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Antiarrhythmic Drugs Flashcards

1
Q

What are the pharmacodynamics of procainamide?

A 
1. Na+ channel blocker 
A. Slow phase 0 depolarization 
B. ⬇️ upstroke 
C. ⬇️conduction 
D. Prolong QRS duration
E. ⬆️ threshold for excitability 
F. ⬇️automaticity
  1. K channel blocker —> class 3 activity + little Na channel blocking —> by its metabolite NAPA:
    A. Prolong APD
    B. ⬆️ QT interval —> may undergo torsades de pointes
    C. ⬆️ ERP
    D. Rapid acetylators
    E. Acc of ⬆️ levels of NAPA in patients with renal failure
  2. Ganglionic blockade
    A. ⬇️ PVR —> HT during rapid IV infusion
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2
Q

What is procainamide eff against?

A

Eff against most atrial and ventricular arrhythmias but long term therapy is avoided bcz:

  1. Inconvenient administration route
  2. Lupus like syndrome:
    A. Serositis : inflammation of the serous membrane
    B. Arthritis
    C. Arthralgia

REMITS IF THE DRUG IS DISCONTINUED

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3
Q

Arrange class 1 acc to anti-muscarinic eff?

A

disopyramide > quinidine > procainamide

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4
Q

What are the atropine-like SE in disopyramide?

A 
Dry mouth
constipation
urinary retention
blurred vision 
precipitation of glaucoma
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5
Q

What can be caused by disopyramide?

A

Torsades de pointes.

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6
Q

What are the characteristics of the another drug req to be taken with disopyramide?

A

Slows AV conduction when treating AF or atrial flutter

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7
Q

What are the eff of disopyramide?

A

Negative inotropic effect

Avoided in patients with ❤️ failure

Not 1st line antiarrythmic drug

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8
Q

What is disopyramide contraindicated with?

A

A. Obstructive Uropathy
B. Glaucoma
C. Decompansated ❤️ failure

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9
Q

What are the general indications of class 1A?

A
  1. Treatment of ventricular tachycardia associated with acute MI —> in patients with preserved LV function —> for diso and pro only
  2. Treatment of supraventricular arrhythmia for all 3–> off - label
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10
Q

What are the routes of administration of D Q P?

A

D: oral / IV

Q: oral / IV

P: IM / IV

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11
Q

What are the general SE of class 1A ?

A
  1. Torsades de pointes
  2. Antimuscarinic effects
  3. Quinidine: GIT disturbances & cinchonism ( ⬆️ doses )
  4. Procainamide:
    A. Arthralgia & arthritis ( LONG TERM )
    B. ⬇️ PVR and cause HT —> ganglion blocker
  5. Disopyramide: may precipitate in ❤️ failure
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12
Q

Arrange the class 1 acc to their ability to block Na channel ?

A

C > A > B

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13
Q

Arrange the class 1 acc to their ability to block K channel ?

A

A > C > B

See drawings slide 15

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14
Q

What are class 1B drugs ?

A

Lidocaine

mexiletine

phenytoin

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15
Q

What are the pharmacodynamics of class 1 B

A
  1. Block Na channels in act and inact state
  2. Exerts greater eff on Na channels in depolarized cells than in normal cells
  3. Minimal eff on phase 0 depolarization —> No eff on QRS duration but
    A. ⬆️ threshold for excitability
    B. ⬇️ automaticity
5. Shorten phase 3 depolarization:
A. ⬆️ K effluent 
B. ⬇️ APD 
C. ⬇️ QT interval 
D. ⬇️ ERP 
E. no eff on conduction velocity
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16
Q

What are the adverse effects of lidocaine?

A
  1. Least cardiotoxic used Na channel blocker —> proarrhythmic effect + no worsening of impaired conduction
  2. CNS side effects
  3. Liver dysfunction affects the dosage
  4. Hypotension (large doses).
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17
Q

What are the CNS side effects of lidocaine?

A
  1. Neurologic paresthesia
  2. muscle twitching
  3. tremor
  4. nausea
  5. hearing disturbances
  6. dizziness
  7. confusion
  8. slurred speech
  9. seizures

Common in ELDERLY patients or when a bolus injection is given too rapidly.
( sudden rise in the dose )

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18
Q

How can liver dysfunction affect the dosage?

A
  1. Inhibit P450 —> decrease the dose —> ex: cimetidine
  2. Induce P450 —> increase the dose —> ex:
    A. Rifampin
    B. Phenytoin
    C. Barbiturate
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19
Q

What is mexiletine ?

A
  1. Prodrug of lidocaine —> used for ventricular arrhythmia
  2. Similar antiarrhythmic and electrophysiological props to lidocaine
  3. NO vagolytic effects
  4. Used as an adjunct to other antiA drugs ex:
    A. Amiodarone
    B. quinidine
    C. Sotalol
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20
Q

What is mexiletine used for?

