Cardiac arrhythmias occur when the heart beats with an irregular rhythm. There are two main types - bradycardia, which is a slow heart rate below 60 bpm, and tachycardia, which is a fast heart rate over 100 bpm. Arrhythmias can be caused by coronary artery disease, electrolyte imbalances, heart muscle changes after injury or surgery. Symptoms include palpitations, dizziness, chest pain, fainting. Treatment depends on the type of arrhythmia but may include sodium channel blockers, beta blockers, drugs that prolong the action potential, calcium channel blockers, or other drugs like adenosine or magnesium.

1. Arrhythmia
ABDULLAH
M.Pharm (Pharmacy Practice) 1st Sem
Faculty of Pharmacy
Jamia Hamdard

2. DEFINATION
Cardiac Arrhythmia is a condition in which
the heart beats with an irregular or
abnormal rhythm.

3. ABNORMAL RHYTHM
CAN BE OF TWO EXTREME FORMS
1. Bradycardia - Cardiac beats below 60
beats per minute .
2. Tachycardia – Cardiac beat above 100
beats per minute.

4. ETIOLOGY
Coronary artery disease.
Electrolyte imbalances in your blood
(such as sodium or potassium).
Changes in your heart muscle.
Injury from a heart attack.

5. Healing process after heart surgery.
Irregular heart rhythms can also occur in
"normal, healthy" hearts.
Ischemic Heart Disease
Drugs related
Others

6. Arrhythmia Presentation
(SYMPTOMS)
Palpitation.
Dizziness.
Chest Pain.
Dyspnea.

7. Fainting.
Sudden cardiac death
Swelling
Shortness of Breath
Exercise Intolerance

8. Mechanism of Arrhythmias
Bradycardia
1. SA node : Slowed / Absent
Causes
• Decreased Sympathetic Signals
• Increased Parasympathetic Signals
• SA node Damage

10. 2. Blockage of Conduction from SA node
 AV node Blockage
Causes
• Ischemia
• Fibrosis
• Viral Infection
RESULTS in HEART ATTACK

12. LEFT BUNDLE BRUNCH BLOCK (LBBB)
• No Impulse conduction through Bundle
Brunch
• Action Potential transferred through Right
Ventricle to Left Ventricle
RESULTS in Wide QRS complex

14. Tachycardia
1. Increased Pacemaker Activity (SA
Node)- Sinus Tachycardia
 Causes
• Increased Sympathetic Signals
• Decreased Parasympathetic Signals
• SA node Dysfunction
 Example : Sick Sinus Syndrome

15. 2.Re-entry Tachycardias
 Atrial Fibrillation

16. • loss of the normal organised propagation
of electrical activity
• atria fibrillate, they no longer contract in a
mechanically useful way
• a degree of stasis to blood flow and
predisposing to clot (thrombus) formation
within the chambers

17.  VentricularFibrillation

18. • Uncoordinated contraction of
the Cardiac Muscle
• Quiver rather than contract properly
• Commonly identified arrhythmia in
Cardiac Arrest patients
• As a consequence, Sudden Cardiac Death

19.  Wolf Parkinson White Syndrome (WPW)

20. • WPW is caused by the presence of an
abnormal accessory electrical conduction
pathway between the atria and
the ventricles.
• Electrical Signals through abnormal
pathway stimulate the ventricles to contract
prematurely
• A unique type of supraventricular
tachycardia referred to as
an ”atrioventricular reciprocating
tachycardia”.

21.  Atrioventricular nodal re-entrant
tachycardia
• Most common regular supraventricular
tachycardia
• Re-entry circuit forms within or just next
to the atrioventricular node.
• Same as WPW except reentry is in or
around AV node

22. 3. Delayed Repolarization

23. Causes
• Ischemia
• Drugs related (Potassium Blockers)
• Electrolyte Imbalance

24.  Effects
Long QT interval
R on T Phenomenon
Premature Ventricular Beat
Ventricular Fibrillation

26. PHARMACOTHERAPY

27. Class Action Drugs
I A. Na Channel blockers Quinidine, procainamide
I B. Na Channel blockers Lidocaine
I C. Na Channel blockers Flecainide
II Beta-adrenergic blockers Propranolol, esmolol
III Prolong repolarization Amiodarone, Sotolol
Dofetalide, ibutilide
IV Calcium channel blockers Verapamil, diltiazem

28. Class I: Sodium Channel
Blockers
(Local Anesthetics)

29.  Class 1A agents:
• Procainamide
• quinidine
• disopyramide
 Effects on cardiac activity
•  conduction

30. •  refractory period ( (K+) and  Na
inactivation)
•  automaticity
•  increase threshold (Na+)
 Quinidine has anticholinergic (atropine
like action) to speed AV conduction used
with digitalis, β blocker or Ca channel
blocker
• Quinidine is also an alpha receptor
antagonist

31.  Uses
 Quinidine : maintain sinus
rhythms in atrial fibrillation and
flutter and to prevent
recurrent tachycardia and
fibrillation
 Procainamide: acute treatment of
supraventricular and ventricular
arrhythmias

