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Year 3 > Antiarrythmia Drugs > Flashcards

Antiarrythmia Drugs Flashcards

1
Q

Molecular mechanism of action of Lidocaine (aka Lignocaine)?

A

Inactivates voltage gated Na+ channels

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2
Q

What tissues/organs does Lidocaine/Lignocaine act on?

A

Nerves, cardiac muscle

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3
Q

What physiological effects does Lidocaine/Lignocaine have on the body?

A

Decreases conduction in excitable tissue

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4
Q

Potential side effects of Lidocaine/Lignocaine?

A

CNS activation/depression, hypotension

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5
Q

What type of anti-arrhythmic drug increases the negative inotropic effect of beta blockers?

A

Lidocaine/Lignocaine

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6
Q

Mnemonic for Class I-IV anti-arrhythmic drugs?

A

“NaB a Pot (of) Milk”

  1. Na+
  2. Beta blockers
  3. K+
  4. CCB’s
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7
Q

Example of Class 1 anti-arrhythmic drug?

A

Class I (Na+ channel blockers) = Flecainide

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8
Q

Example of Class 2 anti-arrhythmic drug?

A

Class 2: Beta blockers: Atenolol

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9
Q

Example of Class 3 anti-arrhythmic drug?

A

Class 3: K+ channel blockers
Amiodarone
Dronedarone

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10
Q

Example of Class 4 anti-arrhythmic drug?

A

Class 4: CCB
Verapamil

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11
Q

Lignocaine (Class 1b antiarrythmic drug) has what type of effect on action potential duration?

A

Shortens AP duration

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12
Q

Flecainide (Class 1c anti-arrhythmic drug) has what type of effect on action potential duration?

A

No effect on AP duration

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13
Q

Class 1 antiarrythmics… the faster the heart rate, the ________ the block.

A

Greater

(So they inhibit tachycardias, but allow normal heart rates)

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14
Q

Which anti-arrhythmic drug is indicated for paroxysmal (intermittent) AF?

A

Flecainide (Na+ channel blocker)

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15
Q

What is the drug of choice in WPW syndrome?

A

Flecainide (Na+ channel blocker)

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16
Q

What is the main contraindication for Flecainide?

A

Established IHD

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17
Q

What investigation should be ordered after starting a patient on Flecainide? (Or changing the dose?)

A

ECG- Can cause QT prolongation

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18
Q

List 4 main side effects of Flecainide

A
  1. QT prolongation (pro-arrhythmia)
  2. Increases pacing threshold (ie pacemaker needs to deliver more energy to activate contraction)
  3. Dizziness
  4. Blurred vision
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19
Q

Class Ic antiarrhythmic agent used to manage atrial fibrillation and paroxysmal supraventricular tachycardias

A

Flecainide

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20
Q

Common indications for this class II antiarrythmic drug include AF (reduces the ventricular rate, and in paroxysmal AF, to maintain sinus rhythm), and supraventricular tachycardia to restore sinus rhythm

A

Atenolol (Beta blocker)

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21
Q

MOA of Atenolol?

A

Act via Beta-1 adrenoreceptors in the heart to reduce force of cardiac contraction and speed of conduction

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22
Q

Contraindications/warnings for Atenolol?

A

Avoid in asthma

NEVER GIVE BETA BLOCKERS TO SOMEONE IN ACUTE HEART FAILURE! Contraindicated in heart block and severe hypotension

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23
Q

Common adverse effects of Atenolol

A

Fatigue, cold extremities, HA, GI upset

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24
Q

Drug treatment recommended for management of ectopic beats?

A

Low dose beta-blocker such as Propranolol

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25
Q

Class 1c anti-arrythmics such as ____________ and beta blockers can be used as second line management for __________________ (as they are less effective, but less toxic than Amiodarone)

A

Flecainide

Paroxysmal AF

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26
Q

Mechanism of action of Class III anti-arrythmic (Amiodarone)?

A

Potassium channel blocker

** Prolongs the action potential (QT PROLONGATION)

Stabilises ventricular and atrial myocytes. Slows AV node conduction. Blocks accessory pathways.

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27
Q

This class III anti-arrythmic is used in a wide range of sustained tachyarrhythmias including AF, atrial flutter, supraventricular tachycardia, VTach, and refractory Vfib. It is generally only used if other tx (drugs or electrical cardioversion) are ineffective or contraindicated

A

Amiodarone
Dronedarone

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28
Q

Contraindications/warnings for amiodarone

A

Severe hypotension
Heart block
Active thyroid disease

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29
Q

Drug of choice in acute VTach?

A

IV Amiodarone
(If that fails, emergency DC cardioversion)

30
Q

What are the three best ventricular-stabilising drugs?

A

Beta blockers (eg Bisoprolol)
Amiodarone (if there is a recurrence of arrythmia on Beta Blocker)
IV Lignocaine

31
Q

List four anti-arrythmic drugs known to cause bradycardia

A

Beta blockers (Bisoprolol)
Verapamil/Diltiazem
Amiodarone
Digoxin

32
Q

Which of the anti-arrythmic drugs is most lipid-soluble, with a very long half life (around 30 days?)

A

Amiodarone

33
Q

Important adverse effects:
Pneumonitis –> lung fibrosis
Hepatitis
Thyroid dysfunction (remember iodine)
Skin photosensitivity
BLUE-GREY DISCOLOURATION of the skin
Corneal microdeposits
Peripheral neuropathy, tremor
Pro-arrythmia (potentially)

A

Amiodarone

34
Q

Four components of regular monitoring for patients on Amiodarone?

