Anti-Arrhythmic Drugs 1

Question 1

Phase 4 involves

Answer 1

Na/K ATPase

Question 2

SA Node

Answer 2

Pacemaker of the heart

• Do not need external stimulaus
• They have a constant Na and Ca leakage which is what leads to the beginning of the AP through slow Na channels opening

Question 3

Delay in spread?

Answer 3

Yes, because you need the atria to contract before the ventricles contract

Question 4

AV and Purkinje Fibers and AP?

Answer 4

They can but they don’t because the have lower BPM than the SA node

Question 5

Effective Refractory Period

Answer 5

Cardiac muscles is refractory to re-stimulation during the AP
A normal cardiac impulse cannot re-excite an already excited area during this time

Question 6

Atria ERP vs Ventricle ERP

Answer 6

Atria ERP is half the time that the ventricles is

Question 7

Anti-arrhythmic drugs may alter the rhythmicity of the heart by:

Answer 7

1) Decreasing the slop of phase 4 (depolarization) - so it takes the heart longer to recover (beta blockers)
2) Elevating the threshold potential (Na and Ca channel blockers)
3) Increasing the maximum diastolic potential - so it delays the next AP (adenosine)
4) Increasing the duration of the AP (K channel blockers)

Question 8

Through all mechanisms of anti-arrhythmic drugs, there will be ___?

Answer 8

Lesser number of AP at a given period of time

Question 9

Class 1 Anti-Arrhythmics

Answer 9

Na Channel Blockers

Reduces slop of phase 0 and increase threshold

Question 10

Class 2 Anti-Arrhythmics

Answer 10

Beta-blockers

blocks sympathetic and decreases the slop of phase 4

Question 11

Class 3 Anti-Arrhythmics

Answer 11

K-channel blockers

Delays repolarization and increases AP time and EPR

Question 12

Class 4 Anti-Arrhythmics

Answer 12

Ca-channel blockers

Blocks L type calcium channels which elevates threshold and affects phase 2

Question 13

Advantages of Vaughan classification system

Answer 13

Convenient way of classifying by primary MOA
Useful short hand
Within a class they have similar adverse effects
Good starting point

Question 14

Disadvantages of Vaughan classification system

Answer 14

Drugs within a class do not necessarily have same effects
Almost all drugs are dirty drugs
Metabolites contribute to many actions and AE

Question 15

Sodium Channel Blockers MOA

Answer 15

Bind the channels at the open or closed but not resting state
They release at phase 4 to allow the channel to recover

Question 16

Class Ib

Answer 16

Fast recovery
Shows effects on fast heart rate
(Weak drugs)
- Lidocaine, mexiletine

Question 17

Class Ic

Answer 17

Slow recovery
Shows effects at all heart rates
(Strong drugs)
- Flecainide, propafenone

Question 18

Class Ia

Answer 18

Intermediate
Effects depend on the rate
- Disopyramide (quinidine, procainamide)

Question 19

Flecainide (Tambocor)

Answer 19

Class Ic Slow Recovery
Potent Na channel blocker
Blocks some delayed rectifier K and Ltype Ca channels

Question 20

Flecainide Na channel blockade results in:

Answer 20

Slowing of conduction in all part of the heart esp His-Purkinje
Inhibition of abnormal automaticity
Delayed AP in faster HR
Acts at normal HR and prolongs QRS

Question 21

Flecainide Elimination and Metabolism

Answer 21

H/R

CYP2D6 and 1A2

Question 22

Flecainide AE

Answer 22

Pro-arrhythmic and heart block
Blurred vision
Exacerbation of HF

Question 23

Flecainide Caution

Answer 23

Patients with severe liver and renal impairment**, HF and electrolyte imbalance

Question 24

Flecainide Contraindications

Answer 24

2nd and 3rd degree AV block or right bundle branch block
Cardiogenic shock
CAD

Question 25

Propafenon (Rythmol)

Answer 25

Clasic 1c
Potent Na channel blocker with slow recovery
Most efficient in maintaining the sinus rhythm and modest with ventricular arrhythmias

Question 26

Propafenone Elimination and Metabolism

Answer 26

hepatic

CYP2D6

Question 27

Propafenone AE

Answer 27

Proarrhythmic effects
Exacerbation of HF
Bradycardia and bronchospasms

Question 28

Propafenone Caution

Answer 28

Patients with severe liver impairment and heart failure

Question 29

Propafenone Contraindications

Answer 29

Severe HF
Prolongs PR and QRS intervals
SA, AV and ventricular disorders
Bradycardia
Marked hypotension
Electrolyte imbalance

Question 30

Disopyramide (Norpace)

Answer 30

Class Ia 
Na blocker (increase threshold potential and decrease automaticity) with intermediate recovery
Blocks K channels (prolongation of AP) and L type Ca-channels 
Vagal inhibition  (anti-cholinergic effects)

Question 31

Disopyramide (norpace) Elimination and Metabolism

Answer 31

H/R

CYP3A4

Question 32

Disopyramide AE

Answer 32

Proarrhythmic effects
Exacerbation of HF
Heart block
Dry mouth 
Constipation
Urinary retention 
Precipitation of glaucoma

Question 33

Disopyramide Caution

Answer 33

Patients with severe liver and renal

Impairment and HF

Question 34

Disopyramide Contraindications

Answer 34

Cardiogenic shock
QT prolongation
2nd and 3rd degree AV block

Question 35

Lidocaine (Xylocaine)

Answer 35

Class Ib
Na blocker with fast recovery (weak)
Automaticitiy is decreased by increasing the threshold potential and reducing the slop of phase 4

Question 36

Lidocaine is not useful for the treatment of:

Answer 36

Arrhythmias

Question 37

Lidocaine Elimination and Metabolism

Answer 37

H/R

CYP3A4

Question 38

Lidocaine AE

Answer 38

Seizures when a large dose
Tremor, dysarthria
Nystagmus

Question 39

Mexiletine (Mexitil)

Answer 39

Class Ib
Weak Na channel blocker
Analog of lidocaine suitable
Chronic oral therapy
NOT USEFUL FOR ATRIAL ARRHYTHMIAS

Question 40

Mexiletine Elimination and Metabolism

Answer 40

H/R

CYP2D6 and CYP1A2

Question 41

Mexiletine AE

Answer 41

Proarhythmic effect
Exacerbation of HF
Upper GI distress
Lightheadedness 
Coordination difficulties