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House Pharmacology > Anti Arrythmics > Flashcards

Anti Arrythmics Flashcards

1
Q

Cardiac arrhythmia

Also known as cardiac ______ or _______, is a group of conditions in which the heartbeat is _______,_____, or _______

A

dysrhythmia

irregular heartbeat

irregular, too fast, or too slow.

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2
Q

Cardiac arrhythmia

An abnormality of impulses in terms of _____,_______ , or _______

Usually (symptomatic or asymptomatic?) .

A

site of origin, rate or conduction.

asymptomatic

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3
Q

Cardiac arrhythmia

When symptoms are present, these may include palpitations miss heartbeats, light-headedness, syncope, shortness of breath, or chest pain.

T/F

A

T

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4
Q

While most arrhythmias are (serious or not serious?) some predispose a person to complications such as _____ or _______. Others may result in cardiac arrest and death.

A

Not serious

stroke or heart failure

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5
Q

There are four main types of arrhythmias: ______,_____,______,_____

A

extra beats, supraventricular tachycardias, ventricular arrhythmias, and bradyarrhythmias.

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6
Q

Anti-Arrhythmic agents are drugs clinically used in treating or preventing abnormalities in _______ and _____

A

Heart rate and rhythm

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7
Q

Heart rate is the ____________

Normal Heart Rate is ____ to ______

A

number of heart beat occurring within a minute

60 to 100 bpm

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8
Q

Heart rhythm is the _____________________

Normal Heart rhythm is regular with _____ contracting before ______

A

pattern in which the heart beats

atrium; ventricles

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9
Q

Heart rate and rhythmic are determined by four major properties of the Heart

______
_______
_______
_______

A

EXCITABILITY
RHYTHMICITY
CONDUCTIVITY
CONTRACTILITY

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10
Q

MECHANISM

Excitation of SA and AV

Phase 0
_______

Phase 3
_________

Phase 4
____________

A

Ca2+ Influx

K+ Efflux

Ca2+ influx, Na+ influx , K+efflux

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11
Q

MECHANISM
Excitation of Atrium and Ventricle

Phase 0- ____

Phase 1-______

Phase 2- _______

Phase 3- _____

Phase 4- _______

A

Na+ influx

Rapid K+ efflux

Ca2+ influx

K+ efflux

Na+/K+ ATPase( resting membrane potential)

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12
Q

If the arrhythmia arises from ____,______, or _______ it is called supraventricular arrhythmia

If the arrhythmia arises from the ———- it is called ventricular arrhythmia

A

atria, SA node, or AV node

ventricles

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13
Q

Cardiac cell undergo depolarization and repolarisation to form cardiac action potential about ___ times per minute.

A

6

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14
Q

In the atria, purkinje, and ventricles the AP curve consists of ___ phases

In the SA node and AV node, AP curve consists of __ phases

A

5

3

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15
Q

Pacemaker cells (automatic cells) have ______ membrane potential so they can generate AP _______

A

unstable

spontaneously

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16
Q

In Plateau phase of AP generation ,

It’s Due to (fast or slow?) inward current caused by _____channels (__-type _____ channels) opening which also leads to cardiac muscle ———.

A

Slow ; Ca2+

L; Ca2+

contraction

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17
Q

In phase 4 of regular AP generation,

Spontaneous _____ to threshold where critical voltage activates ____+ channels. If this phase is steeper, then heart rate ___eases. Involves the spontaneous action of various channel types.

