Classification.defination .MOA and synthesis of antiiarythimic drugs

1. 1
Wilsita Snehal Dsouza
III PHARM D
19Q0807

4. 1- SA node generates
action potential and
delivers it to the atria
and the AV node
2- The AV node delivers
the impulse to purkinje
fibers
3- purkinje fibers
conduct the impulse to
the ventricles
Other types of
conduction that occurs
between myocardial
cells:
When a cell is
depolarized 
adjacent cell
depolarizes along
Normal conduction pathway:

5. Phase 0 : rapid depolarisation
(inflow of Na+)
Phase 1: partial repolarisation (inward
Na
+
current deactivated, outflowof K+)
Phase 2 : plateau (slow inward
calcium current)
Phase 3: repolarisation (calcium
current inactivates, K+outflow)
Phase 4 : pacemaker potential
(SlowNa+ inflow, slowing of K+
outflow) ‘autorhythmicity’
II
I
III
IV
5

6. 2. VOLTAGE- GATED Na+ Channels

7. 3. EFFECTIVE REFRACTORY PERIOD
ERP :
It is also called Absolute refractory period (ARP)
• In this period the cell can’t be excited
• Takes place between phase 0 and 3

8. ECG showing wave segments
Contraction
of atria
Contraction
of ventricles
Repolarization
of ventricles
8
- Recording of electrical activity of the heart
- Net sum of depolarisation and
repolarisation potentials of all myocardial
cells
- P-QRS-T pattern
- P - atrial depolarisation
- QRS -ventricular depolarisation
- T - ventricular repolarisation

9. 4 . Arrhythmia
“ Cardiac arrhythmias is the abnormality of rate,
origin and conduction of impulses.”
• Bradycardia – heart rate slow (<60beats/min)
• Tachycardia – heart rate fast (>100beats/min)
Causes of
arrhythmia
arteriosclerosis
Coronary artery
spasm
Heart block
Myocardial
ischemia

10. MECHANISMS OF ARRHYTHMIAS
1. Enhanced or ectopic pacemaker activity
2. After depolarization :
a) Early after depolarization(EAD)
b) Delayed after depolarization(DAD)
3. Re-entry arrhythmias

11. 1. Enhanced or ectopic pacemaker activity
• There is an increase in the pacemaker activity.
• It causes phase- 4 directly reach into the threshold
potential.
• Ectopic means some other abnormal tissues in the
heart is acting as the pacemaker and it is exciting
your heart. This can be due to ischemia,
atherosclerosis or some damage to cardiac tissue
which causes ectopic pace activity.

12. 2. After depolarization
• EAD and DAD
• EAD: As the name indicates, after the
depolarization (phase 2) any abnormal signal can
excite the heart tissue and generate the impulse
before it reaches the resting membrane potential.
• DAD: It has just reached phase 4and there is
again generation of impulse

13. 3. Re-entry arrhythmias
• Re-entry means the beat is entering again to the same location.
• Two types of conduction:
- Antegrade
- Retrograde
• Generally atria excites ventricle- Antegrade
• Ventricle is exciting your atria- Retograde, which is abnormal.
• Re-entry either takes place at the AV node which is known as AV
nodal reentrant tachycardia or else it can take place at accessory
pathway.
• Accessory pathway is the abnormal pathway which can directly
excite the ventricle. ( Wolff-Parkinson White syndrome)

14. 5. Types of Arrhythmias
• Sinus rhythms : Sinus bradycardia
Sinus tachycardia
• Atrial rhythms : Atrial flutter
Atrial fibrillation
AVNRT
• Ventricular rhythm : Ventricular tachycardia
Ventricular fibrillation
A-V block
Paroxysmal supraventriculr tachycardia

15. Sinus rhythms
• Normal sinus rhythms – 60 to 100 bpm
• Most common variations of sinus rhythms include
Sinus bradycardia - When SA node fires less than 60
times per min resulting in a slow heart beat, <60 bpm.
It is considered normal during sleep.
Sinus tachycardia - When SA node fires more then
100 times per minute resulting in a fast heart beat,
>100 bpm . It may be normal during physical
exercise.

