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CPT > Lecture 8 - Antiarrhythmics > Flashcards

Lecture 8 - Antiarrhythmics Flashcards

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1
Q

What is the process of generating an action potential in a cardiac myocyte?

A

AP arrives from neighbouring cells
VG Na+ channels open
Na+ influx (rapid upstroke)
Slight repolarisation as K+ efflux occcurs
Plateau happens as Ca2+ start to be influxed and K+ continues to be effluxed
VG Ca2+ channels close and VG K+ channels open K+ continues to be effluxed so rapid repolarisation occurs
VG K+ channels close
RMP is returned to and maintained by Na/K+ ATPase

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2
Q

Go to slide 4:

Describe what’s happening in Step 0 of the Cardiac myocyte AP:

A

AP arrives from neighbouring cells
VG Na+ channels open
Na+ influx (rapid upstroke/depolarisation)

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3
Q

Go to slide 4:

Describe what’s happening in Step 1 of the Cardiac myocyte AP:

A

Slight repolarisation as K+ efflux occcurs

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4
Q

Go to slide 4:

Describe what’s happening in Step 2 of the Cardiac myocyte AP:

A

Plateau happens as Ca2+ start to be influxed and K+ continues to be effluxed

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5
Q

Go to slide 4:

Describe what’s happening in Step 3 of the Cardiac myocyte AP:

A

VG Ca2+ channels close and VG K+ channels open K+ continues to be effluxed so rapid repolarisation occurs

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6
Q

Go to slide 4:

Describe what’s happening in Step 4 of the Cardiac myocyte AP:

A

Voltage gated K+ channels close
RMP is returned to and maintained by Na/K+ ATPase

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7
Q

What principle generates the pacemaker potential at the SAN?

A

Funny current

Where HCN channels are always open leading to gradual movemtn of Na+ into the SAN cells

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8
Q

What are the stages to generating an action potential in the SAN (Pacemaker potential)?

A

HCN channels are open so Na+ gradually moves into SAN cells producing the Funny Current
Once threshold met, rapid depolarisation/upstrokek occured due to Ca2+ influx through L-Type voltage gated calcium channels
At peak, Voltagee gated Ca2+ channels close and Voltage gated K+ channels open allowing K+ efflux so REPOLARISATION occurs

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9
Q

What is the 4 main classes of Anti-arrhythmetic drugs in the Vaughan Williams classification?

A

Class I (Voltage gated Na+ channel Blockers)
Class II (Beta blockers)
Class III (Voltage gated K+ channel Blockers)
Class IV (Calcium Channel Blocker)

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10
Q

What are the 3 classes of Class I anti-arrhythmetic drugs?

A

Class 1A
Class 1B
Class 1C

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11
Q

What is the best example of a Class 1B anti-arrhytmetic?

What channels does it block?

A

Lidocaine

Voltage gated Sodium channels

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12
Q

What is the best example of a Class 1C anti-arrhythmetic drug?

What channel does it block?

A

Flecainide

Voltage gated sodium channels

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13
Q

What is the general principle for how Class I anti-arrhythmetic drugs work?

A

Block the VG sodium channels slowing the intital upstroke/making it take longer for the upstroke/rapid depolarisation to occur in the cardiac myocytes

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14
Q

How do Class IB anti-arrythmetics work?

What is an example of a Class IB anti-arrhythmetic?

A

Target cardiac myocytes ONLY IN VENTRICLES

Causes a blockade of VG Na+ channels preventing additional impulses occurring

Lidocaine

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15
Q

What type of tissue do Class IB preferentially target?

Give an example of a Class IB anti-arrhthymetic:

So what condition is it good for?

A

Damaged heart tissue

Lidocaine

Myocardial Infarction

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16
Q

What is the relative speed by which Class IB anti-arrhthymetics dissociate from the voltage gated sodium channels?

A

Rapidly dissociate/unblock

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17
Q

How does the action of Class IC anti-arrhythmetics differ to Class IB?

