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PHARMACOLOGY > ANTIRRYTHMIA > Flashcards

ANTIRRYTHMIA Flashcards

1
Q

Give the significance of antirrythmias

A

1) Most common cause of death in MI
2)

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2
Q

Arrythmias mainly occur due to two main causes

A

1) Improper impulse generation (abnormal automaticity)
2) Improper impulse conduction

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3
Q

Action potentials in the heart can be of two types

A

1) Pacemaker action potentials
2) Myocardial action potentials

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4
Q

Give the phases of the pacemaker action potential

A

1) Phase 1 - Pacemaker potential
Slow positive increase in the membrane potential until it reaches threshold
2)Depolarization
3) Repolarization

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5
Q

Give the phases of the myocardial action potential

A

Phase 0 - rapid influx of sodium
Phase 1 - transient efflux of potassium
phase 2 - influx of calcium that is electrically balanced by the efflux of potassium
Phase 3 -
Phase 4

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6
Q

Give the classification of the Antiarrhythmic drugs

A

Class IA
Class IB
Class IC
Class II
Class III
Class IV
Miscellaneous

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7
Q

All Class one drugs block which channel (Local anaesthetics)

A

Sodium channel

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8
Q

Give examples of :
CLASS IA DRUGS
CLASS IB DRUGS
CLASS IC DRUGS

A

CLASS IA DRUGS
Quinidine
Disopyramide
Procainamide
CLASS IB DRUGS
Lidocaine
Mexiletine
CLASS IC DRUGS
Flecainide
Propafenone

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9
Q

Give the Mechanism of action of the Class IA drugs

A

1) Blocking the sodium channels -affect phase 0
2) Block the potassium channels - repolarization leading to delayed repolarization thus a prolonged AP

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10
Q

What is the effect of the class IA agents

A

1)Prolong the AP thus leading to Torsade de pointes
2)

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11
Q

Prolonged Action potential in the ecg is shown by

A

Prolonged QT interval - due to potassium channel blockade

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12
Q

Blocking the sodium channels by class IA drugs causes

A

Slow conduction velocity in the atria, purkinje and ventricles

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13
Q

Give :
1) ROA of Quinidine
2) Adverse effects of Quinidine
3) Metabolism of Quinidine
4) DDI

A

1) Oral
2) Cinchonism (blurred vision, tinnitus , headache , psychosis) , GIT problems , autoimmune reactions
3) CYP3A4 into active metabolites
4) i)Inhibits CYP2D6 and P glycoprotein
ii) Reduces clearance of digoxin

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14
Q

Both Quinidine and Disopyramide are metabolized using

A

CYP3A4

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15
Q

Give the PK of Procainamide

A

Procainamide may be given by IV or IM and is well absorbed orally. It is acetylated to N-acetylprocainamide (NAPA) that is eliminated in the kidney.

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16
Q

Give the A/E of Procainamide

A

Hypotension
A reversible syndrome similar to SLE

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17
Q

what may worsen class one drug toxicity

A

Hyperkalemia

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18
Q

Give two types of drugs that may be used to treat overdose of the class 1A drugs

A

1) Sodium lactate for drug induced arrhythmias
2) Pressor sympathomimetics for hypotension

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19
Q

Give two examples and ROA of the class 1b drugs

A

Lidocaine - IV or IM
Mexiletine - orally

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20
Q

Give two MOA of the class 1b drugs

A

1) Sodium channel blockade
2) Increase phase 3 repolarization thus reduced AP and reduced or unchanged QT interval

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21
Q

What type of tissue do the class 1b drugs affect

A

1) Ischemic tissue
2) Depolarized Purkinje or ventricular tissue
(Rarely have an effect on atrial tissue)

22
Q

Class 1b agents usually have little effect on normal cardiac cells thus little effect on the ECG, explain?