A

Annual CXR
6-monthly LFT’s
6-monthly TFT’s
Regular ECG’s (QT prolongation)

35
Q

This drug is a class III anti-arrythmic agent that does not contain iodine, and is less lipophilic than amiodarone. Shorter half life. Less effective than amiodarone

A

Dronedarone

36
Q

Indications for Dronedarone?

A

Used to maintain sinus rhythm in paroxysmal AF (but only as a last resort)

37
Q

Adverse effects/toxicity of Dronedarone?

A

Can cause liver dysfunction, monitor LFT’s

38
Q

Drugs that act on the AV node?
(AABCD)

A

Amiodarone
Adenosine
Bisoprolol
CCB (Verapamil & Diltiazem)
Digoxin

39
Q

Best drugs for ventricular tachycardias?

A

Beta blockers (eg Bisoprolol)
Amiodarone
Sometimes IV magnesium

40
Q

First line drug class for most tachyarrythmias?

A

Beta blockers

41
Q

This drug class acts to block the L-type voltage-gated Calcium channel found in cardiac tissue, resulting in a decrease of intracellular calcium.

Can also act to relax the smooth muscle in arterioles, decrease the force of contraction in cardiac muscle, and decrease conduction through the AV node

A

Calcium channel blockers

(amlodipine, verapamil, diltiazem)

42
Q

Which, of the three main CCB’s, has the strongest vasodilatory effect?

A

Amlodipine

43
Q

Which, of the three main CCB’s, has the strongest effect on decreasing heart rate and cardiac contractility?

44
Q

Which, of the three main CCB’s, is useful for both arrhythmias AND angina?

45
Q

This drug class is useful to use in AF, as they help to slow ventricular rate by blocking the AV node

A

CCB’s, particularly Diltiazem

46
Q

What drug would be indicated for terminating a SVT in an asthmatic patient?

A

Verapamil, as Adenosine is contraindicated in asthmatic patients

47
Q

Which calcium channel blockers can be used for prevention of SVT’s?

A

Verapamil or Diltiazem

48
Q

Drug of choice (used IV) for terminating SVT’s?

49
Q

The mechanism of action of this drug is to block AV node conduction via the A1 receptor, activating delayed rectifier K+ channels. THis hyper-polarises cardiac tissue, slowing the pacemaker potential.

50
Q

Which drug (given IV in SVT’s) helps to reveal occult accessory pathways, such as those in WPW syndrome?

51
Q

Common side effects of this drug include chest tightness, breathlessness, dizziness, nausea, and hypotension (vasodilation).

It is also contra-indicated in asthmatic patients as it causes bronchoconstriction

52
Q

This is a physiologically active nitrogenous plant-derived substance that blocks Muscarinic receptors (M1-M5) (ie anti-cholinergic)

53
Q

Which drug acts to INCREASE SA node rate and AV conduction (via M2 receptor), therefore INCREASING heart rate?

A

Atropine

(essentially the opposite action to Adenosine)

54
Q

Indications: sinus bradycardia (acute with symptoms- acute MI, vaso-vagal syncope)
2nd or 3rd degree block AT the AV node (ie with NARROW complexes).
Note that this drug is ineffective for heart block BELOW the AV node

55
Q

Mechanism of action: Inhibits the Na/K ATPase (sodium pump); binds to extracellular K+ binding site, leading to an increase in intracellular Na+. It also inhibits Na+/Ca+ exchange, leading to accumulation of intracellular Ca+.

56
Q

The actions of this drug are to slow AV node conduction. It’s also positively inotropic via an increase in intracellular Ca+ (increases the force of contraction) and negatively chronotropic (reduces the heart rate)

57
Q

This drug is used to SLOW heart rate in AF. It has a NARROW THERAPEUTIC WINDOW, and can cause a wide range of arrhythmias (Especially with hypokalemia, as it competes with K+ on its binding site)

58
Q

What types of changes would you see on an ECG in “Digoxin effect?”

A

“Reverse tick” in the S-T segment

59
Q

Examples of drugs that act on the sinus node?

A

Bisoprolol (class II)
Ivabradine

60
Q

Examples of drugs that act on atrial muscle?

A

Flecainide (class 1c)
Bisoprolol (class II)
Amiodarone (class III)

61
Q

Examples of drugs that act on the AV node?

A

Bisoprolol (class II)
Amiodarone (class III)
Verapamil & Diltiazem (class IV)
Digoxin
Adenosine

62
Q

Examples of drugs that act on the left ventricle muscle?

A

Lignocaine (class 1b)
Flecainide (class 1c)
Bisoprolol (class II)
Amiodarone (class III)
Magnesium

63
Q

Examples of drugs that act on accessory pathways?

A

Flecainide (class 1c)
Amiodarone (class III)

64
Q

Choice of drug for preventing atrial tachycardia?

A

Beta blockers (eg Bisoprolol)

65
Q

Choice of drug for preventing AVNRT?

A

Beta blockers (eg Bisoprolol) or Verapamil

66
Q

Drug of choice for preventing activation of accessory pathways?

A

Flecainide or amiodarone

67
Q

These drugs are atrial stabilisers, which help to maintain sinus rhythm in AF

A

Beta blockers (eg Bisoprolol)
Flecainide
Amiodarone

68
Q

These drugs are AV node blockers, can be used to slow heart rate in AF

A

Beta blockers (eg Bisoprolol)
Diltiazem
Digoxin
Amiodarone

69
Q

Drug of choice for sinus tachycardia?

A

Beta blockers
Ivabradine

70
Q

Drug of choice for bradycardia?

A

Atropine
Isoprenaline

71
Q

The Vaughn-Williams drug classes ____ and ____ act on cardiac electrical tissue. These drugs may be PRO-arrythmic; risk related to prolongation of the QT and QRS intervals on ECG

A

1 (Na+ channel blockers)
3 (K+ channel blockers)

Year 3 (23 decks)

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