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Pharmacology CP > Anti-Arrhythmic Drugs > Flashcards

Anti-Arrhythmic Drugs Flashcards

1
Q

What is an arrhythmia?

A
  • Disturbance of normal cardiac rhythm
  • Site: atrial, junctional, ventricular
  • Rate: tachycardia or bradycardia
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2
Q

What are the four basic mechanisms for arrhythmias?

A
  • Delayed after depolarisation- raised intracellular ion levels
  • Ectopic pacemakers- encouraged by SNS activity
  • Re-entry- diseases myocardium
  • Heart block- disease in conducting system (AVN)
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3
Q

How do drugs correct arrhythmias?

A
  • Anti-Arrhythmics act by
  • Suppressing abnormal impulses
  • Altering re-entry circuit- slowing it by disturbing rhythm
  • If rhythm removed that is self-amplifying, breaks amplification
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4
Q

Why do arrhythmias occur?

A
  • Abnormal impulse generation (automaticity), e.g. ectopic pacemakers
  • Abnormal impulse conduction (e.g. re-entry)
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5
Q

How does an impulse conduct through the heart?

A
  • Slow depolarisation at SA node- reaching threshold triggers AP
  • Pacemaker potential
  • Extended plateau in Purkinje fibres and ventricles-sustained contractions due to Ca influx extending duration of AP
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6
Q

What happens at phase 0 of cardiac action potential and what drugs can be used?

A
  • Rapid depolarisation
  • Fast sodium influx
  • Drugs: sodium channel blockers- class 1
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7
Q

What happens at phase 1 of cardiac action potential?

A
  • Partial repolarisation
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8
Q

What happens at phase 2 of cardiac action potential and what drugs can be used?

A
  • Plateau (calcium influx)
  • Sustaining action potential
    Drugs:
  • Class 2- β blockers, β receptors linked to Ca influx
  • Class 4- calcium channel blockers
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9
Q

What happens at phase 3 of cardiac action potential and what drugs can be used?

A
  • Repolarisation (potassium efflux)
  • Hyperpolarisation
    Drugs:
  • Class 3- potassium channel blockers
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10
Q

What happens at phase 4 of cardiac action potential and what drugs can be used?

A
  • Pacemaker depolarisation (slow sodium and calcium influx in SA and AV nodes)
  • Baseline
  • Pacemaker tissue- potential that slowly depolarises there and triggers the next action potential
    Drugs
  • Class 2 β blockers also work here due to calcium influx
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11
Q

What miscellaneous drug can be used to alter ion current in cardiac AP?

A
  • Digoxin (glycoside)
  • Inhibits primary pump–>inhibit secondary pump
  • Na/K ATPase- primary exchanger for ion balance
  • Ca/Na passive exchanger- uses primary gradient
    • Blocks sodium re-entry so more calcium in cell
    • Alter rhythm- calcium determines heart rhythm
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12
Q

What is the pacemaker current?

A
  • If (funny) current in SAN and AVN carries Na+ ions in at resting voltage- slow depolarisation
  • Pacemaker depolarisation- largely Ca influx
  • Slow L-type Ca channels also important in AVN
  • Target of class 4 drugs
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13
Q

How does sympathetic nervous system affect the heart?

A
  • Circulating Adr/NA acting on β-1 adrenoceptors
  • Increases funny current in pacemaker tissues
  • Increases slope of pacemaker depolarisation in phase 4
  • Reaches threshold sooner
  • Next heart beat occurs sooner, increases heart rate
  • β-1 blockers (class 2 anti-arrhythmics)
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14
Q

How does parasympathetic nervous system affect the heart?

