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Pharmacology > Antidysrhythmic Drugs (52) > Flashcards

Antidysrhythmic Drugs (52) Flashcards

1
Q

Rate

A

Frequency/unit time

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2
Q

Rhythm

A

Regularity of irregularity of the beating `

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3
Q

Electrical activity leads to

A

Mechanical activity

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4
Q

Electrical activity spreads throughout heart tissues in a co ordinated manner though

A

Ion channels in cell membrane

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5
Q

Dysrhythmia

A

Any deviation form the normal rate and rhythm of the heart

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6
Q

Arrhythmia

A

No rhythm

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7
Q

Asystole

A

No heartbeat

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8
Q

Tachydysrhythmias

A

HR is increased

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9
Q

Bradydysrhytmias

A

HR is slowed

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10
Q

What is more common tachydysrhytmias or bradydysrhytmias

A

Tachy dysrhytmias

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11
Q

Tachy dysrhytmias caused from

A

Drugs and other treatments

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12
Q

Brady dysrhytmias caused by

A

Atropine

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13
Q

Many causes of dysrhytmias (5)

A

-ischemic heart disease
-myocardial infarction
-cardiomyopathy
-myocarditis
-electrolyte imbalances

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14
Q

Antidysrhytmias

A

Drugs used for treatment and prevention of disturbances in cardiac rate and/or rhythm

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15
Q

Anti dysrhytmias most suppress

A

Abnormal electrical impulse formation or conduction

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16
Q

Cardiac electrical activity cells

A

SA, AV, purkinje, ventricular

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17
Q

Electrical activity differs with

A

Each cell type

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18
Q

Movement of ions across the cardiac cell membrane results in

A

AP generation

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19
Q

AP leads to

A

Contraction of the myocardial muscle

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20
Q

Action potentials differ between

A

Cardiac cell types

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21
Q

(SA and AV node cells) AP depends on

A

Ca2 influx
-via Ca channels

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22
Q

(Ventricular/atrial cardiac muscle cells) AP starts with

A

Na influx causing depolarizaiton
-via Na channels

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23
Q

(Ventricular/atrial cardiac muscle cells) AP ends with

A

K efflux = repolarization
-via K channels

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24
Q

Order of an ECG

A

P wave

PR interval

QRS complex

ST segment

T wave

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25
Q

Symptoms of dysrhytmias

A

-palpitations
-dizziness
-fainting
-dyspnea

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26
Q

Can dysrhytmias be asymptomatic

A

Yes

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27
Q

Supraventricular tachycardia

A

SVT 120-250 beats/min

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28
Q

Three P’s of Supraventricular tachycardia

A

Paroxysmal
Persistent
Permanent

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29
Q

Supraventricular tachycardia: paroxysmal

A

Episodic, start suddenly, and returns to normal within 24 hours

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30
Q

Supraventricular tachycardia: persistent

A

Episodes longer than seven days
-usually treatment needed to return the heart to a normal rhythm

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31
Q

Supraventricular tachycardia: permanent

A

Dysrhythmia lasts for more than a year despite medications and other treatments

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32
Q

What is most common type of Supraventricular tachycardia

A

Atrial fibrillation

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33
Q

Atrial flutter is a

A

Supraventricular tachycardia

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34
Q

Supraventricular tachycardia is a problem with

A

Ventricular muscle

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35
Q

Non sustained Supraventricular tachycardia

A

<30 sec

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36
Q

Sustained Supraventricular tachycardia

A

> 30 sec

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37
Q

Supraventricular dysrhythmias affect

A

Ventricular contraction rate
-AV block desirable

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38
Q

Ventricular Dysrhythmia is are more dangerous than

A

Supraventricular

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39
Q

Antidysrhymthic drugs have a large

A

Variety of drugs

40
Q

Antidysrhymthic drugs are characterized by

A

How drugs alter heart function

41
Q

Vaughan Williams classification

A

Four classes of drugs plus an “other category”

42
Q

Which Antidysrhymthic can cause dysrhythmias?

A

All Antidysrhymthic can cause dysrhytmias

43
Q

Name the four classes of drugs + other category included in the Vaughan

A

Class I - Na channel blockers
Class II - B blockers
Class III - K channel blockers
Class IV - calcium channel blockers

Other - adenosine, digoxin

44
Q

Class I

A

Na channel blockers
-stops AP from starting, and from depoalrization

45
Q

By blocking Na channels, you are slowing

A

Depolarization

46
Q

Class Ia examples

A

Quinidine

-procainamide, disopyramide

47
Q

Class Ia __ atrial and ventricular rates

A

Slows

48
Q

Class Ia also delays ____ similar to what class of drugs

A

Repolarization
-similar to class III

49
Q

Class Ia increases the

A

APD
-what is this

50
Q

Class Ia is used for

A

ACUTE onset atrial fibrillation

51
Q

Four examples of acute onset atrial fibrillation

A

-premature atrial contractions
-premature ventricular contractions
-ventricular tachycardia
-wolff Parkinson white syndrome

