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Cardiovascular: pharmacology > Arrhythmias and Anti-arrhythmic drugs > Flashcards

Arrhythmias and Anti-arrhythmic drugs Flashcards

1
Q

There are two main electrical dysfunction mechanisms. You can have defects in impulse ______ or impulse ______.

A

There are two main electrical dysfunction mechanisms. You can have defects in impulse formation or impulse conduction.

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2
Q

what are the two defects in Impulse formation?

A
  1. SA node automaticity is interrupted or altered (missed beats, ectopic beats)
  2. triggered activity
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3
Q

There are physiological ways that the SA node activity is modulated e.g. by the ANS (e.g. sinus tachycardia, sinus arrhythmia (this is quite common in _____ people)
However it is also pathological - for example ____ _______.

A

There are physiological ways that the SA node activity is modulated e.g. by the ANS (e.g. sinus tachycardia, sinus arrhythmia (this is quite common in young people)
However it is also pathological - for example latent pacemakers.

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4
Q

what are latent pacemakers?

A

these are pacemakers outwith the SA node which are just waiting to take over the pacemaking activity i.e overdrive suppression is lost.

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5
Q

which two circumstances allow latent pacemakers to activate?

A
  1. when the SA node AP firing frequency is pathologically low or when there is a problem with the conduction of the SA node
  2. might also occur if a latent pacemaker firs at a rate which is faster than the SA node firing rate.
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6
Q

with a low SA node firing frequency you get an ______ escape beat - latent pacemaker initiates the impulse e.g. the AP is not generated by SA node activity, it has escaped the normal overdrive.

A

escape beat - latent pacemaker initiates the impulse e.g. the AP is not generated by SA node activity, it has escaped the normal overdrive.

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7
Q

when might SA node firing frequency be low?

A

during intense vagal stimulation

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8
Q

with a fast latent pacemaker firing frequency you get an ____ beat

A

ectopic

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9
Q

give some causes of an ectopic rhythm

A

ischaemia, hypokalaemia, increased sympathetic activity, fibre stretch

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10
Q

what are the two kinds of triggered activity?

A

EAD, DAD

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11
Q

which part of the heart often causes EAD?

A

the purkinje fibres

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12
Q

during which two phases do EADs incite the AP?

A

phase 2 (terminal plateau) and phase 3 (repolarisation)

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13
Q

In phase 2 what is the EAD mediated by ?

A

Ca channels - the repolarisation happens quicker than it would normally

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14
Q

In phase 3 what is the EAD mediated by ?

A

Na channels - they recover from inactivation

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15
Q

what is EAD associated with?

A

prolongation of AP and drugs (e.g. sotalol) prolonging the QT interval (the interval between depolarisation and repolarisation).

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16
Q

what dangerous rhythm can EAD lead to?

A

ventricular fibrillation

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17
Q

when do DADs occur?

A

after complete repolarisation

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18
Q

what are DADs associated with?

A

Ca overload

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19
Q

what provokes the Ca overload in DAD?

A

catecholamines, digoxin, heart failure

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20
Q

what are the three mechanisms for defects in impulse conduction?

A

re-entry, conduction block, accessory tracts

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21
Q

what is re-entry?

A

a self sustaining electrical circuit (anatomically may be due to parallel conduction pathways) which stimulates an area of myocardium repeatedly/ rapidly

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22
Q

re-entry
1. normal conduction:
We have a conduction pathway in the heart (possibly the purkinje fibres) which divides into two branches. There is a ______ area between the two branches. APs will travel down both branch 1 and 2 and from these branches they will enter into a mass of _____. The APs try to negotiate their way around the ____ area and this is not normally a problem. The two APs from branch 1 and 2 then meet in the ____ and ______ each other

A

We have a conduction pathway in the heart (possibly the purkinje fibres) which divides into two branches. There is a non-excitable area between the two branches. APs will travel down both branch 1 and 2 and from these branches they will enter into a mass of ventricle. The APs try to negotiate their way around the non-excitable area and this is not normally a problem. The two APs from branch 1 and 2 then meet in the middle and extinguish each other

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23
Q

Re-entry
2. abnormal conduction:
There is _______ conduction block meaning that the AP in branch 1 is ____ but the AP in branch 2 _____ ____ forward - (anterograde conduct).

A

There is unidirectional conduction block meaning that the AP in branch 1 is fine but the AP in branch 2 cannot conduct forward - (anterograde conduct).

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24
Q

re-entry conditions are satisfied if

  • the AP is not allowed to progress down its normal direction of branch i.e. unidirectional block - anterograde conduction ______
  • the AP can go in the wrong direction but _____ slowly. The AP goes down branch 1, it then goes round the island of non-conducting tissue however, there is no _______ of AP. The AP will continue in a right hand direction but will also go up branch 2 very slowly in a ______ conduction.
A
  • the AP is not allowed to progress down its normal direction of branch i.e. unidirectional block - anterograde conduction prohibited
  • the AP can go in the wrong direction but abnormally slowly. The AP goes down branch 1, it then goes round the island of non-conducting tissue however, there is no extinguishing of AP. The AP will continue in a right hand direction but will also go up branch 2 very slowly in a retrograde conduction.
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25
Q

why is the slow retrograde in re-entry important?