A

depolarisation; Na

incr

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18
Q

Mechnisms of Arrhythmogenesis

Divided into 2

_______
_______

A

Abnormal impulse generation

Abnormal impulse conduction

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19
Q

Mechnisms of Arrhythmogenesis

Abnormal impulse generation can either be _______ or ———

A

Automatic rhythms

Triggered rhythms

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20
Q

Mechnisms of Arrhythmogenesis

Abnormal impulse conduction can either be _______ or ———

A

Conduction block or re-entry

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21
Q

Mechnisms of Arrhythmogenesis

Automatic rhythms can either be ________ which means _____ or ——— which means _____

A

Ectopic focus; AP arises from sites other than SA node

Enhanced normal automaticity; increased AP from SA node

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22
Q

Mechnisms of Arrhythmogenesis

Triggered rhythms can either be ________ or ———

A

Delayed afterdepolarization

Early afterdepolarization

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23
Q

Conduction block is when __________

A

This is when the impulse is not conducted from the atria to the ventricles

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24
Q

Mechnisms of Arrhythmogenesis

Conduction block has _____ types

List them

A

3

First degree
Second degree
Third degree

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25
Q

Mechnisms of Arrhythmogenesis

Re-entry can either be ——— or _____

A

Circus movement or reflection

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26
Q

Dihydropiridines works on the _____ while the non- Dihydropiridines works on the _________

A

Blood vessels, thereby leading to reflex tachycardia

Heart gan gan

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27
Q

Arrhythmias

Examples under Sinus rhythm

?????

A

Sinus arrhythmia
Sinus tachycardia
Sinus bradycardia

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28
Q

Arrhythmias

Examples under atrial arrythmia

A

Paroxysmal Atrial Tachycardia
Atrial Flutter
Atrial Fibrillation

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29
Q

Arrhythmias

Examples under nodal arrhythmia

A

AV Nodal blocks
Nodal re-entrant arrhythmia

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30
Q

Arrhythmias

Examples under ventricular arrhythmia

A

Paroxysmal Ventricular Tachycardia
Ventricular Tachycardia
Ventricular Fibrillation

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31
Q

Sinus Tachycardia: high sinus rate of ____-___ beats/min, occurs during _____ or other conditions that lead to ______________

A

100-180; exercise

increased SA nodal firing rate

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32
Q

Atrial Tachycardia: a series of __ or more consecutive _______ occurring at a frequency >____/min

A

3

atrial premature beats

100

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33
Q

Paroxysmal Atrial Tachycardia (PAT): tachycardia which ___________________

A

begins and ends in acute manner

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34
Q

Atrial Flutter: sinus rate of _____-___beats/min.

A

250-350

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35
Q

Atrial Fibrillation:_______ atrial
depolarizations.

A

uncoordinated

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36
Q

AV blocks
A __________ within the ______ , occasionally in the _______, that impairs impulse conduction from the atria to the ventricles.

A

conduction block

AV node

bundle of His

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37
Q

Ventricular Flutter - ventricular depolarizations >____/min.

A

200

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38
Q

Ventricular Fibrillation -________ ventricular depolarizations

A

uncoordinated

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39
Q

2 main things used in DIAGNOSIS of arrhythmias

______
______

A

Pulse
Electrocardiogram (ECG

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40
Q

A Regular irregular Pulse can be caused by ???

A

Heart block
Sinus arrhythmia

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41
Q

An IRegular irregular Pulse can be caused by ???

A

Atrial arrhythmia
Ventricular tachycardia

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42
Q

P wave = _______

QRS wave=———-

T wave _________

A

Atrial depolarization

Ventricular depolarization

Ventricular repolarization

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43
Q

Describe the following

PR interval

QRS interval

QT interval

A

Start of P wave to start of QRS wave

Start of QRS wave to end of QRS wave

Start of QRS wave to end of T wave

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44
Q

Describe the following

PR Segment

ST segment

A

End of P wave to start of QRS wave

End of QRS wave to start of T wave

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45
Q

End of QRS wave is also knows as ______

A

J point

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46
Q

COMPLICATIONS caused by heart arrhythmias

_____tension
___________
_____ failure
_______ shock
______
______

A

Hypo

Thromboembolism

Heart
Cardiogenic
Cardiac arrest
Stroke

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47
Q

Pharmacologic Rationale & Goals

The ultimate goal of antiarrhythmic drug therapy:
Restore normal ______ and _____

Prevent _______________ from occurring.

