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ICOM-Cardio > Cardio-Pharm I- Antidysrhythmic Agents I > Flashcards

Cardio-Pharm I- Antidysrhythmic Agents I Flashcards

1
Q

The ability for a cell to respond to an external electrical stimulus (usually in the form of an action potential):

A

excitability

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2
Q

The ability for a cell or region of cells to initiate an action potential:

A

automaticity

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3
Q

The ability of a cell or region of cells to receive and/or transmit an action potential:

A

conductivity

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4
Q

The ability to alter the rate of electrical conduction

A

dromotropism

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5
Q

The inability of a cell to receive and transmit an action potential:

A

refractoriness

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6
Q

What is the action potential duration (APD)?

A

Phase 0 to the next phase 0

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7
Q

What is the effective refractory period (ERP)? or absolute refractory period

A

phase 0 to about the middle of phase 3 - cell cannot be stimulated by an external force.

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8
Q

Why is the slope in phase 4 not flat like a non-nodal action potential?

A

As Ca2+ comes into the cell in phase 4, the resting potential tends to depolarize.

When phase 4 reaches the threshold, it depolarizes automatically

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9
Q

Which ions cause the rapid depolarization in nodal and non-nodal action potential in phase 0?

A

Non-nodal - Na+

Nodal - Ca+2

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10
Q

Phase 3 of both nodal and non-nodal action potentials are both due to what movement of what ion?

A

K+ leaving the cell

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11
Q

Na+ channel blockers (type I anti-dysrhythmic) will affect which type of rhythm?

A

conduction rhythm

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12
Q

What type of cardiac action potential will be affected by Ca2+ channel blockers (type 4 anti-dysrhythmic)?

A

nodal action potentials (SA and AV node) - affect nodal dysrhythmia

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13
Q

What do we call anything above or at the level of the AV node?

A

supraventricular

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14
Q

Supraventricular dysrythmias affect which part of the heart?

A

mainly the AV and SA node (primarily treated with drugs that affect phase 0)

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15
Q

Ventricular dysrythmias are mainly treated with which group of drugs?

A

Drugs that affect mainly Na+ and K+ (phase 0 and phase 3)

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16
Q

The sympathetic nervous system affects which parts of cardiac functionality?

A

SA node • Atria • AV node • His-Purkinje • Ventricle

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17
Q

The parasympathetic nervous system affects which parts of cardiac functionality?

A

• SA node • Atria • AV node

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18
Q

What are the 2 major categories of dysrhythmias?

A

supraventricular and ventricular

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19
Q

What does it mean to have a regular vs irregular rhythm?

A

Regular means that there is a one to one ratio between atrial and ventriclar contraction (QRS complex to every P wave)

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20
Q

What are the consequences of dysrhthmia when it comes to compromise of mechanical performance?

A

decreased efficiency = decreased SV = decreased CO

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21
Q

What are the consequences of dysrhthmia when it comes to Prodysrhythmic/Dysrhythmogenic?

A

it can progress to something worse - conversion of v. tachycardia to v. fibrillation

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22
Q

What are the consequences of dysrhthmia when it comes to thrombogenesis?

A

• atrial flutter & fibrillation contribute to increased stroke incidence

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23
Q

Increased PR interval

A

First degree AV node block

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24
Q

Not all P waves pass

A

2nd degree heart block

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25
Q

no P/QRS relationship

A

3rd degree heart block

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26
Q

Class Ia antidysrhythmics (Na+ channel blockers):

A

quinidine, procainamide, disopyramide

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27
Q

Class Ib (Na+ channel blockers) anytidysrhytmics:

A

lidocaine, phenytoin

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28
Q

Class Ic (Na+ channel blockers) antidysrythmics:

A

flecainide

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29
Q

Class II antidysrythmic:

A

propanolol

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30
Q

Class III antidysrhytnmics:

A

amiodarone, sotalol, ibutilide

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31
Q

Class IV antidysrhythmics:

A

verapamil, diltiazem

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32
Q

Class V antidysrhymics (misc. group):

A

adenosine, digoxin, atropine

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33
Q

What type of tissue deals with this type of action potential?

A

Non-nodal tissue where phase 0 depolarization is due to Na+ influx

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34
Q

What type of tissue deals with this type of action potential?

