Cardiac Arrhyhtmic Drugs Flashcards

1
Q

Give the broad mechanism of action for ALL Class 1 anti arrhythmic drugs

A

Voltage gated Na+ channel blockers

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2
Q

Briefly describe the mechanism of action for Class 1A anti arrhythmic drugs in terms of cellular effects

A

Binds to open or inactivated sodium channels, preventing sodium influx.
This slows the rapid upstroke during phase 0.

It also blocks calcium channels and inhibits potassium channels.
This slows the speed of conduction and increases the length of the refractory period.

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3
Q

What effects do Class 1A drugs have on an ECG

A

Increases the size of QRS complex

Increases the size of QT

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4
Q

Name the main drugs of Class 1A

A

Quinidine and Procainamide

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5
Q

How are Class 1A drugs metabolised

A

Hepatic metabolisation

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6
Q

Describe the therapeutic use of Quinidine

A

Used to maintain sinus rhythms in atrial fibrillation and flutter.

Helps prevent recurrence.

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7
Q

Describe the therapeutic use of Procainamide

A

Used in the acute IV treatment of supraventricular and ventricular cardiac arrhythmias.

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8
Q

List some fo the main ADRs of Class 1A drugs and why these may happen

A

Hypotension - due to the reduced cardiac output

Proarrhythmia - can lead to the generation of a new arrhythmia like Torsades de Points (increase QT interval)

CNS side effects - dizziness, confusion, insomnia etc.
Gastrointestinal side effects

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9
Q

Briefly describe the mechanism of action for Class 1B anti arrhythmic drugs in terms of cellular effects

A

Blocks active and inactivated sodium channels.
This decreases the speed of the upstroke in phase 0.

Shortens phase 3 repolarization, decreasing the length of the action potential.

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10
Q

What effects do class 1B drugs have on an ECG in a normal heart

A

Class 1B drugs do not have an affect on an ECG in a normal heart.

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11
Q

True or False: Class 1B drugs do not show ECG changes in hearts with structural damage

A

False: in fast beating or ischaemic hearts, class 1B drugs show an increase in QRS complex.

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12
Q

Are class 1B drugs used more often in acute or chronic cases

A

Acute

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13
Q

In which situation would class 1B anti arrhythmic drugs be used

A

In an acute situation to treat ventricular tachycardia.

Especially if heart has ischaemic damage.

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14
Q

What is the method of class 1B anti arrhythmic metabolisation

A

Hepatic

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15
Q

What are the common side effects of class 1B anti arrhythmic drugs

A

CNS effects and Gastric distress is most common.

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16
Q

Name different kinds of class 1B anti arrhythmic drugs

A

Lidocaine and Mexiletine

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17
Q

What is a sign of lidocaine toxicity

A

Nystagmus

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18
Q

Briefly describe the mechanism of action for Class 1C anti arrhythmic drugs in terms of cellular affects

A

Suppresses phase 0 upstroke in Purkinje and myocardial fibres.
This drastically slows conduction in all cardiac tissue.

It increases the threshold, leading to a decrease in automaticity.

Blocks K+ channels, which leads to an increase in action potential duration.

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19
Q

What effects do class 1C anti arrhythmic drugs have on an ECG

A

Increases the PR interval.
Increases the QRS complex.
Increases the QT level.

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20
Q

Describe the common uses for class 1C anti arrhythmic drugs

A

Used to treat supra-ventricular arrhythmias (fibrillation and flutter) by maintaining sinus rhythm.

It can also be used to treat refractory ventricular arrhythmias (2 or more ventricular arrhythmic episodes requiring medical attention in a 24 hour period).

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21
Q

True or False: Class 1C anti arrhythmic drugs can be used to treat supra-ventricular arrhythmias in patients with structural heart disease

A

False.

Class 1C anti arrhythmic cannot be used to restore sinus rhythm in patients with structural heart disease.

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22
Q

Name the main class 1C anti arrhythmic drugs

A

Felcainide and Propafenone

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23
Q

What is the method of administration for Flecainide

A

Oral administration

24
Q

What is the method of administration for Propafenone

A

IV administration

25
Q

What is the method of class 1C anti arrhythmic drug metabolisation

A

Hepatic

26
Q

What are the common side effects of class 1C anti arrhythmic drugs

A

CNS effects and gastric distress are most common.

27
Q

True or False: the use of Propafenone should be avoided with asthma patients

A

True.

Due to its β-blocking effects, it may cause bronchospasms.

28
Q

Give the broad mechanism of action for ALL Class 2 anti arrhythmic drugs

A

β-adrenoreceptor blockers.

29
Q

Briefly describe the mechanism of action for class 2 anti arrhythmic drugs in terms of cellular effects

A

Increases the action potential duration and refractory period in the AV node.
This slows AV conduction velocity, decreasing heart rate and contractility.