A

sinus rhythm and conduction

more serious and possibly lethal arrhythmias

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48
Q

Antiarrhythmic drugs are used to:

decrease ________

change the duration of the ___________

suppress _________

A

conduction velocity

effective refractory period (ERP)

Abnormal automaticity

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49
Q

With regards to management of atrial fibrillation, Class _____ and _____ are used in _______ control as medical cardioversion agents while Class ____ and _____ are used as ____ control agents.

A

I and III ; rhythm

II and IV ; rate

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50
Q

There are _____ main classes in the Singh Vaughan Williams classification of antiarrhythmic agents

A

five

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51
Q

Class I agents interfere with the _______

Class II agents are __________agents. Most agents in this class are ______

A

sodium (Na+) channel.

anti-sympathetic nervous system

beta blockers.

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52
Q

Class III agents affect __________

Class IV agents affect ———— and the ______

Class V agents work by _________

A

potassium (K+) efflux.

calcium channels ; AV node.

other or unknown mechanisms.

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53
Q

Anti-arrhythmic drug

Class I - Fast Channel Blockers

Ia - _______,______,______

Ib - ________,_____,________ , Tocaininde

Ic - ______ ,_______ ,________, Indecainide, Moricizine

A

Quinidine, Disopyramide, Procainamide

Lidocaine, Phenytoin, Mexilitine

Ecainide, Flecainide, Propafenone,

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54
Q

Anti-arrhythmic drug

Class II - ________
Propanolol, Acebutolol, Atenolol, Betaxolol, Bisoprolol, Esmolol, Labetalol, Metoprolol, Nadolol, Oxprenolol, Penbutolol, Pindolol, Sotalol, Timolol

A

Beta Blockers

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55
Q

Anti-arrhythmic drug

Class III

_______,_______,_____

A

Bretylium, Amiodarone, Sotalol

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56
Q

Anti-arrhythmic drug

Class IV - Calcium Channel Blockers

______,_______

A

Verapamil, Diltiazem

57
Q

Anti-arrhythmic drug

Unclassified - ______,______ ,_____

A

Digoxin, Adenosine, Mg

58
Q

Anti arrhythmic mech of action

Class 1 : are Na+ channel blockers

_________ effect
(Positive or negative ?) inotropic action

A

Local anaesthetic

Negative

59
Q

Anti arrhythmic mech of action

Class 1( A ): it ______ duration of __________ and _______

Have ____ channel blocking effect

_________ & hypotensive effects.

A

prolongs

action potential & refractory period.

K+ ; Antimuscarinic

60
Q

Anti arrhythmic mech of action

Class I(B): ______ the duration of _______

A

Shorten

action potential & refractory period

61
Q

Anti arrhythmic mech of action

– Class1(C) : ______ on the duration of ______

A

No effect

action or refractory period.

62
Q

Anti arrhythmic mech of action

Class III: K+ channel blockers,

________ duration of action potential and refractory period.

63
Q

Class 1(A) Quinidine:

______ plant

It ____ open & inactivated_____ channel

Block _____ channel

A

Cinchona

Block; sodium

potassium

64
Q

Quinidine

_______ inotropic effect

___________ effect

A

Negative

Antimuscarinic

65
Q

Quinidine

– Prolong _____________ on the ECG

A

Q-T interval

66
Q

Quinidine

Well absorbed _____

(Low or High?) bound to plasma protein

A

orally

High

67
Q

Quinidine

Metabolized in the ____
Excreted via _____ with 20% unchanged

A

liver

Kidney

68
Q

Quinidine

Has ____ blocking and ______ properties

Drug interaction with ____

A

K+

antimuscarinic

Digoxin

69
Q

Adverse effects of quinidine

1- Cardiac effects
A) Due to _____ effect ,in A.Flutter or A.fibrillation, may precipitate _________

A

antimuscarinic

ventricular tachycardia

70
Q

Adverse effects
1- Cardiac effects

Syncope
_________

A

Torsade de pointes

71
Q

Adverse effects
1- Cardiac effects

Cardiac stand still (____) in patients with ______ syndrome .