A

Ventricular arrhythmia

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21
Q

What is phenytoin used for?

A
  1. Young children with ventricular tachycardia
  2. Treatment of congenital prolonged QT syndrome
  3. Partial seizures
  4. Generalized tonic-clinic seizures
  5. Status epilepticus
22
Q

What are the AE of phenytoin?

A
  1. Nystagmus: rapid involuntary movement of the eyes
  2. Diplopia: double vision
  3. Ataxia: loss of control of bodily movements
  4. Sedation
  5. Gingival hyperplasia
  6. Hirsutism: giving hair on atopic places (another drug that has this side effect is minoxidil)
23
Q

What does phenytoin do ( not what it is used for) ?

A
  1. inducer of P450 enzyme
  2. affects the plasma levels of other antiarrhythmic drugs such as: A. mexiletine
    B. lidocaine
    C. quinidine
  3. Drug displacement from blood proteins (90% bound to proteins)
24
Q

What are the pharmacokinetics of lidocaine, mexiletine, and phenytoin?

A

L —> IV —> loading dose followed by infusion —> bcz of ⬆️ first pass metabolism after 1st administration ( metabolism results in toxic prods affecting the CNS )—> unusual to continue IV for longer than 48 hrs

M & P —> active after ORAL administration

25
Q

What are the general clinical uses ?

A
  1. Treatment of ventricular tachycardia and fibrillation during acute MI —> LIDOCAINE
  2. Used especially for Ventricular Arrhythmias and re-entrant arrhythmias —> to counteract digitalis induced tachycardia
26
Q

What are the drugs in class 1C?

A

Flecainide

propafenone

27
Q

What is the MoA of class 1C?

A
  1. Block Na+ channels potently
  2. Decrease the conduction velocity in fast response tissues
  3. largely prolong the QRS complex.
  4. Does not prolong AP or QT interval in normal cells.
  5. Propafenone possesses weak beta-blockade .
28
Q

What is class 1C drugs used for?

A
  1. Supraventricular arrhythmias —> maintain sinus rhythm in absent structural heart disease
  2. Flecainide should NOT be used in patients with:( increased mortality rate)
    A. LV dysfunction
    B. recent acute MI
  3. Limited use due to their fetal proarrhythmic properties and their tendency to exacerbate HF and heart block.
29
Q

What are the drug in class 2?

A

BETA-BLOCKERS

ex: Propranolol, Timolol, Metoprolol, Esmolol, Labetalol, Carvedilol

30
Q

What are the effects of drugs in class 2?

A
  1. ⬇️ phase 4 depolarization in SA node
  2. Prolong depolarization
  3. Slow down conduction via AV node
  4. Prolong refractory period
  5. Supp of ventricular ectopic depolarization (but < than Na+ channel blockers)
  6. In patients recovering from acute MI —> prevent:
    A. recurrent infarction
    B. Sudden death
31
Q

What is BB ( class 2 ) used for?

A

Treatment and prophylaxis of:

  1. Paroxysmal Supra ventricular tachycardia
  2. Atrial fibrillation

ESMOLOL —> ultra short acting B1 selective antagonist —> acute arrhythmias

32
Q

What are the side effects of class 2?

A

Smooth muscle spasm

Bronchospasm

Cold extremities

Impotence

NEGATIVE inotropic eff

Insomnia

Depression

Last 2 bcz it penetrates the CNS

33
Q

What are the drugs of class 3?

A 
Amiodarone
Bretylium
Dofetilide
Ibutilide
Sotalol
Dronedarone
Vernakalant
34
Q

What are the eff of class 3?

A
  1. Prolongs phase 3 of AP
  2. Prolong APD

By
A. blocking K channel
B. delaying repolarization (long QT interval)

thus
prolonging ERP.

35
Q

What property can class 3 drugs display ?

A

Reverse-use dependence property upon chronic administration except amiodarone

36
Q

What are the props of class 3 drugs?

One general and the rest are specific for each drug

A
  1. Variability in causing torsades de pointes despite sig QT-interval prolongation
  2. AMIODARONE:
    A. blocks inactivated Na channels
    B. weak adrenergic and calcium channel blocking actions That:
  3. decreases HR
  4. causes peripheral vasodilation after IV administration.
  5. SOTALOL: Block B-receptors + class 3 activity
  6. BRETYLIUM: interferes with the release of catecholamines ( pretty cat )
  7. DOFETILIDE: ( دوا fit )
    A. negative chronotropic effects ( ⬇️HR )
    B. NO negative inotropic effect ( 🚫⬇️contraction )
    C. less organ toxicity then amiodarone
  8. Dronedarone:
    A. broad MoA like amiodarone but does not cause thyroid dysfunction nor pulmonary toxicity
    B. It increases risk of death, stroke, and HF, thus it’s contraindicated in acute decompensated/advanced HF
7. VERNAKALANT 
A. multi-ion channel inhibitor 
B. used for AF since it: 
1. increases atrial ERP 
2. slows conduction over the AV node
3. does not change QT interval on ECG or heart rate.
37
Q

What are the pharmacokinetics of amiodarone and what are the routes of administration?

