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Pharmacology > Antidysrhythmics > Flashcards

Antidysrhythmics Flashcards

1
Q

Phase 4 for the working myocardial cells begins when

A

membrane potential is taken to a transmembrane potential of -90mV

Potassum efflux

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2
Q

Phase 4 for the working myocardial cells ends when

A

membrane potential reaches -70 mV

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3
Q

Phase 0 represents

A

rapid depolorization up to 20 mV

Sodium influx

*Vmax (rate of rise) reflects myocardial contractility

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4
Q

Phase 1 represents

A

Early/fast Repolorization

Fast sodium channels close
Transient Potassium outward current

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5
Q

Phase 2 (plateau) represents

A

Calcium influx

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6
Q

What are the three functions of the inward calcium current

A

Prolong refractory period
Delivers calcium to inside of myocardium (electromechanical coupling)
Activates SR to release intracellular calcium stores

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7
Q

Phase 3 represents

A

Repolarization

Massive reflux of Potassium

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8
Q

When does the relative refractory period begin

A

during the last half of phase 3

  • Calcium channels can reopen at -30 mV if stimulated
  • Sodium channels can reopen at -70 mV if stimulated
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9
Q

phase 4 for the myocardial pacemaker cells begins when

A

cell has reached full repolorization of -70mV

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10
Q

phase 4 for the myocardial pacemaker cells ends when threshold potential reaches

A

-40 mV

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11
Q

What are three determinants of the frequency of discharge of the cardiac pacemaker cells and what is the effect

A

rate of phase 4 depolarization
the threshold potential
resting transmembrane potential

  • increase in HR
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12
Q

How can you increase the HR while maintaining the rate of depolarization

A

making the threshold potential more negative or

making the resting transmembrane potential less negative

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13
Q

What effect does the PSNS (AcH) have on the slope of phase 4 myocardial pacemaker cells

A

decreases the rate of rise&raquo_space;>decrease in HR

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14
Q

What effect does SNS (epi/Norepi) have on the slope of the phase 4 myocardial pacemaker cells

A

increasing rate of rise»>increase in HR

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15
Q

Dysrhythmias are caused by what two factors

A

abnormal pacemaker activity or

abnormal impulse spread

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16
Q

What are the four major mechanisms used to tx dysrhythmias

A

Sodium channel blockade
Calcium channel blockade
Prolonging the effective refractory period
Blocking the Sympathetic autonomic effects

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17
Q

Class I antidysrhythmias largely work by

A

blocking sodium channels during phase 0 depolarization»>decrease in depolarization and conduction velocity

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18
Q

Class I’s are further subdivided into

A

Class Ia, Ib, Ic

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19
Q

Class 1a’s inhibit sodium influx and possess what three other unique properties

A

prolongs AP duration
prolongs the effective refractory period
lengthens repolarization via potassium blockade

*Prodysrhythmic (prolongs QT and depresses conduction)

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20
Q

Class 1b’s inhibit sodium influx and posess what three other unique properties

A

shortens AP duration in normal cardiac cells
prolongs AP duration in ischemic tissues
decreases spontaneous phase 4 depolorization rate»decreases HR

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21
Q

Class 1c’s inhibit sodium influx and posess what other unique properties

A

ONLY effects AP duration of purkinje fibers
QRS widens via inhibition of His-purkinje network

*Prodysrhythmic (causes SVT)

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22
Q

Class II’s are

A

B-adrenergic antagonists

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23
Q

Class II’s work by

A

decreases rate of phase 4 depolarization
decreases conducton velocity overall
decreases inotropy at higher doses

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24
Q

Class III work by

A

blocking potassium ion channels resulting in:
prolongation of cardiac repolarization
prolongation of AP duration
prolongation of effective refractory period

  • prolongs QT interval
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25
Q

Class IV are

A

calcium entry blockers

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26
Q

Name the Class Ia antidysrhythmic agents

A

Procainamide Police
Disopyramide Department
Quinidine Question

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27
Q

What is the MOA for Quinidine

A

decreases the slope of phase 4 depolarization in PACEMAKER cells

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28
Q

What is Quinidine used to tx

A

Recurrent SVT
Atrial fibrillation with rapid ventricular response
PVC
VT

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29
Q

Quinidine is mainly metabolized by

A

liver

*Induces P450 system

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30
Q

What other effects does quinidine have

A

a-adrenergic blockade»vasodilation»>hypotension

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31
Q

What effect will high doses of quinidine have on the myocardium

A

depression»decreased contractility

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32
Q

What paradoxical effect can be seen with patients taking quinidine in Sinus rjythm

