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Pharm term 2 module 1 > Antiarrhythmics > Flashcards

Antiarrhythmics Flashcards

1
Q

What does the SA node do

A

Electrical impulse at regular intervals that allow for contraction

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2
Q

What is the frequency of the SA node

A

60-100

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3
Q

What happens when the pulse leaves the SA node

A

spreads through atria
enters the AV node

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4
Q

What is the AV node

A

The conduction pathway between atria and ventricle

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5
Q

What structure propagates the impulse to all parts of the ventricle

A

Purkinje fibers

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6
Q

What does premature ventricular depolarization cause

A

Ventricular fibrillation

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7
Q

What are the two mechanisms of arrhythmias

A

Disturbance in impulse formation

Disturbance in impulse conduction

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8
Q

What occurs in the heart during depolarization

A

heart cells are activated

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9
Q

What occurs in the heart during repolarization

A

Cells of the heart are at rest

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10
Q

What is occurring in the heart during the P wave

A

Atrial depolarization

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11
Q

What is occurring in the heart during the T wave

A

Ventricular repolarization

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12
Q

What electrolytes are involved with cardiac action potential

A

Ca2+
Na+
K+

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13
Q

When are the atria re-polarized

A

During the QRS complex (Ventricular contraction)

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14
Q

How do disturbed impulses present

A

Early afterdepolarization (EAD)

Delayed after depolarization (DAD)

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15
Q

When does EAD occur

A

Phase 3

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16
Q

When does DAD occur

A

Phase 4

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17
Q

What causes EAD

A

Triggered by factors that prolong action potential duration in the ventricle

leads to QT prolongation

which ends up as tachycardia, Torsades de pointe, or other arrhythmias

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18
Q

What causes QT prolongation specifically

A

Blockage of rapidly activation delayed rectifier K+ channels

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19
Q

What is intrinsic QT prolongation

A

Congenital

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20
Q

What is extrinsic QT prolongation

A

Drugs or external factors cause QT prolongation

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21
Q

What issues can exacerbate states of long QT syndrome

A

Slow heart rate and hypokalemia

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22
Q

What causes DADs

A

Excess accumulation of intracellular calcium (esp. at fast heart rates)

Can lead to V-Tach

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23
Q

What are some triggers of DADs

A

Digoxin toxicity
excess catecholamines
MI

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24
Q

What node is commonly effected by disturbances in impulse conduction and what is the end result

A

AV node

Various degrees of heart block result

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25
Q

What is occurring during complete heart block

A

There is no conduction from the atria to the ventricles

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26
Q

Why can anti-muscarinic agents sometimes help with heart block

A

b/c AV node is always under influence of parasympathetic system… allows atropine to sometimes be helpful

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27
Q

What is re-entry conduction

A

Impulse re-enters and excited an area of the heart more than once

-can be small or large

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28
Q

Which disease is characterized by re-entry circuit of atrial tissue, AV node, ventricular tissue, and accessory AV connection

A

WPW

Wolfe Parkinson White syndrome

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29
Q

What is enhanced automaticity

A

Acceleration of AP thru normal or abnormal cardiac tissue

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30
Q

How does triggered activity with impulse conduction present clinically

A

A fib
V tach

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31
Q

How do re-entry conductions present clinically

A

Impulse fails to die out after normal activation

AVNRT
WPW

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32
Q

What are the types of arrhythmias

A

Atrial fibrillation
atrial flutter
AV node re-entry (SVT)
Ventricular fibrillation
Ventricular tachycardia

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33
Q

How many classes of anti-arrhythmics are there

A

4

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34
Q

What is the MOA of class 1 anti arrhythmic

A

Sodium channel blockade

  • effect action potential
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35
Q

What is the MOA of class 2 anti- arrhythmics

A

Sympatholytic

Reduce beta adrenergic activity in the heart

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36
Q

What is the MOA of class 3 anti-arrhythmics

A

Manifests as a prolongation of the action potential duration

block the rapid component of the delayed rectifier K+ current

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37
Q

What is the MOA of class 4 anti arrhythmics

A

Blockade of cardiac Ca+ current

Slows conduction in regions where the Ap upstroke is Ca+ dependent (SA & AV) node

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38
Q

What are the classifications of sodium channel blockers

A

A (moderate)
B (weak)
C (strong)

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39
Q

What are the beta blockers for class 2

A

Propranolol
esmolol
Metoprolol

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40
Q

What are the K+ channel blockers in class 3

A

Amiodarone
Ibuttiide
Dofetilide
Sotalol

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41
Q

What are the Ca+ channel blockers for class 4

A

Verapamil
Diltiazem

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42
Q

What is the absolute refractory period (ARP)

