Anti Arrythmic Flashcards

(24 cards)

1
Q

What is the resting membrane potential of a normal cardiac cell?

A

-90 mV

This value represents the electrical charge difference across the cell membrane when the cell is at rest.

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2
Q

What causes depolarization in cardiac cells?

A

Due to Na+ entry through Na+ channels

Depolarization is the process that makes the inside of the cell more positive.

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3
Q

What leads to hyperpolarization in cardiac cells?

A

Due to K+ exit through K+ channels at resting state

Hyperpolarization makes the inside of the cell more negative.

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4
Q

What is the mechanism behind repolarization in cardiac action potentials?

A

Due to K+ exit through K+ channels at depolarization state

Repolarization restores the resting membrane potential after depolarization.

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5
Q

What is the peak value of an action potential in cardiac cells?

A

+30 mV

This value indicates the maximum electrical charge achieved during an action potential.

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6
Q

What is the effect of Na channel blockers on Phase 0 of the action potential?

A

They act by decreasing the slope [dV/dt] of Phase 0

This action slows the rate of depolarization.

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7
Q

What is the effect of K+ channel blockers on action potential duration?

A

They prolong action potential duration [APD] and increase QT interval in ECG

Prolonged QT interval can lead to Torsades de pointes (TDP).

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8
Q

What is the effect of K+ channel openers on action potential duration?

A

They decrease action potential duration [APD]

This can lead to a more rapid recovery of the cardiac cell’s resting state.

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9
Q

What classification system is used for anti-arrhythmic drugs?

A

Vaughan Williams Classification

This classification is based on the predominant mechanism of action of the drugs.

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10
Q

What type of channel blockers are classified as Class I anti-arrhythmic drugs?

A

Na+ Channel Blockers

These drugs primarily act on sodium channels to affect cardiac excitability.

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11
Q

What are the classes of anti-arrhythmic drugs?

A

Class I, Class II, Class III, Class IV, Class V

Class I includes Na+ channel blockers, Class II includes beta blockers, Class III includes K+ channel blockers, Class IV includes Ca2+ channel blockers, and Class V includes others.

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12
Q

What is the primary action of Class I anti-arrhythmic drugs?

A

Na+ channel blockers

Class I drugs block sodium channels affecting the slope of Phase 0.

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13
Q

What are the subclasses of Class I anti-arrhythmic drugs?

A

1a, 1b, 1c

Each subclass has different effects on potassium channels.

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14
Q

What is the effect of Class 1a drugs?

A

Block K+ channels, precipitating TDP

TDP refers to Torsades de Pointes, a type of life-threatening arrhythmia.

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15
Q

Name two examples of Class 1a drugs.

A

Quinidine, Procainamide

These drugs can cause QT prolongation.

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16
Q

What is the primary use of Class 1b drugs?

A

Used only for ventricular arrhythmia

Lignocaine is the drug of choice for digoxin-induced ventricular arrhythmias.

17
Q

Name an example of a Class 1b drug.

A

Lignocaine

Phenytoin and Tocainide are also included in this class.

18
Q

What is the primary use of Class 1c drugs?

A

Used for WPW syndrome

The treatment of choice for WPW syndrome is radiofrequency ablation of the aberrant pathway.

19
Q

Name two examples of Class 1c drugs.

A

Encainide, Flecainide

These drugs have specific applications in arrhythmias associated with WPW syndrome.

20
Q

What are the primary actions of Class II anti-arrhythmic drugs?

A

Beta blockers

These drugs are primarily used in tachyarrhythmias.

21
Q

What is the main action of Class III anti-arrhythmic drugs?

A

K+ channel blockers

They play a crucial role in the management of various arrhythmias.

22
Q

Name two examples of Class III drugs.

A

Dofetilide, Dronedarone

Amiodarone and Sotalol are also included in this class.

23
Q

What is unique about Sotalol?

A

Has both Class III and Class II actions

It combines properties of potassium channel blocking and beta-blocking.

24
Q

What is notable about Amiodarone?

A

Longest acting anti-arrhythmic drug (t1/2 > 3 weeks)

It has multiple mechanisms of action including Na+ channel blocking and non-competitive beta-blocking.