A

asystole

sick sinus

72
Q

Torsades de Pointes is a type of very fast heart rhythm (tachycardia) that starts in ___________

A

your heart’s lower chambers (ventricles).

73
Q

Extracardiac adverse effects of quinidine

___tension

______ (headache, dizziness,tinnitus, deafness )

_________ reactions (hepatitis, thrombocytopenia)

GIT, diarrhea,nausea,vomiting

A

Hypo

Cinchonism

Hypersensitivity

74
Q

Quinidine ___eases the plasma level of digoxin by :
a)_____________
b)______________

A

incr

displacement from tissue binding sites

decreasing digoxin renal clearance

75
Q

Procainamide - Actions

Suppresses automaticity by:

•decreasing the rate and amplitude of __________
•prolongs __________
•reduces the ___________
•suppresses ______ activity in the atria and ventricles

A

phase 4 diastolic depolarization

action potential duration

speed of impulse conduction

fibrillatory

76
Q

Procainamide - Actions

____ dependant ______ activity

A

Dose

anticholinergic

77
Q

Procainamide - Actions

_____ Inotrope
•more pronounced in ischemic myocardium

_________ in high doses
•vasodilatation of peripheral vasculature

A

Negative

Hypotension

78
Q

Procainamide is Metabolized to _______

A

N-acetyl Procainamide (NAPA)

79
Q

Torsade de pointes is an adverse effect or indication of procainamide and quinidine?

A

Adverse effects for quinidine
Contraindication for procainamide

80
Q

PROCAINAMIDE

Given through ________ routes

_________ is safer than _____

A

IV, IM and Oral

Continous infusion

bolus

81
Q

PROCAINAMIDE

Excreted via ______

Has —————- properties

A

Kidney

anticholinergic

82
Q

Procainamide - Administration

QRS widens by ______ %
QT interval ______
Total of 17 mg/kg has been administered

A

> 50

prolongation

83
Q

Procainamide - Adverse Effects

Myocardial ________
prolonged QRS, QT, AV conduction, VF and Torsade de pointes

_________
High doses or rapidly administered

_______
angioedema, bronchoconstriction, vascular collapse, febrile episodes, respiratory arrest

A

Depression

Hypotension

Hypersensitivity

84
Q

Lidocaine - Actions

Class ___ antiarrhythmic

blocks ________ channels

A

IB

fast sodium

85
Q

Lidocaine - Actions

decreases slope of phase ____

decreased automaticity in the ______

action potential duration and effective refractory period of His-purkinje is ______eased

A

4

His-purkinje system

incr

86
Q

Lidocaine - Actions

Acts preferentially on _____ tissue

________ the duration of A.P.& R.P.

Effective in _______ arrhythmias.

A

ischemic

Shorten

ventricular

87
Q

Lidocaine

Causes ______ effect on AV conduction

(Depresses or Elevates?) v-fib threshold

A

little or no

Elevates

88
Q

Lidocaine

(Supresses or elevates ?) ventricular ectopy

_____ effect on autonomic nervous system, myocardial contractility and peripheral vascular tone

A

Suppresses

negligible

89
Q

LIGNOCAINE

Given ____ only

Well absorbed _____

(High or Low?) first pass effect by Liver

A

IV

orally

High

90
Q

LIGNOCAINE

Half life is 2 hours

Excreted via ______

Also used as a ________

A

Kidney

Local anesthetic

91
Q

_______ is the First drug of choice in treatment of ventricular arrhythmias

92
Q

Mexiletine

Effective _____
Half-life (8-20hrs ).

