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pharma > 18.antiaarhythmic drugs > Flashcards

18.antiaarhythmic drugs Flashcards

1
Q

What are antiaarhythmic drugs? Give a definition

A

agents that can modify impulse generation and conduction
by different mechanisms
and are used to suppress abnormal rhythms of the heart

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2
Q

what is the classification of antiaarhythmic drugs?

A

according to changes in Action potential produced in isolated cardiac cells:

Class I - Na+ channel blockers
II - beta blockers
III - K+ channel blockers
IV - Ca2+ channel blockers

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3
Q

describe the AP of cardiomyocytes

A

phase 0 = rapid depolarization - entry of Na+ through rapid sodium channels
phase 1 = ** early repolarization** - closing of Na+ and opening of K+ channels
2 = plateau - balance bw K+ exit and Ca2+ entry
3 = late repolarization - further K+ exit
4 = resting membrane potential is established

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4
Q

Which are the two mechanisms of aarhythmias?

A
  1. abnormal automaticity
  2. reentry mechanism
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5
Q

What happens in cases of abnormal automaticity?

A

normally - the SA node sets the pace of contraction for the myocardium

1.If, other cardiac sites show enhanced automaticity, they may generate competing stimuli leading to aarhytmias
2. If myocardial cells are damaged, the remain partially depolarized during diastole - can reach the firing threshold earlier than normal cells = ectopic focus

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6
Q

what happens in reentry mechanism?

A
  1. If a fiber has 2 conduction pathways and there is a unidirectional block in one of them, the impulse will be conducted down the other.
  2. If the block (e.g in B) is in forward direction only, the impulse may travel in retrograde fashion through B and reenter the point of bifurcation.
    -this results in reexcitation of ventricular muscle, ==premature contraction or sustained ventricular aarhythmia
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7
Q

Which are the types of aarhythmias?

A
  1. SUPRAVENTRICULAR if they arise from atria, SA or AV node
    e.g atrial flutter, sinus tachycardia
  2. VENTRICULAR from the ventricles
    e.g ventricular premature beats
  3. CONDUCTION abnormalities
    e.g AV block
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8
Q

Describe the action of Class I antiaarhytmics

A

1.act by blocking the voltage-sensitive Na+ channels (like local anesthetics)
2. slow the rate of Phase 0 of AP
decreasing the conduction velocity
and decreasing the reentry
3. are divided into 3 groups:
A-moderate block
B-mild block
C-marked block

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9
Q

Describe class IA and give an example of a drug

A

e.g Qinidine sulfate tab.200mg

  1. block Na+ channels - slow phase 0
  2. block K+ channels - delay phase 3 /rapid repol./

=prolong AP duration and refractory period
=slow conduction

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10
Q

Which are the effects of class IA antiaarhytmics

A
  1. antimuscarinic
  2. negative inotropic
  3. hypotensive (a1 adrenolytic)
  4. proaarhythmic action
    —for supraventricular and ventricular aarthymias
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11
Q

IV procainamide is used for?

A

1.hemodynamically stable ventricular tachycardia

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12
Q

Quinidine - class IA antiaarhythmic
pharmacokinetics
1-absorbtion
2-metabolism
3-excretion

A

1-well absorbed orally
2-highly bound to plasma proteins
and metabolized in liver (active metabolite)
3- 20% via urine

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13
Q

Cardiac ADRs of Quinidine

A

1.aarhythmia - ventricular tachycardia (torsade de pointes), prolong the QT
2. antimuscarinic effect- increase AV conduction - tachycardia and increased ventricular rate
3. Hypotension due to a1 blocking effect - quinidine syncope after 1st dose

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14
Q

Extracardiac ADRs of quinidine

A

1.cinchonism (headache, dizziness, tinnitus, deafness)
2. hypersensitivity reactions (hepatitis, thrombocytopenia)
3.GIT - nausea, vomiting, diaarhea

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15
Q

Drug interactions of Quinidine

A

increases plasma level of digoxin by
1-displacement from tissue binding sites
2-decreasing digoxin renal clearance

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16
Q

Procainamide tab.250mg class IA
pharmacokinetics
what is its absorption?

A

1.well-absorbed after oral administration
2.i.v rarely used because it can cause hypotension if infused too rapidly

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17
Q

Procainamide tab.250mg class IA
pharmacokinetics
metabolism?

A

1-short half life (2-3hrs)
2-by acetylation in the liver to N-acetylprocainamide, which is responsible for drug-induced development of LUPUS ERYTHEMATOUS

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18
Q

Procainamide tab.250mg class IA
pharmacokinetics
excretion?

