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ESA4 - Clinical Pharmacology > Anti-Arrhythmic Drugs > Flashcards

Anti-Arrhythmic Drugs Flashcards

1
Q

What is an arrhythmia?

A

Arrhythmias are a group of conditions in which the heart beat is irregular, too fast or too slow - this results in the rate and/or timing of cardiac contraction that is insufficient to maintain normal cardiac output

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2
Q

What are the symptoms of arrhythmias?

A

If any:

Palpitations, syncope, dizziness

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3
Q

What are the 4 main types of arrhythmia?

A
  • Supraventricular tachycardia (eg a fib, atrial flutter)
  • Ventricular arrhythmias (eg v fib, ventricular tachycardia)
  • Extra beats (premature atrial or ventricular contractions)
  • Bradyarrhythmias
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4
Q

What happens in phase 0 of the fast cardiac action potential?

A

Influx of Na+ - depolarisation

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5
Q

What happens in phase 1 of the fast cardiac action potential?

A

Rapid inactivation of Na+ channels

Transient opening of K+ channels, K+ out of cell

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6
Q

What happens in phase 2 of the fast cardiac action potential?

A

Opening of L type calcium channels
Movement of Ca2+ into the cell, which is very very slowly repolarising
This phase is responsible for the large duration of the AP

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7
Q

What happens in phase 3 of the fast cardiac action potential?

A

Rapid repolarisation phase

L type calcium channels close

K+ moves out of the cell

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8
Q

What is happening in phase 4 of the fast cardiac action potential?

A

This is diastole

In the standard non-pacemaker cell the voltage is roughly -90mV

Maintained by Na/K/ATPase which moves 3 Na+ out of the cell and 2 K+ in

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9
Q

Which cardiac cells do fast action potentials occur in?

A

Non pacemaker cells eg ventricular myocytes

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10
Q

What are Class I antiarrhythmics?

A

Sodium channel blockers

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11
Q

Give 3 examples of Class I antiarrhythmics

A 
Quinidine (class Ia)
Lidocaine (class Ib)
Flecainide (class Ic)
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12
Q

What are class II antiarrhythmics?

A

Beta blockers

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13
Q

Give two examples of class II antiarrhythmics

A

Propranolol, bisoprolol

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14
Q

What are class III antiarrhythmics?

A

Potassium channel blockers

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15
Q

Give 2 examples of class III antiarrhythmics

A

Amiodarone, sotalol

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16
Q

What are class IV antiarrhythmics?

A

Calcium channel blockers

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17
Q

Give an example of a class IV antiarrhythmic

A

Verapamil

18
Q

What are class V antiarrhythmics?

A

Additional antiarrhythmic drugs like adenosine and digoxin

19
Q

What is meant by use-dependent block?

A

Only blocks voltage gated Na+ channels in open or inactive state so preferentially blocks damaged depolarised tissue

20
Q

Describe the action of Class I antiarrhythmics on depolarisation

A

Block the fast sodium channels responsible for the rapid depolarisation (phase 0) of the fast cardiac APs.

Decreases amplitude of AP as reduces slope

Decreases conduction velocity in non-nodal tissue

21
Q

Why do class I agents have no effect on nodal tissue?

A

Act on sodium channels that are responsible for phase 0 of the fast action potential, nodal tissue uses slow action potential

22
Q

Why are there 3 subtypes of class I antiarrhythmics?

A

This is because some sodium channel blockers increase the effective refractory period, some decrease it and some have no effect

Class Ia - increase ERP
Class Ib - decrease ERP
Class Ic - no effect on ERP

23
Q

What are the overall mechanisms of action of class I antiarrhythmics?

A
  • Block sodium channels
  • Class Ia increases ERP, class Ib decreases ERP, class Ic has no effect on ERP
  • Decrease automaticity
24
Q

How do the subtypes of class I antiarrhythmics differ in their efficacy for reducing the slope of phase 0?

A

Ic > Ia > Ib

25
Q

What are the side effects of class I antiarrhythmics?

A

Class Ia - hypotension, proarrythmia, GI effects

Class Ib - Abdominal upset, dizziness

Class Ic - proarrythmia, CNS and GI effects

26
Q

What effects can quinidine (class Ia) have on an ECG?

A

Increased QRS
Longation of QT
+/ PR prolongation

27
Q

What effects can lidocaine (class Ib) have on an ECG?

A

Increased QRS in fast beating/ischaemic tissue

28
Q

What is the mechanism of action of lidocaine?

A

Class Ib - sodium channel blocker

Increased depolarisation threshold making the heart less likely to initiate or conduct early APs that may cause an arrythmia

29
Q

How does flecainide work?

A

Class Ic - sodium channel blocker, slows upstroke of cardiac AP

Greatest effect on His-Purkinje system and ventricular myocardium

Effect increases as the HR increases (use-dependence)

30
Q

How do propanolol and bisoprolol differ in terms of selectivity?

A

Propanolol affect b1 and b2 but bisoprolol mostly affects b1 (more cardioselective)

31
Q

What are the cardiac effects of class II agents?

A

Increased APD and refractory period in AV node to slow AV conduction velocity

Decrease phase 4 depolarisation (catecholamine dependent)

32
Q

What effects can a class II agent have on ECG?

A

Increased PR, decreased HR

33
Q

What are the side effects of class II agents?

A

Bronchospasm (beware patients with asthma)
Hypotension

*Don’t use in partial AV block

34
Q

What are the cardiac effects of amiodarone?

A

Increase refractory period
Increased APD
Decreased speed of AV conduction

35
Q

What effects can amiodarone have on ECG?

A

Increased QT, increased PR, increased QRS, decreased HR

36
Q

What are the side effects of amiodarone?

A

Pulmonary fibrosis, hepatic injury, increased LDL, thyroid disease, photosensitivity

37
Q

What are the cardiac effects of class IV agents?

A

Slows conduction through AV node
Increases refractory period in AV node
Increases slope of phase 4 in SAN to slow HR

38
Q

What effects can a class IV agent have on ECG?

A

Increased PR

Increased or decreased HR depending on blood pressure response and baroreflex

39
Q

What are the side effects of class IV agents?

A

GI effects, hypotension

40
Q

How is adenosine administered?

A

Rapid IV bolus

41
Q

What are the cardiac effects of adenosine?

A

Decreases APD, hyperolarisation, increases refractory period in AV node

Slows AV conduction!

42
Q

How does digoxin work as an antiarrhythmic?

A

Slows AV conduction and HR

Inhibits Na/K/ATPase - increases intracellular Na+ which decreases NCX and increases Ca2+

This lengthens phase 4 and phase 0 of AP which decreases HR

ESA4 - Clinical Pharmacology (20 decks)

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