Anti-arrhythmic drugs Flashcards
Phases of action potential(AP) (atria&
ventricles):
• Phase —: rapid depolarization with fast influx of
Na+→ Na+ channels are rapidly inactivated.
——————- determines
conduction —————–
0
Maximal rate of dep. (Vmax)
velocity
Phases of action potential(AP) (atria&
ventricles):
• Phase ————-: early fast repolarization: rapid out flux of————.
1
repolarization
K+
the most effective
Amiodarone(cordarone)
Phase ————: delay in repolarization (plateau) slow
Ca++ influx &————- K+ efflux
2
equal
Phase 3: rapid repolarization due to———— out flux
K+
someone has sever bradycardia what should he use ?
Atropine
Phase 4: ———– → Resting membrane
potential (diast.) due to active pump of Ca++&Na+
in exchange of K+
full repolarization
Pathophysiology of dysrhythmia:
• there is an abnormality in the ———– of origin of the impulse, its rate or
regularity, or its ————-.
site
conduction
I. Disturbance in impulse generation
1. Increased automaticity of automatic tissue (↑———–
Depolarization) {e.g. with increased sympathetic Activity}→——————-
slope of diastolic
tachyarrhythmia
I.Disturbance in impulse generation
. Decreased automaticity of automatic tissue→ ————–
(↑————tone).
Brady arrhythmia
vagal
I. Disturbance in impulse generation
Development of automaticity in ———- tissues (ectopic
pace-maker or slow responses) due to that, cell remain partially depolarized (Slow diastolic depolarization) as in ————, ————–,
————– Stimulation).
non automatic
ischemia
digitalis
sympathetic
II. Disturbance in conduction:
———–: one impulse re-enters and excites the heart more than once.
• -Normally (in some areas) cardiac impulse bifurcates into two branches in order to supply the entire ventricle.
• -These branches conduct at ——- velocities. Then meet and extinguish one another and never re-enters point of bifurcation.
Re-entry
equal
Enumerate in order drug used in cardiac arrhythmia ?
1- ————————–dec. slope of phase 4
2—————————dec slope of phase 4 and slow AV conduction
3- ———————–inc. ERF (Duration of action potential
4- ————————–dec. slope of phase 4 and slow AV conduction
5- ————————–dec. slope of phase 4 ,slow AV conduction,hyperpolarization (Dec. RMP) and___________Trap Na+ channel in inactive
state for longer time
1- Sodium Channel Blocker 2- Beta Blocker 3-Potassioum channel Blocker 4- Calcium channel Blocker 5-Miscellneous ( Adenosine) and (Mg++)
•Enumerate the Mechanism of action of anti-arrhythmic drugs
5 tings
1•-They restore normal rhythm, decrease ectopic pacemaker activity and block re-entry through:
• -Blockade of Na, K & Ca channels.
• - Decrease cardiac sympathetic activity.
• -Prolongation of refractoriness.
• -↑ dose, normal tissue is affected → arrhythmia (proarrythmogenic)
Class 1 Membrane stabilizers ; Sodium channel blockers
- -Block Na channels →slows the rate of rise of phase 0 of the action potential thus ↓ maximal rate of depolarization (Vmax) → ↓conduction velocity (CV) & ↓ excitability.
- -Inhibit spontaneous diastolic depolarization of automatic tissue → ↓rate of discharge.
Classification of Class 1 according to Effect on APD & CV:
• 1a: ——————-Moderate,inc. ERF
• 1b: —————-Weak,De. ERF
• 1c: —————Strong
quinidinen
lidocaine ,mexiletine
Flecainide
Class II = Beta Adrenoceptors blockers (———
,———–, ————–):
propranolol-metoprolol-esmolol
Mechanisms of Beta Blocker
3 things
1• Block intrinsic sympathetic activity → ↓ slope of phase 4 spontaneous depolarization of
automatic tissue.
2• Protect against sympathetic induced ectopic pacemaker activity.
3• - Prolong AV conduction and decreasing HR &
contractility.
Class III = K Channel blockers (———&————) :
mechanism 1 things
amiodarone -sotalol
• Delay repolarization → ↑ APD → ↑ ERP → block re- entry.
Class IV = Ca Channel blockers (————):
mechanism 3 things
verapamil
• - Block slow Ca current (slow conduction):
• 1- Slow SAN firing rate & AVN conduction.
• 2- Suppress slow responses (ectopic pacemaker activity).
• 3- Decrease slope of phase 4 depolarization of
automatic tissues.
Mechanism of Class IA of Sodium channel blocker?
Moderate block on Na+ channel (phase 0)
• Slow conduction velocity
• Prolong ERP (more time between depolarization (i.e.,
more time between heartbeats) _dec HR
Quinidine
Autonomic effects:
Therapeutic uses:4
Adverse effects:5 Adverse effects
1- atropine – like action, α- blocking activity,
slight negative inotropic effect.
2–Broad spectrum oral drug especially effective in AF or flutter refractory to other agents. But never alone because it increases AV conduction and HR {can induce tachycardia in
normal individuals (atropine- like action)}
• - Re-entry arrhythmias
Adverse effects:
• - Serious effects, largely replaced by verapamil.
• 1- Cardio toxicity: Quinidine syncope or sudden arrythmogenic
death.
• - Vent. Tachycardia hence digitalis or verapamil are given
before quinidine in AF or flutter to block AVN conduction.
• 2- Cinchonism (headache, blurred vision, tinnitus, disorientation
and psychosis).
• 3- GIT upset.
• 4- Thrombocytopenia.
• 5- ↑ serum level of digitalis (↓ clearance).
Quinidine never use alone why ?
because it increases AV conduction and HR {can induce tachycardia in normal individuals (atropine- like action)}
Procainamide (class Ia): • Na channel blocker 2 Adverse effects
• Therapeutic uses:
• - Broad spectrum, especially used in treatment of ventricular arrhythmia during myocardial infarction.
• -Rarely used due to development of systemic Lupus Erythematosis( up to 30%) and CHF (-ve inotropic),sever hypotension and CNS adverse
effects(depression, psychosis and hallucinations).
