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Systemic Pharmaco > Anti-Arrhythmics > Flashcards

Anti-Arrhythmics Flashcards

1
Q

What is the resting membrane potential?

A

-70mV

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2
Q

What ions are responsible for maintaining the resting membrane potential? Do they have a higher intracellular or extracellular concentration?

A

K+: high intracellular

Na+, Ca2+, Cl-: high extracellular

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3
Q

How many action potential phases are in the normal sinus rhythm?

A

Phase 0 to phase 4

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4
Q

What happens in each action potential phase?

A

Phase 0: Upstroke

  • Na+ channel opens, Na+ enters cell
  • RMP becomes more positive

Phase 1: Early-fast repolarisation

  • Transient outward K+ channel, K+ exits cell
  • RMP becomes a bit more negative

Phase 2: Plateau

  • Ca2+ channel opens, Ca2+ enters cell
  • RMP prevented from being more negative (exiting K+) by entry of Ca2+

Phase 3: Repolarisation

  • Inward rectifying K+ channels open, K+ continues to moves out of cell
  • RMP becomes more negative

Phase 4: Diastole
- Cell undercomes complete relaxation

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5
Q

What is the effective refractory period (ERF)? It lasts throughout which action potential phases?

A

Phase 0 to Phase 3 (just before Phase 4)

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6
Q

What is the importance of the ERF?

A

Important to prepare muscles for depolarisation. Another action potential cannot be generated during this time

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7
Q

What is the action potential duration (APD)? It lasts throughout which action potential phases?

A

Phase 0 to Phase 4

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8
Q

What is the importance of the APD? What is the difference in duration btwn ERP and APD?

A

Theoretically, don’t have to wait for Phase 4 to have another action potential, it can occur immediately after ERP but this is abnormal.

Physiologically, APD is longer than ERP

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9
Q

What does the P wave in an ECG represent?

A

Atrial depolarisation

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10
Q

What does the PR internal in an ECG represent?

A

The time between the onset of atrial depolarisation and ventricular depolarisation

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11
Q

What does the QRS complex represent in an ECG?

A

Ventricular depolarisation

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12
Q

What does the QT interval in an ECG represent? What is the significance of this?

A

Ventricular depolarisation and repolarisation

It is a rough estimate of the duration of an ventricular action potential from Phase 0 to Phase 4

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13
Q

What is excitability?

A

The cell can change its internal electrical balance to reach threshold.

Mechanism for depolarisation to occur.

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14
Q

What is automaticity?

A

The cell can generate an electrical impulse without being stimulated (automatic).

Mechanism for basal depolarisation until threshold is reached

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15
Q

What is conductivity?

A

The cell can transfer an electrical impulse to the next cell.

Mechanism for spread of depolarisation.

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16
Q

What are the classes of anti-arrhythmic drugs?

A

Class 1A, 1B, 1C: Na+ channel blockers

Class II: ß-blocker

Class III: K+ channel blocker

Class IV: Ca2+ channel blocker

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17
Q

What is an example of a Class 1A Na+ channel blocker?

A

Procainamide

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18
Q

What is the MOA of procainamide?

A
  1. Reduce rate of Phase 0 depolarisation
  2. Prolong Phase 3 repolarisation
  3. Reduce conductivity and automaticity
  4. Increase ERP and APD
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19
Q

What is an example of a Class 1B Na+ channel blocker?

A

Lidocaine

20
Q

What is the MOA of lidocaine?

A
  1. Reduce rate of Phase 0 depolarisation
  2. Shorten Phase 3 repolarisation
  3. Reduce automaticity (little effect on conductivity)
  4. Reduce APD
    - APD becomes shorter than ERP (usually APD longer than ERP)
  5. No change in ERP
21
Q

What is an example of a Class 1C Na+ channel blocker?

A

Flecainide

22
Q

What is the MOA of flecainide?