A

if means that branch 1 is no longer refractory - ie has recovered from inactivation so the AP meets excitable tissue once more without an impulse having to come from the point before branching

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26
Q

what is the movement of APs in a circle called?

A

circus movement

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27
Q

what is first degree AV block?

A

the tissue conducts all impulses but more slowly than usual

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28
Q

what happens in intermittent block?

A

the tissue conducts some impulses but not others - example second degree AV block

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29
Q

accessory tracts - some individuals possess electrical pathways that bypass the _____. Conduction through accessory pathways is relatively ____-

A

some individuals possess electrical pathways that bypass the AV node
conduction through accessory pathways is relatively rapid

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30
Q

name a common accessory tract pathway

A

bundle of kent

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31
Q

in accessory tracts the ventricles receive impulses from both the ____ and _____ pathways - can set up the condition for a ______ loop predisposing to tachyarrhythmias

A

ventricles receive impulses from both the normal and accessory pathways - can set up the condition for a re-entrant loop predisposing to tachyarrhythmias

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32
Q

name an antiarrhythmic drug which is not entirely selective blocker of Na, K or Ca channels

A

amiodarone

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33
Q

name two drugs which do not fit into the vaughn williams classification

A

adenosine and digoxin

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34
Q

what is the channel target for class 1 drugs ?

A

VA Na channels

35
Q

Class 1a:

associate and dissociate from Na channels at a______ rate. They ___ rate of rise of AP and_____ the refractory period

A

Class 1a:
associate and dissociate from Na channels at a moderate rate. They slow rate of rise of AP and prolong the refractory period

36
Q

Class 1b:

associate and dissociate from Na channels at a ____ rate. Prevent premature beats

A

Class 1b:

associate and dissociate from Na channels at a rapid rate. Prevent premature beats

37
Q

Class 1b:

associate and dissociate from Na channels at a ____ rate. Depress c______

A

Class 1b:

associate and dissociate from Na channels at a slow rate. Depress conduction

38
Q

name a class 1a drug

A

disopyramide

39
Q

name a class 1b drug

A

lignocaine

40
Q

name a class 1c drug

A

flecainide

41
Q

what is the channel target for class II drugs ?

A

beta adrenoceptors (as antagonists)

42
Q

what is the action of Class II

A

decrease the rate of depolarisation in SA and AV node

43
Q

name a class II drug

A

metoprolol

44
Q

what is the channel target for class III drugs ?

A

VA K channels (plus others)

45
Q

what is the action of Class III

A

prolong the AP duration - increasing refractory period

46
Q

name a class III drug

A

amiodarone

47
Q

what is the channel target for class IV drugs ?

A

VA Ca channels

48
Q

what is the action of Class IV

A

slow conduction in SA and AV nodes. Decrease the force of cardiac conduction

49
Q

name a class IV drug

A

verapamil

50
Q

which class of drugs are used in WPW?

A

classs 1

51
Q

what are the three conformational states that Na channels exist in? the relative time spent in each depend upon firing frequency

A
  1. resting - nonconducting state
  2. open (conducting state)
  3. inactivated (refractory period)
52
Q

Na channel: During high frequency firing (e.g. tachyarrhythmias) relatively more time is spent in the ____ and _____ states.

A

During high frequency firing (e.g. tachyarrhythmias) relatively more time is spent in the open and inactivated states.

53
Q

Class 1 agents bind preferentially to these targeting areas of the myocardium in which firing frequency is ____ in a use-dependent manner without preventing the heart from beating at normal frequencies.

A

Class 1 agents bind preferentially to these targeting areas of the myocardium in which firing frequency is highest in a use-dependent manner without preventing the heart from beating at normal frequencies.

54
Q

what do class I agents do to the conducting state?

A

they block it

55
Q

what do class I agents do to the inactivated state?

A

they stabilise it

56
Q

Class 1 agents dissociate from the Na channel when it is in the ____ state (i.e. during ____)

A

Class 1 agents dissociate from the Na channel when it is in the resting state (i.e. during diastole)

57
Q 
class I drugs: 
Thus, if heart rate increases, less time is available for \_\_\_\_\_\_ and more time available for \_\_\_\_\_\_. Steady state block increases, particularly for agents with slow dissociation rates. LIKE CLASS 1C.
A

Thus, if heart rate increases, less time is available for unblocking (dissociation) and more time available for blocking (association). Steady state block increases, particularly for agents with slow dissociation rates. LIKE CLASS 1C.