Decreases the amount of phase 4 depolarisation as it is catecholamine dependent.

30
Q

Class 2 anti arrhythmic drugs are most commonly used to treat what conditions

A

Used to treat tachyarrhythmias caused by increased sympathetic activity.

They are also used to treat atrial flutter and fibrillation.

They can be used to treat AV nodal reentrant tachycardia.

31
Q

Describe the effects a class 2 anti arrhythmic drug would have on an ECG

A

It would increase the PR interval.

It would lower the patients heart rate.

32
Q

Name the main class 2 anti arrhythmic drugs

A

Metoprolol
Propranolol
Atenolol
Esmolol

33
Q

What is the method for administration for Metoprolol

A

IV or Oral administration

34
Q

What is the method of administration for Propranolol

A

Oral or IV administration

35
Q

What is the method of administration for Esmolol

A

IV administration

36
Q

True or False: Esmolol is a very short acting drug and is used to treat acute arrhythmias

A

True.

37
Q

How are class 2 anti arrhythmic drugs metabolised

A

Hepatically

38
Q

What are the common side effects of class 2 anti arrhythmic drugs

A

CNS effects
Bronchospasms (non selective β-blockers)
Hypotension

39
Q

Should you use class 2 anti arrhythmic drugs in AV block or ventricular failure

A

No.

This can increase the conduction block and risk of heart failure.

40
Q

Which class 2 anti arrhythmic drug is most commonly used

A

Metoprolol (selective β-blocker)

41
Q

Give the broad mechanism of action for ALL class 3 anti arrhythmic drugs

A

K+ channel blocker

42
Q

Briefly describe the mechanism of action for class 3 anti arrhythmic drugs in terms of their cellular effects

A

Block potassium channels, which causes the potassium efflux during cardiac repolarisation.
This prolongs action potential duration, without changing the Phase 0 depolarisation or the resting membrane potential.

This prolongs the refractory period.

43
Q

Name the two main class 3 anti arrhythmic drugs

A

Amiodarone and Sotalol

44
Q

Describe the mechanism of action for Amiodarone specifically

A

Demonstrates class 1, 2, 3, and 4 anti arrhythmic effects as well as α-blocking activity.

Blocks K+ channels, prolonging action potentials and increasing the refractory period.

Blocks Na+ channels, decreasing phase 0 depolarisation and conduction of the action potential.

Increases action potential threshold.

Acts as a β-blocker and a Ca+ channel blocker, decreasing phase 4

Blocks Ca+ channels. decreasing the speed of AV conduction by prolonging refractory period of AV node.

45
Q

What are the effects of amiodarone on an ECG

A

Increases PR interval.

Increases QRS complex.

Increases QT wave.

Decreases heart rate.

46
Q

Outline the uses of class 3 anti arrhythmic amiodarone

A

It is a wide spectrum anti arrhythmic.

It is used in treatment of most arrhythmias - particularly supra ventricular and ventricular tachyarrhythmias.

47
Q

What are the main adverse side effects of class 3 anti arrhythmic - amiodarone

A

There are multiple side effects of amiodarone, the main ones being:

  • pulmonary fibrosis
  • hepato-toxicity
  • increase in LDL cholesterol
  • thyroid disease
  • photosensitivity
  • optic neuritis (transient blindness)
48
Q

What are some common drug to drug interactions with amiodarone

A

Digoxin and Warfarin usage and dosage will need to be monitored extensively.

Beware of drugs that are metabolised by CYP1A2, CYP2C9, CYP2D6, and P-glycoprotein, as amiodarone inhibits them.

49
Q

What is the method of administration for amiodarone

A

Oral or IV

50
Q

True or False: Amiodarone has a half life of approximately 3 months

A

True.

51
Q

What is the method of elimination for class 3 anti arrhythmic Amiodarone

A

Hepatic

52
Q

Describe the mechanism of action for Sotalol specifically

A

K+ channel blocker, allowing for an increase in the refractory period and overall action potential duration.

As a ß-blocker, it slows phase 4 conduction along with AV conduction.

53
Q

Describe the effects class 3 anti arrhythmic Sotalol has on an ECG

A

Increase QT interval.

Decrease heart rate.

54
Q

What is the method of absorption of Sotalol

A

Oral

55
Q

What are the therapeutic uses of sotalol

A

Maintenance of normal sinus rhythm in cases of atrial fibrillation or flutters.

It is also used in the treatment of ventricular arrhythmias.

56
Q

What are some of the key adverse side effects of class 3 anti arrhythmic sotalol

A
  • Proarrhythmia
  • Fatigue
  • Insomnia
57
Q

True or False: Sotalol would also have mild ß-blocker side-effects

A

True.

These include fatigue, dizziness, and weakness.