A

1.kidney - adjust dose in patients with renal failure

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19
Q

ADRs of Procainamide

A

1.SLE symptoms - arhtralgia, fever, pleural-pericardial inflammation
2.asystole or ventricular aarhythmia
3.hypersensitivity - fever, agranulocytosis
4.hypotension
5.GIT nausea, diarrhea

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20
Q

class IB action of these drugs

A

1.block Na+ channels - slow phase 0
2.open K+ channels - accelerate phase 3 - rapid rep.
3.shorten duration of AP and RP
4.suppress aarthythmias caused by automaticity
5.NO effect on conduction velocity

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21
Q

therapeutic use of class IB

A

1.ventricular aarhythmias arising during myocardial ischemia
or due to digoxin toxicity
2.NO effect on atrial or AV nodal aarhythmias
(do not act on conduction velocity)

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22
Q

Name drugs that belong to class IB

A

1.Lidocaine - amp.0,5%, 1%, 10ml
2.Phenytoin tab.100mg

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23
Q

Lidocaine Pharmacokinetics
1.absorption

A

1.well absorbed after oral administration
BUT
2.undergoes first pass metabolism
so either rapid i.v administration
or slow i.v infusion

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24
Q

Lidocaine Pharmacokinetics
distribution

A

1.large volume of distribution
2.crosses placental and BBB - CNS side effects!

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25
Q

Lidocaine Pharmacokinetics
halflife
metabolism
excretion

A

1.short -2hr
2.in liver
3.by kidney

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26
Q

Therapeutic use of Lidocaine

A

in emergency treatment of ventricular aarhythmias

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27
Q

ADRs of Lidocaine

A

CNS
initially excitation -
1. drowsiness,
2. numbness,
3. agitation
4. confusion

after that
1.unconsciousness
2.respiratory and CVS depression

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28
Q

What is phenytoin used for?

A

it is an antiepileptic drug with antiaarhythmic action
—used for ventricular aarhytmias due to digoxin toxicity

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29
Q

name the drug interactions of phenytoin

A

is an enzyme INDUCER (increases metabolism of other drugs)

30
Q

ADRS of phenytoin

A

1.depression of CNS
2. nystagmis
3.gingival hyperplasia
4.osteoporosis
5.hyperglycemia

31
Q

How do class IC antiaarthymic work?

A

1.block Na+channels - slow phase 0
2.NO effect on duration of AP
3.slow conduction in myocardial tissue
4.reduce automaticity by increasing the threshold potential

32
Q

name a drug of class IC antiaarthythmic

A

Propafenone caps.225mg

33
Q

Propafenone
absorption

A

good oral absorption

34
Q

propafenone metabolism

A

first pass with short term use
—increase in dose leads to unproportionally increase in concentration

35
Q

metabolism and excretion of propafenone

A

1.liver by hydroxylation
2.kidney

36
Q

therapeutic use of Propafenon

A

SUPRAVENTRICULAR AND VENTRICULAR AARHYTHMIAS
1.prevention of paroxysmal atrial fibrillation
2.paroxysmal supraventricular tachycardia

37
Q

Propafenon ADRs

A

proaarthymic drug causing
1-worsening of existing aarhythmia
2-de novo occuring ventricular tachycardia

negative inotropic effect
1-metallic taste
2-constipation

38
Q

which are the drugs in class II antiaarhythmic drugs

A

Beta Blockers

39
Q

Beta blockers effects

A

1.slow phase 4
2.negative chronotropic effect (decreases HR)
3.negative dromotropic effect - slow AV conduction
4.negatice bathmotropic effect - decrease abnormal automaticity

40
Q

therapeutic use of BB

A

SUPRAVENTRICULAR AND VENTRICULAR AARHYTHMIAS
1.stress and exercise induced
2.atrial fibrillation and flutter
3.AV nodal tachycardia
4.protection against sudden cardiac death

41
Q

Class III antiarrhythmic drugs function

A
  1. block K+ channels
  2. inhibit repolarization (phase 3)
  3. prolong effective refractory period and duration of AP
  4. do NOT alter phase 0
42
Q

name 2 drugs in class III antiaarhythmic drugs

A

1.amiodarone tab.200mg
2.sotalol tab.80mg

43
Q

Pharmacodynamics of Amiodarone

A
  1. Contains iodine and is related structurally to thyroxine.

complex effects:
Class I action – blocks Na+ channels;
ClassII action – blocks beta receptors;
Class III action – blocks K+ channels;
Class IV action – blocks Ca2+ channels.actions.

=main effect is blocking of K+ channels.

