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pharmacology > Anti-arrhythmic drugs > Flashcards

Anti-arrhythmic drugs Flashcards

1
Q

Phases of action potential(AP) (atria&
ventricles):
• Phase —: rapid depolarization with fast influx of
Na+→ Na+ channels are rapidly inactivated.
——————- determines
conduction —————–

A

0
Maximal rate of dep. (Vmax)
velocity

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2
Q

Phases of action potential(AP) (atria&
ventricles):
• Phase ————-: early fast repolarization: rapid out flux of————.

A

1
repolarization
K+

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3
Q

the most effective

A

Amiodarone(cordarone)

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4
Q

Phase ————: delay in repolarization (plateau) slow

Ca++ influx &————- K+ efflux

A

2

equal

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5
Q

Phase 3: rapid repolarization due to———— out flux

A

K+

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6
Q

someone has sever bradycardia what should he use ?

A

Atropine

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7
Q

Phase 4: ———– → Resting membrane
potential (diast.) due to active pump of Ca++&Na+
in exchange of K+

A

full repolarization

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8
Q

Pathophysiology of dysrhythmia:
• there is an abnormality in the ———– of origin of the impulse, its rate or
regularity, or its ————-.

A

site

conduction

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9
Q

I. Disturbance in impulse generation
1. Increased automaticity of automatic tissue (↑———–
Depolarization) {e.g. with increased sympathetic Activity}→——————-

A

slope of diastolic

tachyarrhythmia

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10
Q

I.Disturbance in impulse generation
. Decreased automaticity of automatic tissue→ ————–
(↑————tone).

A

Brady arrhythmia

vagal

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11
Q

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).

A

non automatic
ischemia
digitalis
sympathetic

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12
Q

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.

A

Re-entry

equal

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13
Q

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

A 
1- Sodium Channel Blocker
2- Beta Blocker
3-Potassioum channel Blocker
4- Calcium channel Blocker
5-Miscellneous ( Adenosine) and (Mg++)
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14
Q

•Enumerate the Mechanism of action of anti-arrhythmic drugs

5 tings

A

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)

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15
Q

Class 1 Membrane stabilizers ; Sodium channel blockers

A
  • -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.
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16
Q

Classification of Class 1 according to Effect on APD & CV:
• 1a: ——————-Moderate,inc. ERF
• 1b: —————-Weak,De. ERF
• 1c: —————Strong

A

quinidinen
lidocaine ,mexiletine
Flecainide

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17
Q

Class II = Beta Adrenoceptors blockers (———

,———–, ————–):

A

propranolol-metoprolol-esmolol

18
Q

Mechanisms of Beta Blocker

3 things

A

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.

19
Q

Class III = K Channel blockers (———&————) :
mechanism 1 things

A

amiodarone -sotalol

• Delay repolarization → ↑ APD → ↑ ERP → block re- entry.

20
Q

Class IV = Ca Channel blockers (————):

mechanism 3 things

A

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.

21
Q

Mechanism of Class IA of Sodium channel blocker?

A

Moderate block on Na+ channel (phase 0)
• Slow conduction velocity
• Prolong ERP (more time between depolarization (i.e.,
more time between heartbeats) _dec HR

22
Q

Quinidine
Autonomic effects:
Therapeutic uses:4
Adverse effects:5 Adverse effects

A

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).

23
Q

Quinidine never use alone why ?

A

because it increases AV conduction and HR {can induce tachycardia in normal individuals (atropine- like action)}

24
Q 
Procainamide (class Ia): 
• Na channel blocker
2 Adverse effects
A

• 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).

25
Q

Disopyramide (class Ia): ?

A

Similar to quinidine with marked anticholinergic & -ve inotropic effects.
• -Broad spectrum used in ventricular, supraventricular, WPW syndrome
• - Contraindicated in CHF.
• NB: hyperkalemia increases conduction toxicity of
class I , which is treated by sodium lactate.

26
Q

Lowest potency to block Na+ channel • Shorten repolarization

A

Class Ib

27
Q 
Lidocaine (class IB): 
4 things
A

• -Na channel blocker.
• -No effect on atrial or AVN conduction → ineffective in supraventricular arrhythmias (AF, Flutter, SVT).
• -selective on chronically depolarized ventricular
tissue in myocardial ischemia and digitalis
toxicity.
• Given parentally only.

28
Q

Adverse effects of Lidocaine

2 things

A

Adverse effects:
• 1- The least cardio toxic antiarrhythmic. But in diseased heart may precipitate heart block.
• 2- Parasthesia, tremors, dizziness, slurred speech,
disturbed hearing.