A

Increased HR

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33
Q

What effects does quinidine have on neuromuscular transmission

A

decrease transmission

  • potentiates NMB
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34
Q

What are two common SE with quinidine

A

N/D

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35
Q

What are contraindications to quinidine

A

VT caused by QT prolongation

AV blocks

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36
Q

Procainamide is an amide analog of

A

procaine

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37
Q

Procainamide is similar to quinidine except:

A

less prolongation of QT interval

less antimuscarinic properties

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38
Q

Procainamide is metabolized by

A

Kidney (40-60%)
Liver (60-40%)»>NAPA (active metabolite that depends on kidney for excretion)

*Beware in Patients with renal disease

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39
Q

Do Plasma cholinesterase effect Procainamide

A

NO

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40
Q

What are the contraindications to Procainamide

A 
Shock
Myasthenia gravis
AV Block
Renal failure
CHF
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41
Q

Disopyramide has similar electrophysiologic profile as quinidine and procainamide, but differs with the degree of

A

antimuscarinic effect

*More pronounced

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42
Q

What are SE associated with Disopyramide

A

More pronounced myocardial depressant effects (negative inotropic)

Serious anticholinergic effects seen in patients with glaucoma, prostated, myasthenia gravis, severe constipation

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43
Q

Disopyramide is contraindicated in

A 
Uncompensated HF
Glaucoma
Hypotension
untreated UTI
Significant QT prolongation
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44
Q

Class Ib antidysrhythmics work by

A

inhibition of fast sodium channels (phase 0)

shortens AP in normal heart tissues

lengthens AP duration in ischemic tissues (thus preventing re-entry and retrograde conduction)

decreases rate of spontaneous phase 4 depolarization

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45
Q

Name the Class 1b antidysrhythmic agents

A

Tocainide The
Lidocaine Little
Mexiletine Man
Phenytoin Paul

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46
Q

Lidocaine is used to tx

A

Ventricular dysrhythmias such as:

PVC
VT
V fib prevention

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47
Q

What is the therapeutic plasma concentraton of lidocaine

A

1-5 mcg/mL

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48
Q

Can lidocaine be given PO

A

No, extensive first-pass hepatic metabolism

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49
Q

What is the IV bolus therapeutic level of lidocaine

A

1-2 mg/kg

*immediate IV infusion at 1-4 mg/min

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50
Q

Do not exceed what

A

3 mg/kg within one hour period

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51
Q

What are contraindications with Lidocaine

A

SA, AV block
Stoke-Adams Syndrome
WPW syndrome
Sinus bradycardia

52
Q

Therapeutic levels of Lidocaine will produce what s/s

A 
1-5 mcg/mL
Numbness of tongue
Light-headedness
Tinnitus
Visual disturbances
53
Q