A

• Nodal tissue where phase 0 depolarization is due to Ca+2 influx

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35
Q

What does it mean when the ERP/APD ratio is increased?

A

It decreases exciteability (Na+ channel blockers)

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36
Q

Class I Agents – General

Block voltage-sensitive Na+ channels to varying degrees in tissues of the heart • tend to slow VMAX (phase ) • reduce/increase automaticity, delay conduction, prolong ERP • ERP/APD ratio increased/decreased • useful in varying degrees for dysrhythmia and/or digitalis or MI-induced dysrhythmia

A

conductile; 0; reduce; increased; ventricular

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37
Q

What is the overall effect in Class I antidysrhythmics?

A

a decrease in ventricular exciteability

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38
Q

Class Ia Agents can block Na+, K+, and Ca2+ channels: what are the effects of each of these channels?

A

‘Moderate’ binding to Na+ channels • moderate effects on phase 0 depolarization

K+ channel blockade • delayed phase 3 repolarization • prolonged QRS and QT

Ca+2 channel blocking effect at high doses • depressed phase 2 and nodal phase 0

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39
Q

Can class Ia agents be used for supraventricular and ventricular dysrhythmia?

A

yes

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40
Q

Class Ib agents work mainly with what type of ion channel and what it is the effect?

A

‘Weak’ binding to Na+ channels

• weak effect on phase 0 depolarization due to rapid ‘on-off’ receptor kinetics

this is unique MOA actually increases exciteability as demonstrated in the figure

41
Q

Which class and subtype of antidysrhythmics work good in use in digitalis and MI-induced dysrhythmia?

A

Class Ib agents: lidocaine, phenytoin

42
Q

What are the effects of Class Ic antidysrhythmics agents and why are they used less often?

A

‘Strongest’ binding to Na+ channels

• slow ‘on-off’ kinetics with marked effects on phase 0 depolarization (can be completely blocked)

lengthened QRS and APD, QT unchanged

• lengthened PR (depressed AV nodal conduction)

(very potent, can stop heart, only used in certain cases)

43
Q

Class II agents are mainly compromised of :

A

β-adrenergic antagonists

44
Q

β-receptors are G-protein-coupled to Ca+2 channels and therefore class II antidysrhythmic agents will effect primarily on which type of action potential?

A

nodal phase 0 depolarization

45
Q

Though mainly B-blockers, Class II antidysrhythmic agents also have effects on:

A

SA nodal automaticity (phase 4) depression,

AV nodal conduction,

decreased ventricular contractility

46
Q

Class II agents are mainly used for which type of dysrhymia?

A

supraventricular dysryhtmia

47
Q

Class III agents mainly have effects on which ion channels?

A

K+

48
Q

Though class III agents mainly effect K+ channels, they also have effects on Ca2+, Na+ as well as (direct or indirect)

A

B-receptors

49
Q

The action of Class III agents on K+ channels have what effect on action potential?

A

prolong phase 3 repolarization; ↑QT

50
Q

Which class of agents are also useful for ventricular re-entry/fibrillatory dysrhythmia?

A

Class III agents

51
Q

Class IV agents, in general, act directly on which type of ion channel?

A

Ca+2 channel antagonists (direct calcium channel blockers) - hence mainly work on depressed SA nodal automaticity, AV nodal conduction

52
Q

Because Class II and IV agents work on all Ca2+ channels, their use can depress SA nodal automaticity and AV nodal conduction, however Ca2+ channels are all over the ventricular muscle as well and these agents can also:

A

decrease ventricular contractility (Class II and IV agents)

53
Q

Quinidine, Ia

  • bark alkaloid, d-isomer of quinine
  • Use: and dysrhythmia due to effects on nodal (↓automaticity) and non-nodal tissue (↑QRS and ↑)
  • PK: extensive protein binding and active metabolites results in rather long t½
  • dosage adjustment required in dysfunction and elderly with reduced renal function
A

cinchona; supraventricular/ventricular; QT; plasma; renal

54
Q

How do we resolve long QT syndrome produced by drugs?

A

treat with other drugs

55
Q

quinidine, Ia (cont.)

