You are on page 1of 48



 Any deviation from the normal rhythm of

the heart


 Drugs used for the treatment and

prevention of disturbances in cardiac
Resting Membrane Potential:
 This difference in the electronegative
 Results from an uneven distribution of ions
(sodium, potassium, calcium) across the cell
 An energy-requiring pump is needed to
maintain this uneven distribution of ions.
 Sodium-potassium ATPase pump
Heart and Conduction System
Resting Membrane Potential
of a Cardiac Cell
The Active Membrane cell
Action Potential

 A change in the distribution of ions causes cardiac

cells to become excited.

 The movement of ions across the cardiac cell’s

membrane results in the propagation
of an electrical impulse.

 This electrical impulse leads to contraction

of the myocardial muscle.

Four Phases
 The SA node and the Purkinje cells each have
separate action potentials.
Action Potentials: Phases
(SA Node)
Action Potentials: Purkinje Fiber

Non-pacemaker action potential

Phase 1: partial
Due to rapid efflux of

Phase 2: plateu
Phase 0: fast Due to Ca++
upstroke influx
Due to Na+
Phase 3:
Due to K+ efflux

Phase 4: resting

NThe slope of phase 0 = conduction velocity

Also the peak of phase 0 = Vmax
Action Potentials: Intervals

 It is also called absolute

refractory period (ARP) :

 In this period the cell can’t

be excited

 Takes place between phase

0 and 3

If the arrhythmia
arises from atria,
SA node, or AV
node it is called

If the arrhythmia
arises from the
ventricles it is
called ventricular
Factors precipitate
• May includes :
• Ischemia, hypoxia, electrolytes
disturbance, excessive
catecholamines exposure , drug
Mechanisms of

1- Disturbances in impulse formation.

• Vagal stimulation or β- receptor blocking

drugs slow normal pacemaker .

• Acceleration of pacemaker by
hypokalemia or β- adrenoceptor stimulants.

• Development of ectopic pacemakers.-­ 

2- Disturbances in impulse conduction

• May result from block ( nodal block or

bundle branch block .
• Reentry :
• circus movement
In which one impulse reenters and
excites areas of the heart more than
• Some forms of reentry are anatomical
in shape as in Wolff- Parkinson –White
Abnormal Heart Rhythms
Arrhythmia BPM
tachycardia 150-250
bradycardia <60
atrial flutter 200-350
atrial fibrilation >350
prem. atrial cont. variable
prem. vent. cont. variable
vent. fibrilation variable
Pharmaceutical Treatment
Pharmacologic Rationale & Goals

 Aimed at preventing life-threatening conditions by

The ultimate
restoring goal of antiarrhythmic drug
normal rhythm
oActs on the normal
Restore myocardium where
sinus the impulses
rhythm are
and conduction
o Prevent more serious and possibly lethal
 Some fromheart
drugs influence occurring.
rate, others influence
movement of ions (Nadrugs are used to:
and Ca)
decrease conduction velocity
change the duration of the effective refractory
period (ERP)
suppress abnormal automaticity
Vaughan Williams Classification

 Class 1
 Class Ia
 Class Ib
 Class Ic

 Class II
 Class III
 Class IV
 Other
Vaughan Williams Classification

Class I
 Membrane-stabilizing agents
 Fast sodium channel blockers
 Divided into Ia, Ib, and Ic agents, according
to effects
Vaughan Williams Classification

Class I
 General Class I agent
 Has characteristics of all three subclasses
 Used for symptomatic ventricular and life-
threatening dysrhythmias
Vaughan Williams Classification
Class Ia
quinidine, procainamide, disopyramide
 Block sodium channels
 Delay repolarization
 Increase the APD
 Used for atrial fibrillation, premature atrial
contractions, premature ventricular contractions,
ventricular tachycardia, Wolff-Parkinson-White syndrome
Vaughan Williams Classification

Class Ib
tocainide, mexiletine, phenytoin, lidocaine
 Block sodium channels
 Accelerate repolarization
 Decrease the APD
 Used for ventricular dysrhythmias only
(premature ventricular contractions, ventricular
tachycardia, ventricular fibrillation)
Vaughan Williams Classification

Class Ic
encainide, flecainide, propafenone
 Block sodium channels (more pronounced
 Little effect on APD or repolarization
 Used for severe ventricular dysrhythmias

