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PHAR20300 > ANTIDYSRHYTHMICS > Flashcards

ANTIDYSRHYTHMICS Flashcards

1
Q

What is arrhythmia?

A

Absence of rhythm

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2
Q

What is dysrhythmia?

A

Disturbance in rhythm

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3
Q

How are dysrhythmias classified?

A

Site of origin, effect and frequency of occurrence

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4
Q

What are the possible sites of origin of dysrhythmias?

A

Atrial
Ventricular
Junctional (supraventricular)

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5
Q

What is meant by a true dysrhythmia?

A

A very disorganised rhythm

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6
Q

What is meant by tachycardia?

A

Heart beat too fast

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7
Q

What is meant be bradycardia?

A

Heart beat too slow

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8
Q

What is paroxysmal supraventricular tachycardia?

A

Happens in attacks, rapid but regular heart beat

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9
Q

What are ectopic heartbeats?

A

Skipped or extra heartbeats leading to irregular heart rate and heart rhythm

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10
Q

What is multifocal atrial tachycardia?

A

electrical impulses arriving from multiple locations within atria

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11
Q

What is ventricular fibrillation?

A

Rapid heartbeat initiated within ventricles. It is characterised by 3 or more consecutive premature ventricular beats

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12
Q

What is the most common type of bradydysrhythmia?

A

Heart block - communication between atria and ventricles is disrupted

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13
Q

What is the difference between first, second and third degree heart block?

A

First: slowed conductance through AVN
Second: some atrial impulses fail to make it through to ventricles
Third: no conduction from atria to ventricles - complete heart block

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14
Q

What is asystolic arrest?

A

Complete cessation of electrical activity - bradydysrhythmia

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15
Q

What are the five main mechanisms that lead to dysrhythmia?

A

Ectopic pacemakers - conducting tissue other than SAN initiate heart beat
Delay after depol - build up on Ca2+ in cells leading to train of APs
Re-entry circuits - Tissue damage leads to AP travelling in circles
Congenital abnormalities - additional conducting pathways between atria and ventricles
Heart block - damage to conducting pathways disrupts signalling between atria and ventricles

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16
Q

Ectopic foci lead to an odd shaped ___ wave on ECG

A

P

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17
Q

Heart rate increase if rate of ectopic focus exceeds rate of SAN. True or false?

A

True

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18
Q

What takes place in AF that leads to abnormal impulse generation?

A

Atrial myocytes contract independently, each atria potentially acts as ectopic focus so there is no coordinated contraction of atria so QRS complex occurs at irregular intervals

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19
Q

Ventricular fibrillation can be a result of ectopic foci or re-entry circuits. True or false?

A

True

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20
Q

Ventricular fibrillation is a true arrhythmia. True or false?

A

True

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21
Q

In ventricular fibrillation, the ventricles are not coordinated in contraction and there is no ____ wave on ECG

A

QRS

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22
Q

What is Wolff-Parkinson-White syndrome?

A

A congenital abnormality where there are additional conducting pathways between the atria and ventricles known as Kent bundles.
Signals go via AVN and Kent bundles leading to atrial flutter - ventricles try to keep up pace with atria - sudden death possible
Kent bundles can also set up re-entry circuits

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23
Q

Can Kent bundles be surgically removed?

A

Yes - if one or two present usually surgically removed

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24
Q

All dysrhytmias are abnormal and dangerous. True or false?

A

False - sinus dysrhythmia is an alteration of HR brought about by breathing - particularly common in young people

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25
Q

What is the VW system?

A

main classification system used for anti-dysrhythmic drugs

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26
Q

In the VW system, which receptors are targeted in the different classes?

A 
Class I - Na channels
Class 2 - B1 receptor
Class 3 - K channel
Class 4 - Calcium channel 
Unclassified - various
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27
Q

What are the main drugs in the classes of VW system?

A

Class I - Lidocaine
Class 2 - Atenolol
Class 3 - Amioderone
Class 4 - Verapamil

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28
Q

Which class of the VW system is further subdivided into a, b and c?

A

Class 1

29
Q

How do class 1 drugs in the VW system work?

A

They block sodium channels in a use-dependence manner (preferentially block open and inactivated channels). They share this mechanism with local anaesthetics

30
Q

Which class does lidocaine belong to and how is it administered?

A

Class 1b - IV because metabolised by the liver so not given orally

31
Q

What is lidocaine’s clinical use?

A

Ventricular dysrhythmia

32
Q

What class do procainamide and disopyramide belong to?

A

1a

33
Q

What class does flecainide belong to?

