ANTIARRYTHMICS DRUGS

1. Anti-arrhythmics
Dr.ZIKRULLAH

2. Arrhythmia
• Arrhythmia is a term for any of a large
and heterogeneous group of conditions
in which there is abnormal electrical
activity in the heart.
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3.  Arrhythmias may be due to:
 improper impulse generation
 impulse conduction.
 These manifest as abnormalities of:
 rate or
 regularity or
 as disturbances in the normal sequence of
activation of atria and ventricles.
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4. Causes of arrhythmias
A. Altered automaticity:
1. Sinus node(sinus tachy or brady)
2. ↑ vagal activity
3. ↑ sympathetic activity
4. Ectopic foci
5. Triggered Automaticity
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5. B. Abnormal impulse conduction
• Heart blocks may produce bradyarrhythmias.
• Reentry circus conduction may produce
tachyarrhythmias.
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6. FACTORS UNDERLYING ARRHYTHMIAS
• Arterial hypoxemia
• Electrolyte abnormalities (↓K⁺ or ↓Mg⁺⁺
predispose to ventricular dysrhythmias).
• Acid-base abnormalities (alkalosis >> acidosis)
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7. • Altered autonomic nervous system activity
(↑ Symp activity predisposes to ventricular
dysrhythmias as VT / VF
• Drugs (beta blockers , Clonidine and other
sympatholytics, narcotics, adenosine,
antiarrythmics class I and III )
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8. Treatment
• In many patients, the correction of
identifiable precipitating events is not
sufficient to suppress cardiac ectopic
dysrhythmias, and therefore specific cardiac
antidysrhythmic drugs may be administered.
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9. DYSRHYTHMIAS REQUIRE TREATMENT
• 1. Persists despite removing the
precipitating cause
• 2. Hemodynamic function is compromised
• 3. Predisposes to more serious cardiac
dysrhythmias
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10. Therapeutic effects are achieved by:
1. sodium- or calcium-channel blockade
2. prolongation of effective refractory
period
3. blockade of sympathetic effects on
the heart.
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11. 11

12. Class I - membrane stabilizers
• depress depolarization of cardiac cell
membrane
• by restricting entry of fast sodium current
resulting in reduction in the maximum rate of
rise of phase 0 of the action potential.
• This leads to slower rate of conduction,
increased threshold for excitation and
prolongation of the effective refractory period.
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13. Ia
• lengthen action potential
• slow rate of rise of phase 0
• prolong repolarization
• prolong refractoriness by blocking potassium
channel
• prolong PR, QRS, QT
• moderate-marked sodium channel blockade
• eg quinidine, procainamide, disopyramide
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14. Ib
• shorten action potential
• shorten repolarization
• shorten QT
• raise fibrillation threshold
• mild-moderate sodium channel blockade
• eg lignocaine, mexilitine, phenytoin,
propafenone
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15. Ic
• no effect on length of action potential
• markedly reduces rate of rise of phase 0
• markedly prolongs PR and QRS complex
• marked Na channel blockade
• prolong refractoriness by blocking potassium
channels
• eg flecainide
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16. Class II
• decrease potential for arrhythmias to
develop in response to catecholamines
• eg bretylium: blocks release of sympathetic
transmitters
• beta blockers: competitive antagonists and
also block possible arrhythmogenic effect of
cAMP.
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17. Class III
• - K channel blockers: prolong duration of
action potential with resulting prolongation of
effective refractory period
• - eg amiodarone, sotalol, disopyramide,
bretylium
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18. Class IV
• calcium channel blockers
• slow SAN pacemaker cells and AVN
conduction by direct blockade of Ca channels
• have inportant effects on upper and middle
parts of the AV node
• may have particular value in blocing one limb
of a re-entry circuit
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19. Site of action
• SAN, atrium
- Ia eg quinidine, disopyramide
- II beta blockers
- III eg amiodarone
- IV ? verapamil
- ? digoxin
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20. 20

21. PSVT
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22. AVN
• - Ia ? disopyramide
• - Ic eg flecainide
• - II beta blockers
• - III amiodarone
• - IV verapamil
• - digoxin
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23. Anomalous pathway
• - Ia disopyramide, quinidine
• - Ic flecainide (most effective)
• - III amiodarone
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24. Ventricle
• - Ia disopyramide, quinidine
• - Ib lignocaine, mexilitine
• - Ic flecainide
• - II bretylium
• - III amiodarone
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25. VT/VF
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26. EFFICACY AND RESULTS
• Suppression of ventricular ectopy using a
cardiac antiarrhythmic drug does not prevent
future life-threatening arrhythmias and may
increase mortality
• Survivors of cardiac arrest have a high risk of
subsequent ventricular fibrillation, and the
treatment of these patients with amiodarone
results in fewer life-threatening cardiac
events.
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27. DECISION TO TREAT CARDIAC
DYSRHYTHMIAS
• The benefit of antiarrhythmic drugs is clearest
when it results in the immediate termination
of a sustained tachycardia
• β-adrenergic antagonists decrease mortality
after an acute myocardial infarction
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28. 28

