for study purpose

1. WELCOME
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2. ARRHYTHMIA
Presentation By: Sarath D
First Semester M.Pharm.
Pharmacy Practice
CPS, TVM.
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3. CONTENTS
 INTRODUCTION
 EPIDEMIOLOGYAND PREVALENCE
 AETIOLOGY
 PATHOPHYSIOLOGY
 CLINICAL MANIFESTSTIONS
 DIAGNOSIS
 MANAGEMENT
 ROLE OF PHARMACIST
 CONLUSION
 REFERENCES
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4. INTRODUCTION
Arrhythmia is an abnormal cardiac rhythm, usually involving a change in rate or
regularity, and is monitored by an electrocardiograph.
 Bradycardia.
 Tachycardia.
 Flutter/ Fibrillation.
 Premature Contraction.
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5. EPIDEMIOLOGY
• Patients who have pre-existing cardiac disorders including heart failure, hypertension or
a recent infarction.
• Older age.
• More common in pregnancy and following surgery.
• Women have a higher risk of drug induced arrhythmia.
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6. PREVALENCE
• It is estimated that 3.9 million people in USA have cardiac rhythm disturbance and
results in 7,30,000 hospital admissions in each year.
• It is prevalent in community-dwelling adults, affecting >2% of individuals.
• The abnormalities occur at a rate of 0.5% per year.
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7. AETIOLOGY
Irregular heart beat is not always related to an underlying condition. It may be caused by:
• Alcohol abuse.
• Drug abuse.
• Smoking.
• Excessive caffeine consumption.
• Mental stress.
• Certain medications/Dietary supplements.
• CCF.
• Age.
• Diabetes.
• Hypertension.
• Hyperthyroidism.
• Myocardial Infarction.
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8. RISK FACTORS
 Cardiac problems, such as coronary artery
disease and cardiomyopathy.
Hyperthyroidism or Hypothyroidism.
 Electrolyte disturbances, such as low
potassium levels.
 Severe emotional stress.
 Alcohol abuse.
 Infections, such as viral myocarditis and lyme
disease.
 Old age.
 Inherited gene defects.
 Hypertension.
 Too much caffeine.
 Illegal drugs.
Obesity.
 Some medications.
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9. PATHOPHYSIOLOGY
ACTION POTENTIAL
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10.  Phase 0- Depolarization:
Voltage gated Na+ channel open.
 Phase 1- Initial Repolarization:
Voltage gated Na+ channels close and voltage gated K+ channel begins to open.
 Phase 2- Plateau Phase:
Voltage gated Ca2+ channels open, K+ efflux continuous results Myocytes contraction.
 Phase 3- Rapid Repolarization:
Voltage gated Ca2+ channels close, slowly opens voltage gated K+ channels.
 Phase 4- Resting Potential:
High K+ permeability.
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11. PATHOPHYSIOLOGY
• Abnormal impulse generation.
• Rate of impulse generation at the tissue exceeds than that of SA node causes tachycardia.
• Chemicals such as Digitalis, Catecholamines.
• Conditions such as Hypoxemia, Electrolyte abnormality.
• Phase 4 diastolic interval increases.
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12. ARRHYTHMATIC MECHANISM
 ABNORMAL IMPULSE FORMATION
 ABNORMAL IMPULSE PROPAGATION
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13. ABNORMAL IMPULSE FORMATION
1. ABNORMAL AUTOMATICITY
 Pacemaker Activity. Enhances activity of SA node.
 Causes rhythm disturbances.
 Impulse may be the result of injury.
 Normal - Special Cardiac Cell.
 Diseased Stage.
 Affected On Phase 4.
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14. 2. TRIGGERED ACTIVITY
 When cells are at rest Abnormal Electric Impulses are formed.
 Two Major Forms:
1. Early after Depolarisation: Increased inward movement of Ca2+ Ions. Na+/Ca2+
transport occur. Prolong cardiac Repolarisation. Phase 2/3 of normal cardiac potential
is interrupted. Leads to polymorphic Ventricular Tachycardia with long QT interval,
known as Torsade De Pointes.