16. Atrial Flutter
• It is caused by an electrical impulse that travels around in a localized cells
forming a loop.
• Most commonly located in the right atrium.
• For each cycle around the loop there is one contraction of the atria.
• The atrial rate is rapid btw 250 and 400 beats per min. Ventricular rate is
however slower due to refractory properties of AV node.
• The AV node blocks part of atrial impulses from reaching the ventricles.
Only one out of 3 atrial impulses makes its way to the ventricle. The
ventricular rate is therefore 3 times slower than the atrial rate. This is an
example for 3:1 heart block.
ATRIAL RHYTHMS

17. Atrial Fibrillation
• Caused by multiple electrical impulses that are initiated
randomly from the ectopic sites in and around the atria.
• These unsynchronised cardiac electrical signals cause the atria
to quiver or fibrillate rather than contract.
• The atrial rate at atrial fibrillation can be extremely high, but
most of the electrical impulses do not pass through the AV
node to the ventricles.

18. AVNRT
• It is caused by a small re-entrant pathway that falls directly to
the AV node.
• Every time the impulses passes through the AV node it is
transmitted down to the ventricles.
• The atrial rate and the ventricular rate is therefore identical.
• The heart rate will be 150 to 250 bpm.

19. Ventricular Tachycardia
• V- tach is commonly caused by a single strong firing
site in one of the ventricles.
• Impulses starting from the ventricles produces
ventricular premature beats ranging from 100- 250
bpm.
Ventricular Fibrillation
• Caused by multiple weak ectopic sites in the ventricles.
• These unsynchronised cardiac electrical signals cause the
ventricle to fibrillate rather than contract.
• Heart can pump little or no blood.
• V-Fib can quickly lead to cardiac arrest.
VENTRICULAR RHYTHMS

20. PSVT
• It may either result from AVNRT or as a part of Wolff- Parkinson White
syndrome.
• In AVNRT a small extra pathway exists in or near the AV node. If an
electrical impulse enters this pathway, it may start travelling in a circular
pattern that causes heart to abruptly start beating fast.
• PSVT can occur when the doses of the heart medicines are too high.
AV blocks
A conduction block within the AV node , occasionally in the bundle of His,
that impairs impulse conduction from the atria to the ventricles.

21. Class I: Block sodium channels –
Membrane Stabilizing agents
Ia (quinidine, procainamide, disopyramide)
Ib (lignocaine,phenytoin)
Ic (flecainide,propaferone)
Class II: ß-adrenoceptor antagonists
Antisympathetic Drugs
eg : propranolol,atenolol, sotalol
Class III: Prolong action potential and prolongrefractory period
(suppress re-entrant rhythms) – Prolonging cardiac action
eg : amiodarone, dronedarone
Class IV: Calcium channel antagonists. Impair impulse propagation
in nodal and damaged areas - Interference with calcium conductance
eg: verapamil,diltiazem
21
6. ANTIARRHYTHMIC DRUGS/ ANTIDYSRHYTHMIC
DRUGS/ ANTIFIBRILLATORY DRUGS

23. 23
Procainamide
Quinidine
Disopramide

26. 26
Lignocaine

29. 29
Flecainide
Morcizine
Propafenone

32. 32
Atenolol

34. Amiodarone
Dronedarone

37. class mechanism action notes
I Na+ channel blocker
Change the slope of
phase 0
Can abolish
tachyarrhythmia
caused by reentry
circuit
II β blocker
↓heart rate and
conduction velocity
Can indirectly alter K
and Ca conductance
III K+ channel blocker
1. ↑action potential
duration (APD) or
effective refractory
period (ERP).
2. Delay repolarization.
Inhibit reentry
tachycardia
IV Ca++ channel blocker
Slowing the rate of rise in
phase 4 of SA node(slide
12)
↓conduction velocity
in SA and AV node

38. Other antiarrhythmics
1. Adenosine :
– Purine nucleotide having short and rapid action
– Mechanism of action: AcetylCholine sensitive K+
channels and causes membrane hyperpolarization
through interaction with A1 type of adenosine
GPCRs on SAnode
– IV suppresses automaticity, AV conduction and
dilates coronaries
– Drug of choice for PSVT
– Adverse events:
• Nausea, dyspnoea, flushing, headache
2. Atropine: Used in sinus bradycardia
3. Digitalis: Atrial fibrillation and atrial flutter
4. Magnesium SO4: digitalis induced arrhythmias

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