Used in chronic treatment of ______ arrhythmias.

A

orally

ventricular

93
Q

Mexiletine

Effective in relieving chronic pain due to _________ and ______

Adverse effects - _______ side effects

A

diabetic neuropathy& nerve injury.

Neurologic

94
Q

Class1(c)- Flecainide

_____ effect on the duration of A.P.& R.P.

Approved for _______________ arrhythmias.

A

No

refractory ventricular

95
Q

Class1(c)- Flecainide

Pro or Anti arrhythmic?

96
Q

Class1(c) -Propafenone

Has a weak ________ effect.

A

β-blocking

97
Q

Class1(c) -Propafenone

Used to maintain sinus rhythm in patients with _______ arrhythmias including AF.

A

supraventricular

98
Q

Class1(c) -Propafenone

Adverse effects :

________________, constipation .

A

Metallic taste

99
Q

Compare between class IA, IB , and CI drugs as regards effect on Nat channel & ERP

• Sodium-channel blockade: _____ >___ >____

• Increasing the ERP:___>___>___ (lowered)

A

IC; IA; IB

IA; IC; IB

100
Q

Specific ADVERSE EFFECTS of class 1 drugs

Quinidine: _______,_____ reaction , G.I disturbance, ______ toxicity

Procainamide: _______

Lignocaine: _______ effect

A

Cinchonism; Hypersensitivity; Digoxin

Hypersensitivity

Neurological

101
Q

Specific ADVERSE EFFECTS of class 1 drugs

Mexiletine: ______ effect

Propafenone :______,_______

A

Neurological

Metallic taste, Constipation

102
Q

INDICATIONS for class 1 drugs

_______
_______
________

A

Atrial flutter
Atrial fibrillation
Ventricular arrhythmia

103
Q

Esmolol - Very (short or long?) acting used for ______ and ——— arrhythmias

A

Short

intraoperative & acute

104
Q

Esmolol

______ half life of ______

A

ultra-short

9 minutes

105
Q

Beta Blockers -

Contraindicated
• in > _____ degree heart block

•_______ or _______

•Caution with _______

A

first

CHF or cardiogenic shock

calcium channel blockers

106
Q

MECHANISM OF ACTION of beta blockers

Binds and blocks Beta adrenergic receptors on the heart

Inhibit PHASE ____ at _____

A

4; SA node

107
Q

Class 2 drugs

Decreased slope of ___________

Prolonged ________

A

phase 4 depolarization

repolarization

108
Q

Class 3- Amiodarone

cardiac effects

______ channel blocking
_______ channel blocking
______ channel blocking
____________ blocking

A

Sodium

Potassium

Calcium

β- adrenoceptor

109
Q

Class 3- Amiodarone

Extracardiac effect

Peripheral _______

A

vasodilation

110
Q

Pharmacokinetics of amiodarone

Given ______

(Slow or Fast?) onset of action

(Short or Long?) half-life(_____).

A

orally

Slow

Long; 13-103 hrs

111
Q

Pharmacokinetics of amiodarone

Is highly lipo______ , is concentrated in many tissues.
Eliminated by ______ mostly as (active or inactive ?) metabolites.

A

philic

liver

Active

112
Q

Clinical uses of amiodarone

Recurrent & refractory ventricular & supraventricular arrhythmias .

Arrhythmias associated with ________.
In maintaining sinus rhythm in patients with AF.