2. Delayed after Depolarisation: Inward movement of calcium increases. Usually in Phase
4.
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15. ABNORMAL IMPULSE PROPAGATION
RE-ENTRY
 Due to abnormality of conduction.
 Re circulation of impulse in the Heart causes repetitive activation without generation of a new
impulse.
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16. CLINICAL MANIFESTATIONS
 Dizziness or Collapse because of a poor blood supply to the Brain.
 Shortness of breath because of poor Oxygenation.
 Angina associated with a poor Coronary circulation.
 Increased Cardiac workload arising from a Tachycardia.
 Weakness.
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17. DIAGNOSIS
 Patient Medication History Review include Family History, Diet and Lifestyle.
 ECG.
 Holter Monitor: A wearable device to record the Heart’s Rhythm.
 Echocardiogram.
 Chest X Ray.
 Tilt Table Test: Records Blood Pressure, Heart Rhythm and Heart Rate on a beat-by-beat basis as the
table is tilted to different angles
 Electrophysiology Test.
 Blood Urine Test.
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18. ELECTROPHYSIOLOGICAL TESTING:
Intra Cardiac Procedures to determine location of Ectopic Foci.
LABORATORY FINDINGS:
 Serum K+ Level >5 mEq/L (Normal range: 3.7-5.2 mEq/L).
 Serum Ca Level <4.5 mEq/L (Normal range: 4.4-5.2 mEq/L).
 Serum Mg Level <1.3 mEq/L (Normal range: 1.3-2.1 mEq/L).
HIS BUNDLE STUDY:
Can locate the origin of a Heart Block or Re-Entry pattern.
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19. ECG CHANGES
 P Wave- Atrial Depolarization.
 QRS Complex- Ventricular Depolarization.
 T Wave- Ventricular Repolarization.
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20. NORMAL ECG TACHYCARDIA
BRADYCARDIA
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21. MANAGEMENT
AIM OF TREATMENT:
• Control the Heart rate within a relatively normal range.
• Restore a normal Heart Rhythm, if possible.
• Treat Heart disease/condition that may be causing Arrhythmia.
• Reduce other risk factors for Heart disease and Stroke.
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22. 1. PHARMACOLOGICAL MANAGEMENT
DRUGS USED IN ARRHYTHMIA:
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CLASS ACTIONS DRUGS
I A Na+ Channel Blocker Quinidine, Procainamide
I B Na+ Channel Blocker Lidocaine, Mexiletine
I C Na+ Channel Blocker Propafenone, Flecainamide
II Beta Blocker Propranolol, Esmolol, Sotalol
III K+ Channel Blocker Amiodarone, Dronedarone,
Dofetilide, Ibutilide
IV Ca2+ Channel Blocker Verapamil, Diltiazem
V Unknown Mechanism Digoxin

23. CLASS I
Slows down sodium channel current in phases 0 and 4 of Action Potential.
Used in Ventricular Tachyarrhythmia.
Lidocaine is not used orally; given as IV regimen in doses-
 4mg/Min For 30 Min
 2mg/Min For 2 Hrs.
 1mg/Min To Continue.
Effective in Atrial & Ventricular Arrhythmia.
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24. CLASS II
Beta Blockers.
Used with Alpha Blockers.
Contraindicated in patients with Asthma and COPD.
IV Drugs – Atenolol, Metoprolol, Esmolol.
Drug of choice- Esmolol.
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25. CLASS III
Prolong action potential; bring uniformity among different cell types.
Amiodarone blocks Na channel- have Class I and II activity.
Sotalol is a racemic mixture:
 D isomer- Class III activity
 L isomer- Beta Blocker
Used in Wolf Parkinson White Syndrome.
Long half life (30days)- Slow onset of action
 200 mg TID for 7 days
 200 mg BD for 7 days
 200 mg OD
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26. CLASS IV
Verapamil and Diltiazem inhibit slow channel conduction through AV node.
