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Pharm exam 5 > Antiarrhythmics > Flashcards

Antiarrhythmics Flashcards

1
Q

what channels/receptors do class III agents effect

A

K+, Ca2+, Na+ channels & autonomic receptors

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2
Q

main effect of class III agents

A

prolong phase 3 repolarization; increase QT

Effective in many types of arrhythmias

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3
Q

what are the class III agents

A

Amiodarone

Ibutilide

Dofetelide

Dronedarone

Sotalol

(AIDDS)

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4
Q

class III

Blocks K+ channels –> prolongs refractoriness and APD

Blocks Na+ channels that are in the inactivated state

Block Ca2+ channels –> slows SA node phase 4

Slows conduction through the AV node

Noncompetitive blockade of α-, β-, and M receptors

Explains diverse antiarrhythmic actions

A

Amiodarone

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5
Q

clinical applications of amiodarone

A

Conversion and slowing of Af, maintaining sinus rhythm in Af (rx of choice)

AV nodal reentrant tachycardia

IV for acute termination of VT or VF and is replacing lidocaineas first-line therapy for out-of-hospital cardiac arrest

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6
Q

explain pharmacology of amiodarone

A

highly lipophilic

metabolize to DEA: DEA has antiarrythmic potency >/= amiodarone

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7
Q

what may be responsible for early recurrence of arrhythmias after discontinuation or rapid dose reduction of amiodarone

A

Until all tissues are saturated, rapid redistribution out of the myocardium

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8
Q

most serious adverse rxn to amiodarone

other SE

A

most serious: lethal pulmonary fibrosis

Hyperthyroidism or hypothyroidism

elevated serum hepatic enzyme levels

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9
Q

what should be checked when someone is taking amiodarone

A

Check PFTs (CXR/3 months), LFTs, & TFTs when using amiodarone

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10
Q

MOA of Ibutilide

A

Blocks the rapid component of the delayed rectifier K+ current –> slows cardiac repolarization.

Activation of slow inward Na+ current --> prolong AP.
(other class III are not acting on Na+)
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11
Q

therapeutic use of ibutlide

A

IV: acute conversion of atrial flutter and atrial fibrillation to NSR (20 min

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12
Q

SE of ibutilide

A

Excessive QT-interval prolongation and Torsades de Pointes.

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13
Q

MOA of dofetilide

A

Dose-dependent blockade of delayed rectifier K+ current (IKr) (blockade IKrincreases in hypokalemia)

Does not block other K+ channels.

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14
Q

clinical use of dofetilide

A

Restore & maintenance of normal sinus rhythm in patients with Afib.

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15
Q

SE of dofetilide

A

Dose-dependent QT interval prolongation and ventricular proarrhythmia

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16
Q

MOA of sotalol

A

Has both β-blocking & AP-prolonging actions.

acting on K+ channe

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17
Q

clinical use of sotalol

A

Life-threatening ventricular arrhythmias

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18
Q

SE of sotalol

A

Dose-related torsades de pointes

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19
Q

class IV agents

A

Verapamil

Diltiazem

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20
Q

what channels do class IV agents blcok

A

Ca2+

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21
Q

action of class IV agents

A

depressed SA nodal automaticity,

AV nodal conduction,

decreased ventricular contractility

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22
Q

what interval is increased by class IV

A

PR interval

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23
Q

which Ca2+ subunit contains pores

A

alpha1

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24
Q

Ca2+ channel blockers (CCBs) interfere with the entry of Ca2+into cells through voltage-dependent _____ channels.

A

L- and T-type Ca2+

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25
Q

where are CCB major cardiovascular sites of action

A

vascular smooth muscle cells
cardiac myocytes
SA and AV nodal cells

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26
Q

By binding to specific sites in Ca2+ channel subunits,CCBs diminish the degree to which the Ca2+ channel pores _____

A

open in response to voltage depolarization

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27
Q

which CCBs mainly effect the vasculature

A

Dihydropyridine (DHP): Nifedipine

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28
Q

which CCBs mainly effect the heart?

A

Non-dihydropyridine (NDHP)

Phenylalkylamine - Verapamil

Benzothiazepine - Diltiazem

–used as antiarrhythmics

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29
Q

for CCBs where is vasodilation more seen

A

more marked in arterial and arteriolar vessels than on veins

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30
Q

which CBCs have Negative chronotropic and dromotropic effectsare seen on the SA and AV nodal conducting tissue

A

NDHP agents only (verapamil, diltiazem)`

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31
Q

ratio of vasodilation to negative inotropy for the protoype CCBs?

A

10 : 1 for nifedipine,

1 : 1 for diltiazem and verapamil.

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32
Q

do CCBs have effect on non-cardiovascular smooth muscles

will skeletal muscles respond to CCBs?