44
Q

Application of Amiodarone

A

1.orally - but incomplete oral absorption
2. i.v

45
Q

Amiodarone volume of distribution

A

large
- extensively taken up by tissues
- especially adipose tissue

46
Q

What is the correct dose of Amiodarone?

A

has long half life ca.1-6months
-give 6-8tab initially and then 1 per day

47
Q

Metabolism and excretion of Amiodarone

A
  1. liver
  2. bile excretion
48
Q

ADRs of Amiodarone

A
  1. pulmonary fibrosis
  2. Corneal micro-deposits (may cause halos around lights).
  3. Hypo- or hyperthyroidism !!!
  4. Photosensitivity of the skin
  5. skin pigmentation
  6. Peripheral neuropathy.
  7. Hepatitis.
49
Q

Therapeutic use of amiodarone

A

Severe refractory supraventricular and ventricular tachyarrhythmias.

50
Q

which is the most commonly employed antiaarhytmic?

A

amiodarone

51
Q

drug interactions of amiodarone

A
  1. Increases plasma digoxin levels
  2. Inhibits some CYP isoenzymes
  3. increases plasma concentration of anticoagulants (Warfarin)
    +
    lipid lowering drugs (statins e.g. simvastatin ).
52
Q

pharmacodynamics of sotalol

A
  1. Non-selective beta-blocker - suppresses phase 4 (spontaneous depolarization)
  2. also blocks K+ channels and
  3. prolongs the duration of action potential and effective refractory period.
53
Q

absorption of Sotalol

A

hydrophilic BB - good oral absorption

54
Q

metabolism and excretion of sotalol

A

1.does NOT cross BBB
2.NOT metabolized
3.excreted by kidneys

55
Q

therapeutic uses of Sotalol

A
  1. Ventricular arrhythmias and supra-ventricular tachycardia.
  2. Especially effective in prevention of sustained ventricular tachycardia.
56
Q

ADRs of Sotalol

A
  1. ADRs of beta blockers
    +
  2. Proarrhythmic effect - polymorphic ventricular tachycardia (because it increases ERP).
57
Q

What does IVA antiaarhythmic drugs do?

A

1.Block Ca2+ channels
2. inhibit Phase 2.
3. slow conduction in Ca2+ current-dependent tissues
like AV node.

58
Q

which are the therapeutic uses of class IVA antiaarhythmic drugs?

A
  1. effective in AV nodal arrhythmias, where the action potential largely results from Ca2+ entry rather than Na+ entry.
  2. only against supraventricular arrhythmias
    (atrial and A-V nodal arrhythmias).
59
Q

class IV antiaarhythmic drugs
-which are the groups of Ca2+ channel blockers

A

Dihydropyridines;
Non-dihydropyridines.

60
Q

what does dihydropyridines do?

A
  1. mainly block Ca2+ channels in blood vessels and 2. cause vasodilation decreased BP.
  2. used as antihypertensive and antianginal drugs.
61
Q

which are the non-dihydropyridine ca2+ channel blockers?

A

1.verapamil tab.40 or 80mg
2.diltiazem tab.60 and 90mg

62
Q

Action of non-dihydropyridine Ca2+ blockers

A

mainly block Ca2+ channels in heart and cause:
1. (-) inotropic effect – decreased contractility;
2. (-), chronotropic effect – bradicardia;
3. (-) dromotropic effect – slowed A-V conduction;
4. (-) and bathmotrpic effect - decreased
automaticity.

used as
antiaarhythmic
antihypertensive
and antianginal agents.

63
Q

Absorption of non-dihydropyridine Ca2+ channel blockers

A

good oral

64
Q

distribution and metabolism of of non-dihydropyridine Ca2+ channel blockers

A

1.first pass effect - low bioavailability
2. large volume of distribution
3. cross BBB and placental barrier
4. bile excretion

65
Q

ADRS of non-dihydropyridine Ca2+ channel blockers

A

1) Heart failure – due to (-) inotrpic effect.
2) Bradicardia – due to (-) chronotropic effect.
3) A-V block – due to (-) dromotropic effect.
4) Constipation (Verapamil).

66
Q

which are the IVB anttiarhythmic drugs

A

adenosine

67
Q

administration and halflife of adenosine

A

i.v
very short half life - less than 2sec

68
Q

pharmocodynamics of adenosine

A
  1. Acts on adenosine receptors in the sinoatrial node and causes bradycardia.
  2. no (-) inotropic and arrhythmogenic effect.
69
Q

therapeutic use of adenosine (4b)

A

supraventricular tachycardia

70
Q

ADRs of adenosine

A
  1. Hypotension.
  2. Bronchoconstriction (wheezing) – asthma is
    contraindication.
  3. Flushing.

pharma (17 decks)

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