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Drugs: From molecules to man > Antidysrhythmic Agents > Flashcards

Antidysrhythmic Agents Flashcards

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Organic Chemistry 101 flashcards
1
Q

Generally, how is the heart electrically controlled?

A

the SA node initiates the cycle, the AV relays the impulse to the ventricles.
Purkinje fibres and the bundle of His spread impulses through the ventricles

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2
Q

How are dysrhythmias classified?

A

based on the site of origin and the type of dysrhythmia

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3
Q

what are the 3 sites of origin for a dysrhythmia?

A

Atrial (supraventricular)
Junctional (supraventricular)
ventricular

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4
Q

what are the 3 types of dysrhythmia?

A
  • True arrythmias
  • Tachycardias
  • Bradycardias
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5
Q

what are true arrythmias?

A

very disorganised rhythm

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6
Q

what are tachycardias?

A

too fast HR

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7
Q

what are bradycardias?

A

too slow HR

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8
Q

What are the risk factors for dysrhythmias? (4)

A

CHD, heart valve disorders, blood chemistry disorders, drugs (beta blockers, psychotropics, sympathomimetrics, caffeine, amphetamines, cocaine, some antidysrhythmic drugs)

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9
Q

what are the 5 causes of Disrhythmias?

A 
ectopic pacemakers
delayed after depolarization
re-entry circuits 
congenital abnormalities
heart block
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10
Q

what are re-entry circuits?

A

when there’s an area of damaged tissue which conduct impulses better in one direction, resulting in a never-ending loop of conduction

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11
Q

what’s atrial fibrillation?

A

when HR speeds up
shown in ECG by misshapen P waves
serious but not immediately life-threatening
insufficient pumping to ventricles

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12
Q

what are ectopic pacemakers?

A

when cardiac tissue other than the SA node initiates heart beats

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13
Q

what’s delayed after depolarization?

A

build up of calcium in cells leading to a train of action potentials

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14
Q

what are congenital abnormalities causing dysrhythmias?

A

additional pathways between atria and ventricles

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15
Q

how can ectopic pacemakers be corrected?

A

surgically

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16
Q

what type of dysrhythmia do ectopic pacemakers tend to cause?

A

tachycardia

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17
Q

What’s Wollf-Parkinson White syndrome?

A

a congenital disorder of impulse control

causes an abnormal conducting bridge between atria and ventricles –> giant re-entry circuit

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18
Q

how is an atrio-ventricular block seen on an ECG?

A

several P waves in a row (atrial depolarization/contraction)
no QRS waves- (ventricular depolarization)
this means atrial contraction isn’t always being followed by ventricular contraction

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19
Q

What do Vaughan- Williams Class I drugs target?

A

sodium channels

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20
Q

what do vaughan williams Class II drugs target?

A

beta- 1 adrenoreceptors

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21
Q

what do vaughan williams class III drugs target?

A

Potassium channels

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22
Q

what do vaughan williams class IV drugs target?

A

Calcium channels

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23
Q

How is amiodarone classified by the vaughan-williams classification?

A

class III

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24
Q

how is Adenosine classified by the vaughan-williams system?

A

unclassified

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25
Q

What does Amiodarone do?

A

blocks K+ channels- prolonging the AP
this means that depolarisation doesn’t happen so quickly
also blocks Na+ (I) and Ca2+ (IV) channels

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26
Q

What can Amiodarone treat? (4)

A

Supraventricular and ventricular Arrhythmias
Wolff-Parkinson- White syndrome
Atrial fibrillation/flutter

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27
Q

How long does it take for a stable concentration of Amiodarone to be reached?

A

weeks/monthhs

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28
Q

How long does it take for Amiodarone to completely leave the system?

A

100s of days

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29
Q

how is Amiodarone administered?

A

orally or i.v. injection

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30
Q

give 3 side effects of Amiodarone (give 3)

A
  • Microcrystals in cornea (increased dazzle from lights)
  • phototoxic reaction from crystals turns skin slate grey
  • can damage/affect thyroid
  • hepatoxicity (liver damage)
  • Affects respiration
  • bradycardia/ conduction disturbances
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31
Q

How is Adenosine classified by the BNF?

A

useful for supraventricular arrhythmias

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32
Q

how is Adenosine classified by the Vaughan-Williams system?`

A

unclassified

33
Q

What can adenosine be used to treat? (3)

A
  • paroxysmal supraventricular tachycardia
  • ventricular tachycardia associated with Wolff- Parkinson- White syndrome
  • Supraventricular tachycardia that may occur during general anaesthesia
34
Q

what setting is adenosine used in?

A

hospital setting

35
Q

How quickly do the effects of adenosine occur after being administered?

