Anti-arrhythmias Flashcards
Phase 0
- Rapid depolarization
- Fast Na+ influx
Phase 1
- Partial repolarization
- K+ ion efflux
- Na channels inactivated
Phase 2
- Plateau achieved
- Slow Ca2+ influx
- K+ continues efflux
Phase 3
- Repolarization
- Ca2+ channels close
- K+ efflux continues
- Membrane voltage becomes negative
Phase 4
-Pacemaker potential
- K+ channels close
- Some K+ influx
- Resting membrane voltage maintained until depolarization signaled to proceed to phase to phase 0
Involvement of SNS
- Beta 1 receptor
- Positive inotropy and chronotropy
- Reduced cardiac efficiency
Involvement of PNS
- M2 receptor
- negative inotropy and chronotropy
- inhibition of AV conduction
- reduce automacity
Precipitating factor After-depolarization
- triggered depolarization interferes with action potential
- May be early P2&3 or delayed P4
- precipitate sustained firing
Precipitating factors re-entry
- Propagating impulse fails to stop
- Cardiac excitement continues
- Heart is continuously stimulated> tachycardia
Precipitating factors ectopic pacemaker activity
- Other cardiac tissues adopt pacemaker activity
- normal cells spontaneously depolarize> tachycardia
Precipitating factors heart block
- Fibrosis/ ischaemic damage to conduction system
- Atria and ventricle beats independently of each other
- bradycardia
Types of heart blocks
- 1st degree: slow conduction, all impulses reach ventricle
- 2nd degree: some impulses blocked> severe bradycardia
- 3rd degree: all impulses> bradycardia
MOA of class I drugs
- Blocks voltage gated Na+ channels> reduces amplitude and slope of phase 0
Class I drugs
- disopyramide (Int diss)
- Lidocaine (Fast diss): marked first-pass met
- Flecainide (Slow diss)
Side Effects of Class I drugs
- Anticholinergic SE
- Drowsiness, Dizziness
- Bradycardia
MOA of Class II drugs
Blocks beta adrenergic stimulation> reduces AV conduction> increases refractory period
- act on Phase 2&4
Class II drugs
Propanolol atenolol
MOA of Class III drugs
-Blocks voltage gated K+ channels> prolonging cardiac action potential
- Blocking repolarizing K+ channels> Increases refractory period
- Act on phase 3
Class III drug and its side effects
- Amiodarone t1/2 142Days
- photosensitivity, pulmonary fibrosis, hypo-hyperthyroidism
MOA of Class IV drugs
Block voltage gates Ca channel> slow conduction in SA&AV nodes> shortens plateau> reduce myocardial infarction
- Reduced after-depolarization and ectopic beats
- Acts on phase 2
Class IV drugs
- Verapamil, diltiazem
MOA of adenosine
- not classified by Vaughan Williams classification system
- Activates adenosine A1 receptors> hyperpolarizes pacemaker cells> slows conduction velocity> negative chronotropy effects
Adenosine considerations
- 10sec T1/2
- metabolized in 2 ways:
- Deaminated by adenosine deaminase to inosine
- Adenosine kinase may recycle and re-phosphorylate it to adenosine monophosphate
Adenosine side effects
Chest pains
Shortness of breath
Dizziness
Nausea