Lidocaine levels reaching 7 mcg/mL will produce what s/s

A

Muscular twitching

54
Q

Lidocaine levels of 10 mcg/mL will produce what s/s

A

Unconsciousness

Convulsions

55
Q

Lidocaine levels of 15 mcg/mL will produce what s/s

A

coma

56
Q

Lidocaine levels of 20 mcg/mL will produce what s/s

A

Respiratory arrest

57
Q

Lidocaine levels of 25-30 mcg/mL will produce what s/s

A

CVS depression

58
Q

Lidocaine toxicity should be tx by

A

stopping lidocaine
100% 02
Seizure control

59
Q

Mexiletine is an orally active amine of

A

Lidocaine

60
Q

What is mexiletine used to tx

A

chronic suprression of VT

61
Q

What effect does mexiletine have on hemodynamic system

A

none

62
Q

What effect does mexiletine have on QT interval

A

none»>less prodysrythmic

63
Q

What effect does mexiletine have on vagolytics

A

none»>no reflex tachycardia

64
Q

Class Ic antidysrhythmics work by

A

Inhibition of the His-purkinje fast sodium channels (phase 0)»>QRS widening

*Causes significant Supraventricular prodysrhythmic properties

65
Q

Name the Class Ic agents

A

Flecanide For
Propafenone Pushing
Encainide Ecstasy

66
Q

Flecanide is used to tx ventricula dysrhythmias with what exception

A

must have normal LV function d/t its negative inotropic effects

67
Q

Encainide is different than flecanide only in

A

less negative inotropic activity

68
Q

What class Ic agent is the only agent useful for supraventricular dysrhythmias

A

Propafenone

69
Q

Class II antidysrhythmics are AKA

A

beta-adrenergic antagonists

70
Q

SE associated with beta-adrenergic antagonists include

A 
PR interval prolonged
brady
progressive AV block
myocardial depression
hypotension
bronchospasm (b2)
71
Q

Although Esmolol is beta 1 selective antagonism, at high doses, what is noted

A

b2 antagonism

72
Q

What is the half-life of esmolol

A

9 minutes (very short acting)

73
Q

how is esmolol metabolized

A

ester hydrolysis by red cell esterases

*redistribution half-life is 2 minutes

74
Q

Name the b1 selective antagonists

A

AA BB EM

75
Q

Class III antidysrhythmic agents work by

A

blocking potassium channels»prolongs repolarization

increases AP duration

QT interval prolonged»>prodysrhythmic

76
Q

Name Class III antidysrhythmic agents

A 
Bretylium
Amiodarone
Dronedarone
Sotalol
Azimilide
Dofetilide
Tedisamil
Ibutilide

*IT BAD, SAD

77
Q

Bretylium works by

A

strongly blocking potassium channels in purkinje networks

causes an initial release of NE»>then Inhibits NE release»then inhibits NE reuptake

78
Q

Amiodarone is a class III antidysrrhythmic with that has wide spectrum of

A

activity

79
Q

Amiodarone is used to tx what three dysrhythmias

A

SVT
Ventricular tachydysrhythmias
WPW

80
Q

Amiodarone has what effect on ALL cardiac tissues

A

prolongs the effective refractory period

  • SA node, atrium, AV node, HIS-Purkinje system, ventricle, adn accessory bypass tracts
81
Q

What similarities does amiodarone share with the other classes of antidysrhythmics

A

blocks sodium channels ( class 1a activity)

noncompetively blocks b-adrenoreceptors (class II activity)

prolongs APD/repolorization of potassium channel blockade (class II activity)

weak calcium channel blocker-class IV activity

  • also blocks a-adrenergic receptors»vasodilation
82
Q

What effect does amiodarone have on coronary arteries

A

dilates and increases coronary blood flow

*antianginal

83
Q

Peak plasma concentration of amiodarone is achieve in how many days

A

15-30 (orally)

84
Q

How long does the pharmacological effects of amiodarone last after being D/C’d

A

45-60 days

85
Q

Amiodarone is extensively metabolized into what ACTIVE form

A

desethylamiodarone

86
Q

Desethylamiodarone is excreted by the

A

lacrimal glands

skin

biliary tract

*NO renal excretion

87
Q

What is the IV loading dose of amiodarone

A

150 mg over 10 minutes

88
Q

How much amiodarone should be given over next 6 hours

A

360 mg

89
Q

How much amiodarone should be given over next 18 hours

A

540 mg

90
Q

What is the maintenance infusion of amiodarone

A

0.5 mg/min

91
Q

How much amiodarone should be given as a supplemental infusion for breakthrough dysrhythmias

A

150 mg

92
Q

What is the major SE associated with amiodarone

A

Pulmonary toxicity

*predisposed to ARDS, must keep Fi02 < 0.3

93
Q

What endocrine gland is effected by amiodarone

A

thyroid (hyper/hypo thyroidism)

*inhibits peripheral conversion of T4 to T3

94
Q

What hematologic component is effected by amiodarone

A

directly depresses vitamin K-dependent clotting factors (II, VII, IX, X)