Calcium channel blockers.
Adenosine is an indirect calcium antagonist.
Adenosine is a Bronchoconstrictor, cause flushing, chest pain.
Verapamil has a greater dilatory effect on systemic arteries used in HT and angina.
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27. CLASS V
Digoxin
Inhibits conduction through AV node.
Narrow therapeutic range: 1-2mg/ml.
Renal and hepatic elimination is possible.
Adverse effects :
Cardiac : Ventricular Tachycardia, SA node arrest, Heart Block.
Non cardiac : Anorexia, Nausea ,Vomiting, Fatigue, Confusion, Abnormal color vision, Diarrhea.
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28. 28
ECG
ASYSTOLE
Adrenaline
1mg I.V.
Pacing
VENTRICULAR FIBRILATION OR
PULSELESS VENTRICULAR
TACHYCARDIA
DC shocks
× 3
Adrenaline
1mg I.V.
DC shocks × 3
(repeat as often as required)
ELECTROMECHANICAL
DISSOCIATION
Adrenaline
1mg I.V.
(Repeat as often as
required)
EMERGENCY TREATMENT OPTION FOR ARRHYTHMIAS IN ADULTS

29. ARRYTHMIA TREATMENT ALGORITHM
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30. 2. NON-PHARMACOLOGICAL MANAGEMENT
Life style changes.
• Losing weight if overweight.
• Quitting smoking.
• Decreasing intake of caffeine or alcohol.
• Stopping drug abuse.
• Avoiding certain over-the-counter medications such as decongestants and certain herbal
remedies such as cola nut, ephedra.
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31.  Devices: Implantable Cardioverter Defibrillator (ICD) which is a small battery-
powered device placed in the chest to detect and stop irregular heartbeats
 Cardiac Ablation: A non surgical technique that neutralizes parts of the abnormal
electrical pathway (tissue) that causing Arrhythmia.
Cardiac Surgery: It is an invasive procedure where surgeons will remove abnormal sites.
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32. ROLE OF PHARMACIST
Pharmacists play a vital role in the management of Atrial Fibrillation (AF) patients taking
Antiarrhythmics.
KEY RESPONSIBILITIES ARE;
 Discussing adverse events and administration requirements.
 Reviewing drug interactions.
 Recommending monitoring parameters.
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33.  Encouragement and realistic reassurance.
 Advice the patient family and friends.
 Suggest to avoid smoking, cocaine, alcohol, stressful conditions.
 Give informed consent about interventions.
 Give instructions about the storage conditions of the medicines.
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34. CONCLUSION
Arrhythmia is defined as loss of cardiac rhythm, especially irregularity of heartbeat. Arrhythmia
is most commonly occur in old age and patients who have pre-existing cardiac disorders. The early
detection and management can reduce the risk of the disease. Pharmacological and non-pharmacological
methods can be used for the management of the disease. However, due to the nature of the side effects or
monitoring requirements of antiarrhythmics, therapy selection should be based first upon safety and then
upon efficacy.
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35. REFERENCES
1. Roger Walker and Clive Edwards. Clinical Pharmacy and Therapeutics: Arrhythmia by D. Scott
2003;3:321-333.
2. Joseph T Dipiro et al. Pharmacotherapy, A Pathologic Approach: The Arrhythmias by Cynthia A
Sanoski and Jerry L Bauman 2014;9:227-9.
3. K D Tripathi. Essentials of Medical Pharmacology: Cardiovascular Drugs 2019;8:521-3.
4. Eric T Herfindal, Richard A Helms, David J Quan, Dick R Gourley. Text Book of Therapeutics:
Cardiac Arrhythmias by Tien M H Ng, J Jason Sims and Mark A Gill 2006;8:537-544.
5. WWW.bing.com/search?q=non+pharmacological+management+of+arrhythmias&FORM=HDRSC1
.
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36. THANK YOU
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