 May be used in atrial fibrillation/flutter

Vaughan Williams Classification
Class II
Beta blockers: atenolol, esmolol, petaprolol,
 Reduce or block sympathetic nervous system
stimulation, thus reducing transmission of impulses in
the heart’s conduction system
 Depress phase 4 depolarization
 General myocardial depressants for both
supraventricular and ventricular dysrhythmias
Vaughan Williams Classification
Class III (potassium channe;l blocker): amiodarone, bretylium, sotalol,

 Increase APD

 Prolong repolarization in phase 3

 Used for dysrhythmias that are difficult to treat

 Life-threatening ventricular tachycardia or fibrillation, atrial fibrillation or

flutter—resistant to other drugs

 Sustained ventricular tachycardia

 Ibutilide is specifically indicated only for treatment of recent-onset atrial

fibrillation and flutter.

 Patients taking amiodarone must have baseline and serial pulmonary

function tests in order to monitor for potential pulmonary toxicity.
Vaughan Williams Classification

Class IV
verapamil, diltiazem
 Calcium channel blockers
 Depress phase 4 depolarization
 Used for paroxysmal supraventricular
tachycardia; rate control for atrial
fibrillation and flutter
Vaughan Williams Classification

Other Antidysrhythmics
digoxin, adenosine
 Have properties of several classes and are
not placed into one particular class

 Cardiac glycoside

 Inhibits the sodium-potassium ATPase pump

 Positive inotrope—improves the strength of cardiac contraction

 Allows more calcium to be available for contraction

 Used for CHF and atrial dysrhythmias

 Monitor potassium levels, drug levels, and

for toxicity

adenosine (Adenocard)
 Slows conduction through the AV node
 Used to convert paroxysmal supraventricular tachycardia to
sinus rhythm
 Very short half-life
 Only administered as fast IV push
 May cause asystole for a few seconds
 Other side effects minimal
Antidysrhythmics: Side Effects

ALL antidysrhythmics can cause dysrhythmias!!

 Hypersensitivity reactions
 Nausea
 Vomiting
 Diarrhea
 Dizziness
 Blurred vision
 Headache
Principles in the clinical use of
 Eliminate the cause. Precipitating factors must be
recognized and eliminated if possible (hypoxia or
electrolyte abnormalities (especially hypokalemia or
hypomagnesemia), hyperthyroidism or cardiac disease

 Make a firm diagnosis. A firm arrhythmia diagnosis

should be established. For example, the misuse of
verapamil in patients with ventricular tachycardia
mistakenly diagnosed as supraven- tricular tachycardia
can lead to catastrophic hypotension and cardiac arrest.
Principles in the clinical use of
 Determine the baseline condition. Underlying heart
disease is a critical determinant of drug selection for a
particular arrhythmia in a particular patient.

 Question the need for therapy. The mere identification

of an abnormality of cardiac rhythm does not
necessarily require that the arrhythmia be treated.

 consider benefit & risk : reduction of arrhythmia-

related symptoms vs he risk of an adverse reaction is
clearly related to high dosages or plasma
1st: Reduce thrombus formation by using anticoagulant warfarin

2nd: Prevent the arrhythmia from converting to ventricular arrhythmia:

First choice: class II drugs:
•After MI or surgery
•Avoid in case of heart failure

Second choice: class IV

Third choice: digoxin

•Only in heart failure of left ventricular dysfunction

3rd: Conversion of the arrhythmia into normal sinus rhythm:

Class III:
IV ibutilide, IV/oral amiodarone, or oral sotalol

Class IA:
Oral quinidine + digoxin (or any drug from the 2nd step)
Use direct current in
Class IC: case of unstable
Oral propaphenone or IV/oral flecainide hemodynamic patient
Premature ventricular beat (PVB)
First choice: class II
•IV followed by oral
•Early after MI Avoid
Second choice: amiodarone class IC
after MI


First choice: Lidocaine IV

•Repeat injection

Second choice: procainamide IV

•Adjust the dose in case of renal failure

Third choice: class III drugs

•Especially amiodarone and sotalol
(IA, IC, class III) torsades de pointes.

Classes II and IV bradycardia (don’t combine the two)

In atrial flutter use (1st ↓impulses from atria to ventricular to

prevent ventricular tachycardia)
1. Class II
2. Class IV
3. Digoxin.
2nd convert atrial flutter to normal sinus rhythm use:
1. Ibutilide
2. Sotalol
3. IA or IC.
If you use quinidine combine it with digoxin or β blocker
(because of its anti muscarinic effect)

Avoid IC in myocardial infarction because it ↑ mortality