29. Lidocaine
• Lidocaine is used principally for the suppression
of ventricular dysrhythmias (premature
ventricular contractions, ventricular tachycardia),
having minimal effects on supraventricular
tachydysrhythmias
• The efficacy of prophylactic lidocaine therapy for
preventing ventricular fibrillation after acute
myocardial infarction has not been documented,
and its use is no longer recommended.
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30. • In adult patients with normal cardiac output,
hepatic function, and hepatic blood flow, an
initial intravenous administration of lidocaine,
2 mg/kg, followed by a continuous infusion of
1 to 4 mg/min should provide therapeutic
plasma lidocaine concentrations of 1 to 5
µg/mL.
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31. Mechanism of Action
• delays the rate of spontaneous phase 4
depolarization by preventing or diminishing
the gradual decrease in potassium ion
permeability.
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32. • Lidocaine is essentially devoid of effects on the
ECG or cardiovascular system when the plasma
concentration remains <5 µg/mL .
• Hypotension
• Bradycardia
• sizzures
• Its metabolites may possess cardiac
antiarrhythmic activity.
• CNS depression, apnea, cardiac arrest
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33. Amiodarone
• potent antiarhythmic, antiadrenergic effect
• activity against refractory supraventricular and
ventricular tachydysrhythmias.
• In the presence of VT or VF that is resistant to
electrical defibrillation, amiodarone (300
mgIV) is recommended.
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34. • Administered over 2 to 5 minutes, a dose of 5
mg/kg IV produces a prompt antidysrhythmic
effect that lasts up to 4 hours.
• prolonged elimination half-time of this drug.
• After discontinuation of chronic oral therapy,
the pharmacologic effect of amiodarone lasts
for a prolonged period (up to 60 days)
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35. • It prolongs the effective refractory period of
all cardiac tissues, including the sinoatrial
node, atrium, atrioventricular node, His-
Purkinje system, and ventricle.
• minor negative inotropic effect.
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36. Propanolol and esmolol
• β-Adrenergic antagonists are effective for the
treatment of cardiac dysrhythmias related to
enhanced activity of the sympathetic nervous
system
• perioperative stress, thyrotoxicosis,
pheochromocytoma
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37. • controlling the rate of ventricular response in
patients with atrial fibrillation and atrial
flutter.
• The usual oral dose of propranolol for the
chronic suppression of ventricular
dysrhythmias is 10 to 80 mg every 6 to 8
hours.
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38. SIDE EFFECTS
• Bradycardia
• Hypotension
• Myocardial depression
• Bronchospasm
• Congestive heart failure
• Heart block
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39. VERAPAMIL AND DILTIAZEM
• Intravenous verapamil is highly effective in
terminating PSVT.
• 75 to 150 µg/kg over 1 to 3 minutes, followed
by a continuous infusion of about 5 µg/kg per
minute to maintain a sustained effect.
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40. DOFETILIDE and IBUTILIDE
• are effective for the conversion of recent
onset atrial fibrillation or atrial flutter to
normal sinus rhythm.
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41. • MEXILETINE and TOCAINIDE
orally effective amine analog of lidocaine that is
used for the chronic suppression of ventricular
cardiac tachydysrhythmias.
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42. ADENOSINE
• slows the conduction of cardiac impulses
through the atrioventricular node.
• treatment of PSVT and WPW syndrome
• The usual dose of adenosine is 6 mgIV
followed, if necessary, by a repeat injection of
6 to 12 mgIV about 3 minutes later.
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43. Side effects
• Flushing
• Headache
• Dyspnea
• Chest discomfort
• Nausea
• Atrioventricular heart block
• Bronchospasm
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44. DIGOXIN
• Digitalis preparations, such as digoxin, are
effective cardiac antidysrhythmics for the
stabilization of atrial electrical activity and the
treatment and prevention of atrial
tachydysrhythmias.
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45. • Digoxin toxicity can produce increased
ventricular ectopy and, when coupled with
bradyarrhythmias caused by digoxin toxicity,
may predispose to sustained polymorphic
ventricular arrhythmias and VF
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46. • Drugs administered for the chronic
suppression of cardiac dysrhythmias pose little
threat to the uneventful course of anesthesia
and should be continued up to the time of
anesthesia induction.
• The majority of cardiac dysrhythmias that
occur during anesthesia do not require
therapy
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47. • For these reasons, the pharmacologic
treatment of cardiac arrhythmias is principally
used to treat atrial fibrillation and atrial flutter
that is not responsive to catheter ablation
treatment and for patients with implantable
cardioverter-defibrillator devices who are
receiving frequent but needed electrical
shocks.
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48. VT/VF
• Sustained polymorphic VT, ventricular flutter,
and VF all lead to immediate hemodynamic
collapse.
• Emergency asynchronous defibrillation is
therefore required, with at least 200-J
monophasic or 100-J biphasic shock.
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49. • If the arrhythmia persists, repeated shocks
with the maximum energy output of the
defibrillator are essential to optimize the
chance of successful resuscitation.
• Intravenous lidocaine and/or amiodarone
should be administered but should not delay
repeated attempts at defibrillation.
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50. Catheter and Surgical Ablative Therapy
• Ablation therapy is currently considered an
alternative to additional pharmacologic
therapy trials in patients with recurrent
symptomatic AF or AF associated with poor
rate control who have failed an initial attempt
at rhythm control with pharmacologic
management.
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51. Bradyarrythmias
• Pacing in SA nodal disease is indicated
to alleviate symptoms of bradycardia.
• Surgical implantation of electrical leads
attached to a pulse generator.
• Pulse generator can sense electrical
activity generated by the heart and only
deliver electrical impulses when
needed.
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52. Thank you
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