A

1c

34
Q

Class 1c drugs are useful in preventing paroxysmal atrial fibrillation. True or false?

A

True

35
Q

Class 1c drugs should be used after heart attacks. True or false?

A

False - avoid after heart attacks - sudden death likely

36
Q

B1 antagonists are particularly useful if sympathetic nervous system is involved in dysrhythmia. True or false?

A

True

37
Q

B1 blockers are useful for supraventricular and ventricular disrhythmia. True or false?

A

True

38
Q

What are the unwanted side effects of beta blockers?

A 
Bronchoconstriction 
Heart block
Hypoglycaemia 
Cold extremities
Vivid dreams
39
Q

What is one of the weaknesses of VW system?

A

Some drugs act by more than one mechanism

40
Q

How does amiodarone work?

A

By blocking potassium channels (also blocks sodium and calcium)

41
Q

What is amiodarone useful for treating?

A

Supraventricular, ventricular dysrhythmias and WPW syndrome, AF

42
Q

How do potassium channel blockers work in reducing heart rate?

A

Potassium channel activation contributes to repolarisation so by blocking the channels, action potentials are prolonged and so is the refractory period therefore there is a decrease in heart rate

43
Q

Which drug is an analogue of the thyroid hormone?

A

Amioderone

44
Q

Amioderone is very lipophilic. True or false?

A

True

45
Q

What are the ways in which amioderone is administered?

A

Orally or IV into a central vein

46
Q

Although amioderone reduces heart rate, it alters the force of contraction, which isn’t good. True or false?

A

False - doesn’t alter the force of contraction

47
Q

What does cardiac rhythm depend on?

A

Ion channel activity and calcium ion concentration

48
Q

What is the structure of calcium channels (and sodium channels)?

A

Large proteins formed from an alpha subunit and a beta subunit. The alpha subunit consists of 4 pseudo-subunits.
The pseudo-subunits have 6 transmembrane domains with a membrane dipping domain between the 5th and 6th transmembranes.
The 4th transmembrane is charged and acts as a voltage sensor

49
Q

Voltage gated channels can exist in three states. What are they?

A

Resting
Open
Inactivated

50
Q

What is verapamil used for?

A

Prophylactically for paroxysmal supraventricular tachycardia and also in patients with AF to decrease ventricular rate

51
Q

Is Verpamil safe to use for patients with WPW?

A

No - dangerous

52
Q

Class IV drugs act on which type of calcium channel?

A

L-type

53
Q

What are unwanted side effects of amiodarone?

A

Thyrotoxicosis
Hepatoxicity
Bradycardia
Micro-crystals in the cornea

54
Q

What are the major side effects of verapamil?

A

AVN block

Reduction in CO

55
Q

Which drug has a mechanism of reducing after-depolarisations?

A

Verapamil

56
Q

What causes after-depolarisations to take place?

A

Build up of calcium in cell due to repeated stimulation which triggers chain of APs

57
Q

Ziconotide is a drug that blocks which type of calcium channel?

A

N-type

58
Q

What are weaknesses of VW system?

A

Excludes some potential sites for antidysrhythmic drugs
Doesn’t allow for the fact that some drugs have multiple mechanisms of action
Does not all for the fact that drug action on diseased tissue may differ from that on healthy tissue

59
Q

What is digoxin used for?

A

Heart failure

60
Q

Antidysrhytmic effects of digoxin are largely mediated by which nerve?

A

Vagus

61
Q

Ziconotide requires intrathecal delivery. True or false?

A

True

62
Q

Ziconotide has a narrow therapeutic window. True or false?

A

True

63
Q

How does digoxin work?

A

It increases vagus nerve activity which:
reduces SAN firing rate
reduces AVN conduction velocity
reduces ventricular rate

64
Q

Digoxin has a narrow therapeutic index. What happens if it is given at a toxic dose?

A

Increases sympathetic tone - dysrhythmia -
depolarisation
increases afterdepolarisations
increases ectopic beats

65
Q

How is digoxin toxicity treated?

A

Stop digoxin administration
Correct hypokalaemia by giving KCl orally/infusion
Give propranolol/phenytoin

66
Q

How does adenosine work?

A

Activation of adenosine leads to activation of K+ channels and so hyperpolarisation, reducing AP duration and inhibiting Ca2+ channels.

67
Q

What can adenosine be used for?

A

Supression of:
Supraventricular tach
Ventricular tach - WPW
PSVT

68
Q

Why can’t adenosine be used chronically?

A

Because it’s plasma half life is 10s

PHAR20300 (25 decks)

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