Antiarrhythmic Drugs
Deviation Cardiac Rhythm
from
°
the normal
pattern of is
known as
Arrhythmia .
Cardiac Action Potential
Phase 0 :
Nat channel
opens
•
causing Depolarization .
Rate
of Depolarization
°
depends No onMat .
☐
channels
open
.
Antiarrhythmic
•
Class I
slow
Drugs can
or block Phase 0 in
Phase I Fast Response fibers
°
.
.
•
Nat channels are inactivated
•
In some His -
Purkinje cells ,
transient outward Kt currents
and inward a
-
currents contribute to
"
Notch
"
& Overshoot .
Antiarrhythmic Drugs have no
significant Effect here
•
Phase 2 :
Plateau which slow
phase in
influx of
"
• a Ca in
balanced
by late appearing - outward K+ current .
Antiarrhythmic drugs have no
significant effects .
Phase 3 :
Re polarisation phase in which
delayed rectifier K+ current
°
current dies out
rapidly
"
increases as Ca as ca
"
channels
close .
slow this Repolarization
•
Class -11
Antiarrhythmic drugs phase .
Phase 4 :
• Return of Membrane to
Resting Potential -
maintained
by
activity ☐
Nat / K+ ATPase .
•
This in
Resting Membrane
potential .
associated Diastole
This
phase is with
•
.
Nat channels
• Exists in 3
conformation :
state
(a)
Resting or
Ready
(b)
Open / Active state
(c) Inactivated or
state
Refractory
•
Channel has 2 Gates :
(is M ( activating )
(in h ( inactivating )
Inactivation of gate it stays
•
h in slower ,
so
, open longer
and Nat channel in active .
Heart Rate
ANS
Regulation of
Nodal tissue Mode innervated
SA in
heavily by both
•
esp
.
PANS & SANS
fibers activating Mz & Pt Receptors , resp
.
• Phase 4 slope is increased
by :
A cAMP via P
,
Receptor Activation
& Slowed
by a CAMP
from Mz Receptor Activation .
Increase in cAMP Decrease in CAMP
in Increase
upstroke velocity in slows the Rate g diastolic
in
pacemakers by increase de polarisation via K+ current
of cast current
and thus decrease Heart
Rate .
Shorten duration
(2) AP
by
increase Potassium current 121 P blockers prevent CAMP
of
(3) Increase Heart Rate formation ,
with
primary
effects on SA & Av Nodes .
Cardiac Action Potential with Ecg
•
Phase 0 & I QRS Complex
( Depolarization )
Phase
• 2 57
Segment
( Plateau Phase )
•
Phase 3 T wave
( Repolarization )
f-
Singh & Vaughan William’s Classification of Antiarrhythmic Drugs
•
Class I Mat Channel Blockers
• Class I Beta Blockers
•
Class II Kt Channel Blockers
"
• Class II Ca channel Blockers
Class Miscellaneous
I
Drugs
•
.
Class 1 : Na Channel Blockers
•
Class ?
Antiarrhythmic Agents interfere with the
activity
Nat channels
of .
•
All these drugs can decrease the
slope of phase 0 ( Imax)
• More
frequently the Nat channels
open ,
greater will be
blockade
by
these
drugs .
Further divided a/c to Action on Kt channels :
① Class IA :
state )
•
Antiarrhythmic ,
blocks
fast Nat channels ( in
open
.
•
Also blocks K+ channels thus
delaying Re
polarisation
resulting in
prolonged Action Potential duration .
Prolonged QT interval .
Drugs : ii. Quinoline
iii, Procainamide
Quinidine :
channel state
•
Blocks
fast Nat in
open
4 also K+ channel .
Causes conduct
receptor
'
•
Muscarinic blockade ,
came HR & Av
-
On .
Vasodilation
•
May cause via ✗ block with
possible
reflex tachycardia .
Orally effective
•
As Quinoline in derivative g
→
• Adverse
Effects : ( is Cinchonism cinchona
plant .
I
(a)
Tinnitus (e) Visual Disturbances
(b)
Vertigo if , Mental
changes .
(c) Deafness
(d) Headache
ciii Nausea ,
Vomiting & Diarrhea
eiiis
Hypotension
civs
Hypoglycemia
in
Prolongation y QRS
iris 19 QT interval
( Ii
Drug Interaction :
Hyperkalemia enhances
effect
iii. Displaces digoxin from Tissue
binding
a site
Enhancing toxicity
Procainamide :
•
less muscarinic receptor block
Metabolised
• via H -
acetyltransferase to N -
acetyl procainamide
•
Adverse effects : ii.
systemic lupus erythematosus ( SL E)
like syndrome in 30%
Hema to
iii.
