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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

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

A
  • Mainly for AFib and AFlutter (supraventricular tachycardias)
  • Premature ventricular contractions
  • WPW syndrome
25
Q

List 4 ADRs of Class IC Antiarrythmitics

A
  • 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
Q

When giving a Class IC Antiarrythmitic, why do we also give an AV node blocker?

A

To prevent the ‘Flecainide Flutter effect’ caused by increased ventricular responsiveness to supraventricular tachycardia

27
Q

Describe the administration of the following Class II Antiarrythmitics;

  • Propranolol
  • Bisoprolol
  • Metoprolol
  • Esmolol
A

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
Q

Describe the effects of Class II Antiarrythmics

A
  • Increased refractory period and AP duration in AV node
  • Decreased Phase 4 depolarisation (catecholamine-dependent)
  • Prolonged PR, Reduced HR
29
Q

Describe the uses of Class II Antiarrythmics

A
  • Sinus tachycardia
  • Treat re-entrant arrhythmias at AV node
  • Prevent ventricular tachycardia caused by AFib/ AFlutter (slowed AV conduction)
30
Q

List 2 ADRs of Class II Antiarrythmics

List 3 contraindications

A
  • Bronchospasm
  • Hypotension
  • Partial AV block
  • Asthma
  • Acute heart failure (only when heart is stable, including stable heart failure)
31
Q

Describe the administration of Amiodarone (Class III Antiarrythmitic)

A

Oral or IV (half life of 3 months)

32
Q

Name a drug that has both Class II and III effects

A

Sotalol

33
Q

Describe the effects of Amiodarone (Class III Antiarrythmitic)

(Has actions of all 4 classes, so most effective)

A
  • Increased refractory period and AP duration
  • Reduced Phase 0 + 4 depolarisation
  • Increased AP threshold
  • Reduced AV conduction
  • Prolonged PR, QRS, QT
  • Reduced HR
34
Q

Describe the use of Amiodarone (Class III Antiarrythmitic)

A

Most arrhythmias (Mostly AFib and VTach)

35
Q

List the ADRs of Amiodarone

A
  • Thyroid disease
  • Pulmonary fibrosis
  • Hepatic injury
  • Photosensitivity and Optic neuritis
  • Increased LDL-C
36
Q

How should Digoxin and Warfarine dose change if Amiodarone is added to a prescription?

A

Digoxin- Lower dose (Increased toxicity)

Warfarin- Lower dose + Monitoring

37
Q

Describe the administration of Sotalol

A

Oral

38
Q

Describe the effects of Sotalol (Class III Antiarrythmitic)

A
  • Increased refractory period and AP duration
  • Slowed Phase 4 depolarisation
  • Slowed AV Conduction
  • Prolonged QT and reduced HR
39
Q

Describe the uses of Sotalol

List 3 ADRs

A

Supraventricular and ventricular tachycardia

  • Proarrythmia
  • Fatigue
  • Insomnia
40
Q

Describe the administration of Verapamil and Diltiazem

A

Verapamil: Oral or IV

Diltiazem: Oral only

41
Q

Describe the effects of Class IV Antiarrythmitics

A
  • 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
Q

Describe the uses of Class IV Antiarrythmitics

A
  • Control ventricle rate during supraventricular tachycardia (especially asthma or where Beta blockers can’t be used)
  • Treat supraventricular tachycardia around AV node
43
Q

List 2 ADRs of Class IV Antiarrythmitics

List 4 contraindications

A
  • GI problems (constipation)
  • Possible Bradycardia/ Asystole if Beta blocker is being used
  • Partial AV block
  • Hypotension
  • Heart Failure
  • Unstable Angina
44
Q

When can we give Ca blockers with Beta blockers?

A

If a pacemaker is present to prevent asystole

45
Q

How is Adenosine administered?

Describe its mechanism and cardiac effects

A
  • 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
Q

List 2 uses of Adenosine

List 2 ADRs

A
  • Treat re-entrant supraventricular arrhythmias
  • Diagnosis of Coronary Artery Disease (Scans)
  • Bradycardia
  • Asystole
47
Q

Describe the administration, mechanism and effects of Ivabradine

A

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
Q

List the ADRs and uses of Ivabradine

A

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
Q

Describe the mechanism and uses of Digoxin

A

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
Q

List 3 ADRs of Digoxin

A
  • Bradycardia
  • GI Disturbance
  • Low therapeutic window/ index
51
Q

List 3 Contraindications of Digoxin

List 2 DDIs

A
  • Heart block
  • Renal Failure
  • Hypokalaemia
  • Diuretics that can cause Hypokalaemia
  • Amiodarone
52
Q

Which antiarrythmitics are the safest, but have the least efficacy?

A

Beta blockers and Non-Dihydropine Ca blockers

Amiodarone is opposite

53
Q

Describe the mechanism, effects and uses of Atropine

A

Mechanism: Muscarinic antagonist

Effects: Block vagal activity to increase AV conduction and HR

Uses: Treating vagal bradycardia

54
Q

List 4 ADRs of Atropine

A
  • Dry mouth
  • Dizzy
  • Headache
  • Anxiety
55
Q

List 3 contraindications of Atropine

A

Where antimuscarinic action unwanted;

  • Urinary retention
  • Glaucoma
  • GI obstruction

CPT (19 decks)

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