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Pharmacology > Antiarrhythmic Drugs > Flashcards

Antiarrhythmic Drugs Flashcards

1
Q

What is the value of cardiac action potential

What is it produced by

A

-90mV

K+ channels - High permeability to K+ ions

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2
Q

What are the phases of cardiac myocyte action potential

A

Phase 0 - VG Na channels, fast depolarising current
Phase 1 - K channels, transient repolarisation
Phase 2 - L type Ca channels, slow depolarising current, systole
Phase 3 - K channels, repolarisation
Phase 4 - resting membrane potential, diastole

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3
Q

What are the main causes of arrhythmias

A

Abnormal impulse generation

Abnormal impulse conduction

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4
Q

What are the phases of pacemaker action potential

A

Phase 0: L type Ca channel, slow depolarising current
Phase 3: K channel, repolarisation
Phase 4: HCN channel, Funny current If, automatic gradual depolarisation to threshold

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5
Q

What are the mechanisms of abnormal impulse formation

A

Automatic rhythms

Triggered rhythms

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6
Q

What are the types of abnormal automatic rhythms

A

Enhanced automaticity - pacemaker cells of nodes

Ectopic focus - pacemaker cells at sites other than nodes

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7
Q

What are types of triggered rhythms

A

Delayed after-depolarisations: AP arising immediately after previous AP
Early after-depolarisation: AP arising from plateau phase

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8
Q

What are types of abnormal impulse conduction

A

Conduction block
Re entry: incomplete unidirectional conduction block causing circus of depolarisation
Accessory pathway: WPW syndrome - pathway between A+V bypassing AVN

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9
Q

What is effective refractory period

A

Period after AP initiation when Na channels are inactivated and another AP cannot be generated

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10
Q

What are the classes of antiarrhythmic drugs

A

Class I: Na channel blockers
Class II: Beta blockers
Class III: K channel blockers
Class IV: Ca channel blockers

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11
Q

What is the mechanism of action of class I agents

A

Inhibit VG Na channels
Slow conduction of phase 0
Slow depolarisation
Prolong ERP

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12
Q

How are Class I agents classified

A

According to rate of dissociation

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13
Q

Give examples of Class Ia agents

A

Procainamide

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14
Q

What is the mechanism of action of class Ia

A

Moderate rate of dissociation

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15
Q

What are ECG changes with Class Ia agents

A

Broad QRS

Prolonged QT

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16
Q

What are indications of Class Ia agents

A

Procainamide

Acute IV for SVT + VT

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17
Q

What are side effects of Class Ia agents

A 
Hypotension 
Proarrhtymic: Torsades de Pointes 
Dizziness
Confusion
Seizure
Lupus like syndrome
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18
Q

Give examples of class Ib agents

A

Lidocaine

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19
Q

What is mechanism of action of Class Ib agents

A

Rapid dissociation rate
Inhibits inactivated Na channels
Inhibits depolarisations too close to previous AP in fast/ischaemic tissue
Minimal effect on conduction in normal tissue

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20
Q

What are indications of Class Ib agents

A

VT - especially post MI

NOT in atrial arrhythmias

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21
Q

What are contraindications of Lidocaine

A

HF
Seizures
Nystagmus

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22
Q

Give examples of class Ic agents

A

Flecainide

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23
Q

What is mechanism of action of class Ic agents

A

Slow dissociation rate

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24
Q

What are indications of Class Ic agents

A

AF
Atrial flutter
Premature ventricular contractions
WPW Syndrome

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25
Q

What must Flecainide be prescribed with when treating for Atrial flutter

A

Beta blockers
Slowed rate of flutter in atria leads to increased conduction of flutter at AVN
Increase ventricular response to SVT
Thus need to block conduction at AVN

26
Q

What are contraindications of Flecainide

A

Structural heart disease, IHD

Associated with arrhythmias and sudden deaths

27
Q

Give examples of Class II agents

A 
Bisoprolol
Propranolol
Atenolol 
Esmolol 
Sotalol
28
Q

What are PK properties of Class II agents

A

Bisoprolol: long Acting, once daily regime, oral
Propranolol: short acting, oral or IV
Esmolol: v short acting(seconds)