A

Time during which another stimulus will not lead to another AP

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43
Q

What is the relative refractory period (RRP)

A

Interval following ARP in which a 2nd stimulus in inhibited, but not impossible

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44
Q

What is the effective refractory period (ERP)

A

Time in which a cell does not produce a new AP (Phase 0,1,2,3)

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45
Q

In someone who has sinus tachycardia, what drug class will you use to treat them

A

Class II and IV

46
Q

If someone has Afib or A flutter, what drug class will you use to treat them

A

Class 1A, 1C, II, III, IV, digoxin

*ventricular rate control is important goal and anticoagulant is required

47
Q

What class of drugs will you use to treat someone with paroxysmal SVT

A

Class IA, IC, II, III, IV or adenosine

48
Q

How would you treat someone with an AV block

A

Atropine

*break parasympathetic hold on the node

49
Q

How would you treat someone with VTach

A

Class I, II, III

50
Q

How would you treat someone with PVCs IF they need treatment

A

Class II, IV, Magnesium

51
Q

And how would you treat someone who is in digoxin toxicity

A

Class IB
Magnesium sulfate

52
Q

What drugs are class IA anti arrhythmics

A

Quinidine
Procainamide
Disopyramide

53
Q

What is the MOA of class IA drugs

A

Blocks cardiac Na+ channels
-decrease conduction velocity and delayed depolarization

54
Q

What is the use for Quinidine

A

Broad spectrum agent against SVT and ventricular dysrhythmias

*primary indication is long term suppression of SVT, Aflutter, Afib, and sustained VT

55
Q

When is procainamide used

A

Acute atrial or ventricular arrhythmia
-can tx WPW
-largely replaced by amoiderone

56
Q

What are the class IB anti arrhythmics

A

Lidocaine
Mexiletine

57
Q

When is Lidocaine used in the cardiac problems

A

Used ONLY for short term treatment of ventricular dysrhythmias

-particularly prevention of fib after cardioversion

58
Q

When is mexiletine used

A

Oral analogue of lidocaine used for chronic tx of ventricular dysrhythmias

59
Q

What is the MOA of class IB agents

A

-Blocks the Na+ channels
-decrease conduction(AP)
-greater effect on cells with long AP (not atrial cells)
-shorten phase 3

60
Q

What are the class IC agents

A

Flecinide
Propafenone

61
Q

What is the MOA of IC cardiac agents

A

Block Na+ and K+ channels
-slowly dissociate from resting sodium channels in purkinje and myocardial fibers
-slows phase 0 depolarization

*contraindicated in those with heart disease

62
Q

When is flecinide used

A

Maintenance therapy for supra ventricular dysrhythmia (Afib etc)

63
Q

When is propafenone used

A

Maintenance therapy of atrial arrhythmias
-can prevent paroxysmal SVT in patients with AVRT

64
Q

When is metoprolol used

A

Most widely used beta blocker in the treatment of cardiac arrhythmias

65
Q

What is the MOA for metoprolol

A

Selectively antagonizes beta 1 receptors

66
Q

What is the MOA for propranolol

A

Nonselective beta blocker
-decreases the rate at which the SA nose fired
-red conduction velocity in AV node

67
Q

When is propranolol used

A

Very useful for tx of dysrhythmias caused by excessive sympathetic stimulus.
-Sinus tachy
-Severe recurrent VT
-Paroxysmal atrial tachycardia from emotion / exercise

68
Q

When is esmolol used

A

Immediate treatment of ventricular rates in patients with Supraventricular arrhythmias only

69
Q

What is the MOA of Esmolol

A

Cardioselective beta-1 blocker
-decrease rate at which SA node fires

70
Q

What is the MOA of Amiodarone

A

K+ blocker -delayes depolarization of fast potentials

-Na+ and Ca+ channel blockade as well

71
Q

What is the MOA of Sotalol

A

Nonselective beta blocker and K+ channel blocker

72
Q

When is Sotalol used

A

Life threatening ventricular dysrhythmias

cardioversion and maintenance of NSR in patients with afib

*not commonly used because a loading dose while inpatient is required

73
Q

When is amiodarone used

A

Highly effective against both atrial and ventricular dysrhythmias

74
Q

What is the MOA of Dronederone and Dofetilide

A

K+ channel blocker
-delays depolarization of fast potentials

75
Q

When is Dronedarone used

A

Maintain NSR in patients with aflutter and afib

76
Q

When is Dofetilide used

A

Highly symptomatic atrial dysrhythmias

77
Q

What is the MOA of class 4 agents

A

Ca2+ channel blocker
-slows SA nodal automaticity
-delays AV nodal conduction
-reduces myocardial contractility