A

Class IB agents usually associate and dissociate rapidly from the sodium channels thus usually affect the cells when there is rapid depolarization and repolarization

23
Q

Give ROA of Lidocaine

A

Lidocaine may be given by IM or IV but never orally due to its very high first pass effect and the its metabolites are potentially cardiotoxic

24
Q

What CYP Isoenzyme metabolizes Mexiletene

A

CYP2D6

25
Q

Lidocaine is metabolized by two main CYP isoenzymes to less active metabolites , name them

A

CYP1A2 AND CYP3A4

26
Q

Give two main clinical uses of Lidocaine

A

1) Acute ischemic ventricular arrhythmias
2) Polymorphic VT or VT storm (WITH Amiodarone)

27
Q

Give the main use for Mexiletine

A

Combined with Amiodarone to treat chronic ventricular arrhythmias

28
Q

Give A/E of Lidocaine

A

Nystagmus, slurred speech, paresthesia, agitation and confusion

29
Q

What increases the toxicity of Class IB agents

A

Hyperkalemia

30
Q

Give two types of Class IC agents

A

Flecainide and Propafenone

31
Q

Of the two Class IC agents which one has a B-blocking effect and is thus C/I in patients with?

A

Propafenone, Asthma (may cause bronchospasm)

32
Q

Both Flecainide and Propafenone being Class I agents block sodium channels although one only blocks potassium channels, which one

A

Flecainide

33
Q

Class IB and IC agents usually differ in dissociation from the cardiac cells, explain and their consequent effects

A

Class IB agents dissociate rapidly from the sodium channels thus have little effect on normal cardiac cells and the ECG.
Class IC agents dissociate slowly from the sodium channels thus have prominent effects on normal cardiac cells and show QRS duration increase and a slight PR interval increase on the ECG

34
Q

give the
1) ROA of Flecainide and Propafenone
2) Metabolism of Flecainide and Propafenone

A

1) Both orally
2) Flecainide CYP2D6 and Propafenone (CYP1A2, CYP3A4 AND CYP2D6)

35
Q

Give the uses of:
1) Flecainide
2) Propafenone

A

1) Flecainide :
Atrial flutter and fibrillation
Refractory ventricular arryhythmias
2) Propafenone
Atrial fibrilation/flutter
Paroxysmal supraventricular tachycardia

36
Q

Flecainide is generally well tolerated, and its few side effects include?

A

Nausea, dizziness, blurred vision

37
Q

What are inotropic agents and which type is Flecainide

A

Inotropic agents alter the force of muscular contractions
It is a negative inotropic agent thus it reduces the force and thus can worsen chronic heart failure

38
Q

Class 2 Antiarrhythmic drugs are also called

A

Beta blockers

39
Q

Give the examples of beta blockers

A

Metoprolol
Atenolol
Esmolol
Propranolol

40
Q

In ECG the beta blockers show which changes

A

An increase in the PR interval

41
Q

An increase in the PR interval is usually due to

A

An increase in conduction time from the atrium to the ventricle via the AVN

42
Q

What is the mechanism of beta blockers (4)

A

1) Blocking B1 receptors
2) Prolong AV conduction
3) Reduce heart rate
4) Reduce myocardial contractility
5) Reduce AV refractory period

43
Q

Give the class three agents

A

AID2S
Amiodarone
Ibutilide
Dofetilide
Dronedarone
Sotalol

44
Q

What is the MOA of the class three agents

A

They block potassium channels thus prolong AP and are seen as QR interval prolongation in the ECG

45
Q

The most efficacious of the antiarrhythmic drugs is

A

Amiodarone

46
Q

Give the A/E of Amiodarone

A

1) Pulmonary fibrosis
2) Neuropathy
3) Hepatotoxicity
4) Microcrystalline corneal deposits
5) Optical neuritis
6) Blue-grey skin discoloration
7) Thyroid dysfunction
8) Paresthesia and tremor

47
Q

Give two examples of calcium channel blockers

A

Verapamil and Diltiazem

48
Q

Give the mechanism of the calcium channel blockers

A

Blocking the calcium channels and blocking the conduction rate through the AV node

48
Q

Give the mechanism of the calcium channel blockers

A

Blocking the calcium channels and blocking the conduction rate through the AV node

49
Q

Class 4 agents show what change in the ECG

A

Increase in the PR interval due to blockade of AV nodal conduction from atrium to ventricles

50
Q

Give he Dihydropyridine calcium channel blockers

A

Amlodipine
Nicardipine
Nifedipine
Felodipine

51
Q

Torsades de pointes on ecg is shown by prolongation in

A

QT interval

PHARMACOLOGY (17 decks)

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