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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
What must Flecainide be prescribed with when treating for Atrial flutter
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
What are contraindications of Flecainide
Structural heart disease, IHD | Associated with arrhythmias and sudden deaths
27
Give examples of Class II agents
``` Bisoprolol Propranolol Atenolol Esmolol Sotalol ```
28
What are PK properties of Class II agents
Bisoprolol: long Acting, once daily regime, oral Propranolol: short acting, oral or IV Esmolol: v short acting(seconds)
29
What is mechanism of action of Class II agents
``` 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
What are indications for Class II agents
Sinus tachycardia Convert AVNRT Protect ventricles from high atrial rates
31
What are side effects of Class II agents
Bronchospasm | Hypotension
32
What are contraindications of Class II agents
Asthma
33
What is mechanism of action of Class III agents
``` Block K channels Slow repolarisation (phase 3) Prolong ERP ```
34
Give examples of class III agents
Amiodarone | Sotalol
35
What are PK properties of amiodarone
Oral, IV | T1/2 3 months
36
What is mechanism of action of amiodarone
Inhibit K channels: prolong ERP Inhibit Na channels: slow conduction, prolong ERP Inhibit Beta adrenoceptor: slow AVN conduction
37
What are indications of amiodarone
Most arrhythmias: atrial, nodal, ventricular | When other drugs failed
38
What are side effects of amiodarone
``` Optic neuritis (transient) Photosensitivity Thrombophlebitis at injection site (use central veins) Pneumonitis/pulmonary fibrosis Hepatitis/liver fibrosis Raised LDL Hyperthyroidism (contains iodine) ```
39
What monitoring is required for amiodarone
LFT, TFT, ECG, U+E, CXR at baseline | TFT+LFT 6 monthly
40
What is mechanism of action of sotalol
Inhibit K channels: prolong ERP | Inhibit beta adrenoceptor: slow AVN conduction
41
What are indications for sotalol
SVT | VT
42
What are side effects of sotalol
``` Torsades de Pointes Insomnia Fatigue Bronchspasm Hypotension ```
43
Give examples of Class IV agents
Verapamil | Diltiazem
44
What is mechanism of action of Class IV agents
``` Inhibit L type Ca channels Slow conduction velocity at Phase 0 Decrease HR Slow conduction at AVN Negative inotropic effect ```
45
What are indications for Class IV agents
``` SVT Prophylaxis Convert SVT (replaced by adenosine due to negative inotropic effect) ```
46
What are contraindications of Class IV agents
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
What is mechanism of action of adenosine
``` Bind to A1 GPCR in AVN Inhibit adenylyl cyclase Activate K channels Inhibit Ca channels Slow conduction at AVN ```
48
What are indications for Adenosine
Convert AVNRT | Distinguish between SVTs
49
What are PK properties of adenosine
Admin: rapid IV bolus | Short T1/2 (seconds)
50
How can adenosine be used to distinguish between SVTs
If SVT continues after IV bolus treatment, re-entry loop unlikely to occur at AVN
51
What is mechanism of action of Vernakalant
Inhibits atrial specific K channels Prolong ERP in atria Thus slow atrial conduction
52
What are indications of Vernakalant
Convert AF
53
What are side effects of Vernakalant
Taste disturbances Hypotension AV block
54
What is mechanism of action of Ivabradine
Inhibit HCN channels at SAN Slow HR Without affecting BP
55
What are side effects of Ivabradine
Flashing lights | Teratogenicity
56
What are indications of Ivabradine
Sinus tachycardia | Tachycardia in HF and IHD
57
What is mechanism of action of Digoxin
Cardiac glycoside Stimulate vagal activity Slow HR, Slow AVN conduction
58
What are indications of Digoxin
AF Atrial flutter (Not first line - ineffective)
59
What is mechanism of action of Atropine
Selective muscarinic antagonist Block vagal activity Increase HR, increase AVN conduction
60
What are indications for Atropine
Sinus bradycardia

Pharmacology (19 decks)

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