78
Q

When is verapamil used

A

Slow ventricular rate afib/flutter
-terminate SVT caused by an AV nodal reentrant circuit

*Rate controlling drug

79
Q

When is diltiazem used

A

Slow ventricular rate afib/flutter
-terminate SVT caused by an AV nodal reentrant circuit

*IV form often given in ER for afib with RVR

80
Q

When is Digoxin used

A

Primary indication is HF
-also used in the tx of supra ventricular tachydysrhythmias

81
Q

When is Adenosine used

A

DOC for termination Paroxysmal SVT
-WPW syndrome

82
Q

When is atropine used

A

Aborts life threatening second degree/complete heart block

83
Q

What is the MOA of atropine

A

Competitive blockade at muscarinic receptors

84
Q

What is the MOA of adenosine

A

Decrease automaticity in SA node and greatly slows conduction through AV node

Inhibits cAMP-induced calcium influx

85
Q

What is the MOA of Digoxin

A

Inhibits Na+/K+/ ATPase pump
-shortens refractory period in atria and ventricles and prolongs refractory period in AV node

86
Q

What are the adverse effects of Quinidine

A

Cinchonism (Tinnitus, HA, Nause, vertigo, psychosis)
-hypotension
-widen QRS complex & prolonged QT interval
-Drug interactions w/ digoxin & class 3 agents

87
Q

What are some adverse effects of procainamide

A

SLE-like effects
-hypotension
-widen QRS complex and prolonged QT interval

88
Q

What are the adverse effects of lidocaine

A

Drowsiness
-confusion
-paresthesias
-toxic dose can cause seizures and respiratory arrest

89
Q

What are the adverse effects of Mexiletine

A

N/V and neurologic side effects

90
Q

What are some of the adverse side effects of Flecainide

A

Widen QRS
Prolonged PR
Contraindicated in those with structural heart damage

91
Q

What are the pharmacokinetics of Mexiletine

A

Hepatic
narrow TI

92
Q

What are the pharmacokinetics of Lidocaine

A

IVV only
Rapid hepatic metabolism
plasma levels easily controlled

93
Q

What are the adverse effects of Propafenone

A

N/V
bronchospasm
widen QRS
prolonged PR
can cause HF

94
Q

What are the adverse effects of Metoprolol

A

Bradycardia
reduced cardiac output
AV heart block
Prolonged PR

95
Q

What are the adverse effects of propranolol

A

Heart failure
AV heart block
Sinus arrest
Hypotension
bronchospasm
prolonged PR

96
Q

What are the adverse effects of esmolol

A

Prolonged PR
Hypotension
bradycardia
heart block
HF

97
Q

What are the pharmacokinetics of esmolol

A

IV infusion only
very short half life (9min)

98
Q

What are the adverse effects of sotalol

A

Bradycardia
AV block
prolonged QT and PR
CAN TRIGGER TORSADES

99
Q

What are the adverse effects of amioderone

A

Lung fibrosis
visual impairment
thyroid toxicity
hypotension
hepatotoxicity
avoid in younger patients
Widen QRS

100
Q

What are the pharmacokinetics of amioderone

A

Metabolized by liver
very long half life (20-100 days)
oral or IV

101
Q

What are the adverse reactions of dronedarone

A

Diarrhea
skin reactions
weakness
hepatotoxicity
can trigger torsade
Contraindicated and those with HF

102
Q

What are the pharmacokinetics of dronedarone

A

Shorter half life than amioderone (24 hours)

103
Q

What are the adverse reactions of dofetilide

A

Prolonged QT
can trigger Torsades

104
Q

What are the adverse effects of verapamil

A

Bradycardia
AV block
heart failure
hypotension
peripheral edema
constipation
*adjust for renal impairment

105
Q

What are the adverse effects of Diltiazem

A

Bradycardia
AV block
HF
peripheral edema

106
Q

What are the adverse effects of Digoxin

A

Cardiotoxicity
N/V
visual disturbances

107
Q

What are the adverse effects of adenosine

A

Prolonged PR interval
Sinus Brady
Dyspnea
Facial flushing
chest discomfort / pain

108
Q

What are the adverse effects of atropine

A

Xerostomia
blurred vision
photophobia
incr. intraocular pressure
Urinary retention
anhidrosis
tachycardia
asthma

109
Q

What are the pharmacokinetics of Atropine

A

Parenteral admin

110
Q

What are the pharmacokinetics of Adenosine

A

IV bolus as close to the heart as possible

Very short half life (1-10 seconds)

111
Q

What is the pharmacokinetics of Digoxin

A

Oral / IV
Narrow TI
Need loading dose

Pharm term 2 module 1 (3 decks)

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