2. Normal conduction pathway:
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
3.
4. ARRHYTHMIA (ABNORMAL OR IRREGULAR RHYTHM)
If the arrhythmia
arises from the
ventricles it is
called ventricular
arrhythmia
If the arrhythmia
arises from atria,
SA node, or AV
node it is called
supraventricular
arrhythmia
Causes of
arrhythmia
arteriosclerosi
s
Coronary
artery spasm
Heart block
Myocardial
ischemia
5.
6. MECHANISMS OF ARRHYTHMOGENESIS
Abnormal impulse
generation
Automatic
rhythms
Ectopic focus
Enhanced normal
automaticity
Triggered rhythms
Delayed
afterdepolarization
Early
afterdepolarization
↑AP from SA node
AP arises from sites
other than SA node
7. Abnormal
conduction
Conduction
block
1st degree 2nd degree 3rd degree
Reentry
Circus
movement
Reflection
This is when the impulse is
not conducted from the
atria to the ventricles
1-This
pathway is
blocked
2-The impulse from
this pathway travels
in a retrograde
fashion (backward)
3-So the cells here will
be reexcited (first by the
original pathway and the
other from the
retrograde)
8.
9. Supraventricular Arrhythmias
Sinus Tachycardia: high sinus rate of 100-180 beats/min, occurs during
exercise or other conditions that lead to increased SA nodal firing rate
Atrial Tachycardia: a series of 3 or more consecutive atrial premature beats
occurring at a frequency >100/min
Paroxysmal Atrial Tachycardia (PAT): tachycardia which begins and ends in
acute manner
Atrial Flutter: sinus rate of 250-350 beats/min.
Atrial Fibrillation: uncoordinated atrial depolarizations. 500 beats/min
Types of Arrhythmia
15. 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.
16. Ventricular Premature Beats (VPBs): caused by ectopic
ventricular foci; characterized by widened QRS.
Ventricular Tachycardia (VT): high ventricular rate caused by
abnormal ventricular automaticity or by intraventricular
reentry; can be sustained or non-sustained (paroxysmal);
characterized by widened QRS; rates of 100 to 200
beats/min; life-threatening.
Ventricular Flutter: ventricular depolarizations >200/min.
ventricular Arrhythmias
Types of Arrhythmia
21. PHARMACOLOGIC RATIONALE &
GOALS
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:
decrease conduction velocity
change the duration of the effective refractory period (ERP)
suppress abnormal automaticity
22. ANTYARRHYTHMIC DRUGS
•Most antiarrhythmic drugs are pro-arrhythmic (promote
arrhythmia)
•They are classified according to Vaughan William into
four classes according to their effects on the cardiac
action potential
23. ANTYARRHYTHMIC DRUGS
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
↓conduction velocity in SA
and AV node
24. Class I – blocker’s of fast Na+ channels
Subclass IA
Cause moderate Phase 0 depression
Prolong repolarization
Increased duration of action potential
Includes
Quinidine – 1st antiarrhythmic used,
treat both atrial and ventricular
arrhythmias, increases refractory period
Procainamide - increases refractory
period but side effects
25. QUINIDINE
Isomer of anti malarial drug Quinine
Pharmacological Actions
Automaticity: depresses re entry of sodium into cell during depolarization, and there by
depresses diastolic depolarization – decreases automaticity.
Excitability: depresses excitability and thus make ectopic impulse ineffective.
Conduction Velocity: reduces conduction velocity, increases refractory period and reduces
excitability restore rhythm to normal.
Refractory period: depresses potassium efflux during repolarization and thus prolong
refractory period.
A. V. node conduction: depresses conduction between atria and purkinje system.
Contractility: depresses entry of calcium ions – reduces contractility.
26. QUINIDINE
Pharmacokinetic parameter
Completely absorb from gut.
Excreted through kidney.
Side effect
Cinchonism characterized by, tinnitus (Ringing in the ear), vertigo, blurring of vision.
Embolism: sudden restoration of normal rhythm, may dislodge the mural thrombi attached
to auricular appendages. This may occlude the blood vessels causing embolism (obstruction
of an artery, typically by a clot of blood or an air bubble).
27. QUINIDINE
Therapeutic uses
Atrial fibrillation
Atrial Flutter
Paroxysmal supraventricular tachycardia
Ventricular arrhythmias.
Side effect
Quinidine sulphate – 200 mg t. i. d. oral
Quinidine gluconate – 200 mg oral
28. PROCAINAMIDE
Definite depressant effect on S. A. Node.
Reduces Excitability.
Reduces conduction velocity.
Prolongs refractory period.
Less potent than quinidine.
Rapidly and completely absorbed from gut.
Nausea, bitter taste, anorexia are common side effect.
Used in ventricular arrhythmia
29. Subclass IB
Weak Phase 0 depression
Shortened depolarization
Decreased action potential duration
Includes
Lidocane (also acts as local anesthetic)
– blocks Na+ channels mostly in
ventricular cells, also good for
digitalis-associated arrhythmias
Phenytoin – anticonvulsant that also
works as antiarrhythmic similar to
lidocane
30. LIGNOCAINE
Local anesthetic.
Decreases duration of action potential.
Enhances conduction velocity.
Increases membrane responsiveness.
Shortens duration of action potential.
Reduces re-entry type of circuitous transmitters.
Always administered I/V
Excreted unchanged in urine.
Used to treat ventricular arrhythmias.
31. Subclass IC
Strong Phase 0 depression
No effect of depolarization
No effect on action potential duration
Includes
Flecainide (initially developed as a local
anesthetic)
Slows conduction in all parts of heart,
Also inhibits abnormal automaticity
Propafenone
Also slows conduction
Weak β – blocker
Also some Ca2+ channel blockade
32. Class II – β–adrenergic blockers
Based on two major actions
1) blockade of myocardial β–adrenergic receptors
2) Direct membrane-stabilizing effects related to Na+ channel blockade
Propranolol
causes both myocardial β–adrenergic blockade and membrane-stabilizing effects
Slows SA node and ectopic pacemaking
Can block arrhythmias induced by exercise or apprehension
Prolongs nodal refractory period.
Completely absorbed through gut, metabolized by liver and excreted in urine.
33. Class III – K+ channel blockers
Developed because some patients negatively
sensitive to Na channel blockers (they died!)
Cause delay in repolarization and prolonged
refractory period
Amiodarone – prolongs action potential by
delaying K+ efflux but many other effects
characteristic of other classes
Bretylium – first developed to treat
hypertension but found to also suppress
ventricular fibrillation associated with myocardial
infarction
34. Class IV – Ca2+ channel blockers
Inhibit influx of Calcium through
cardiac cell membrane into cardiac
cell.
slow rate of AV-conduction in
patients with atrial fibrillation
Also called peripheral vasodilators.
Includes
Verapamil – blocks Na+ channels
in addition to Ca2+; also slows SA
node in tachycardia
Diltiazem