

66
Q

adenosine* MOA

A

activates K+ and inhibits influx of calcium in SA node, atrium and AV node.
Works in AV node»SA node

67
Q

why do we like adenosine?

A

Half-life: 10 seconds

68
Q

S/E of adenosine?

A

*flushing (20%), SOB and chest *burning (10%), less common HA, low BP, nausea and paresthesias, bronchospasm

69
Q

Uses of adenosine?

A
  • 1st choice for conversion of SVT to sinus rhythm because works and is gone fast
  • Slows conduction through AV node & increases AV node refractory period
  • In fact AV node conduction can be completely blocked for a few seconds, resulting in brief asystole
70
Q

uses of magnesium?

A
  • To treat digitalis induced ventricular arrhythmias
  • To suppress drug-induced torsades de pointes
  • To treat supraventricular arrhythmias associated with magnesium deficiency
71
Q

MOA of magnesium?

A

IV, Magnesium is a very common intracellular cation with many roles in normal cardiac function

72
Q

MOA potassium?

A
  • Increasing potassium in the blood depresses ectopic pacemakers (tissue other than the conduction system depolarizing) and slows conduction
  • Too high or too low can increase arrhythmias, so need to normalize
73
Q

principles of antiarrhythmics?

A
  • Treatment of many arrhythmias are complicated & often handled by cardiologist
  • Not all arrhythmias need to be treated
  • If there is a risk of sudden death implantable defibrillator is the only thing to decrease mortality
  • Atrial fibrillation is a common arrhythmia often treated in primary care
  • Remember: Any drug that treats arrhythmias can cause one
74
Q

What is A-fib?

A

Disorganized electrical impulses

75
Q

options for a-fib?

A

BB or CCB

Pharm 5 (8 decks)

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