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SA 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
  • occur due to automatic or triggered activity, re-entry due to a scar
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2
Q

Describe the movement of ions in the fast cardiac action potential

A
  1. 0 → sodium enters the cell via funny channels and causes depolarisation
  2. 1 → K leaves the cell causing early depolarisation
  3. 2 → ca moves from the sarcoplasmic recticulum inside the cell via t type channels
  4. 3 → K starts to move out of the cell causing depolarisation
  5. Na/K ATPase resets it to normal
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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)
  • takes longer to depolarise the cell
  • Minor effects on action potential duration (APD)
  • eg: Flecainide and propaferone*
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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

→ heart will beat more slowly, with less force and lower blood pressure

→ block actions of adrenaline

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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)

slows depolarisation

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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
  • refractory period is increased
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7
Q

Describe the movement of ions in the slow cardiac action potential

A
  1. this occurs in the SAN or the AV node
  2. 4 → slow Na channels / spontaneous depolarisation
  3. 0 → depolarisation
  4. 4 → K leaves the cell and causes depolarisation
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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

conduction block: impulse is not conducted from the atria to the ventricles

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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) → slowed down
  • Raises the threshold so takes longer to reach and slows heart down
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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) / reduced conduction in tissues
  • Increase ERP (effective refactory period)
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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

what does automaticity mean

A

Pacemaker cells ability to create an action potential and spontaneously depolarise

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15
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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16
Q

Provide two examples of Class IA anti-arrhythmic agents

A
  • Procainamide
  • Quinidine
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17
Q

How are Class IA anti-arrhythmic agents administered?

A
  • Oral preparation
  • IV preparation
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18
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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19
Q

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

A
  • ↑ QRS
  • ± PR
  • ↑ QT
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20
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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21
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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22
Q

Provide two examples of Class IB anti-arrhythmic drugs

A
  • Lidocaine
  • Mexiletine
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23
Q

How are Class IB anti-arrhythmic agents administered?

A
  • Lidocaine: IV preparation
  • Mexiletine: oral preparation

start out with lodicaine and then once stable move onto mexiletine

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24
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
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25
Q

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

A
  • No effects in normal / fast beating / ischaemic
  • ↑ QRS
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26
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
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27
Q

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

A
  • Less proarrhythmic than Class 1A
  • CNS effects: dizziness & drowsiness
  • Abdominal upset
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28
Q

Provide two examples of Class IC anti-arrhythmic drugs

A
  • Flecainide
  • Propafenone
29
Q

How are Class IC anti-arrhythmic agents administered?

A
  • Oral preparation
  • IV preparation
30
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 (action potential duration) (K+) and ↑ refractory period (esp in rapidly depolarising atrial tissue)
31
Q

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

A
  • ↑PR
  • ↑QRS
  • ↑QT
32
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 (congenital condition where the heart suddenly starts beating very fast for a period of time)
33
Q

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

A
  • Proarrhythmia and sudden death (esp chronic use) → need stable ventricles and valves
  • Increase ventricular response to supraventricular arrhythmias (flutter)
  • CNS effects
  • GI effects
34
Q

Provide two examples of Class II anti-arrythmic agents

A
  • Propranolol
  • Bisoprolol
35
Q

How are Class II anti-arrhythmic agents administered?

A
  • Propranolol: Oral, IV
  • Bisoprolol: Oral
36
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)
37
Q

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

A
  • ↑PR
  • ↓HR
38
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)
39
Q

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

A
  • Bronchospasm
  • Hypotension

Don’t use in partial AV block or heart failure or if there are any major conducting problems

40
Q

Provide an example of a Class III anti-arrythmic agents

A

Amiodarone

41
Q

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

A
  • Oral preparation
  • IV preparation

it has a VERY high half life of (3 months)

42
Q

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

A
  • ↑ refractory period and ↑APD (block K+) ↓ phase0 and conduction (Na+)
  • ↑ Threshold
  • ↓ Phase 4 (β block and Ca2+ block)
  • ↓ Speed of AV conduction
43
Q

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

A
  • ↑ PR
  • ↑ QRS
  • ↑ QT → if you prolong too much then you will risk getting torsades de pointes
  • ↓ HR
44
Q

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

A

Very wide spectrum: effective for most arrhythmias but lots of side effects

45
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)
46
Q

Provide two examples of Class IV anti-arrythmic agents

A
  • Verapamil
  • Diltiazem
47
Q

How are Class IV anti-arrhythmic agents administered?

A
  • Verapamil: oral/IV preparation
  • Diltiazem: oral preparation
48
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
49
Q

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

A
  • ↑ PR
  • ± HR (depending on BP response and baroreflex)
50
Q

Describe the uses of Class IV anti-arrhythmic drugs

A
  • Control ventricles during supraventricular tachycardia
  • Convert supraventricular tachycardia (re-entry around AV)
51
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

52
Q

How can adenosine be administered?

A

Rapid IV

53
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
54
Q

Describe the effect of adenosine on cardiac activity

A

Slows AV conduction

55
Q

Describe the uses of adenosine

A
  • Convert re-entrant supraventricular arrhythmias
  • Hypotension during surgery
  • Diagnosis of CAD
56
Q

Describe the mechanism in which digoxin functions

A
  • Enhances vagal activity (↑K+ currents, ↓Ca2+ currents, ↑refractory period)
  • Slows AV conduction and slows HR
57
Q

Describe the use of digoxin

A

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

58
Q

where do fast action potentials occur vs slow action potentials?

A

cardiac tissue vs SA/AV node

59
Q

what is the re-entry mechanism?

A

due to a circuit within the myocardium, occurs when a propagating impulse fails to die out after normal activation of the heart and persists as a result of continuous activity around the circuit to re-excite the heart after the refractory period has ended;

60
Q

what is the Vaughan-williams classification

A
61
Q

what is sotalol used for and how does it do this

A

Class III drug:

→ Supraventricular and ventricular tachycardia

increases APD and refactors period in atrial and ventricular tissue

slow phase 4 ( B blocker)

slow AV conduction

62
Q

effects of Sotalol on ECG

A

increased QT

reduced HR

63
Q

side effects of sotalol

A

proarrhythmia, fatigue and insomnia

64
Q

orthodromic vs antidromic tachycardia

A

orthodromic is when the impulses are being sent in the right direction

65
Q

Ivabradine

A

→ very good for treating POTS with the preventing sudden increase in heart beating

66
Q

Atropine

A
  • anti-arrhythmic drug
  • selective muscarinic antagonist
  • blocks vagal activity to speed AV conduction and increase HR
  • treats bradycardia
67
Q

efficacy of anti-arrhythmic drugs

A

but the safety and tolerability reduces as you move up to using amidarone

68
Q

considering anti-platelet drug dipyridamole, what are some drug interactions with adenosine

A

dipyridamole inhibits cellular uptake of adenosine so increase adenosine in the AV node

this might

SA Clinical Pharmacology & Therapeutics (36 decks)

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