  • Therapeutic Use: • atrial flutter and , paroxysmal tachycardia (PAT), Paroxysmal tachycardia (PSVT), etc. • tachycardia
  • Adverse Effects ( discontinue use):
  • nausea, vomiting, diarrhea
  • (tinnitis, hearing loss, blurred vision)
  • due to α-adrenergic blocking effect
  • dysrhythmogenicity ( due to drug induced increases in QT interval)
A

fibrillation; atrial; supraventricular; ventricular; 33%; cinchonism;

hypotension; torsades de pointes

56
Q

What is this pathology when you have longer and longer prolongation of QT interval?

A

Tordades de pointes (twisted points)

57
Q

How do you treat torsades de pointes?

A

Treatment usually involves the application of parenteral MgSO4

58
Q

procainamide, Ia

similar pharmacology and use as

  • procainamide has no ester linkage, ∴ little CNS access
  • PK: metabolism depends on hepatic activity and renal function
  • of procainamide excreted unchanged in urine
  • rapid-acetylators: t½=2.5-3hrs • slow-acetylators: t½>5hrs (30-40% of patients)
A

quinidine; N-acetyltransferase; 70%

59
Q

procainamide, Ia (cont.)

  • Adverse Effects:
  • slow-acetylators develop an upon chronic use (reversible on discontinuation)
  • GI nausea and vomiting are very common
  • decreased renal function may be

• mental confusion and

A

SLE-like syndrome; prodysrhythmic; torsade de pointes

60
Q

SLE-like syndrome can be cause by which type Ia antidysrhyhmic and what are the symptoms?

A

procainamide

arthralgia, pericarditis, fever, weakness, skin lesions, lymphadenopathy, anemia and hepatomegaly

61
Q

Which antidysrythmic inhibits reentry mechanisms in ventricular tissue which suppresses spontaneous ventricular depolarizations and has preferential action on ischemic tissue with excellent use in post-MI or digoxin-induced tachycardia?

A

lidocaine, Ib

62
Q

Lidocaine, Ib, is unique in that it may actually lengthen/shorten the ERP and APD within the His-Purkinje system, which would increase in exciteabilty in normal concuction pathways

A

lengthen

63
Q

Though lidocaine can increase/decrease ERP which increases/decreases exciteability in normal tissue, it can actually go into necrotic cells and increase/depress conduction (prolong ERP) which increases/decreases exciteability.

A

decrease

increase

depress

decreases

64
Q

Which antidysrhythmic inhibits reentry mechanisms in ventricular tissue, intitially suppressing spontaneous ventricular depolarizations

A

lidocaine, Ib

65
Q

Lidocaine, lb, is administered by which method only and how is it metabolized?

A

IV administration and extensive hepatic metabolism into active metabolites, no excretion of unchanged drug

66
Q

Which antidysrhythmic has a potent Na+ channel blockade (slow on-off kinetics) whcih markedly depresses cardiac conduction?

A

flecainide, Ic -hence not used clinically often

67
Q

Flecainide, Ic, because of its potency is only used to treat?

A

refractory life-threatening ectopic ventricular dysrhythmia

by prolonging phase 0 and widening QRS

68
Q

Propranolol is which type of antidysrhythmic?

A

Class II, competitive, β-receptor antagonists- indirect Ca2+ channel blocker as well

69
Q

What are 3 other Class II antidysrhythmics other than propranolol and which receptors to they work on?

A

esmolol (β1, β2), metoprolol (β1), acebutolol (β1)

70
Q

Which antidysrhythmic competes with adrenergic transmitters for binding at sympathetic sites in SA and AV nodes, atrial, and ventricular tissue?

A

Class II, propranolol

71
Q

Propranolol, II, being an indirect Ca2+ blocker has effect on phase in nodal or dysrhythmia, but also can have an effect on cardiac in ventriclar tissue.

A

0

supraventricular

contractility

72
Q

The overall effect of propranolol, II, is ? It also ↓conduction in atria, AV node, ventricles; ↓SA/AV nodal automaticity

A

↓HR/CO (↑ERP)

73
Q

Propranolol, II, is excellent in the use for which pathologies?

A

atrial flutter & fibrillation, PAT, and digoxin-induced dysrhythmia

74
Q

propranolol, II

  • PK: for sustained treatment of dysrhythmia
  • extensive first-pass metabolism = bioavailability
  • IV dosage provides immediate effects
  • wide distribution to , placenta, breast milk, etc.
A

PO

25%

BBB

75
Q

Propranolol, II

  • Adverse Effects:
  • , asystole (heart completely stops, AV node completely blocked)
  • with non-selective antagonists
  • withdrawal effect due to receptor up-regulation
A

hypotension

bronchospasm

rebound

76
Q

Always consider IV administration of antidysrhythmics as low/high dose.

