CPT > Antiarrythmitics > Flashcards

Antiarrythmitics Flashcards

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1
Q

What is an Arrhytmia?

A

Heart condition involving disturbances in;

  • Pacemaker impulse formation
  • Impulse conduction
  • or a combination of the two

Results in a rate/ timing of contraction that is insufficient to maintain normal CO

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2
Q

Which cells use the Fast Cardiac Action Potential

A
  • Atrial and cardiac Myocytes

- Cells in Purkyne tissue

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3
Q

List the Phases of the fast cardiac action potential

A

Phase 0: Depolarisation
Phase 1: Initial repolarisation
Phase 2: Plateau phase

Phase 3: Major repolarisation
Phase 4: Spontaneous depolarisation

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4
Q

What are the mechanisms of action of Classes I-IV of antiarrythmitics

A

Class I: Na blockers

Class II: Beta blockers

Class III: K blockers

Class IV: Ca blockers

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5
Q

How do Class I Antiarrythmitics affect the Fast cardiac AP?

Name 2

A
  • Slowing of Rapid Depolarisation phase
  • Minor effects on AP Duration
  • Lidocaine
  • Flecainide
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6
Q

How do Class II Antiarrythmitics affect the Fast cardiac AP?

Name 2

A
  • AP duration increased
  • Reduced depolarization in phase 4 (Na-K ATPase)
  • Bisoprolol
  • Metoprolol
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7
Q

How do Class III Antiarrythmitics affect the Fast cardiac AP?

Name 2

A
  • Slowed repolarisation-> Increased AP duration and Refracory Period
  • Amiodarone
  • Sotalol
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8
Q

How do Class IV Antiarrythmitics affect the Fast cardiac AP?

Name 2

A
  • AP duration increased
  • Decreased phase 4 depolarization
    (Also affects plateau phase)
  • Diltiazem
  • Verapamil
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9
Q

List the Phases of the Slow cardiac AP (SA/ AV node conduction)

A

Phase 0: Depolarisation (‘Funny’ current slow Na channels)

Phase 3: Repolarisation

Phase 4: Spontaneous depolarisation

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10
Q

How do Ca blockers affect the Slow Cardiac AP

A
  • Slowed depolarisation

- Lengthened refractory period

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11
Q

How do Beta agonstis affect the Slow Cardiac AP

A
  • Speed up Phase 4 spontaneous depolarisation
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12
Q

How do Adenosine and Muscarinic antagonists affect the Slow Cardiac AP

A
  • Slow down spontaneous depolarisation
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13
Q

Arrhythmias can be caused by abnormal impulse generation, which can be due to Automatic or Triggered rhythms.

Name 2 types of triggered rhythm

A
  • Delayed afterdepolarisation
  • Early afterdepolarisation

(Automatic rhythms- Sinus tachycardia, Ectopic impulses)

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14
Q

Arrhythmias can be due to Abnormal conduction.

What are 2 types?

A
  • Conduction block (Degrees 1,2,3)

- Re-entry (Circus movement, Reflection)

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15
Q

List the intended actions of drugs used to treat Arrhythmias due to;

  • Abnormal impulse generation
  • Abnormal impulse conduction
A

Abnormal generation;

  • Decrease Phase 4 slope
  • Raise threshold for AP generation

Abnormal conduction;
- Reduce conduction velocity/ increase length of refractory period

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16
Q

Describe the pathology of Wolf-Parkinson-White Syndrome (WPW)

A

Additional tissue provides an accessory pathway for impulses to re-enter atria from ventricles

(Re-entry loop)

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17
Q

Briefly compare Class IB and IC Antiarrythmitics

Give examples

A

IB;

  • No change in Phase 0
  • Lidocaine, Mexiletine

IC;

  • Marked change in Phase 0
  • Flecainide, Propafenone
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18
Q

List 4 Class V Antiarrythmitics

A
  • Adenosine
  • Digoxin
  • Atropine
  • Ivabradine
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19
Q

Describe the administration of Lidocaine, Mexiletine and Flecainide

A

Lidocaine- IV only
Mexiletine- Oral only

Flecainide- IV or Oral

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20
Q

Describe the effects of Class IB Antiarrythmitics

A
  • Fast binding offset kinetics
  • No change in Phase 0 in normal tissue

In Fast Beating/ Ischaemic tissue;

  • Reduced Phase 0 conduction
  • Prolonged QRS segment
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21
Q

Describe the uses of Class IB Antiarrythmitics

A
  • Acute Ventricular Tachycardia (or to prevent)

- Not used in atrial or AV junction arrhythmias (not effective)

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22
Q

List 3 ADRs of Class IB Antiarrythmitics

A
  • Abdominal upset (N + V)

- Dizziness and drowsiness

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23
Q

Describe the effects of Class IC Antiarrythmitics

Study These Flashcards
A
  • Slow binding offset kinetics
  • Significantly slowed Phase 0-> Prolonged refractory period (especially in rapidly depolarising tissue)
  • Decreased Automacity and increased AP threshold
  • Prolonged PR, QRS and QT
24
Q

