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(LUSUMA) Clinical Pharmacology & Therapeutics > S3) Cardiac Arrhythmias > Flashcards

S3) Cardiac Arrhythmias Flashcards

1
Q

What is an arrhythmia?

A
  • An arrhythmia is a heart condition arising due to disturbances in pacemaker impulse formation and/or contraction impulse conduction
  • It results in a rate and/or timing of myocardial contraction that is insufficient to maintain normal CO
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2
Q

Describe the movement of ions in the fast cardiac action potential

A
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3
Q

Describe the effect of drugs blocking Na+ channels on the fast cardiac action potential

A
  • Marked slowing conduction in tissue (phase 0)
  • Minor effects on action potential duration (APD)
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4
Q

Describe the effect of beta blockers on the fast cardiac action potential

A

Diminish phase 4 depolarisation and automaticity

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5
Q

Describe the effect of drugs blocking K+ channels on the fast cardiac action potential

A

Increased action potential duration (APD)

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6
Q

Describe the effect of calcium channel blockers on the fast cardiac action potential

A
  • CCBs decrease inward Ca2+ currents resulting in a decrease of phase 4 spontaneous depolarization
  • Effect plateau phase of action potential
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7
Q

Describe the movement of ions in the slow cardiac action potential

A
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8
Q

Outline the mechanisms of arrhythmogenesis due to abnormal impulse generation

A
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9
Q

Outline the mechanisms of arrhythmogenesis due to abnormal conduction

A
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10
Q

Describe the two possible actions of anti-arrhythmic drugs in terms of abnormal generation

A
  • Decrease the phase 4 slope (in pacemaker cells)
  • Raises the threshold
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11
Q

Describe the two possible actions of anti-arrhythmic drugs in terms of abnormal conduction

A
  • Decrease conduction velocity (phase 0)
  • Increase ERP
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12
Q

Why are anti-arrhythmic drugs used?

A

Anti-arrhythmic drugs are used to:

  • Decrease conduction velocity
  • Change the duration of ERP
  • Suppress abnormal automaticity
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13
Q

What are the different types of anti-arrhythmic drugs?

A
  • Class I: Na+ channel blockers
  • Class II: beta-adrenergic blockers
  • Class III: K+ channel blockers (prolong repolarisation)
  • Class IV: Ca2+ channel blockers
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14
Q

Describe the actions of the different types of class I anti-arrhythmic drugs

A
  • Class IA – Moderate phase 0
  • Class IB – No change in phase 0
  • Class IC – Marked phase 0
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15
Q

Provide two examples of Class IA anti-arrhythmic agents

A
  • Procainamide
  • Quinidine
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16
Q

How are Class IA anti-arrhythmic agents administered?

A
  • Oral preparation
  • IV preparation
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17
Q

Describe the four effects of Class IA anti-arrhythmic agents on cardiac activity

A
  • Decrease conduction – ↓ phase 0 of the action potential (Na+)
  • Increase refractory period – ↑ APD (K+) and ↑ Na+ inactivation
  • Decrease automaticity – ↓ slope of phase 4, fast potentials
  • Increase threshold (Na+)
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18
Q

Describe the effects of Class IA anti-arrhythmic drugs on the ECG

A
  • ↑ QRS
  • ± PR
  • ↑ QT
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19
Q

Describe the uses of Class IA anti-arrhythmic drugs

A
  • Quinidine: maintain sinus rhythms in atrial fibrillation and flutter, prevent recurrence, Brugada syndrome
  • Procainamide: acute IV treatment of supraventricular and ventricular arrhythmias
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20
Q

Identify 5 side-effects of Class IA anti-arrhythmic drugs

A
  • Hypotension (reduced CO)
  • Proarrhythmia e. g. Torsades de Points (↑ QT interval)
  • Dizziness & confusion
  • Gl effects (common)
  • Lupus-like syndrome (esp. procainamide)
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21
Q

Provide two examples of Class IB anti-arrhythmic drugs

A
  • Lidocaine
  • Mexiletine
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22
Q

How are Class IB anti-arrhythmic agents administered?

A
  • Lidocaine: IV preparation
  • Mexiletine: oral preparation
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23
Q

Describe the five effects of Class IB anti-arrhythmic agents on cardiac activity

A
  • Fast binding offset kinetics
  • No change in phase 0 in normal tissue (no tonic block)
  • APD slightly decreased (normal tissue)
  • ↑ increase threshold (Na+)
  • ↓ phase 0 conduction in fast beating or ischaemic tissue
24
Q

Describe the effects of Class IB anti-arrhythmic drugs on the ECG

A
  • No effects in normal / fast beating / ischaemic
  • ↑ QRS
25
Q

Describe the uses of Class IB anti-arrhythmic drugs

A
  • Acute use in ventricular tachycardia (esp. during ischaemia)
  • Not used in atrial arrhythmias or AV junctional arrhythmias
26
Q

Identify 3 side-effects of Class IB anti-arrhythmic drugs

A
  • Less proarrhythmic than Class 1A
  • CNS effects: dizziness & drowsiness
  • Abdominal upset
27
Q

Provide two examples of Class IC anti-arrhythmic drugs

A
  • Flecainide
  • Propafenone
28
Q

How are Class IC anti-arrhythmic agents administered?