95
Q

Sotalol at low doses behaves as a ——–, and at high doses behaves as a ——–

A

b-blocker

class III antidysrhythmic

*prolongs the APD in the atria, ventricles, and accessory bypass tracts

96
Q

Is sotalol a prodysrhthmic

A

YES

*because of this, it is restricted to use in life threatening situations

97
Q

What are unique features of the pharmacokinetics of sotalol

A

does not bind to plasma proteins and is not metabolized

excreted unchanged by kidneys (lower with renal failure)

98
Q

Ibutilide is a class III antidysrhythmic that is indicated for

A

a-fib

a-flutter

*slows repolarization and prolongs APD

99
Q

Name the three Class IV antidysrthmics and their MOA

A

Verapamil

Diltiazem

Nefedipine

*calcium channel blocker

100
Q

Phenylalkylamines and benzothiazepines are calcium channel blockers that are selective for

A

AV node

101
Q

Dihydropyridines are CCB taht are selective for

A

arteriolar beds

102
Q

What is the MOA of

A

selectively blocks the inward transfer of calcium through slow calcium channels in heart and vasculature

103
Q

What is the effect of CCB on the heart

A

decreased HR
decreased contractility
decreased SA/AV nodal conduction

  • prevents recurrent SVT
  • reduces the ventricular rate in a. fib
104
Q

What is the effect of CCB on the vascular smooth muscles

A

vasodilation»relaxation

105
Q

Verapamil and diltiazem also block

A

fast sodium channels

106
Q

Verapamil is a

A

phenylalkylamine

107
Q

Verapamil binds to which portion of the L-type calcium channel

A

intracellular portion when the channel is in an OPEN state (occludes the channel)

108
Q

What are two isomer of verapamil and their MOA

A

dextro-isomer act upon fast sodium channels

levo-isomer acts upon the calcium channels

109
Q

What effect does verapamil have on the SA node

A

direct depressant

110
Q

What is verapamil effective in treating

A

SVT (a fib, a-flutter with RVR)

111
Q

Nifedipine is a

A

dihydropyridine calcium antagonist

112
Q

Nifedipne binds to which side on the calcium channel

A

outer gate of the slow calcium channel

113
Q

Nefedipine primarily acts on the

A

arterial smooth muscles

114
Q

Nefedipine is used to tx what four conditions

A

prinzmetal’s angina
raynaud’s phenomenon
essential HTN
pulmonary HTN

115
Q

Nifedipine is rapidly oxidized by

A

light

*must be given immediately if drawn into a syringe

116
Q

What is the MOA of digoxin

A

inhibition of sodium-potassium ATPase pumpe

117
Q

What is the effect of blocking the NA/K+ atpase pump

A

increases intracelluar sodium

decreases extrusion of calcium leading to greater intracellular calcium availability»>greater contractility (INOTROPISM)

118
Q

What effect does digoxin have on phase 0

A

decreased d/t inhibition of outward transport of sodium

119
Q

What effect does digoxin have on the APD

A

decreases it d/t shortened phase 2

120
Q

By enhancing PSNS tone, digoxin has what three effects on the heart

A

decreased SA node activity

prolongs absolute (effective) refractory

suppresses conduction across AV node

121
Q

What percentage of digoxin is excreted unchanged by the kidneys

A

75%

122
Q

Digoxin competes with what electrolyte

A

potassium

*with low level of potassium, digoxin activity increases

123
Q

What are the three main body systems effected by digoxin toxicity

A

Heart- brady, dysrhythmias r/t increased SNS tone secondary to arterial hypoxemia

GI- d/t increased vagal tone, increase Ach activity in the gut

Nervous system- d/t blocking Na/KATPase dependent photoreceptors (amblyopia, scotoma, trigeminal neuralagia)

124
Q

Name four methods of correcting digoxin toxicity

A

d/c digoxin
correct hypoxemia/hypokalemia
treat dysrhythmias
Give DIGIBIND

125
Q

What is the three MOA of adenosine

A

slows conduction through AV node

interrupts re-entry pathways through AV node

restores SR in SVT and WPW patients

126
Q

What is the initial dose of adenosine and the repeat dose

A

6 mg IV RAPID (1-2 seconds)

12 mg repeat dose with refractory dysrhythmia

Pharmacology (27 decks)

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