Describe the uses of Class IC Antiarrythmitics

Study These Flashcards
A
  • Mainly for AFib and AFlutter (supraventricular tachycardias)
  • Premature ventricular contractions
  • WPW syndrome
25
List 4 ADRs of Class IC Antiarrythmitics
- Can be pro arrhythmic - Sudden death, especially chronic use in patients with coronary artery disease (MI, NSTEMI, Structural disease) - Increases ventricular response to supraventricular tachycardia (Slowing of Afib-> VTach) - CNS and GI effects like Class IB Antiarrythmitics (Ab upset, Dizzy, Drowsy)
26
When giving a Class IC Antiarrythmitic, why do we also give an AV node blocker?
To prevent the ‘Flecainide Flutter effect’ caused by increased ventricular responsiveness to supraventricular tachycardia
27
Describe the administration of the following Class II Antiarrythmitics; - Propranolol - Bisoprolol - Metoprolol - Esmolol
Propranolol- Oral or IV Bisoprolol- Oral only Metoprolol- Oral or IV (BD/ TDS as it is short acting) Esmolol- IV only (very short acting)
28
Describe the effects of Class II Antiarrythmics
- Increased refractory period and AP duration in AV node - Decreased Phase 4 depolarisation (catecholamine-dependent) - Prolonged PR, Reduced HR
29
Describe the uses of Class II Antiarrythmics
- Sinus tachycardia - Treat re-entrant arrhythmias at AV node - Prevent ventricular tachycardia caused by AFib/ AFlutter (slowed AV conduction)
30
List 2 ADRs of Class II Antiarrythmics List 3 contraindications
- Bronchospasm - Hypotension - Partial AV block - Asthma - Acute heart failure (only when heart is stable, including stable heart failure)
31
Describe the administration of Amiodarone (Class III Antiarrythmitic)
Oral or IV (half life of 3 months)
32
Name a drug that has both Class II and III effects
Sotalol
33
Describe the effects of Amiodarone (Class III Antiarrythmitic) (Has actions of all 4 classes, so most effective)
- Increased refractory period and AP duration - Reduced Phase 0 + 4 depolarisation - Increased AP threshold - Reduced AV conduction - Prolonged PR, QRS, QT - Reduced HR
34
Describe the use of Amiodarone (Class III Antiarrythmitic)
Most arrhythmias (Mostly AFib and VTach)
35
List the ADRs of Amiodarone
- Thyroid disease - Pulmonary fibrosis - Hepatic injury - Photosensitivity and Optic neuritis - Increased LDL-C
36
How should Digoxin and Warfarine dose change if Amiodarone is added to a prescription?
Digoxin- Lower dose (Increased toxicity) | Warfarin- Lower dose + Monitoring
37
Describe the administration of Sotalol
Oral
38
Describe the effects of Sotalol (Class III Antiarrythmitic)
- Increased refractory period and AP duration - Slowed Phase 4 depolarisation - Slowed AV Conduction - Prolonged QT and reduced HR
39
Describe the uses of Sotalol List 3 ADRs
Supraventricular and ventricular tachycardia - Proarrythmia - Fatigue - Insomnia
40
Describe the administration of Verapamil and Diltiazem
Verapamil: Oral or IV Diltiazem: Oral only
41
Describe the effects of Class IV Antiarrythmitics
- Increased refractory period in AV node - Reduced Phase 4 depolarisation - Slowed AV conduction - Prolonged PR - Mostly lowers HR (depends on BP and Baroreceptor reflex)
42
Describe the uses of Class IV Antiarrythmitics
- Control ventricle rate during supraventricular tachycardia (especially asthma or where Beta blockers can’t be used) - Treat supraventricular tachycardia around AV node
43
List 2 ADRs of Class IV Antiarrythmitics List 4 contraindications
- GI problems (constipation) - Possible Bradycardia/ Asystole if Beta blocker is being used - Partial AV block - Hypotension - Heart Failure - Unstable Angina
44
When can we give Ca blockers with Beta blockers?
If a pacemaker is present to prevent asystole
45
How is Adenosine administered? Describe its mechanism and cardiac effects
- IV bolus (very rapid acting, half life of seconds) - Alpha1 receptor agonist-> Activation of K+ channels= AV + SA node hyperpolarisation - Effects: Slowed AV conduction and reduced HR
46
List 2 uses of Adenosine List 2 ADRs
- Treat re-entrant supraventricular arrhythmias - Diagnosis of Coronary Artery Disease (Scans) - Bradycardia - Asystole
47
Describe the administration, mechanism and effects of Ivabradine
Administration: Oral (2.5mg bd upto 10mg bd) Mechanism: Blocks ‘Funny current’ in SA node Effects: Slows SA node-> Slows HR (No effect on BP)
48
List the ADRs and uses of Ivabradine
Side effects; - Flashing lights/ Visual disturbance (will reduce with time) - Headache, Dizziness - Possible teratogen Uses; - Reduce sinus tachycardia - Reduce HR in Heart Failure + Angina
49
Describe the mechanism and uses of Digoxin
Mechanism; - Enhanced vagal activity (Increased K currents + refractory period, reduced Ca current) - Slows AV conduction and HR Uses; - To reduce ventricular rates in AFib/ AFlutter
50
List 3 ADRs of Digoxin
- Bradycardia - GI Disturbance - Low therapeutic window/ index
51
List 3 Contraindications of Digoxin List 2 DDIs
- Heart block - Renal Failure - Hypokalaemia - Diuretics that can cause Hypokalaemia - Amiodarone
52
Which antiarrythmitics are the safest, but have the least efficacy?
Beta blockers and Non-Dihydropine Ca blockers | Amiodarone is opposite
53
Describe the mechanism, effects and uses of Atropine
Mechanism: Muscarinic antagonist Effects: Block vagal activity to increase AV conduction and HR Uses: Treating vagal bradycardia
54
List 4 ADRs of Atropine
- Dry mouth - Dizzy - Headache - Anxiety
55
List 3 contraindications of Atropine
Where antimuscarinic action unwanted; - Urinary retention - Glaucoma - GI obstruction
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