A

Wolff Parkinson syndrome

113
Q

Adverse effects of amiodarone

__________ discoloration & ______ .

Corneal microdeposits leading ____,_____,_______

pulmonary ______

A

Gray- blue skin; photodermatitis

corneal opacity ,optic neuritis, blindness

fibrosis

114
Q

Adverse effects of amiodarone

hypo or hyperthyroidism

Nausea & constipation

Hepatic impairment

_______ effects

A-V block & bradycardia

A

neurological

ISEOLUWA, just look at it, you are tired

115
Q

Drug interactions of amiodarone

__________ leading to _____

______ leading to ____ toxicity

_________ has an additive effect

A

Oral anticoagulant; bleeding

Digoxin; digoxin

β- blockers

116
Q

Bretylium - Actions

Class ____

______ effects

A

3

Biphasic

117
Q

Bretylium - Actions

Class 3

Biphasic effects

_________ effects last 20 minutes

Then
____________ 45 to 60 minutes after administration

A

Norepinephrine release

Blocks release of norepinephrine

118
Q

Bretylium - Actions

Class 3

Affects phase ____ (_____)

prolongs refractoriness

  • (pro or anti?) fibrillatory
A

3; repolarization

Anti

119
Q

Sotalol

Is used for the treatment of :

_____________ arrhythmias.

To maintain sinus rhythm in patients with _________.

A

Life- threatening ventricular

atrial fibrillation

120
Q

_______ is used For treatment of supra & ventricular arrhythmias in pediatric age group.

121
Q

Specific ADVERSE EFFECTS of Amiodarone

_______ discoloration

_______ disorder

_______ dysfunction

A

Gray-blue skin

Corneal

Thyroid

122
Q

INDICATIONS of class 3 drugs??

A

All arrhythmias

123
Q

Class IV
Calcium channel blockers e.g. Verapamil, Diltiazem

Their main site of action is ______ and ________

Effective only in _____ arrhythmias

A

A.V.N & S.A.N.

atrial

124
Q

Class IV
Calcium channel blockers

Second drugs of choice for the treatment of ______________

A

paroxysmal supraventricular tachycardia

125
Q

Calcium channel blockers are effective in Wolff Parkinson White syndrome

T/F

A

F

Not effective in Wolff Parkinson White syndrome

126
Q

Class IV

Adverse effect
Negative inotropic effect causes heart failure, AV block

T/F

127
Q

MECHANISM OF ACTION of class 4 drugs

Binds and Blocks Calcium channels on the heart

Inhibit
•_________
•PHASE __ at ______ and _____

A

All PHASE 4

0

SA and AV node

128
Q

Adenosine - Actions

Negative Chronotropic effects on ___________

Blockade of the ______

A

SA and AV node

AV node

129
Q

Adenosine - Binds to specific __________ coupled adenosine receptors (____) leading to opening of ____ channel and hence ______.

A

G protein -

A1&A2; K+

hyperpolarization

130
Q

adenosine leads to a ____eased influx of calcium

131
Q

Adenosine - Pharmacokinetics

Very (slow or rapid?) onset of action .

(Short or Long?) half- life (______)

Given as a rapid _____ injection

A

Rapid

Short; seconds

IV Bolus

132
Q

Adenosine - Pharmacokinetics

For the acute termination of _____________ tachycardia ( paroxysmal
attack) First choice.

A

re-entrant supraventricular

133
Q

Drug Interactions of adenosine

Less effective with adenosine receptor blockers (_______ or ________)

More effective with uptake inhibitors as __________

A

Caffeine or theophylline

dipyridamole

134
Q

MECHANISM OF ACTION of Adenosine

Inhibits PHASE ___ at ___________

A

0

SA and AV node

135
Q

INDICATIONS of Adenosine

_________________ tachycardia

A

Paroxysmal supraventricular

136
Q

MECHANISM OF ACTION of Magnesium

Direct: ________________

Indirect: _____________

A

Binds and blocks Na+, K+ ATPase pump

Binds and blocks Calcium channel

137
Q

MECHANISM OF ACTION of Magnesium

Inhibits PHASE _______

A

4, 3 and 0

138
Q

ADVERSE EFFECT of Magnesium

_______
____

A

Hypermagnesemia
Hyperkalemia

139
Q

_______ can be used to treat Torsade de pointes

House Pharmacology (50 decks)

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