Antiarrythmitics Flashcards
(55 cards)
What is an Arrhytmia?
Heart condition involving disturbances in;
- Pacemaker impulse formation
- Impulse conduction
- or a combination of the two
Results in a rate/ timing of contraction that is insufficient to maintain normal CO
Which cells use the Fast Cardiac Action Potential
- Atrial and cardiac Myocytes
- Cells in Purkyne tissue
List the Phases of the fast cardiac action potential
Phase 0: Depolarisation
Phase 1: Initial repolarisation
Phase 2: Plateau phase
Phase 3: Major repolarisation
Phase 4: Spontaneous depolarisation
What are the mechanisms of action of Classes I-IV of antiarrythmitics
Class I: Na blockers
Class II: Beta blockers
Class III: K blockers
Class IV: Ca blockers
How do Class I Antiarrythmitics affect the Fast cardiac AP?
Name 2
- Slowing of Rapid Depolarisation phase
- Minor effects on AP Duration
- Lidocaine
- Flecainide
How do Class II Antiarrythmitics affect the Fast cardiac AP?
Name 2
- AP duration increased
- Reduced depolarization in phase 4 (Na-K ATPase)
- Bisoprolol
- Metoprolol
How do Class III Antiarrythmitics affect the Fast cardiac AP?
Name 2
- Slowed repolarisation-> Increased AP duration and Refracory Period
- Amiodarone
- Sotalol
How do Class IV Antiarrythmitics affect the Fast cardiac AP?
Name 2
- AP duration increased
- Decreased phase 4 depolarization
(Also affects plateau phase) - Diltiazem
- Verapamil
List the Phases of the Slow cardiac AP (SA/ AV node conduction)
Phase 0: Depolarisation (‘Funny’ current slow Na channels)
Phase 3: Repolarisation
Phase 4: Spontaneous depolarisation
How do Ca blockers affect the Slow Cardiac AP
- Slowed depolarisation
- Lengthened refractory period
How do Beta agonstis affect the Slow Cardiac AP
- Speed up Phase 4 spontaneous depolarisation
How do Adenosine and Muscarinic antagonists affect the Slow Cardiac AP
- Slow down spontaneous depolarisation
Arrhythmias can be caused by abnormal impulse generation, which can be due to Automatic or Triggered rhythms.
Name 2 types of triggered rhythm
- Delayed afterdepolarisation
- Early afterdepolarisation
(Automatic rhythms- Sinus tachycardia, Ectopic impulses)
Arrhythmias can be due to Abnormal conduction.
What are 2 types?
- Conduction block (Degrees 1,2,3)
- Re-entry (Circus movement, Reflection)
List the intended actions of drugs used to treat Arrhythmias due to;
- Abnormal impulse generation
- Abnormal impulse conduction
Abnormal generation;
- Decrease Phase 4 slope
- Raise threshold for AP generation
Abnormal conduction;
- Reduce conduction velocity/ increase length of refractory period
Describe the pathology of Wolf-Parkinson-White Syndrome (WPW)
Additional tissue provides an accessory pathway for impulses to re-enter atria from ventricles
(Re-entry loop)
Briefly compare Class IB and IC Antiarrythmitics
Give examples
IB;
- No change in Phase 0
- Lidocaine, Mexiletine
IC;
- Marked change in Phase 0
- Flecainide, Propafenone
List 4 Class V Antiarrythmitics
- Adenosine
- Digoxin
- Atropine
- Ivabradine
Describe the administration of Lidocaine, Mexiletine and Flecainide
Lidocaine- IV only
Mexiletine- Oral only
Flecainide- IV or Oral
Describe the effects of Class IB Antiarrythmitics
- Fast binding offset kinetics
- No change in Phase 0 in normal tissue
In Fast Beating/ Ischaemic tissue;
- Reduced Phase 0 conduction
- Prolonged QRS segment
Describe the uses of Class IB Antiarrythmitics
- Acute Ventricular Tachycardia (or to prevent)
- Not used in atrial or AV junction arrhythmias (not effective)
List 3 ADRs of Class IB Antiarrythmitics
- Abdominal upset (N + V)
- Dizziness and drowsiness
Describe the effects of Class IC Antiarrythmitics
- Slow binding offset kinetics
- Significantly slowed Phase 0-> Prolonged refractory period (especially in rapidly depolarising tissue)
- Decreased Automacity and increased AP threshold
- Prolonged PR, QRS and QT
Describe the uses of Class IC Antiarrythmitics
- Mainly for AFib and AFlutter (supraventricular tachycardias)
- Premature ventricular contractions
- WPW syndrome