A
  • Oral preparation
  • IV preparation
29
Q

Describe the four effects of Class IC anti-arrhythmic agents on cardiac activity

A
  • Very slow binding offset kinetics (>10 s)
  • Substantially ↓ phase 0 (Na+) in normal
  • ↓ automaticity (↑ threshold)
  • ↑ APD (K+) and ↑ refractory period (esp in rapidly depolarising atrial tissue)
30
Q

Describe the effects of Class IC anti-arrhythmic drugs on the ECG

A
  • ↑PR
  • ↑QRS
  • ↑QT
31
Q

Describe the uses of Class IC anti-arrhythmic drugs

A

Wide spectrum use:

  • Supraventricular arrhythmias (fibrillation and flutter)
  • Premature ventricular contractions (caused problems)
  • Wolff-Parkinson-White syndrome
32
Q

Identify 4 side-effects of Class IC anti-arrhythmic drugs

A
  • Proarrhythmia and sudden death (esp chronic use)
  • Increase ventricular response to supraventricular arrhythmias (flutter)
  • CNS effects
  • GI effects
33
Q

Provide two examples of Class II anti-arrythmic agents

A
  • Propranolol
  • Bisoprolol
34
Q

How are Class II anti-arrhythmic agents administered?

A
  • Propranolol: Oral, IV
  • Bisoprolol: Oral
35
Q

Describe the two effects of Class II anti-arrhythmic agents on cardiac activity

A
  • ↑ APD and refractory period in AV node to slow AV conduction velocity
  • ↓ Phase 4 depolarisation (catecholamine dependent)
36
Q

Describe the effects of Class II anti-arrhythmic drugs on the ECG

A
  • ↑PR
  • ↓HR
37
Q

Describe the uses of Class II anti-arrhythmic drugs

A
  • Treating sinus and catecholamine-dependent tachycardia
  • Converting re-entrant arrhythmias at AV node
  • Protecting the ventricles from high atrial rates (slow AV conduction)
38
Q

Identify 2 side-effects of Class II anti-arrhythmic drugs

A
  • Bronchospasm
  • Hypotension

Don’t use in partial AV block or heart failure

39
Q

Provide an example of a Class III anti-arrythmic agents

A

Amiodarone

40
Q

How are Class III anti-arrhythmic agents (amiodarone) administered?

A
  • Oral preparation
  • IV preparation
41
Q

Describe the four effects of Class III anti-arrhythmic agents on cardiac activity (amiodarone)

A
  • ↑ refractory period and ↑APD (K+) ↓ phase0 and conduction (Na+)
  • ↑ Threshold
  • ↓ Phase 4 (β block and Ca2+ block)
  • ↓ Speed of AV conduction
42
Q

Describe the effects of Class III anti-arrhythmic drugs on the ECG (amiodarone)

A
  • ↑ PR
  • ↑ QRS
  • ↑ QT
  • ↓ HR
43
Q

Describe the uses of Class III anti-arrhythmic drugs (amiodarone)

A

Very wide spectrum: effective for most arrhythmias

44
Q

Identify 6 side-effects of Class III anti-arrhythmic drugs (amiodarone)

A
  • Pulmonary fibrosis
  • Hepatic injury
  • Increase LDL cholesterol
  • Thyroid disease
  • Photosensitivity
  • Optic neuritis (transient blindness)
45
Q

Provide two examples of Class IV anti-arrythmic agents

A
  • Verapamil
  • Diltiazem
46
Q

How are Class IV anti-arrhythmic agents administered?

A
  • Verapamil: oral/IV preparation
  • Diltiazem: oral preparation
47
Q

Describe the three effects of Class IV anti-arrhythmic agents on cardiac activity

A
  • Slow conduction through AV (Ca2+)
  • ↑ Refractory period in AV node
  • ↑ Slope of phase 4 in SA to slow HR
48
Q

Describe the effects of Class IV anti-arrhythmic drugs on the ECG

A
  • ↑ PR
  • ± HR (depending on BP response and baroreflex)
49
Q

Describe the uses of Class IV anti-arrhythmic drugs

A
  • Control ventricles during supraventricular tachycardia
  • Convert supraventricular tachycardia (re-entry around AV)
50
Q

Identify 2 side-effects of Class IV anti-arrhythmic drugs

A
  • Asystole (if β blocker is on board)
  • Some GI problems

Caution when partial AV block, hypotension, decreased CO or sick sinus present

51
Q

How can adenosine be administered?

A

Rapid IV

52
Q

Describe the mechanism in which adenosine functions

A
  • Binds α1 receptors and activates K+ currents in AVN & SAN
  • ↓ APD, hyperpolarization → ↓HR
  • ↓ Ca2+ currents – ↑ refractory period in AVN
53
Q

Describe the effect of adenosine on cardiac activity

A

Slows AV conduction

54
Q

Describe the uses of adenosine

A
  • Convert re-entrant supraventricular arrhythmias
  • Hypotension during surgery
  • Diagnosis of CAD
55
Q

Describe the mechanism in which digoxin functions

A
  • Enhances vagal activity (↑K+ currents, ↓Ca2+ currents, ↑refractory period)
  • Slows AV conduction and slows HR
56
Q

Describe the use of digoxin

A

Digoxin is used in treatment to reduce ventricular rates in atrial fibrillation and flutter

(LUSUMA) Clinical Pharmacology & Therapeutics (29 decks)

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