52
Q

Wolff parkinson white syndrome

A

Usually tachy, may cause atrial fib/flutter

53
Q

Class Ib examples

A

Lidocaine

54
Q

Lidocaine

A

Given IV, used to block sodium channels

55
Q

Class Ib

A

-accelerate repolarization
-decrease APD

56
Q

Class Ib is used for

A

Ventricular dysrhytmias ONLY

57
Q

Ventricular dysrhythmias examples (3)

A

-premature ventricular contractions
-ventricular tachycardia
-fibrillation after MI

58
Q

Class Ic examples

A

Flecainide, encainide, propafenone

59
Q

Flecainide, encainide, propafenone

A

Block sodium channels

60
Q

Class Ic

A

Little effect on APD or repolarization

61
Q

Class Ic is used for

A

-Severe ventricular dysrhytmias
-atrial fibrillation

62
Q

Class II

A

B adrenoceptor antagonists

63
Q

Class II: b adrenergic receptors increase

A

Ca influx
-SA and AV AP depend on Ca influx
-therefore B blockers reduce cell activity

64
Q

Class II examples

A

Metoprolol

-esmolol, propranolol, sotalol

65
Q

Class II reduce or block

A

Sympathetic nervous system stimulation
-AV block

66
Q

Class II are general myocardial…

A

Depressants for both supraventricular and ventricular Dysrhythmia is

67
Q

Class III

A

Potassium channel blockers

68
Q

Class III effect on AP

A

AP ends with K efflux for repolarization, so blockage means that AP is prolonged

69
Q

Class III examples

A

Amiodarone

Dofetilide, sotalol, bretylium

70
Q

Class III prolonged

A

Repolarization, a prolonged cardiac AP and extends refractory period of cells

71
Q

Amiodarone affects

A

SA node contractility
-Amiodarone is a potassium channel blocker

72
Q

Amiodarone

A

Very effective drug
-has serious AE if used for 6 months

73
Q

AE of Amiodarone

A

75% serious AE if used for 6 months
-lung fibrosis, thyroid

74
Q

What percentage of Amiodarone is fatal

A

10%

75
Q

Amiodarone is used for

A

-Ventricular tachycardia or fibrillation
-atrial fibrillation
-flutter
-sustained ventricular tachycardia

76
Q

Pros of Amiodarone

A

Ventricular tachycardia or fibrillation, and atrial fibrillation or flutter is resistant to other drugs
-Amiodarone is a very good option

77
Q

Class IV

A

Calcium channel blockers

78
Q

Class IV reduce

A

Cell electrical activity
-blocking Ca influx, which SA and AV AP depend on Ca influx

79
Q

Class IV examples

A

Diltiazem and verapamil

80
Q

CCBs inhibit

A

Ca cell entry
-cardio active

81
Q

Class IV act on

A

AV node
-reducing conduction velocity
-AV block

82
Q

Class IV is used for/not used for

A

Used for - paroxysmal SVT
-rate control for atrial fibrillation and flutter

Not for - ventricular dysrhythmias

83
Q

Unclassified antidysrhythmics

A

Digoxin and adenosine

84
Q

Both digoxin and adenosine decrease

A

AV conduction and SA automaticity

85
Q

Digoxin

A

-av block
-slows HR

86
Q

Adenosine

A

Slows conduction through AV node
-AV block

87
Q

Adenosine is used to

A

Convert paroxysmal supraventricular tachycardia to sinus rhythm

88
Q

Half life of adenosine

A

10 to 20 seconds
-extremely short half life
-need more frequent doses

89
Q

Adenosine is ONLY ADMINISTERED

A

As FAST IV push

90
Q

Adenosine may cause

A

Asystole for a few seconds
-lack of ventricular contractions

91
Q

AE of antidysrhythmic drugs

A

All antidyrhythmics can cause dysrhythmias

92
Q

Ensure that the client knows to notify health care provider of any

A

Worsening of dysrhytmias and
-SOB
-edema
-dizziness
-syncope
-toxicity

93
Q

What should clients learn to be able to do when taking digoxin

A

How to take their own radial pulse for one full minute

94
Q

Clients should notify physician if what happens to pulse, prior to taking medication

A

If the pulse is less than 60 beats/a min before taking next dose of medication

95
Q

Monitor for therapeutic responses such as

A

-decreased BP in hypertensive clients
-decreased edema
-regular pulse rate
-pulse rate without major irregularities
-improved cardiac output

Pharmacology (23 decks)

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