Arrhythmias

1. Arrhythmia
Disturbances in cardiac rhythm i.e
abnormality in site of origin of impulse, its
rate, regularity or conduction.

3. Tachyarrhythmias:
Defined as heart rhythm with a rate in
excess of 100bpm
Bradyarrhythmias:
Defined as heart rhythm with a rate less
than 60 bpm

4.  Atrial:
Sinus tachycardia
Atrial flutter (200-350/min.)
Atrial fibrillation (350-500/min.)
Supraventricular tachycardia
 Ventricular:
Ventricular tachycardia
Ventricular flutter
Ventricular fibrillation

5.  Antiarrhythmic drugs suppress arrhythmias
by blocking flow through specific ion
channels or by altering autonomic function.
 Block of Na+ or Ca2+ channels usually results
in altered threshold, and block of cardiac K+
channels prolongs the action potential.

7. Class I: Na channel blockers
a. IA: Drugs that prolong action potential
duration- Quinidine, procainamide,
disopyramide
b. IB: Drugs that shorten action potential
duration- Lignocaine, mexiletine,
phenytoin
c. IC: Drugs that have minimal effect on
action potential duration- Flecamide

8. Class II -Beta adrenergic blockers:
Propranolol, atenolol, esmolol, metoprolol,
sotalol
Class III- K channel blockers:
Amiodarone, bretylium
Class IV- Calcium channel blockers:
Verapamil, diltiazem
Others:
Adenosine, Digitalis, Atropine

9.  PSVT- Adenosine, Digitalis, Esmolol,
Verapamil
 AF- Esmolol, Verapamil, Amiodarone
also Digitalis
 VT- Lignocaine, Amiodarone
 VF- Lignocaine, Amiodarone
 A-V Block- Atropine, Isoprenaline
 Torsades de pointes- Magnesium Salts

11. Quinidine
 MOA: Quinidine blocks myocardial Na+ channel, reduces
automaticity and depolarization in a frequency dependent
manner. Quinidine blocks Na+ current and multiple cardiac
K+ currents.
 It is used to maintain sinus rhythm in patients with atrial
flutter or atrial fibrillation and to prevent recurrence of
ventricular tachycardia or ventricular fibrillation.
 Pharmacological actions of quinidine:
 Cardiac tissue:
▪ Reduce automaticity
▪ Reduce excitability
▪ Reduce conductivity
▪ Prolong refractory period
▪ Reflex tachycardia
Other action:
• Anti-malarial
• Anti-pyretic
• Decrease B.P (vasodilation)

12. Indications:
 As anti-arrhythmic used in:
 Atrial fibrillation and flutter
 Ventricular fibrillation and flutter
 Paroxysmal supra-ventricular
tachycardia
 Premature supra-ventricular
tachycardia
 Atrial, nodal and ventricular
premature beats
 Also as anti-malarial
 Anti-pyretic
 During digitalis therapy
 Adverse effects:
 Fall in BP
 Vomiting
 Diarrhoea
 Cinchonism:
 Headache, vertigo
 Blurred vision
 Tinnitus
 Contraindications:
 Quinidine
intolerance
 Digitalis
intoxication
 Heart failure
 Hypotension
 hypokalemia

13. Lignocaine
 MOA: It has membrane stabilizing effect by blocking
both activated and inactivated Na+ channels; which
in turn suppresses SA node and also ectopic beats.
 Shortens refractory period and action potential;
make uniform rhythm.
Indications:
 As local anesthetic
 As anti-arrhythmic
 suppressVT
 PreventVF
Adverse effects:
 Bradycardia
 Hypotension
 Seizure
 Nystagmus

14. Propanolol
 It blocks β-receptors in heart, thereby exerts
▪ Negative inotropic effect
▪ Negative chronotropic effect
▪ Depress atrioventricular conduction
▪ Depresses automaticity
 It has:
▪ Anti-arrhythmic effect
▪ Anti-hypertensive effect
▪ Anti-anginal-effect in CVS.

15.  MOA: Prolongs APD and Q-T interval
 Blocks inactivated Na+ channels
 Partially inhibits myocardial Ca2+ channels
 Conduction is slowed and ectopic automaticity is markedly depressed
Cardiac effects
a. Block Na channels (1A), but low affinity for open channels; mainly blocks
inactivated Na channels
b. Block is most pronounced in tissues with long action potentials
c. Weak Ca channel blocker also (Class IV activity)
d. A powerful inhibitor of abnormal automaticity, decreases conduction,
increases refractory period and APD.
e. Has antianginal effects (blocks alpha/beta receptors and Ca channels)
Extracardiac effects:
Vasodilation via block of Ca channels and alpha receptors

16. A. Cardiac
i. Sinus bradycardia, increase QT interval
ii. Negative inotropic action due to block of Ca channels and beta
receptors; but can improve heart failure via vasodilation.
iii. A-V block, paradoxicalVTs.
B. Non-cardiac:
i. Deposits into almost every organ
ii. Reduces clearance of drugs like procainamide, flecainide, quinidine
iii. Thyroid dysfunction (hypo or hyperthyroidism)
iv. Pulmonary fibrosis is most serious adverse effect
v. Paresthesias (tingling, pricking, or numbness)
vi. Photosensitivity
vii. Corneal microdeposits and blurred vision
viii. Ataxia, dizziness, tremor
ix. Anorexia, nausea

17. A. Adenosine: i.v. (15 secs), activates P1 purinergic receptors
(A1) coupled to K channels, ↓CV, ↑refractory period.
A/E: Flushing, hypotension, burning sensation
B. Potassium ions (K+): Depress ectopic pacemakers
- can depress CV → reentrant dysrhythmia
C. Digoxin:
 used to treat atrial flutter and fibrillation
 AV node ↓conduction (vagal stimulation)
 myocardium ↓refractory period
 Purkinje fibers ↑refractory period, ↓conduction
D. Magnesium: used to treatTorsades de Pointes
E. Autonomic agents: used to treat A-V block
β-agonists (Adrenaline) , anticholinergics (Atropine)