A

no

no

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33
Q

non-cardiovascular effect of CCBs

A

CCBs may relax uterine smooth muscle and have been used in therapy for preterm contractions

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34
Q

what CCBs have IV formulations available

A

Verapamil, Diltiazem, Nicardipine, Clevidipine (only IV)

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35
Q

MOA of verapamil

A

↓SA automaticity  ↓HR

↓AV conduction velocity –> ↑PR interval
Increased ERP

Cardiac depression (decrease ventricular contractility and HR)

No effect on ventricular Na+ conduction –> ineffective on ventricular arrhythmia

36
Q

clinical application of verpamil

A

Prevention (PO) or conversion (IV) of nodal arrhythmias: PSVT

Rate control in Afib

37
Q

SE of verapamil

A

Constipation

Exacerbate CHF

38
Q

contraindications of verapmil

A

WPW syndrome with Afib

Ventricular tachycardia

39
Q

MOA of adenosine

A

Activates A1receptors in SA & AV nodes –> open K+ channels –> increase K+ efflux –>

  • SA node hyperpolarization and decrease firing rate
  • Shortening of AP duration of atrial cells
  • Depression of A-V conduction velocity

Activates A2receptor in vasculature –> K+ channels

  • increase endothelial Ca2+ –> increase NO
  • Smooth muscle hyperpolarization –> vasodilation
  • stimulates pulmonary stretch receptors
40
Q

clinical use of adenosine

A

Very effective for acute conversion of paroxysmal supraventricular tachycardia caused by reentry involving accessory bypass pathways.

41
Q

Adenosine pharmacology:

how is adenosine administered?

what blunts adenosines effects?

A

t½=10-15 sec

Must use as IV bolus to a central vein (brachial, antecubital)

Effects blunted by adenosine receptor antagonists: theophylline & caffeine

42
Q

clinical use of magnesium

A

Torsades de pointes

Digitalis-induced arrhythmias

43
Q

what can be used to tx bradycardia

A

atropine (vagal block increases HR)

isoproterenol (B1 stim.)

pacemaker

44
Q

what can be used to tx sinus tachycardia, PSVT

A

vagal stimulation through carotid sinus massage or Valsalva maneuver

45
Q

what are the 4 ways of decreasing spontaneous activity

A

decrease phase 4 slope

increased threshold

increased maximum diastolic potential

increased action potential duration

46
Q

what are two ways to increase refractoriness

A

Na+ channel blockade
- shifts voltage dependence of recovery and so delays the point at which sufficient Na+ channels have recovered prolonging refractoriness

Drugs that prolong AP will also extend ERP point without interacting with Na+ channels

47
Q

Na+ channel blockers bind and block the channels when they are in the 1 and 2 states, but not in the 3 state.

A
  1. open
  2. inactivated
  3. resting
48
Q

State-dependent blockade - consequences:

Slower 1 rates
increases Na+ channel block

2 increases Na+ channel block

A
  1. drug dissociation

2. Tachycardia

49
Q

what are class I agents useful for?

A

***MI induced arrhythmia

  • ventricular dysrhythmia
  • digitalis
50
Q

MOA for class I agents

A
  • *Block fast inward Na+ channels to varying degrees in conductive tissues of the heart**
  • Decrease maximum depolarization rate (Vmax of phase 0)
  • reduce automaticity, delay conduction
  • Prolong ERP –> ERP/APD increased
51
Q

how can class I agents tx re-entry

A

block Na+ channels - decrease excitability

block K+ channels - increase ERP

52
Q

what do class Ia agents include

A

Quinidine, Procainamide, Disopyramide

The Queen Proclaims Disos Pyramid

53
Q

Class Ia agents

‘Moderate’ binding to 1 channels
- moderate effects on phase 0 depolarization

2 channel blockade

  • delayed phase 3 repolarization
  • prolonged QRS and 3
A
  1. Na+
  2. K+
  3. QT
54
Q

primary MOA of quinidine (class Ia)

A

Primary: Block rapid inward Na+ channel:

  • Decreased Vmax of phase 0
  • Slowed conduction (His-Purkinje > atria)
  • Effects greatest at fast HR (state-dependent block)
55
Q

aside from quinidines primary MOA of blocking rapid inward Na+ channels, what else do they do?

  • multiple actions - dose dependent effect
A

Block K+ channels - increase APD

Block α receptors - decrease BP

Block M receptors - increase HR in intact subjects

56
Q

clinical application of quinidine

A

Now mainly used in refractory patients to:

  • Convert symptomatic AF or flutter
  • Prevent recurrences of AF
  • Treat documented, life-threatening ventricular arrhythmias
57
Q

SE of quinidine

A

Diarrhea (most common)

cinchonism (headache, tinnitus, hearing loss, blurred vision)

hypotension due to α-adrenergic blocking effect

proarrhythmic (torsades de pointes – increased QT interval)

58
Q

MOA of procainamide (class Ia)

A

Block rapid inward Na+ channel –> slows
conduction
automaticity
excitability

Blocks K+ channels –> prolongs APD & refractoriness

59
Q

which class I agent has very little vagolytic activity and does not prolong the QT interval to as great an extent

A

procainamide

60
Q

what does procainamide treat

A

Ventricular:
treat documented, life-threatening ventricular arrhythmias

Supraventricular: acute tx of:

  • Reentrant SVT
  • Atrial fibrillation
  • Atrial flutter associated with Wolff-Parkinson-White syndrome
61
Q

SE of procainamide

A

Cardiac:

  • arrhythmia aggravation
  • torsades de pointes

Extracardiac:

  • SLE-like syndrome
  • GI nausea and vomiting
62
Q

when is procainamide contraindicated

A

(contraindicated in long QT syndrome,

history of TdP,

hypokalemia)

63
Q

what are the class Ib agents

A

Lidocaine, Mexiletine

First Aid’s mnemonic: I’d Buy Liddy’s Mexican Taco

64
Q

MOA of class Ib

A

‘Weak’ binding to Na+ channels
- weak effect on phase 0

Accelerated phase 3 repolarization
- shortened APD and QT interval

65
Q

what are class Ib agents good to use for

A

digitalis and MI-induced arrhythmia

66
Q

MOA of lidocaine

A

Blocks inactivated&raquo_space; open Na+ channels - reduces Vmax

Shorten cardiac action potential

Lowers the slope of phase 4; altering threshold for excitability

produces variable effects in abnormal conduction system

  • Slows ventricular rate
  • Potentiates infranodal block
67
Q

Lidocain is more effective in what tissues?

A

ischemic

68
Q

how is lidocaine more effective in ischemic tissues

A

Ischemia causes:

  • Prolonged depolarization
  • Slow-inactivated state of Na+ channel
  • depolarized resting potential (-60 mv)

1) Lidocaine (Ib) blocks I&raquo_space; O –> blocks slow-inactivated Na+ channels that are important in ischemic tissue –> shortens AP
2) Slower dissociation rate –> increase rx effect

69
Q

clinical applications for lidocaine

A

post-MI (best)

70
Q

how should lidocaine be administered

A

Extensive first-pass hepatic metabolism –> IV use.

need multiple loading doses and a maintenance infusion

71
Q

SE of lidocaine

A

rapid bolus: tinnitus, seizure

72
Q

what the class Ic agents?

A

Propafenone, Flecainide

73
Q

MOA of class Ic agents (Propafenone, Flecainide)

A
  • **Strongest binding to Na+ channels (O state)
    a) slow dissociation – strong effects on phase 0 depolarization
    b) *lengthened QRS, less on APD

c) Little effect on repolarization - QT unchanged
d) lengthened PR (depressed AV nodal conduction)

74
Q

MOA of propafenone

A

**Strong inhibitor of Na+ channel

Can inhibits beta-adrenergic R: marked structural similarity to propranolol

75
Q

Clinical application of propafenone

A

ventricular arrhythmias in patients with no or minimal heart disease and preserved ventricular function

76
Q

MOA of flecainide

A

potent Na+ channel blockade –> prolongs phase 0 and widens QRS

***markedly slows intraventricular conduction

77
Q

clinical application for Flecainide

A

use only in the treatment of refractory life-threatening ectopic ventricular arrhythmia

**not considered a first-line agent due to propensity for fatal proarrhythmic effects

78
Q

Class Ic SE

A

Proarrhythmic, especially post-MI

79
Q

what are class Ic agents contraindicated in?

A

structural and ischemic heart disease

80
Q

what are the class II agents

A

Beta adrenergic antagonists

Metoprolol, Propranolol, Esmolol, Atenolol, Timolol, Carvedilol

81
Q

MOA of class II agents (Metoprolol, Propranolol, Esmolol, Atenolol, Timolol, Carvedilol)

A

decrease cAMP, decrease Ca2+ currents –>

  • decrease SA nodal automaticity (phase 4);
  • decrease AV nodal conduction
  • decrease Ventricular contractility
82
Q

what are class II agents effective for?

A

supraventricular arrhythmias due to excessive sympathetic activity

83
Q

Are the only antiarrhythmic drugs found to be clearly effective in preventing sudden cardiac death in patients with prior MI

A

class II agents - beta adrenergic antagonists

Metoprolol, Propranolol, Esmolol, Atenolol, Timolol, Carvedilol

84
Q

what class II agent has a very short half life and is only used IV

  • useful when short termed beta blockade is desired (aortic dissection, critically ill pts, postop HTN)
A

esmolol

85
Q

SE of class II agents

A
  1. Impotence
  2. Exacerbation of COPD & asthma
  3. Bradycardia, AV block, heart failure; mask signs of hypoglycemia
  4. CNS: sedation, sleep alterations
  5. Dyslipidemia: Metoprolol
  6. Exacerbation of Prinzmetal angina: Propranolol
  7. Unopposed alpha1 agonism if given alone in pheochromocytoma or cocaine toxicity, except carvedilol & labetalol (blocking both alpha and beta)
86
Q

main clinical applications of CCBs - both dihydropyridines and nondihydropyridines

A

systemic HTN

angina pectoris

coronary spasm

87
Q

Main clinical applications of CCBs for only nondihydropyridines

A

SVT

Post-infarct

Pharm exam 5 (9 decks)

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