A

20-30s

36
Q

give side effects of adenosine (4)

A
  • severe bradycardia (don’t use in heart block)
  • facial flushing (vasodilator)
  • chest pain
  • dyspnoea/ Bronchospasm- avoid in bronchial asthma
37
Q

give 3 weaknesses of the vaughan- williams system of drug classification

A
  • does not allow for the fact that drugs may have multiple mechanisms of action
  • does not allow for the fact that drug action of disease tissue may differ from that on healthy tissue
  • excludes some potential sites of dysrhythmic drug activities e.g. adenosine
38
Q

what do Vaughan- Williams class I drugs target?

A

Sodium channels

39
Q

Give an important example of a Vaughan- Williams class I drug

A

Lidocaine (Lignocaine)

40
Q

How precisely is lidocaine classified by vaughan williams?

A

Class 1b antidysrhythmic

41
Q

As well as treating dysrhythmias, what else can lidocaine be used for?

A

local anaesthetic

42
Q

How is pain perceived?

A

when bare nerve endings generate an AP that travels up the spinal cord to higher CNS centres to perceive pain.
This AP is activated by Na+ channel activation and terminated by deactivation of Na+ channels and delayed activation of K+ channels

43
Q

As well as Lidocaine, what are 2 other important local anaesthetics to know?

A

procaine and cocaine

44
Q

generally, what is the structure of local anaesthetics?

A

made up of an amine, linker and aromatic ring

45
Q

what is the linker in procaine?

A

ester

46
Q

what is the linker in cocaine?

A

ester

47
Q

what is the linker in lidocaine?

A

amide

48
Q

in procaine and cocaine, where in the body breaks down the ester bond?

A

the blood

49
Q

if the ester bond in procaine and cocaine is broken down in the blood, how does this effect the duration of action?

A

short duration of action

50
Q

in lidocaine, where in the body breaks down the amide bond?

A

the liver

51
Q

if the amide bond is broken down in the liver, how does this effect the duration of action?

A

long duration of action

52
Q

How many forms are local anaesthetics found in the blood?

A

2

53
Q

what are the 2 forms taken by local anaesthetics in the blood?

A

protonated and unprotonated

54
Q

In lower pH do local anaesthetics work better or worse?

A

worse

55
Q

How does the drug get into the cell and activate?

A

The unprotonated form has a lipophilic aromatic group which can travel through the lipid bilayer to enter the cell. This form is inactive, so needs to be protonated inside the cell to become active. (there’s an equlibrium inside and outside the cell between protonated and unprotonated drug)

56
Q

How are class I drugs divided?

A

into 1a, 1b and 1c (slightly different mechanisms)

57
Q

what are the side affects of Class I drugs?

A
  • Affects the CNS (suppresses it/ can cause convulsions)
58
Q

Due to the side affects of Class I drugs, what setting must they be used in and by whom?

A

hospital/ emergency setting by medical personnel

59
Q

what do Vaughan- Williams class II drugs target?

A

B1 Adrenoreceptors (Beta-Blockers)

60
Q

Give 2 examples of Beta-blocker (class II) drugs

A

Propranalol

Atenolol

61
Q

what line of treatment for cardiac arrhythmias are beta blockers?

A

2nd or 3rd

62
Q

what do beta-blockers do to treat arrhythmias?

A

slow the rate of SA node discharge and conduction through the AV node

63
Q

What do Vaughan- Williams class IV drugs target?

A

Calcium channels

64
Q

what do Vaughan-Williams class IV drugs do for arrhythmias?

A

slows SA and AV node conduction

65
Q

what type of arrhythmia causes do class IV drugs treat? (2)

A

after-depolarisation and ectopic pacemakers

66
Q

give 2 examples of class IV drugs

A

Verapamil and Diltiazem

67
Q

what type of Calcium channels do Veramil and Diltiazem treat?

A

L-type

68
Q

what are the clinical uses of Class IV drugs?

A
  • paroxysmal supraventricular tachycardia

- decrease ventricular rate in atrial fibrillation

69
Q

When can Class IV drugs be dangerous to use? (2)

A

in patients with ventricular dysrhythmias and Wolff-Parkinson-White

70
Q

what side effects can Class IV drugs cause? (give 3)

A
  • cardiodepression
  • hypotension
  • AV node block
  • Oedema
  • headache
  • constipation
71
Q

what are the 4 types of calcium channel?

A

L, T, N, P

72
Q

which calcium channels mostly affect the heart?

A

L and T

73
Q

which calcium channels mostly affect the Neuronal system?

A

N and P

74
Q

how many subunits do calcium channels tend to have?

A

at least 5

75
Q

what other channels are calcium channels structurally related to? (2)

A

Na+ and K+

76
Q

what is meant by a drug being use-dependent?

A

the degree of block is proportional to the rate of nerve stimulation

77
Q

what is meant by a drug being non use- dependent?

A

the degree of block is not related to the rate of nerve stimulatio

78
Q

What’s the surgery used to treat dysrhythmias?

A

Cardiac ablation surgery

79
Q

what does cardiac ablation surgery involve?

A

destroying and removing non-functional heart tissue

Drugs: From molecules to man (10 decks)

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