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Randa Al-Harizy
Impulses originate
regularly at a frequency
SAN
of 60-100 beat/ min
AVN
mv Phase 1 Cardiac Action
20
0
Potential
Phase 2
Depolarization
(Plateau Phase)
-20
-40
Phase 3
-60 Phase 0
-80 Phase 4
Resting membrane
Potential
Na +
++
Na
-100 NaNa ++ ++
caca
Na+++
Na ca++
K+
m
Na+ K+ ca++ ATPase
h +++ Na+
KKK
+K
mv Phase 1 Cardiac Action
20
0
Potential
Phase 2
Depolarization
(Plateau Phase)
-20
-40 Phase 4
Phase 3 (only in
-60 Phase 0 pacemaker
cells
-80 Phase 4
R.M.P
Na +
-100 Na++++
Na ++ ++
caca
Na
Na+
Na ca++
K+
m
Na+ K+ ca++ ATPase
h +++ Na+
KKK
+K
Cardiac Arrhythmias
Mechanisms of bradicardias:
Sinus bradycardia is a result of abnormally slow
automaticity while bradycardia due to AV block is caused by
abnormal conduction within the AV node or the distal AV
conduction system.
Normal
Re-enterant
Tachycardia
Atrial Arrhythmias
Sinus arrhythmia:
Sinus tachycardia
• Pharmacological therapy.
• Cardioversion.
• Pacemaker therapy.
• Surgical therapy e.g. aneurysmal excision.
• Interventional therapy “ablation”.
Classification of Anti-Arrhythmic Drugs
Class IV:
Ca ++ channel blockers
- Class II:
Phase 2
(Plateau Phase) - Beta blockers
Phase 1
Class I:
Na + channel blockers.
Phase 3
-
Phase 0 - - Pacemaker potential
Phase 4
Class III:
R.M.P
K + channel blockers
Classification of Antiarrhythmic Drugs
based on Drug Action
CLASS ACTION DRUGS
I. Sodium Channel Blockers
1A. Moderate phase 0 depression and Quinidine,
slowed conduction (2+); prolong Procainamide,
repolarization Disopyramide
1B. Minimal phase 0 depression and slow
conduction (0-1+); shorten Lidocaine
repolarization
1C. Marked phase 0 depression and slow
conduction (4+); little effect on Flecainide
repolarization
II. Beta-Adrenergic Blockers Propranolol, esmolol
III. K+ Channel Blockers Amiodarone, Sotalol,
(prolong repolarization) Ibutilide
IV. Calcium Channel Blockade Verapamil, Diltiazem
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