29
Q

What is mechanism of action of Class II agents

A 
Inhibit Beta1 adrenoceptor
Slow rate of depolarisation of pacemaker potential to threshold 
Slow conduction velocity at Phase 4 
Decrease HR 
Slow conduction at AVN 
Negative inotropic effect
30
Q

What are indications for Class II agents

A

Sinus tachycardia
Convert AVNRT
Protect ventricles from high atrial rates

31
Q

What are side effects of Class II agents

A

Bronchospasm

Hypotension

32
Q

What are contraindications of Class II agents

A

Asthma

33
Q

What is mechanism of action of Class III agents

A 
Block K channels 
Slow repolarisation (phase 3) 
Prolong ERP
34
Q

Give examples of class III agents

A

Amiodarone

Sotalol

35
Q

What are PK properties of amiodarone

A

Oral, IV

T1/2 3 months

36
Q

What is mechanism of action of amiodarone

A

Inhibit K channels: prolong ERP
Inhibit Na channels: slow conduction, prolong ERP
Inhibit Beta adrenoceptor: slow AVN conduction

37
Q

What are indications of amiodarone

A

Most arrhythmias: atrial, nodal, ventricular

When other drugs failed

38
Q

What are side effects of amiodarone

A 
Optic neuritis (transient) 
Photosensitivity
Thrombophlebitis at injection site (use central veins) 
Pneumonitis/pulmonary fibrosis
Hepatitis/liver fibrosis 
Raised LDL 
Hyperthyroidism (contains iodine)
39
Q

What monitoring is required for amiodarone

A

LFT, TFT, ECG, U+E, CXR at baseline

TFT+LFT 6 monthly

40
Q

What is mechanism of action of sotalol

A

Inhibit K channels: prolong ERP

Inhibit beta adrenoceptor: slow AVN conduction

41
Q

What are indications for sotalol

A

SVT

VT

42
Q

What are side effects of sotalol

A 
Torsades de Pointes 
Insomnia
Fatigue
Bronchspasm 
Hypotension
43
Q

Give examples of Class IV agents

A

Verapamil

Diltiazem

44
Q

What is mechanism of action of Class IV agents

A 
Inhibit L type Ca channels 
Slow conduction velocity at Phase 0
Decrease HR
Slow conduction at AVN 
Negative inotropic effect
45
Q

What are indications for Class IV agents

A 
SVT Prophylaxis 
Convert SVT (replaced by adenosine due to negative inotropic effect)
46
Q

What are contraindications of Class IV agents

A

Use with beta blockers: cumulative negative inotropic effect

AF in pt w WPW: conduction block at AVN causes increased transmission through Bundle thus risk of VF

47
Q

What is mechanism of action of adenosine

A 
Bind to A1 GPCR in AVN 
Inhibit adenylyl cyclase
Activate K channels 
Inhibit Ca channels 
Slow conduction at AVN
48
Q

What are indications for Adenosine

A

Convert AVNRT

Distinguish between SVTs

49
Q

What are PK properties of adenosine

A

Admin: rapid IV bolus

Short T1/2 (seconds)

50
Q

How can adenosine be used to distinguish between SVTs

A

If SVT continues after IV bolus treatment, re-entry loop unlikely to occur at AVN

51
Q

What is mechanism of action of Vernakalant

A

Inhibits atrial specific K channels
Prolong ERP in atria
Thus slow atrial conduction

52
Q

What are indications of Vernakalant

A

Convert AF

53
Q

What are side effects of Vernakalant

A

Taste disturbances
Hypotension
AV block

54
Q

What is mechanism of action of Ivabradine

A

Inhibit HCN channels at SAN
Slow HR
Without affecting BP

55
Q

What are side effects of Ivabradine

A

Flashing lights

Teratogenicity

56
Q

What are indications of Ivabradine

A

Sinus tachycardia

Tachycardia in HF and IHD

57
Q

What is mechanism of action of Digoxin

A

Cardiac glycoside
Stimulate vagal activity
Slow HR, Slow AVN conduction

58
Q

What are indications of Digoxin

A

AF
Atrial flutter
(Not first line - ineffective)

59
Q

What is mechanism of action of Atropine

A

Selective muscarinic antagonist
Block vagal activity
Increase HR, increase AVN conduction

60
Q

What are indications for Atropine

A

Sinus bradycardia

Pharmacology (19 decks)

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