ARRHYTHMIAS

1. ARRhYTHMIasis
By
T.V.Subba Rao (M.Pharm)

6. ACTION POTENTIAL IN CARDIAC MUSCLE
1.rapid depolarization
2.partial repolarization
3.Platue
4. Repolarization
5. Pacemaker depolarization

8. Conductivity of impulse
1.Sino atrial node(SA node)
2. Atrial chambers
3.Atrio ventricular node(AV node)
4.Bundle of HIS
5.Purkinje fibres

9. ELECTRO CARDIO GRAM(ECG)
*Einthoven Willem – father of ECG
=>Technique – electrocardiography
=>Instrument – electrocardiograph
=>graphical report – electrocardiogram
USES:
1.Heart rate
2.Heart rhythm
3.Abnormal electrical conduction
4.Poor blood flow to heart muscle(ischemia)
5.Heart attack
6.Coronary artery disease

10. 1. P-Wave :- Atrial depolarization .
2. QRS Complex :- Ventricular depolarization .
3. T-Wave :- Ventricular repolarization .

11. Normal cardiac rhythm:
1. 60 – 100 beats / min .
2. Impulse should originate from SA node .
3. Impulse should follow normal conduction pathway .
4. Impulse should be in normal velocity .

12. 1. impulse origin from SA node
3. 60 – 100 beats / min 2. normal conduction pathway
4. normal velocity

13. >350 fibrillation
350 flutter
250 paroxysmal tachycardia
150 simple tachycardia
100 normal rhythm
60 mild bradycardia
40 moderate bradycardia
20
<20 severe bradycardia

14. TYPES OF CARDIAC ARRTHYMIAS
=>Irregular heartbeat / disturbance in rhythm of heart.
=> Heartbeat may be fast / slow / extra beat / missed beat.
1. SA node :- sinus arrthymias
i. Sinus bradycardia
ii. Sinus tachycardia
iii. Sinus brady and tachy syndrome ( sick sinus syndrome )
2. Atria :- atrial arrthymias
i. Atrial tachycardia
ii. Atrial flutter
iii. Atrial fibrillation

15. 3. AV nodal / junction :- nodal / junctional arrthymias
i. Junctional bradycardia ( heart block )
ii. Junctional tachycardia (wolf Parkinson’s white syndrome )
4. Ventricles :-
i. ventricular tachycardia
ii. Ventricular flutter
iii. Ventricular fibrillation
iv. Ectopic beats ( ischemia )

16. MECHANISMS OF CARDIAC ARRTHYMIAS
1. Enhanced pacemaker activity
2. After – depolarization
i. Early after – depolarization
ii. Delayed after – depolarization
3. reentry

18. REENTRY

19. SYMPTOMS
1.Palpitation
2.Chest discomfort
3.Shortness of breath
4.Dyspnoea
5.fealing of anxiety
6.dizziness

20. DIAGNOSIS
1. Family history
2. Medical history
3. Other heart problems
4. Health habits
5. Emotional stress
 ECG ( Electro Cardio Gram )
24hr Holter monitor
Event monitor
Blood test ( pot and thyroid hormones )

21. HOLTER MONITOR

22. TREATMENT

23. DESIRED OUTCOME
1.Pharmacological treatment
2.Pacemaker therapy
3. Surgical therapy
4. Iinerventional therapy ( ablation )

27. Mechanism of action of anti-arrthymics

30. PROCAINAMIDE (CLASS 1a)
MOA : - Block Na + channels in depolarized state.
TOXICITY : - QT interval prolongation .
PHARMACOKINETICS :-
A – IM , IV , Oral .
M – NAPA (has class iii ) cause Torsade depointes in renal
failure condition
DOSE :- IV loading dose up to 12mg / kg can be given at rate of 0.3 mg / kg /min
followed by maintenance dose of 2-5 mg / min .
=>risk of GI & Cardiac toxicity at plasma con > 8mcg / ml or NAPA con
>20 mcg / ml.

31. LIDOCAINE (CLASS 1b )
MOA :- block activated & inactivated Na + channels .
PHARMACOKINETICS :-
M:- excess 1st pass metabolism ( orally )
so given parenterally .
DOSE :- It has half life of 1-2 hrs .
loading dose 150 – 200 mg for 15 min to achieve plasma level of
2-4mcg / ml .

32. PROPAFENONE (CLASS 1c )
PHARMACOKINETICS:
M :- Liver
half life of 5 – 7 hrs .
DOSE :- Daily dose 450 – 900 mg in 3 divided doses .
USES :- Primarily used for supraventricular arrthymias .
ADVERSE EFFECTS :- metallic taste , constipation .

33. PROPRANOLOL (CLASS II )
MOA :- Decrease depolarization & automaticity in SA node .
DOSE :- IV 1mg / min
oral 40 – 80 mg 2 time day
USES :- It is highly effective in sympathetically mediated arrthymias seen in
heocromacytoma & anesthesia with halothane .
=> digitalis induced tachyarrthymias may be suspended .

34. AMIADARONE (CLASS III)
=>In USA amiadarone is approved for oral & IV to treat serious ventricular
arrthymias .
Broad spectrum ( diff arrthymias )
EXTRACARDIAC : It cause peripheral vasodilation .
TOXICITY : Accumulated in Heart ,Lungs ,Skin and concentrated in Tears .
Dose related Pulmonary toxicity is important adverse effect .
Skin deposition
Blocks T4T3
DRUG INTERACTIONS :Drugs induce CYP3A4 ex: Rifampicin decrease
Amiadarone concentration when coadministered .

35. PHARMACOKINETICS : Bioavailability 35 - 65%
Elimination Half life is 3-10 days
DOSE : Loading dose of 10g is usually achieved with 0.8-1.2g daily doses.
The maintenance dose is 200-400mg daily.

36. VERAPAMIL (CLASS IV )
MOA : Blocks both activated and inactivated
L-type ca+2 channels .
EXTRACARDIAC : It causes peripheral vasodilation , which may be beneficial and
hypertension .
TOXICITY : It causes AV block in large dose used in patients with AV nodal
disease.
PHARMACOKINETICS : ½ life is 7 hours .
Bio availability is on 20 % .
ADVERSE EFFECTS : Constipation , peripheral odema .
DOSE : Initialbolus of 5 mg .

37. DOC FOR CHRONIC THERAPY ( 1st choice )
• PSVT - digoxin , verapamil , propranolol .
• Atrial flutter – amiodarone , quinidine , digoxin .
• Atrial fibrillation –amiodarone , quinidine , digoxin .
• Ventricular tachycardia – amiodarone , dofetilide .
• Torsades de pointes – propranolol .
• Ventricular fibrillation – amiodarone .
• Wolf Parkinson white syndrome – amiodarone , propranolol .

38. ABLATION

39. PACEMAKER

40. REFERENCES
1. K.D. Tripathi
2. Rang and Dale
3. Katzung
4. Goodman and Gilman
5. Net source

41. THANK YOU