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CVR > Anti-arrhythmic drugs > Flashcards

Anti-arrhythmic drugs Flashcards

1
Q

What is the anti-arrythmic drug classification

A

Class 1: Na channel blockers
lidocaine, quinidine, flecainide

Class 2: beta blockers
atenolol, metoprolol

Class 3: drugs delaying repolarisation/ blocks K+ channels
amiodarone, sotalol

Class 4: Ca2+ channel antagonists
verapamil, diltiazem

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2
Q

8 possible causes of arrythmias

A
  • fever
  • heart failure
  • acute myocardial infarction
  • therapetuic e.g. digitalis and abuse drugs (cocaine is pro-arrythmic)
  • acute myocardial infarction
  • hypokalaemia (esp in anorexia nervosa)
  • autonomic dysfunction- nervous system acting too sympathetically than parasympathetically
  • inherited mutations of ion channels- channel neuropathy
  • hyperthyroidism
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3
Q

What is an ectopic beat?

A

Disturbance of the cardiac rhythm in which beats arise from fibres outside of the region in the heart muscle ordinarily responsible for impulse formation

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4
Q

What are the drug targets in arrhythmias?

A

initiation and maintenance of arrhythmias

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5
Q

What may be the cause of a heartbeat originating elsewhere other than the SA node?

A
  • abnormal pacemaking- automaticity
  • failure of conduction to stop at the end of the heart beat causing re-entry

drugs blocking re-entry are more important than drugs blocking abnormal automaticity

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6
Q

what may abnormal automaticity cause?

A

May initiate ventricular tachycardia in infarction

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7
Q

What is a wave front?

A

Is a surface containing points affected in the same way by a wave at a given time.

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8
Q

Mechanism of re-entry

A
  • caused by localised slow conduction
  • wave front may become ragged and meander
  • wave front may split into two
  • may circle around and re-enter its original pathway
  • slow conduction causes a ragged wave front
  • followed by a spiral wave front
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9
Q

How can re-entry cause an arrythmia?

A

If an injury such as ischaemia causes localised unidirectional conduction block and retrograde conduction

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10
Q

What is retrograde conduction

A

it is a conduction backward phenomena in the heart where conduction comes from the ventricles or from the AV node into and through the atria

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11
Q

How to suppress arrhythmias caused by abnormal automaticity?

A

As abnormal automaticity may be due to high beta adrenergic drive

treat with class II beta blockers

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12
Q

How to suppress arrhythmias caused by re-entry?

A

By blocking the conduction of the re-entry wave either directly or indirectly

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13
Q

Mechanism of direct re-entry suppression?

A

Direct conduction block in damaged region/ retrograde conduction region

  • localised block of ion channels responsible for depolarisation in the damage area
  • blocking Na+ channels in the AV node, atria and ventricles
  • blocking Ca2+ channels in the AV node
  • makes cells inexcitable
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14
Q

Mechanism of indirect re-entry suppression?

A
  • target K+ channels
  • block the conduction/ delay repolarisation anywhere in the re-entrant pathway
  • to prolong refractory period
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15
Q

Action of class IV drugs

A

Directly block re-entry in the AV node by blocking Ca2+ channel

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16
Q

Action of class I drugs

A

Directly block re-entry in AV node, atria and sometimes ventricles by blocking Na+ channels

17
Q

Action of class III drugs

A
  • indirectly block re-entry in atria, by blocking K+ channels
  • are indirect re-entry blockers because prolonging the refractory period indirectly blocks Na channels and conduction
  • delays repolarisation/ prolongs refractory period
  • ragged or split wave fronts encounter fewer excitable cells
  • re-entry wave is therefore blocked
18
Q

Why are class III drugs no longer used for ventricular fibrillation?

A
  • originally developed for treating VF causing ventricular repolarisation
  • in ECG, seen as QT prolongation
  • ALL CLASS III DRUGS PROLONG QT
  • but is dangerous and can cause torsades de pointes syndrome

so now used in lose dose for atrial arrhythmias

19
Q

Problems with drugs targeting re-entry

A
  • class I and class IV drugs must selectively target Na and Ca channels in the damaged region
  • however most are not selective enough so cause conduction block in normal tissue
  • can use a lower dose drug but this causes slow conduction block allowing for re-entry of wave front again
  • proarrhythmias
20
Q

How are class IV drugs administered?

A

Verapamil, diltiazem are class IV Ca2+ antagonists

  • bolus i.v. converts re-entry in the AV node to sinus rhythm
  • allows a high concentration to arrive at the AV node to block conduction in the damaged section
  • BUT are vascular selective/ not AV selective
  • this is overcome by iv bolus administration
  • drug hits the AV node in high concentration
  • drug is then diluted in ventricular blood
  • low concentration is pumped out to the rest of the body to produce side effects (vasodilation)
21
Q

Can nifedipine be used to treat arrhythmias?

A

No, it is completely vascular selective

No action on AV node even after iv bolus

22
Q

How is a drug classified as class I or class III?

A

depends on its relative selectivity of action

  • a QT widening drug with no appreciable effects on conduction velocity at therapeutically relevant concentrations is defined as class III
23
Q

How were older antiarrhythmics classified?

A

Class 1a: quinidine
Class 1b: lidocaine
Class 1c: flecainide

24
Q

Class 1a quinidine

A
  • effective against supraventricular arrhythmias
  • lethal ventricular arrhythmias not suppressed
  • substantial class III effects such as QT widening at therapeutic concentrations
  • torsades de pointes is a major side effect
  • sinus tachycardia due to muscarinic antagonism
25
Q

Class 1b lidocaine

A
  • iv only
  • more selective for Na+ channel (versus K+ channel) than class 1a drugs
  • effective against ventricular premature beats
  • BUT no reduction in death in the long term
  • use is declining
26
Q

Class ic flecainide

A
  • used for supraventricular arrhythmias only
  • blocks Na+ channel throughout the heart
  • not selective for damaged tissue!!
  • thus, slows conduction like ischaemia
27
Q

What are the first and second generation of class III drugs?

A

First generation: amiodarone, DL-SOTALOL

Second generation: D-sotalol, dofetilide

28
Q

First generation class 3

A
  • amiodarone for ventricular fibrillation
  • DL- sotalol for supraventricular arrhythmias

adv

  • little or not negative ionotropic effects
  • amiodarone reduces VF in MI

diasd
- side effects of amiodarone preclude long term use: corneal opacities, thyroid dysfunction

29
Q

Second generation class 3

A
  • were originally developed for VF
  • only used against supraventricular arrhythmias
  • highly potent
  • selective against K+ channels
  • D sotalol has no beta adrenergic antagonist effects unlike DL-sotalol
30
Q

Unmet needs in cardiac arrhythmias?

A
  • antiarrhythmic drugs dont affect the cure but merely treat the manifestation

need drugs to

  • achieve selective drug action
  • no pro-arrhythmic liability
  • better overall side effect profile
  • fewer interactions
  • need a good tolerable drug

NEED DRUGS TO TARGET VENTRICULAR FIBRILLATION
- automatic implantable cardiac devices are used but most VF victims die from the first attack

CVR (12 decks)

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