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
Symptoms of dysrhytmias
-palpitations -dizziness -fainting -dyspnea
26
Can dysrhytmias be asymptomatic
Yes
27
Supraventricular tachycardia
SVT 120-250 beats/min
28
Three P’s of Supraventricular tachycardia
Paroxysmal Persistent Permanent
29
Supraventricular tachycardia: paroxysmal
Episodic, start suddenly, and returns to normal within 24 hours
30
Supraventricular tachycardia: persistent
Episodes longer than seven days -usually treatment needed to return the heart to a normal rhythm
31
Supraventricular tachycardia: permanent
Dysrhythmia lasts for more than a year despite medications and other treatments
32
What is most common type of Supraventricular tachycardia
Atrial fibrillation
33
Atrial flutter is a
Supraventricular tachycardia
34
Supraventricular tachycardia is a problem with
Ventricular muscle
35
Non sustained Supraventricular tachycardia
<30 sec
36
Sustained Supraventricular tachycardia
>30 sec
37
Supraventricular dysrhythmias affect
Ventricular contraction rate -AV block desirable
38
Ventricular Dysrhythmia is are more dangerous than
Supraventricular
39
Antidysrhymthic drugs have a large
Variety of drugs
40
Antidysrhymthic drugs are characterized by
How drugs alter heart function
41
Vaughan Williams classification
Four classes of drugs plus an “other category”
42
Which Antidysrhymthic can cause dysrhythmias?
All Antidysrhymthic can cause dysrhytmias
43
Name the four classes of drugs + other category included in the Vaughan
Class I - Na channel blockers Class II - B blockers Class III - K channel blockers Class IV - calcium channel blockers Other - adenosine, digoxin
44
Class I
Na channel blockers -stops AP from starting, and from depoalrization
45
By blocking Na channels, you are slowing
Depolarization
46
Class Ia examples
Quinidine -procainamide, disopyramide
47
Class Ia __ atrial and ventricular rates
Slows
48
Class Ia also delays ____ similar to what class of drugs
Repolarization -similar to class III
49
Class Ia increases the
APD -what is this
50
Class Ia is used for
ACUTE onset atrial fibrillation
51
Four examples of acute onset atrial fibrillation
-premature atrial contractions -premature ventricular contractions -ventricular tachycardia -wolff Parkinson white syndrome
52
Wolff parkinson white syndrome
Usually tachy, may cause atrial fib/flutter
53
Class Ib examples
Lidocaine
54
Lidocaine
Given IV, used to block sodium channels
55
Class Ib
-accelerate repolarization -decrease APD
56
Class Ib is used for
Ventricular dysrhytmias ONLY
57
Ventricular dysrhythmias examples (3)
-premature ventricular contractions -ventricular tachycardia -fibrillation after MI
58
Class Ic examples
Flecainide, encainide, propafenone
59
Flecainide, encainide, propafenone
Block sodium channels
60
Class Ic
Little effect on APD or repolarization
61
Class Ic is used for
-Severe ventricular dysrhytmias -atrial fibrillation
62
Class II
B adrenoceptor antagonists
63
Class II: b adrenergic receptors increase
Ca influx -SA and AV AP depend on Ca influx -therefore B blockers reduce cell activity
64
Class II examples
Metoprolol -esmolol, propranolol, sotalol
65
Class II reduce or block
Sympathetic nervous system stimulation -AV block
66
Class II are general myocardial…
Depressants for both supraventricular and ventricular Dysrhythmia is
67
Class III
Potassium channel blockers
68
Class III effect on AP
AP ends with K efflux for repolarization, so blockage means that AP is prolonged
69
Class III examples
Amiodarone Dofetilide, sotalol, bretylium
70
Class III prolonged
Repolarization, a prolonged cardiac AP and extends refractory period of cells
71
Amiodarone affects
SA node contractility -Amiodarone is a potassium channel blocker
72
Amiodarone
Very effective drug -has serious AE if used for 6 months
73
AE of Amiodarone
75% serious AE if used for 6 months -lung fibrosis, thyroid
74
What percentage of Amiodarone is fatal
10%
75
Amiodarone is used for
-Ventricular tachycardia or fibrillation -atrial fibrillation -flutter -sustained ventricular tachycardia
76
Pros of Amiodarone
Ventricular tachycardia or fibrillation, and atrial fibrillation or flutter is resistant to other drugs -Amiodarone is a very good option
77
Class IV
Calcium channel blockers
78
Class IV reduce
Cell electrical activity -blocking Ca influx, which SA and AV AP depend on Ca influx
79
Class IV examples
Diltiazem and verapamil
80
CCBs inhibit
Ca cell entry -cardio active
81
Class IV act on
AV node -reducing conduction velocity -AV block
82
Class IV is used for/not used for
Used for - paroxysmal SVT -rate control for atrial fibrillation and flutter Not for - ventricular dysrhythmias
83
Unclassified antidysrhythmics
Digoxin and adenosine
84
Both digoxin and adenosine decrease
AV conduction and SA automaticity
85
Digoxin
-av block -slows HR
86
Adenosine
Slows conduction through AV node -AV block
87
Adenosine is used to
Convert paroxysmal supraventricular tachycardia to sinus rhythm
88
Half life of adenosine
10 to 20 seconds -extremely short half life -need more frequent doses
89
Adenosine is ONLY ADMINISTERED
As FAST IV push
90
Adenosine may cause
Asystole for a few seconds -lack of ventricular contractions
91
AE of antidysrhythmic drugs
All antidyrhythmics can cause dysrhythmias
92
Ensure that the client knows to notify health care provider of any
Worsening of dysrhytmias and -SOB -edema -dizziness -syncope -toxicity
93
What should clients learn to be able to do when taking digoxin
How to take their own radial pulse for one full minute
94
Clients should notify physician if what happens to pulse, prior to taking medication
If the pulse is less than 60 beats/a min before taking next dose of medication
95
Monitor for therapeutic responses such as
-decreased BP in hypertensive clients -decreased edema -regular pulse rate -pulse rate without major irregularities -improved cardiac output