Give an example of a Class IC anti-arrhythmetic:

A

The rate of Na+ ion influx is slowed much more strongly than class IB
So depolarisation occurs later than with Class IB (Lidocaine)

Example = Flecainide

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18
Q

What interval do the Class IC anti-arrhythmic drugs affect but this interval is impacted much less than Class IB since the Na+ ion influx happens sooner?

A

QRS interval prolonged with Class IC

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19
Q

What is not affected on an ECG with Class IB anti-arrhythmics but IS with Class IC?

Why is this the case?

A

QRS interval

The Class ICs delay the upstroke of the QRS way more than Class IBs (class IBs dont prolong it enough)

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20
Q

What part of the heart do Class II (beta blockers) target/bind to?

A

SAN

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21
Q

How do Class II anti-arrythmics affect the heart?
(Beta blockers)

A

Decrease the gradient of the funny current (since blocking the B-adrenoceptors reduces sympathetic tone and so inversely increases parasympathetic tone) = slower heart rate

Decreased uptake of of Calcium (leads to weaker contractions)

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22
Q

What is an example of a Class II anti-arryhthmic?

A

Beta blocker

Bisoprolol
Atenolol

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23
Q

What type of anti-arrhythmic is a Class III anti-arrhythmic?

A

K+ Channel blocker

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24
Q

What is the best example of a Class III anti-arrhythmic? (K+ channel blocker)

A

Amiodarone

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25
Q

What part of the heart do Class III K+channel blockers affect?

A

Cardiac myocytes

26
Q

What is the effect of Class III anti-arrhythmics (K+ channel blockers) on the action potential cycle?

A

Prolongs repolarisation (by preventing the K+ efflux)

27
Q

What interval on the ECG do Class III K+ channel blockers affect?

What is an example of a Class III anti-arrhythmic?

A

Prolongs the QT interval
Since it prolongs repolarisation

Amiodarone

28
Q

What are 2 examples of Class IV anti-arrhythmics?

What type of drug are these?

A

Calcium channel blockers (Non dihydropyridines)

Verapamil = phenylalkylamine
Diltiazem = benzothizapine

29
Q

What part of the heart do Class IV (Ca2+ channel blockers) target?

A

SAN
+
Cardiac myocyets
So affects pacemaker potential

30
Q

How do Class IV anti-arrhythmics work?

What are 2 examples?

A

SAN:
Block L-type voltage gated Ca2+ channels
This slows the speed at which the depolarisation/upstroke happens once the threshold potential has been reached

Cardiac myocytes:
Blocks the L-type voltage gated Ca2+ channels which prolongs the plateau phase due to the Ca2+ channel blockade

Verapamil
Diltiazem

31
Q

How do Class IV calcium channel blockers prolong the plateau phase in cardiac myoctes?

A

Reduced rate of influx of Ca2+ leads to a decreased rate of efflux of K+ which leads to a prolonged plateau phase

32
Q

Which class of drug prolongs the QT interval?

What is an example of this drug?

How does it do so?

A

Class III (K+ channel blocker)

Amiodarone

Blocks the K+ channels slowing down/prolonging repolarisation

Repolarisation is the QT interval

33
Q

What drug class causes QRS prolongation?

How does it do this?

What is an example?

A

Class IC

Delays QRS upstroke (Na+ influx) from happening lenghthening the QRS interval

34
Q

What is represented by the PR interval?

A

The time taken for the AV node to conduct the electrical impulse from the atria to the ventricles

35
Q

What classes of anti-arrhythmics prolong the PR interval and so work at the AV node?

A

Beta blockers (Class II)

Calcium Channel blockers (Class IV)

36
Q

What is the negative effect of Amiodarone (Class III) prolonging the QT interval?

A

Can induce arrhythmia

By prolonging the QT interval/repolarisation time too much you increase the risk of getting early after depolarisations and so arrhythmias

37
Q

What are 3 examples of anti-arrhythmic medications that dont fit in the 4 classes?