32. Side effects
• Hypotension, reduced cardiac output
• Proarrhythmia (generation of a new
arrhythmia)
• Dizziness, confusion, insomnia,
seizure (highdose)
• Gastrointestinal effects (common)

33.  Class 1B agents:
• Lidocaine
• mexiletine
• Henytoin
Administration
Lidocaine: iv only
Tocainide and mexiletine: oral

34. Effects on cardiac activity
• APD slightly decreased (normal tissue)
•  increase threshold (Na+)

35.  Uses
• Acute : Ventricular tachycardia and
fibrillation (esp. during ischemia)
• Not used in atrial arrhythmias or AV
junctional arrhythmias
 Side effects
CNS effects: dizziness, drowsiness

36.  Class 1C agents:
• Flecainide
• propafenone
 Effects on cardiac activity
•  automoticity ( threshold)
•  APD (K+) and  refractory
period, especially in rapidly
depolarizing atrial tissue.

37.  Uses
• Wide spectrum
• Used for supraventricular
arrhythmias (fibrillation and flutter)
• Premature ventricular contractions
(caused problems)
• Wolff-Parkinson-White syndrome

38. Side effects
• Proarrhythmia and sudden death
especially with chronic use
• increase ventricular response to
supraventricular arrhythmias
• CNS and gastrointestinal effects like
other local anesthetics

39. CLASS II :BETA-ADRENOCEPTOR-
BLOCKING DRUGS

40.  Class II agents:
• propranolol
• acebutolol
• esmolol
Administration
Propranolol: oral, iv
Esmolol: iv only
(very short acting T½, 9 min)

41. Cardiac effects
•  APD and refractory period in AV node to
slow AV conduction velocity

42.  Uses
• Treating sinus and catecholamine
dependent tachyarrhythmias
• converting reentrant arrhythmias in
AV
• protecting the ventricles from high
atrial rates (slow AV
conduction)

43. Side effects
• bronchospasm
• hypotension
• don’t use in partial AV block or ventricular
failure

44. CLASS III - Drugs That Prolong
Effective Refractory Period By
Prolonging the Action Potential

45.  Class III agents:
• amiodarone
• sotalol
• Ibutilide
• dofetilide
 Amiodarone
Administration
Oral or iv (T 1/2 about 3 months)

46. Cardiac effects
•  increase refractory period and  APD
(K+)
•  conduction (Na+)
•  (β block and Ca++ block)
•  speed of AV conduction

47.  Uses
• Very wide spectrum: effective for most
arrhythmias
 Side effects:
Many serious that increase with time
• Pulmonary fibrosis
• Hepatic injury
• Increase LDL cholesterol
• Thyroid disease
• Photosensitivity

48.  Sotolol
Administration-oral
 Cardiac effects
•  APD and refractory period in
atrial and ventricular tissue

49. Uses
• Wide spectrum: supraventricular and
ventricular tachycardia
Side effects
• Proarrhythmia,
• Fatigue
• insomnia

50.  Ibutilide
Administration- iv infusion
 Cardiac effects
• Result in  APD

51. Uses
• conversion of atrial fibrillation and flutter
Side effects
• Torsades de pointes

52.  Dofetilide
Administration- oral
 Cardiac effects
•  APD and refractory period

53. Uses
• maintain sinus rhythm in atrial fibrillation
Side effects
• restricted use
• Torsades de pointes

54. CLASS IV- CALCIUM CHANNEL-
BLOCKING DRUGS

55.  Class IV agents:
• verapamil
• diltiazem
Administration
verapamil: oral or i.v.
diltiazem: oral

56. Cardiac effects
• slow conduction through AV (Ca++)
•  refractory period in AV node

57.  Uses
• control ventricles during
supraventricular tachycardia
• convert supraventricular tachycardia
(re-entry around AV)
 Side effects
• Caution when hypotension,
decreased CO or sick sinus.Some
gastrointestinal problems

58. ADDITIONAL
ANTIARRYHTHMIC AGENTS

59.  Adenosine
Adminsitration
rapid i.v. bolus, very short T1/2
(seconds)
 Cardiac effects
• Slows AV conduction

60. Uses
• convert re-entrant supraventricular
arrhythmias
• hypotension during surgery, diagnosis of
CAD

61.  Digioxin (cardiac glycosides)
 Mechanism
• Enhances vagal activity(10th Cranial
Nerve)
• ( K+ currents,  Ca++ currents,
refractory period
• slows AV conduction and slows HR

62. Uses
• Treatment of atrial fibrillation and flutter

63. Atropine
Mechanism
• selective muscarinic antagonist
Cardiac effects
• block vagal activity to speed AV conduction and
increase HR
Uses
• treat vagal bradycardia
Magnesium
• treatment for tachycardia resulting from long QT

64. References
 Basic and Clinical Pharmacology Katzung 13 Edition
 Pharmacotherapy Handbook - Ninth Edition by Barbara G.
Wells (Author), Joseph T. Dipiro (Author), Terry L.
Schwinghammer (Author)
 www.youtube.com - Pathophysiology of Cardiac Arrhythmias by
Andrew Wolf
 Wikipedia