A

high, and always monitor

77
Q

Amiodarone, Class III

  • like other class III agents, alters flux during phase 3, ∴↑ and ↑APD
  • utility in refractory dysrhythmia • purported less/more prodysrhythmic potential
A

K+

ERP

ventricular

less

78
Q

amiodarone, III

PK: and IV availability

• t½=1-2 months (extensive distribution with s/s levels in 1-5 months, ∴ aggressive loading doses) • slow hepatic de-ethylation to active metabolite, N-desethyl-amiodarone (DEA)

A

PO

79
Q

amiodarone, Class III

  • Adverse Effects: ( incidence rate in chronic oral administration)
  • GI nausea and vomiting
  • toxicity (10-17%, pneumonitis/ARDS)
  • may elevate enzymes
  • (micro-deposition in the eye)
  • disorders/tumors (iodinated benzofuran chemical structural is similar to thyroxine)
A

75%

pulmonary

liver

photosensitivity

thyroid

80
Q

ibutilide, dofetilide, etc., III

equate with which drug?

A

amiodarone

81
Q

What happens to the PR interval with the use of Class II and Class IV agents that block Ca2+ in AV node?

A

Increased PR interval

82
Q

Verapamil, IV are what kind of ion blocker? And it is useful in the tx of what?

A

Ca2+, useful in tx of supraventricular tachycardia (also can use diltiazem), angina and hypertension (at higher dose)

83
Q

Which type of Ca2+ channels are primarily affected by verapamil, IV?

A

“slow” inward Ca+2 channels in nodal tissue

84
Q

What affect does verapamil, IV, have on ventricular dysrhythmia?

A

ventricular dysrhythmia unaffected (no ventricular Na+ conduction effect)

85
Q

What are the overall effects of verapamil, IV?

A

↓HR (↓SA automaticity), ↑PR, ↓AV conduction

• cardiac depression (↓ ventricular contractility and ↓HR result in ↓SV and ↓CO)

86
Q

IV verapamil, IV is used for ?

PO verapamil, is used for?

A

IV for rapid conversion of SVT

PO for maintenance of recurrent SVT

87
Q

Verapamil, IV is highly which means it sticks around for a while in CNS, placental and breast milk access.

A

lipophillic

88
Q

Hemodialysis is ineffective with which antidysrhythmic?

A

verapamil

89
Q

Which drug is more useful than digoxin for rate control in atrial fib since Ca+2 channel blockade in AV node persists during sympathetic stimulation?

A

verapamil, IV

90
Q

verapamil ADEs:

A

GI constipation

  • hypotension
  • exacerbate CHF
  • AV heart block in combination with β-blockers
  • male sexual dysfunction
91
Q

Verapamil, IV, can also be used as a to lower BP due to extended use. (works on all Ca2+ channel blockers)

A

antihypertensive

92
Q

Why are we concerned about possible GI constipation ADEs with antidysryhtmics?

A

Possible chance of bearing down due to valsalva maneuver consequences

93
Q

Adenosine is considered in what class of antidysrhythmics?

A

Class V or “other”

94
Q

What Class V antidysrhythmic is a purin nucleoside and useful for conversion of reentrant SVT (PAT, PSVT and WPW) to NSR and is comparable to verapamil?

A

adenosine, administered as large rapid acting bolus

95
Q

Adenosine works on which type of receptor to produce complete AV nodal block (temporarily stopping the heart)?

A

Subtype A1 receptors in AV nodal tissue (not to be confused with a1 receptors)

96
Q

What is the overall effect of adenosine, IV, on AV nodal subtype A1 receptors?

A

AV nodal hyperpolarization due to adenosine-stimulated opening of membrane K+ channels

• produces complete AV nodal block

97
Q

Adenosine, IV, is very susceptible to acid degradation which results in a very short ? It also has rapid plasma metabolism in which case needs to be administered where?

A

half-life, 10- 15 seconds

clsoe to the heart in bolus form, not IV

98
Q

Adenosine is used for a action, hopefully the AV nodal conduction will return to NSR

A

conversion

ICOM-Cardio (32 decks)

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