A

Digoxin
Ivabradine
Adenosine

These are considered Class V drugs (miscellaneous)

38
Q

What class of drug is Digoxin?

A

Cardiac glycoside

39
Q

How does digoxin work as an anti-arrhythmic drug?

A

AV node blockade (slows AVN transmission)

Stops the Na+/K+ ATPase leading to activity of the Na+/Ca2+exchanger to cease so levels of Ca2+ in the cells increase increasing the strength of contraction (+ve inotropy)

40
Q

What is digoxin typically used for?

A

Heart failure
Arrhythmias

41
Q

How does Ivabradine work as an anti-arrhythmic?

A

Slows heart rate

Inhibts the pacemaker current at the SAN so slows the rate at which the threshold potential is reached slowing heart rate

42
Q

When is Ivabradine typically used?

A

Angina
Coronary disease
Arrhythmias

43
Q

How does Adenosinei work to treat arrhythmias?

A

Stimulates A1 adenosine receptors at the AV node blocking the AV node preventing/reducing impulse travelling from atria to ventricles

This reduces rate of contraction of ventricles

44
Q

What is adenosine typically used to treat?

A

Supraventricular tachycardia when the heart is beating extremely fast to the point you cant see what the atria are doing on an ECG

45
Q

How long does adenosine last for as an anti-arrhythmic?

A

Couple seconds (very short lasting)

46
Q

What is a contraindication of using class I anti-arrhythmics like Flecainide?

A

Structural heart diseases (changes that occur following MI) since it increases risk of arrhythmias

47
Q

What is a contraindication of using Class II anti-arrhythmics?

A

Consider alternate treatments like CCB (verapamil or diltiazem) if ASTHMATIC

Don’t prescribe with Diltiazem or verapamil

48
Q

Why shouldn’t you prescribe Class II anti-arrhythmias with diltiazem or verapamil?

A

Beta blockers also work on the SAN like the calcium channel blockers (non-dihydropyridines) verapamil and diltiazem

49
Q

What is a contraindication for using class IV anti-arrhythmics (CCB)?

A

HFrEF

50
Q

What are the negative side effects/adverse effects of Class III anti-arrhythmics like Amiodarone?

A

Hepatotoxic
Lung fibrosis
Optic neuritis
Thyroid toxicity
Peripheral neuropathy

51
Q

What is a very effective drug for putting the heart back into sinus rhythm?

A

Amiodarone

52
Q

What are the 2 general ways we get arrhythmias?

A

Generate abnormal impulses (ventricular ectopics)

Or

Conduct impulses abnormally (heart block, re-entry loops or accessory pathways)

53
Q

What is atrial fibrillation?

A

Irregularly irregular contractions/electrical activity of the atria

54
Q

What are the 2 methods by which you can try and stop an atrial fibrillation?

A

Rate control

Rhythm control

55
Q

What is meant by rate control for trying to treat Atrial fibrillation?

A

Slow the rate of transmission from atria to the ventricles

56
Q

What is meant by rhythm control for trying to treat Atrial fibrillation?

A

Stop the abnormal rhythm

57
Q

If we are trying to reduce rate of excitation in atrial fibrillation, what heart structure do we need to target?

A

AV node (needs blocking)

58
Q

What are some drugs that can block the AV node to control rate for Atrial fibrillation?

A

Adenosine (TOO SHORT LASTING, Afib will come back)

CCB (depending on HF status)

B-Blocker (depends on asthma status)

Digoxin (depends of exercise tolerance, lots of exercise people don’t tolerate well)

59
Q

What drugs can be used to terminate the rhythm of Atrial Fibrillation?

A

Flecainide
Amiodarone
Sotalol
Cardio version

60
Q

What type of control, rate or rhythm is best for treating an atrial fibrillation?

A

Young = rhythm control

Most = rate control

61
Q

What class of anti-arrhythmic is sotalol?

A

Class III not Class II

CPT (30 decks)

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