58
Q 
class I drugs 
In \_\_\_\_\_ myocardium, myocytes are partially depolarised and the action potential is of l\_\_\_\_\_ duration thus: 
- The inactivated state of the Na channel is available to Na channel blockers for a \_\_\_\_ period of time 
- The rate of channel recovery from block is \_\_\_\_\_\_
A

In ischaemic myocardium, myocytes are partially depolarised and the action potential is of longer duration thus:
The inactivated state of the Na channel is available to Na channel blockers for a greater period of time
The rate of channel recovery from block is decreased

59
Q 
class I drugs 
Collectively the higher affinity of Na channel blockers for the \_\_\_ and \_\_\_  states of the channel allows them to act \_\_\_\_\_  on ischaemic tissue and block an arrhythmogenic focus at its source. This is because ischaemic myocaytes   are partially \_\_\_\_ - and so ‘The inactivated state of the Na channel is available to Na channel blockers for a greater period of time’ as above.
A

Collectively the higher affinity of Na channel blockers for the open and inactivated states of the channel allows them to act preferentially on ischaemic tissue and block an arrhythmogenic focus at its source. This is because ischaemic myocytes are partially depolarised - and so ‘The inactivated state of the Na channel is available to Na channel blockers for a greater period of time’ as above.

60
Q

which classes of drugs are used for atria (rate control of SVT) ?

A

classes Ic and III

61
Q

which classes of drugs are used for ventricles ?

A

classes 1a Ib, II

62
Q

which classes of drugs are used for AV node (rhythm control of SVT) ?

A

adenosine, dogoxin, classes II, IV

63
Q

which classes of drugs are used for atria and ventricles, AV accessory pathways?

A

amiodarone, sotalol, classes Ia Ic

64
Q

what does adenosine do?

A

activates A1 adenosine receptors coupled to Gi which opens ACh senistive K channels (GIRK) just like ACh would

65
Q

adenosine ______ the AV node briefly so the slope of the pacemaker potential ______, suppressing impulse conduction

A

hyperpolarizes the AV node briefly so the slope of the pacemaker potential decreases , suppressing impulse conduction

66
Q

what is adenosine used to treat?

A

PSVT termination

67
Q

what causes PSVT?

A

re-entry involving the AV node SA node or atrial tissue

68
Q

with adenosine threshold does not changes - just the _______.

A

Threshold does not changes - just the time taken to reach it.

69
Q

what are some side effects of adenosine?

A

anxiety and sense of impending doom

70
Q

what does verapamil do?

A

blocks L-type Ca channels

71
Q

verapamil ____ conduction and _____ refractory period in ___ node and ________

A

slows conduction and prolongs refractory period in AV node and bundle of His

72
Q

what is verapamil used to treat?

A

atrial tachycardia, SVT, atrial fib and flutter, AVRT (wPW)

73
Q

at high doses what may verapamil cause?

A

heart block

74
Q

verapamil should be used with great caution in combination with other drugs that have a ____ inotropic effect - because these already suppress calcium in the cell.

A

It should be used with great caution in combination with other drugs that have a negative inotropic effect - because these already suppress calcium in the cell.

75
Q

what does lignocaine do?

A

rapidly blocks Na channels - blocks inactivated with little effect on open channels

76
Q

Due to rapid unblocking, lidocaine primarily affects Na channels in areas of the myocardium that discharge action potentials at a ____rate (e.g. ischaemic zone)

A

Due to rapid unblocking, this drug primarily affects Na channels in areas of the myocardium that discharge action potentials at a high rate (e.g. ischaemic zone)

77
Q

what is lidocaine used in?

A

ventricular arrhythmias - tachycardias

78
Q

disopyramide is used (orally) to prevent recurrent _____ _____, procainamide (IV) is used to treat ventricular arrhythmias following ___

A

disopyramide is used (orally) to prevent recurrent ventricular arrhythmias, procainamide (IV) is used to treat ventricular arrhythmias following MI

79
Q

what is fleccainide used for?

A

paroxysmal AF - it has a negative inotropic action and may trigger serious ventricular arrhythmias

80
Q

what are propranolol and atenolol used in treatment for?

A

supraventricular tachycardias- basically all of them, AF, AVNRT, AVRT

premature ventricular complex

81
Q

how do amiodarone and sotolol work?

A

they slow repolarization of the AP by block of voltage activated K channels and hence increase in AP duration and the effective refractory period

SUPPRESSES RE-ENTRY

82
Q

what is amiodarone used for treatment in?

A

stable VT, AF, AVNRT

83
Q

Amiodarone is effective when many other drugs have failed and reduces mortality after ____ and in ____

A

Amiodarone is effective when many other drugs have failed and reduces mortality after MI and in congestive heart failure

84
Q

what are some examples of the adverse effects of amiodarone

A
  • pulmonary fibrosis
  • thyroid disorders
  • photosensitivity reactions
  • peripheral neuropathy

Cardiovascular: pharmacology (6 decks)

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