A
  1. Reduce rate of Phase 0 depolarisation
  2. Shorten Phase 3 repolarisation (but not as much as Class 1b)
  3. Reduce conductivity and automaticity
  4. No/little effect on APD/ERP
23
Q

What is the clinical use of flecainide?

A

(not a 1st line drug)

Refractory ventricular tachycardias that tend to progress to VF

24
Q

What is an adverse effect of flecainide?

A

Can lead to sudden death if there is existing ischaemia

25
Q

What are the Class II ß-blockers?

A

Metoprolol, Propranolol

26
Q

What is the MOA of Class II ß-blockers?

A
  1. Reduce/suppress phase 4 depolarisation (slope)
  2. Reduce automaticity
  3. Prolong AV conduction
  4. Reduce HR and contractility (indirect effects on Ca2+ channels)
    - Blocks ß1 receptors in cardiac myocytes  reduces CICR
  5. No change to APD & ERP
27
Q

What are the clinical uses of Class II ß-blockers?

A
  1. Tachycardia caused by sympathetic activation
  2. Atrial fibrillation
  3. AV nodal re-entrant tachycardia
  4. Reduces sudden arrhythmic death (*only med that does this!)
    - Protective
    - Reduces long-term mortality
28
Q

What are the Class III K+ channel blockers?

A

Amiodarone

29
Q

What is the MOA of amiodarone? What other actions does it have?

A
  1. Prolongs Phase 3 repolarisation (no Phase 0 effect)
  2. Increases ERP and APD

Actions w properties of all 4 classes:
1. Block inward rectifying K+ channels Ikr and Iks – Class III (main)

  1. Block Na+ channels (although no Phase 0 effect) – Class I
  2. Block adrenergic receptor – Class II
  3. Block Ca2+ channels – Class IV
30
Q

What is the bioavailability of amiodarone?

A

35-65%

31
Q

How is amiodarone metabolised? Is it metabolised to an active or inactive form?

A

Hepatic metabolism to desethylamiodarone (bioactive)

32
Q

How is amiodarone eliminated? What is the 1/2 life?

A

Eliminated by liver, H½:

  • 3-10d (first 50%)
  • Several weeks (second 50%)
33
Q

After discontinuation, the effects of amiodarone are maintained for how long?

A

1-3 months

34
Q

What are the clinical uses of amiodarone?

A
  1. Maintaining normal sinus rhythm in patients with atrial fibrillation
  2. Prevent re-entrant ventricular tachycardia
35
Q

What are the adverse effects of admiodarone?

A
  1. Symptomatic bradycardia

2. Heart block

36
Q

What are the Class IV non-DHP Ca2+ channel blockers?

A

Verapamil, Diltiazem

37
Q

What is the MOA of Class IV non-DHP Ca2+ channel blockers?

A
  1. Prolong Phase 4 depolarisation (direct Ca2+ channel effect)
  2. Reduce conductivity on AV node
  3. Increase ERP and APD
38
Q

What are the clinical uses of verapamil?

A
  1. Supraventricular tachycardia
  2. Hypertension
  3. Angina
39
Q

What is an adverse effect of verapamil?

A

Hypotension

40
Q

What is the contraindication of verapamil?

A

Pts w pre-existing depressed cardiac function (cardiac failure)

41
Q

What other drug is used as an anti-arrhythmic but is not formally classified as a class?

A

Adenosine

42
Q

What is the MOA of adenosine? When is it used?

A
  1. Suppress atrioventricular nodal conduction (used in emergency)
  2. Increase AV nodal refractory period
  • Stimulates cardiac K+ channel (KACh)
  • Inhibits Ca2+ current
43
Q

What is the half life of adenosine in blood (infusion)?

A

<10s

44
Q

What is a clinical use of adenosine?

A

Supraventricular tachycardia

45
Q

What are the adverse effects of adenosine?

A
  1. Flushing
  2. SOB, chest burning
  3. Induction of AV block or AF
  4. Headache
  5. Hypotension

Systemic Pharmaco (6 decks)

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