2. Cardiac arrythmias results from alterations in the orderly
sequence of depolarisation followed by repolarization in the heart.
OR
Cardiac arrythmias may result in alterations in heart rate or rhythm
and arise from alterations in simple generation or conduction.
2 types: Tachycardia (Heart beat more than normal) and
bradycardia (Heart beat less than normal)
CARDIAC ARRYTHMIAS
Definition
3. ELECTROPHYSIOLOGY – CARDIAC RHYTHM
IMPULSE GENERATION
AND CONDUCTION
Conducting tissue
• SA node,AV
node,bundle of his &
purkije fibers.
Contractile tissue
• Atria and ventricles.
7. Depressed automaticity of SA
node
Enhanced automaticity of SA
node
Ischemia, digitalis,
catecholamine's, acidosis,
hypokalaemia
1) Abnormal impulse
generation
2) TriggeredActivity
•Extra abnormal depolarisation
Due to abnormal
intracellular Ca2+
regulation
8. Conduction
block
Reentry
phenomenon
3) Abnormal impulse conduction
Due to abnormality of conduction , an impulse may
recirculate in the heart and causes repetitive activation
without the need for any new impulse to be generated.
These are called reentrant arrythmias.
9. The ultimate goal of antiarrhythmic drug therapy:
o Restore normal sinus rhythm and conduction
o Prevent more serious and possibly lethal arrhythmias from
occurring.
Antiarrhythmic drugs are used to:
o Decrease conduction velocity
o Change the duration of the effective refractory period
(ERP)
o Suppress abnormal automaticity
Pharmacological goals
10.
11.
12. Class I
IA IB IC
They ↓ automaticity in non-nodal
tissues (atria, ventricles, and purkinje
fibers
They act on open Na+
channels or
inactivated only
Have moderate K+ channel
blockade
13. IA
Quinidine Procainamide Disopyramide Moricizine
Slowing the rate of rise in phase 0
They prolong action potential & ERP
↓ the slope of Phase 4 spontaneous depolarization
↑ QRS & QT interval
14. QUINIDINE
It’s a isomer of quinine- natural alkaloid of CHINCHONA
BARK.
Antimalarial, antipyretic, skeletal muscle relaxant and
atropine like action.
15. Mechanism of action (Pharmacological effects)
1.
Depolarisati
on:
Quinidine
binds to
open and
inactivated
sodium
channels
depress the
sodium
influx,
slowing
deporisation-
repolarisation
cycle
2. Impulse
formation:
direct
effect
Slow down
the
impulses
3. Excitability:
Decrease the
excitability of
cardiac
muscles
So threshold of
an impulse to
initiate cardiac
activity is
increases
So weak
impulses
become
ineffective
4.
Repolarizatio
n:
Increase it by
depression the
K+ efflux
5.
Conduction
velocity:
decreases
16. Quinidine- Extra cardiac effects (Pharmacological
effects)
1. It produces a fall in BP on oral or parenteral
administration--- dur to decrease sympathetic activity and
direct dilation of arteries.
2. If Cardiac output is low- quinidine returns to normal- no
effect on normal CO.
3. It produces relaxant effects in skeletal muscles.
4. It also have anti malarial, anti pyretic and oxytocic
activity.
17. Pharmacokinetics
• Oral – rapid GI absorption and 80% plasma protein binding
• Half life- 6 hours.
• If given parenteral may can cause hypotension
ADVERSE EFFECTS:
Diarrhoea
“Cinchonism” – tinnitus, vertigo, headache, nausea & blurred vision.
200-400 mg orally tds
USES: Ventricular tachyarrythmias
DRUG INTERACTIONS:
• Quinidine can interact the plasma concentration of digoxin, which may in turn lead to
signs and symptoms of digitalis toxicity.
• Cimitidine increases hepatic metabolism of quinidine
18. They shorten Phase 3 repolarization
↓ the duration of the cardiac action potential
IB
Lidocaine Mexiletine Phenytoin
19. LIDOCAINE
• Drowsiness
• Slurred speech
• Confusion and convulsions
• V
A
• Digitalis toxicity
A/E
Uses
the duration of action potential decreases
Mechanism of action
It shorten phase 3 repolarization and decreases the
duration of action potential
20. markedly slow Phase 0 depolarization
slow conduction in the myocardial tissue
minor effects on the duration of action potential
and ERP
reduce automaticity by increasing threshold potential
rather than decreasing slope of Phase 4 depolarization.
IC
flecainide Encainide Propafenone moricizine
21. FLECAINIDE &
ENCAINIDE
Mechanism of action
Flecainide suppresses phase 0 upstroke in purkinje and myocardial
fibers.
This causes marked slowing of conduction in all cardiac tissues, with a
minor effect on the duration of the action potential.
Use- ventricular arrhythmia
A/E –visual disturbances & headache
22. CLASS II DRUGS – PROPRANOLOL, METOPROLOL,
ESMOLOL, ACEBUTOLOL (Beta-blockers)
The primary action of drugs in this class is to suppress adrenergically
mediated ectopic activity.
propranolol have quinidine like direct membrane stabilizing action at
high doses,
but in the clinically used dose range—antiarrhythmic
action is exerted primarily because of cardiac adrenergic blockade.
Propranolol decreases the slope of phase-4 depolarization and
automaticity in SA node, PF and other ectopic foci when this has been
increased under adrenergic influence
25. • K+ channel blockers
• AP / ERP without affecting
phase 0 / 4
Class III
Amiodarone Bretylium Sotalol
26. Amiodarone
Iodine –
containing
Block K+ Na+ ,
Ca++ & β
HR &AV
nodal
conduction
QT prolongation
Uses =VF, VT
&AF
Arrhythmic
death in post MI
LD-150mg slow
IV
MD-1mg/min
for 6hrs
A/E – heart block,
hepatitis,
dermatitis,
Interaction –
digoxin,
diltiazem &
quinidine
27. Mechanism
• Block L-type calcium channels.
• Rate of phase 4 in SA / AVnode
• Slow conduction – prolong Refractory period
• Phase 0 upstroke
Class IV
Verapamil Diltiazem
28.
29. Verapamil
Stronger action on heart than smooth muscle
Used in supraventricular arrhythmia
80-120mg three times a day
A/E – ankle oedema, constipation
C/I – AVblock, hypotention
It digoxin toxicity
Diltiazem
Mixed action
Oral dose 30-90mg 6hourly
30. WHICH OTHER DRUGS……
Adenosine
Naturally occurring nucleoside
Adenosine receptors – inhibits nodal conduction
Used in Reentry & SVT
Ultra short t1/2 (10-20 sec)
A/E – facial flushing, short breath, bronchospasm, metallic taste
Dipyridamole it’s action
3mg IV bolus
31. REFERENCES
Pharmacology - IV edition , Pg.no:196-207
- Lippincotts
Illustrated reviews
Clinical pharmacology - IX edition , Pg.no:497-519
- P.N.Bennett
- M.J.Brown
Essentials of medical pharmacology – K .D. Tripathi Pg.no:508-520
Pharmacology – Rang/ dale
- fifth edition , Pg no:277-280
Modern pharmacology with clinical Applications.
- Sixth edition
- Charles R.Ciaig. Robert E. Stitzel