29
Q

Most potent block Na+ channel
• Markedly slow the rate of depolarization •No change in ERP
• They should be used with caution

A

Class IC

30
Q

Flecainide & Propafenone (class IC)
Mechanism of action
1thing
Clinical uses 3 things

A

 It interacts slowly with Na+ channels  Clinical Uses • - Used in SV arrhythmia, and ventricular arrhythmia (if no HF).
• - Pro-arrythmogenic (5-12%) → ↑ mortality,
AV block, HF; so are restricted to case not
responding to other drugs( class IC is of serious
toxicity)
-They are the most dangerous anti-arrhythmic
class of drugs; use only by experienced providers

31
Q

Class II : β1-blockers

A
  • Decrease sympathetic stimulation
  • They block β1 adrenergic receptors at SA and AV nodes
  • Decrease the slope of phase 4; take longer time to hit threshold
  • decrease Frequency of SA firing and slow av conduction so dec HR
32
Q 
β adrenoceptors blockers (class II agents )
Use of propranolol and metoprolol 
2 things 
Use of Esmolol
1 thing
A

Therapeutic uses:
• (propranolol and metoprolol):
• Supraventricular dysrhythmias particularly
those associated with increased sympathetic
activity.
• - Prophylactic (to prevent ventricular
dysrhythmias) following myocardial infarction
→ ↓ incidence of CHF and sudden
arrythmogenic death.
• - Esmolol (an ultashort acting) is used IV in
acute arrhythmias during surgery or
emergency.

33
Q

• Work primarily on non-nodal cells
• Prolong repolarization (Phase 3)
• Prolong ERP; more time between
depolarization (i.e., more time between heartbeats) • Prolong the action potential

A

Class III: K+ channel blockers

34
Q

Amiodarone
Mechanism 1 thing
Uses

A

• - Heavily iodinated drug.
• Broad spectrum.
• The most efficacious antidysrhythmic drug.
• - Block K channels delaying repolarization
→prolongation of APD and ERP.
• - Na channel & a weak Ca channel blocker and
β receptor blocker (I, IV & II respectively).
• - Slows sinus rate and AVN conduction.
- Used in Re-entry arrhythmia (Wolff Parkinson
White Syndrome).
- High lipid soluble drug, precipitate in many
adipose tissues, cardiac and skeletal muscle,
liver, lung and the thyroid.

35
Q

Adverse effects of Amiodarone ?

7 things

A 
Serious due to long half life →cumulative
(t1/2is many weeks with delayed onset). 
• 1- Alteration of thyroid function 
• 2- Precipitation of corneal deposits. 
• 3- Photosensitivity. 
• 4- Pulmonary infiltrates and fibrosis.
• 5- Proximal myopathy and neuropathy. 
• 6- AV block, sinus bradycardia. 
• 7- Potentiates warfarin & ↑ digoxin and
quinidine levels.
36
Q

Dronedarone

A

• It was approved by the FDA in 2009.
• Less toxic on skin, lung and thyroid gland because it is not
have a iodine in its structure.
• A methylsulfonamide group is added to reduce solubility in fats
• Black box warning in USA, to class IV HF
(lipophilicity)
• t1/2 = 24 hs
• Similar mechanism to amiodarone
• Approved now only for atrial fibrillation or flutter

37
Q

Sotalol (class II and III)
Uses
Adverse effect 1

A

• -Broad spectrum in SV and ventricular
arrhythmias &WPW syndrome.
• -Long term therapy to decrease incidence of
sudden death following myocardial infarction
• - Has a strong antifibrillary effects particularly
in ischemic myocardium.
• -Adverse effects:
• had the lowest rate of acute and long term
complications. Prolongs QT interval as drugs
in class I & syndrome of Torsade de pointes is
a serious complication.

38
Q

Non-dihyropyridine (working on SA and AV nodes)
e.g., Verapamil, Diltiazem
• Slow phase 4 depolarization
• Slow AV conduction (prolong repolarization at AV node)

A

Class IV: Ca++ channel blockers

39
Q

Calcium channel blockers (Verapamil and Diltiazem (classIV)

Therapeutic uses

A

1- Supraventricular tachycardia (prophylaxis inhibits nodal re-entry).
• 2- reduce ventricular rate in AF and flutter.
• CI: in CHF due to their –ve inotropic activity.

40
Q

Mechanism of Adenosine and uses

A

• K channel opener → prolong refractory period and slows CV of AVN.
• -Dilates coronary and peripheral blood vessels.
• - The drug of choice in acute paroxysmal SV tachycardia.
• - Can cause brochospasm ,flushing, headache, chest pain, AV
block and hypotension.
(CI in asthma and heart block),

41
Q

Uses of digoxin

A

Digoxin:

• Controls ventricular response in AF and flutter

pharmacology (6 decks)

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