A

Routes: oral and IV

  1. Structural analog of thyroid hormone
  2. Slow oral abs
  3. Long half life —> 100 days —> most long lasting antiarrhythmic drug —> can give one dose only —> bcz highly lipophilic —> eliminated extremely slowly —> cardiac tissue concentration is 30 times > than plasma concentration
  4. Loading dose —> daily for about 2 weeks —> after that daily maintainance dose
  5. Metabolized by CYP3A4 to an active metabolite
  6. ⬆️ warfarin and digoxin —> must reduce their dose
38
Q

What are the pharmacokinetics of sotalol and dofetelide ?

A

simple pharmacokinetics with
A. complete oral absorption
B. renal excretion mainly.

39
Q

What are the pharmacokinetics of dronedarone?

A

When taken with food its absorption is 2-3 times increased.

Is both a CYP3A4 substrate and inhibitor

40
Q

What are class 3 drugs used for?

A
  1. Ventricular —> NOT Dofetilide / ibutilide / dronedarone
  2. Supraventricular —> such as AF —> NOT Bretylium
  3. Supraventricular and ventricular in pediatrics —> sotalol
41
Q

What are the SE of amiodarone ?

A

A. Torsade de pointes: ⬆️ with cumulative dose—> MAJOOOOOR

B. Corneal microdeposits (yellowish-brown micro crystals) —> if for than 6 months

C. Skin discoloration: dermatological reactions (15-20%) including
photosensitivity (10%), which can result in blue-gray skin color in
sun-exposed areas, and various visual disturbances (10%).

D. Peripheral neuropathy (20-40% incidence, but reversible by
lowering dose)

E. paresthesias

F. ataxia

G. tremors

H. Optic neuritis may progress to blindness

I. Thyroid dysfunction —> Dronaderone is less lipophilic (shorter half-
life), lacks iodine moeities (less thyroid toxicity).

J. Pulmonary fibrosis and interstitial pneumonitis —> Chest x-rays are required every 3 months

K. Hepatotoxicity & hypersensitivity hepatitis —> abnormal liver function tests
(which can be fatal; 30% of patients have elevated serum liver enzymes) and
Constipation (in 20%).

L. Testicular dysfunction

42
Q

What are the therapeutic tests conducted when using class 3 drugs ?

A
  1. Pulmonary function tests
  2. liver function tests
  3. cardiac function
  4. thyroid function
  5. eye exams
43
Q

What are the contraindications of using class 3 drugs?

A
  1. SA or AV node dysfunction
  2. Lung disease
  3. Thyroid disorders
44
Q

What are the drugs in class 4 ?

A

Verapamil

Diltiazem

45
Q

What are the effects of class 4 ?

A
  1. Marked effect in tissues that fire frequently and in
    which their activation rely exclusively on Ca+2 current such
    as SA and AV nodes.
  2. Reduce rate of SA node discharge
  3. slow conduction through AV node
  4. prolong AV node ERP (prolong PR interval)
  5. decrease contractility.
46
Q

When is class 4 used as drug of choice?

A

In PSVT

47
Q

What is the use of verapamil?

A

reduce the ventricular rate in atrial fibrillation and flutter provided patients do not have WPW. ( what is it )

MAIN DRUG USED

48
Q

What does diltiazem differ from verapamil?

A

Relatively more smooth-muscle relaxing effect

Produces less bradycardia

49
Q

What is adenosine?

A
  1. very short half life
  2. Only IV
  3. Activates K+ channels and inhibits Ca++ channels thus causing hyperpolarization.
  4. cAMP production is inhibited by A1 receptor activation by Adenosine.
  5. Inhibits AV node conduction and ­ AV node ERP
  6. Drug of choice in treatment of PSVT.
50
Q

What is digoxin?

A

⬇️ ventricular rate in AF by ⬇️ AV node conduction

⬆️ vagal activity via CNS

51
Q

What is MgCl2?

A

digitalis induced arrhythmias if hypomagnesemia is

present and in patients with torsade de pointes.

52
Q 
What is the indication of each of the following :
Atropine 
CaCl2
Epinephrine 
Isoprenaline
A
  1. Atropine: Indicated for sinus bradycardia.
  2. Calcium chloride: Ventricular tachycardia due to hyperkalaemia
  3. Epinephrine (Adrenaline): Cardiac arrest
  4. Isoprenaline: non-selective β adrenoreceptor agonist Heart block.

Pharma (5 decks)

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