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CVS Pharmacology > Anti-Arrhythmics > Flashcards

Anti-Arrhythmics Flashcards

1
Q

Phases of cardiac potential: how many phases? What are they called?

A

Five phases from 0 - 4

0- rapid depolarisation
1- initial repolarization 
2- plateau phase
3- repolarization 
4- resting potential
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2
Q

What happens in Phase 0?

A

Results from rapid influx of Na+

Depolarisation raises resting membrane potential from -85mV to +20mV. At this point threshold potential has been reached and an all or none action potential response occurs.

Rapid influx Na+ raises membrane potential further to 20mV.

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3
Q

What happens in Phase 1?

A

Initial repolarization:
Voltage gated Na channels close as transmembrane potential becomes sufficiently positive.

Notch caused by transient outward K+ and inward Cl- movement.

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4
Q

What happens in Phase 2?

A

Inward movement of Ca+ ions through slow L-type Ca channels,

and outward movements of K+.

Cancel out each other, and only slow downward slope to repolarisation.

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5
Q

What happens in Phase 3?

A

Repolarization as calcium efflux slows/stops and

K+ movement out via concentration gradient via open K+ channels.

Relative refractory period.

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6
Q

What happens phase 3-4?

A

Resting membrane potential is re-established by 2K+ moving inwards for every 3Na+ outwards

Gives a net outward movement of positive charge.

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7
Q

Mechanisms of Arrhythmia generation (4)?

A
  1. Enhanced automaticity
  2. Abnormal automaticity
  3. Triggered activity
  4. Re-entry (circus movement)
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8
Q

what arrhythmias occur with

  1. enhanced normal automaticity
  2. Abnormal automaticity
  3. Triggered activity
A
  1. Inappropriate sinus tachycardia, by phase 4 depolarisation.
  2. Ectopic atrial tachycardia by phase 4 depolarisation
  3. Torsades de pointes- action potential duration/ early afterdepolarisation

Digixon induced arrhythmia- calcium over load or delayed afterdepolarization.

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9
Q

What are the re-entry arrhythmias?

A

Atrial flutter type 1- conduction and excitability

Wolf Parkinson White - conduction and excitability

Ventricular fibrillation - refractory period vulnerable

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10
Q

How many phases of cardiac cycle do pacemaker cells have?

A

3 phases, - 0, 4 and 3

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11
Q

How is resting membrane potential re-established?

A
  • the resting membrane potential is re-established by 2K+ in and 3Na+ out.
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12
Q

What classification does The Vaughan-Williams Classification Scheme?

A 
5 classes with class 1 (a, b, c) 
1- Na channel blockers (fast, intermediate, slow) 
2- B blockers
3- K channel blockers 
4- Ca channel blockers 
5- work by unknown mechanism
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13
Q

How do Vaughan-Williams Class I work?

Provide examples of the subclasses, effect on action duration and effective refractory period and clinical uses.

A

Drugs reduce the phase 0 slope and the peak of the action potential - decrease membrane excitability and conduction velocity.

a - quinidine, procainamide. (increase ADP + ERP) (AF/SVT)

b - lidocaine (reduced ADP + ERP) (Dig Toxicity/ VF)

c - flecainide (no change) (AF/SVT)

Propranolol also has some Class 1 action.

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14
Q

Side effects of Na channel blockers?

A

CVS side effects - hypotension, bradycardia, arrhythmia

CNS side effects- Two phases: excitatory phase followed by depressive phase with increasingly heavier exposure.

  1. Nervous, anxiety, tremor, dizziness, hallucinations, seizures, psychosis, euphoria
  2. Drowsy, lethargic, slurred speech, confusion, LOC, respiratory depression
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15
Q

Contraindications to Na channel blocker?

A
  1. Syndromes:
    Adam Stokes syndrome
    Wolf Parkinsons White
  2. Conduction defects:
    2/3 heart block
    Serious SA node block without pacemaker
  3. Meds:
    Prior use of amiodarone
    Use of other Class 1 antiarrhythmics
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16
Q

Flecainide:
Uses
Side effects
Avoided?

A

Use: pill in the pocket to terminate AF, treatment of supraventricular tachycardias (inc those in WPW)

Side effects: arrhythmias (Torsades de Pointes), prolonged PR, widened QRS, can be negatively ionotropic effect

Avoid- structural heart diseases

17
Q

Mechanism of B-blocker activity

A

Decreases sympathetic activity on the heart by acting as antagonists at b-receptors (antagonising catecholamines).