I
toxicity
Thrombocytopenia
(a)
(b)
Agranulocytosis
Liii ' C"
Effects ( Tor sa def Prolonged QT
interval .
② Class I B :
Antiarrhythmic : block fast Nat channels
But K+ Channel
opening Properly
•
.
•
A APD ( Atrial premature depolarization ) Due to blocky
slow Nat window currents ,
but this increases
Extends time
diastole &
for Recovery .
These drugs are used
only for Ventricular Arrhythmia
• .
?
ylocain )
lidocaine (
Drugs : ii.
leg no caine ) ( ✗
iii. An exile line
Iii, Tocainide
( in
Phenytoin
lidocaine :
•
Post MI , Open - Heart
surgery .
Digoxin Toxicity
Ventricular
Arrhythmias only .
local Anaesthetics
•
lignocainc in most
commonly used in .
• Side Effects : ii. CNS
Toxicity ( seizures )
least cardio toxic
Liii
of conventional
Anti -
arrhythmia .
• Administered only by 1.x .
M exile line :
Orally Active lignocaeine derivative with all
properties
of lignocaine .
③ Class IC :
•
Block fast Nat channels ,
up
. His -
Purkinje tissue
•
No
effect on APD
No
•
AMS
Effects
Negligible effect
•
on Kt channels .
Drugs :
ci , Flecainide
ii, Encainide
iii. Morici zine
in
Pnopafe none
Flecainide
arrhythmia genic effects
limited became Pro
•
me
of ,
indicated Resistant life threatening
thus
only for & -
ventricular tachycardia or
Refractory supra ventricular
tachycardia .
Flecainide Can be used Parkinson white
• in
Wolff
IN PW )
syndrome . (
Class II : Beta Blockers
•
Prevent P -
Receptor Activation ( B Blockers ) .
which
eventually $ CAMP .
I 5A
Activity
Node
°
& An
Adrenaline
•
They act
by blocking Effect of & Nor adrenal
-
- ine .
treatment
•
Helpful in , supra ventricular Tachycardia .
Decrease slope of Phase 4
of AP in Pacemakers .
Drags : ii. Fsmolol ( shortest acting )
Iii ,
Propranolol
( iiis
Metropol ol
Class III : K Channel Blockers
• Decrease K+ current
by blocking Kt
slowing
Channel thus ,
phase 3 ( Re polarisation ) /
Prolonging Repolarization .
( Effective
• APD Ñ
,
ERP
Refractory Period ) I ,
QT Interval
4
•
These
drugs exhibit Reverse Use
Dependent Prolongation ,
AP duration .
Means Refractoriness Tat Lower Heart Rates .
He
these
preventing
Thus
,
are more
efficacious a
1-
achy arrhythmia than
treating it .
Amiodarone
Dregs : ii.
Iii , Sotalol
(
iii,
Bretyleiem
in Ibulilide
in
Dofetéléde
Amiodarone
Possesses action
•
of all clauses
of Antiarrhythmic drugs .
• Increases APD & ERP in all Cardiac tissues .
tyz > so
days ( ✗
congest Acting )
•
Side
Effects : ii.
Pulmonary fibrosis
•
iiii Blue
pigmentation of skin ( Smurf skin )
Photo
toxicity
Iii)
(
(
in corneal deposits
in
Hepatic Necrosis
evil
Thyroid dysfunction -
So 1- alot
• Decrease K+ current ,
slowing phase 3 .
Non selectin P blocker to
:
P, Blockade
leading
•
IHR , te Au conduction .
Ventricular
Use in
life threatening arrhythmia
•
- .
Side
•
Effect : Torsade .
Class IV : Ca Channel Blockers
"
°
Block slow Cardiac Ca Channels
•
Decrease
phase 0 . I, Phase 4
Decrease Nodal
Activity
•
SA & All .
✗
Digs : cis
erapamil
cii , Diltiazem
Verapamil & Diltiazem
Prototype
"
•
Ca Channel Blockers
•
Uses :
Supra ventricular Tachycardia
• Side
effects : Constipation ( ilerapamil )
Dizziness
Flushing Hypotension
At Block '
Class V : Unclassified
Dregs : ii.
Digoxin
ciis Adenosine
ciii ,
Magnesium
in
Atropine
in Potassium
Adenosine :
• Activates adenosine receptors : I. CAMP
5A Nodal
Activity
& All
• I
,
Urges : Paroxysmal supra ventricular Tachycardia
°
All Nodal
Arrhythmias
•
Administered 111 : 1- in
< 10sec
•
Side
effects :
Flushing
Sedation
Dyspnea
C
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