A
  • Vagus nerve receiving ACh, acting on M2 muscarinic receptor
  • Opens specific K channels (K-ACh channels)- influx
  • Causes SAN hyperpolarisation- less active
  • Pacemaker slow depolarisation reduced
  • Longer to reach threshold
  • Next beat slower, AP delayed, slower HR
  • Atropine blocks Msc receptors- used in bradycardia to increase heart rate
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15
Q

List the classes of anti-arrhythmic drugs

A
  • Class 1-Na channel blockers
  • Class 2- β-adrenoceptor blockers
  • Class 3- K+ channel blockers
  • Class 4- Ca channel blocker
  • Miscellaneous group (or class 5): adenosine, glycosides, atropine
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16
Q

Describe Class 1- sodium channel blockers

A
  • Like local anaesthetics
  • Blocking fast Na channels in phase 0
  • Blocks AP on peripheral nerve- prevents pain and other sensations
17
Q

How can slope be measured?

A
  • Using upstroke velocity- Vmax
18
Q

What is the effect of class 1A on Vmax?

A
  • Disopyramide

- Reduce Vmac and prolong action potential

19
Q

What is the effect of class 1B on Vmax?

A
  • Lidocaine

- Slightly reduce Vmax and shorten action potential

20
Q

What is the effect of class 1C on Vmax?

A
  • Flecainade

- Greatly reduce Vmax but have no effect on AP duration

21
Q

Give examples of class 2 β-adrenoceptor blockers

A
  • E.g. atenolol, metoprolol, propranolol
22
Q

What do class 2 β-adrenoceptor blockers do?

A
  • Block action of Adr/NA on β-1 adrenoceptors on heart muscles/conducting tissue
  • Reduce inward Na+ (If) current in SA nodes, slowing pacemaker depolarisation in phase 4
  • Indirectly reduce Ca influx in phase 2- plateau of AP, phase 4- depolarisations
  • Suppress abnormal pacemakers- e.g. ectopic
  • Strongly reduce AV conduction (increased refractory period) slowing heart rate
23
Q

What do class 3 potassium channel blockers do and give 2 examples?

A
  • Block K+ efflux and repolarisation (phase 3)
  • Extend duration of action potential
  • Class 3- Amiodarone
    • Other actions (Blocks Na and β channels)
    • Long half life
  • Sotalol
    • Class 3 + β blocker (class 2)
24
Q

Give examples of class 4 calcium channel blockers

A
  • E.g. Verapamil (Non-dihydropyridine)

- Dihydropyridine

25
Q

What do non-dihydropyridine type Ca blockers do?

A
  • block slightly different L-type channels in heart as well as peripheral smooth muscle, limiting increase in HR
26
Q

What do dihydropyridine type Ca blockers do?

A

block L-type peripheral vascular smooth muscle- arterial dilation
- Confined to peripheral

27
Q

What do Class 4 Ca channel blockers do in general?

A
  • Blocks voltage-gated L-type Ca channels
  • Shortens repolarisation plateau (phase 2)- reduce intensity and length
  • Decreases AVN conduction- requires Ca
  • Depresses myocardial activity reduced contractility, inotropic + chronotropic effect
28
Q

Give examples of miscellaneous drugs

A
  • Adenosine
  • Atropine (bradycardia)
  • Glycosides
29
Q

What is adenosine used for?

A
  • Used acutely
  • Negative chronotropic effect on SA and AV nodes by activating K+ current and hyperpolarising cells
  • Reducing hypersensitivity
  • Onset 30s during 60-90s, half-life 7s
30
Q

What are glycosides used for?

A
  • Enhances vagal (ACh) activity
  • For atrial fibrillation
  • Positive inotrope used in HF (increases Ca ion conc.)
31
Q

What are the clinical uses of anti-arrhythmics?

A
  • Atropine- Sinus bradycardia
  • Class 2 β-blockers- stress induced
  • Lidocaine (1B)- ventricular
  • Dispryamide (1A), Flecainide (1C) and Amiodarone + Sotalol (3)- Ventricular and supra ventricular
  • Verapamil (4) and adenosine + digoxin- Supraventricular
32
Q

What is an implantable cardioverter-defribillator (ICD)

A
  • Anti-arrhythmics-adverse effects
  • ICDs increasingly used to control arrhythmias
  • Delivers shock -restore normal heart rhythm

Pharmacology CP (11 decks)

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