Prolongs Phase 4 ‘diastolic’ depolarization.

reduces intracellular cAMP levels and therefore reduces Ca influx. Produce bradycardia, depress myocardial contractility, prolong AV conduction.

Useful in treating supraventricular tachycardias.

18
Q

Side effects of B-blockers

A 
Hypotension 
Bradycardia
Heart block
Depression 
Sexual dysfunction 
Impaired glucose handling
19
Q

Mechanism of K+ channel blockers

A

Prolong repolarization by blocking potassium channels, K+ efflux in Phase 3.

  • > prolongs action potential duration and effective refractory period
  • > bradycardia
20
Q

Amiodarone:
Uses
Side effects
Contraindications

A

Uses- treatment of ventricular and supraventricular tachycardias, WPW
Increases APD, ERP

Side effects: 
interstitial lung disease, 
thyroid dysfunction (hypo/hyper), 
abnormal liver enzymes, 
corneal micro deposits 
and photosensitivity

Contra- pregnancy, bradycardia,

21
Q

Mechanism of the Ca channel blocker?

Contra-indications

Side effects

A
  • prevents influx of Ca through slow L-type channels in the AV and SA node, slowing conduction and automaticity.
  • This shortens phase 2 - plateau of cardiac potential.
  • Reduce contractility of the heart.

Contraindication: Should not be used in WPW- precipitate VT.

Side effects: constipation, dizziness, headache, redness on the face, ankle oedema, bradycardia

22
Q

Adenosine mechanism action?

What arrhythmias can it be used to differentiate?

A

AV node block via specific adenosine-A receptors.

Short half life, less than 10 seconds - taken up rapidly by red blood cells.

Can be used to differentiate between VT and SVT. Will only treat SVT.

23
Q

Adenosine side effects and contraindications.

A

Side effects: diaphoresis, metallic taste, nausea, sense of impending doom.

Contra-indications: asthma, decompensated heart failure, long QT syndrome.

24
Q

Digoxin mechanism of action

A

Commonly used for rate control in AF

Action is to inhibit Na/K ATPase in the myocardium. Raises Na intracellular levels - eventually raises Ca and therefore prolongs phase 4 and phase 0 of the cardiac potential.

Also indirectly increases acetylcholine at cardiac muscarinic receptors. Slows conduction and prolonging the refractory period in the AV node and bundle of His.

Weak ionotrope.

25
Q

Digoxin side effects

A

Narrow therapeutic index

  • gynaecomastia, nausea, yellow vision.
  • Hypokalaemia can precipitate side effects as both act at same cardiac receptors.
26
Q

ECG changes in Digoxin toxicity

A

ST depression
Flat T waves
QT interval shortening
“Reverse tick sign”

27
Q

Name some Class 1 anti-arrhythmias.

A

A- quinidine, procainamide (intermediated assoc/ dissoc)

B- lidocaine, phenytoin (fast assoc)

C- flecainide, propafenone (slow assoc)

28
Q

Name class 2 antiarrhythmics

A

Beta blockers

Propranolol
Metoprolol

29
Q

Name some class 3 antiarrhythmics

A

K channel blockers

Amiodarone - class 1-4 activity
Sotalol - also Bblocker
30
Q

Name some class 5 antiarrhythmics

A

Adenosine and Digoxin

- unknown mechanism

31
Q

Lidocaine is contraindicated in which syndrome?

A

Wolf Parkinson White

32
Q

What type of blockade happens in Class 1?

A

Sodium channel block.
Phase 0 prolonged
Increased effective refractory period.
Slows down HR

Good for SVT - AF, WPW tachy

33
Q

Class 2 antiarrhythmics mechanism?
Ion target
Phase target

A

Reduced sympathetic stimulation of heart by blocking B-adrenegeric receptors.

Decreases Phase 4 nodal slope (Na/ Ca slow channel slope)

34
Q

Class 3 antiarrhythmics:
Target ion block
Phase block
Effect on action potential

A

Potassium channel block,
Phase 3 of cardiac myocytes action potential
Prolongs ERP AND QT interval

Contraindicated in long QT syndromes- can trigger VF and VT

CVS Pharmacology (9 decks)

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