ANTIRRYTHMIA Flashcards

(52 cards)

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

25
Lidocaine is metabolized by two main CYP isoenzymes to less active metabolites , name them
CYP1A2 AND CYP3A4
26
Give two main clinical uses of Lidocaine
1) Acute ischemic ventricular arrhythmias 2) Polymorphic VT or VT storm (WITH Amiodarone)
27
Give the main use for Mexiletine
Combined with Amiodarone to treat chronic ventricular arrhythmias
28
Give A/E of Lidocaine
Nystagmus, slurred speech, paresthesia, agitation and confusion
29
What increases the toxicity of Class IB agents
Hyperkalemia
30
Give two types of Class IC agents
Flecainide and Propafenone
31
Of the two Class IC agents which one has a B-blocking effect and is thus C/I in patients with?
Propafenone, Asthma (may cause bronchospasm)
32
Both Flecainide and Propafenone being Class I agents block sodium channels although one only blocks potassium channels, which one
Flecainide
33
Class IB and IC agents usually differ in dissociation from the cardiac cells, explain and their consequent effects
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
give the 1) ROA of Flecainide and Propafenone 2) Metabolism of Flecainide and Propafenone
1) Both orally 2) Flecainide CYP2D6 and Propafenone (CYP1A2, CYP3A4 AND CYP2D6)
35
Give the uses of: 1) Flecainide 2) Propafenone
1) Flecainide : Atrial flutter and fibrillation Refractory ventricular arryhythmias 2) Propafenone Atrial fibrilation/flutter Paroxysmal supraventricular tachycardia
36
Flecainide is generally well tolerated, and its few side effects include?
Nausea, dizziness, blurred vision
37
What are inotropic agents and which type is Flecainide
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
Class 2 Antiarrhythmic drugs are also called
Beta blockers
39
Give the examples of beta blockers
Metoprolol Atenolol Esmolol Propranolol
40
In ECG the beta blockers show which changes
An increase in the PR interval
41
An increase in the PR interval is usually due to
An increase in conduction time from the atrium to the ventricle via the AVN
42
What is the mechanism of beta blockers (4)
1) Blocking B1 receptors 2) Prolong AV conduction 3) Reduce heart rate 4) Reduce myocardial contractility 5) Reduce AV refractory period
43
Give the class three agents
AID2S Amiodarone Ibutilide Dofetilide Dronedarone Sotalol
44
What is the MOA of the class three agents
They block potassium channels thus prolong AP and are seen as QR interval prolongation in the ECG
45
The most efficacious of the antiarrhythmic drugs is
Amiodarone
46
Give the A/E of Amiodarone
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
Give two examples of calcium channel blockers
Verapamil and Diltiazem
48
Give the mechanism of the calcium channel blockers
Blocking the calcium channels and blocking the conduction rate through the AV node
48
Give the mechanism of the calcium channel blockers
Blocking the calcium channels and blocking the conduction rate through the AV node
49
Class 4 agents show what change in the ECG
Increase in the PR interval due to blockade of AV nodal conduction from atrium to ventricles
50
Give he Dihydropyridine calcium channel blockers
Amlodipine Nicardipine Nifedipine Felodipine
51
Torsades de pointes on ecg is shown by prolongation in
QT interval