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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
Class IV are
calcium entry blockers
26
Name the Class Ia antidysrhythmic agents
Procainamide Police Disopyramide Department Quinidine Question
27
What is the MOA for Quinidine
decreases the slope of phase 4 depolarization in PACEMAKER cells
28
What is Quinidine used to tx
Recurrent SVT Atrial fibrillation with rapid ventricular response PVC VT
29
Quinidine is mainly metabolized by
liver *Induces P450 system
30
What other effects does quinidine have
a-adrenergic blockade>>vasodilation>>>hypotension
31
What effect will high doses of quinidine have on the myocardium
depression>>decreased contractility
32
What paradoxical effect can be seen with patients taking quinidine in Sinus rjythm
Increased HR
33
What effects does quinidine have on neuromuscular transmission
decrease transmission * potentiates NMB
34
What are two common SE with quinidine
N/D
35
What are contraindications to quinidine
VT caused by QT prolongation | AV blocks
36
Procainamide is an amide analog of
procaine
37
Procainamide is similar to quinidine except:
less prolongation of QT interval | less antimuscarinic properties
38
Procainamide is metabolized by
Kidney (40-60%) Liver (60-40%)>>>NAPA (active metabolite that depends on kidney for excretion) *Beware in Patients with renal disease
39
Do Plasma cholinesterase effect Procainamide
NO
40
What are the contraindications to Procainamide
``` Shock Myasthenia gravis AV Block Renal failure CHF ```
41
Disopyramide has similar electrophysiologic profile as quinidine and procainamide, but differs with the degree of
antimuscarinic effect *More pronounced
42
What are SE associated with Disopyramide
More pronounced myocardial depressant effects (negative inotropic) Serious anticholinergic effects seen in patients with glaucoma, prostated, myasthenia gravis, severe constipation
43
Disopyramide is contraindicated in
``` Uncompensated HF Glaucoma Hypotension untreated UTI Significant QT prolongation ```
44
Class Ib antidysrhythmics work by
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
45
Name the Class 1b antidysrhythmic agents
Tocainide The Lidocaine Little Mexiletine Man Phenytoin Paul
46
Lidocaine is used to tx
Ventricular dysrhythmias such as: PVC VT V fib prevention
47
What is the therapeutic plasma concentraton of lidocaine
1-5 mcg/mL
48
Can lidocaine be given PO
No, extensive first-pass hepatic metabolism
49
What is the IV bolus therapeutic level of lidocaine
1-2 mg/kg *immediate IV infusion at 1-4 mg/min
50
Do not exceed what
3 mg/kg within one hour period
51
What are contraindications with Lidocaine
SA, AV block Stoke-Adams Syndrome WPW syndrome Sinus bradycardia
52
Therapeutic levels of Lidocaine will produce what s/s
``` 1-5 mcg/mL Numbness of tongue Light-headedness Tinnitus Visual disturbances ```
53
Lidocaine levels reaching 7 mcg/mL will produce what s/s
Muscular twitching
54
Lidocaine levels of 10 mcg/mL will produce what s/s
Unconsciousness | Convulsions
55
Lidocaine levels of 15 mcg/mL will produce what s/s
coma
56
Lidocaine levels of 20 mcg/mL will produce what s/s
Respiratory arrest
57
Lidocaine levels of 25-30 mcg/mL will produce what s/s
CVS depression
58
Lidocaine toxicity should be tx by
stopping lidocaine 100% 02 Seizure control
59
Mexiletine is an orally active amine of
Lidocaine
60
What is mexiletine used to tx
chronic suprression of VT
61
What effect does mexiletine have on hemodynamic system
none
62
What effect does mexiletine have on QT interval
none>>>less prodysrythmic
63
What effect does mexiletine have on vagolytics
none>>>no reflex tachycardia
64
Class Ic antidysrhythmics work by
Inhibition of the His-purkinje fast sodium channels (phase 0)>>>QRS widening *Causes significant Supraventricular prodysrhythmic properties
65
Name the Class Ic agents
Flecanide For Propafenone Pushing Encainide Ecstasy
66
Flecanide is used to tx ventricula dysrhythmias with what exception
must have normal LV function d/t its negative inotropic effects
67
Encainide is different than flecanide only in
less negative inotropic activity
68
What class Ic agent is the only agent useful for supraventricular dysrhythmias
Propafenone
69
Class II antidysrhythmics are AKA
beta-adrenergic antagonists
70
SE associated with beta-adrenergic antagonists include
``` PR interval prolonged brady progressive AV block myocardial depression hypotension bronchospasm (b2) ```
71
Although Esmolol is beta 1 selective antagonism, at high doses, what is noted
b2 antagonism
72
What is the half-life of esmolol
9 minutes (very short acting)
73
how is esmolol metabolized
ester hydrolysis by red cell esterases *redistribution half-life is 2 minutes
74
Name the b1 selective antagonists
AA BB EM
75
Class III antidysrhythmic agents work by
blocking potassium channels>>prolongs repolarization increases AP duration QT interval prolonged>>>prodysrhythmic
76
Name Class III antidysrhythmic agents
``` Bretylium Amiodarone Dronedarone Sotalol Azimilide Dofetilide Tedisamil Ibutilide ``` *IT BAD, SAD
77
Bretylium works by
strongly blocking potassium channels in purkinje networks causes an initial release of NE>>>then Inhibits NE release>>then inhibits NE reuptake
78
Amiodarone is a class III antidysrrhythmic with that has wide spectrum of
activity
79
Amiodarone is used to tx what three dysrhythmias
SVT Ventricular tachydysrhythmias WPW
80
Amiodarone has what effect on ALL cardiac tissues
prolongs the effective refractory period * SA node, atrium, AV node, HIS-Purkinje system, ventricle, adn accessory bypass tracts
81
What similarities does amiodarone share with the other classes of antidysrhythmics
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
What effect does amiodarone have on coronary arteries
dilates and increases coronary blood flow *antianginal
83
Peak plasma concentration of amiodarone is achieve in how many days
15-30 (orally)
84
How long does the pharmacological effects of amiodarone last after being D/C'd
45-60 days
85
Amiodarone is extensively metabolized into what ACTIVE form
desethylamiodarone
86
Desethylamiodarone is excreted by the
lacrimal glands skin biliary tract *NO renal excretion
87
What is the IV loading dose of amiodarone
150 mg over 10 minutes
88
How much amiodarone should be given over next 6 hours
360 mg
89
How much amiodarone should be given over next 18 hours
540 mg
90
What is the maintenance infusion of amiodarone
0.5 mg/min
91
How much amiodarone should be given as a supplemental infusion for breakthrough dysrhythmias
150 mg
92
What is the major SE associated with amiodarone
Pulmonary toxicity *predisposed to ARDS, must keep Fi02 < 0.3
93
What endocrine gland is effected by amiodarone
thyroid (hyper/hypo thyroidism) *inhibits peripheral conversion of T4 to T3
94
What hematologic component is effected by amiodarone
directly depresses vitamin K-dependent clotting factors (II, VII, IX, X)
95
Sotalol at low doses behaves as a --------, and at high doses behaves as a --------
b-blocker class III antidysrhythmic *prolongs the APD in the atria, ventricles, and accessory bypass tracts
96
Is sotalol a prodysrhthmic
YES *because of this, it is restricted to use in life threatening situations
97
What are unique features of the pharmacokinetics of sotalol
does not bind to plasma proteins and is not metabolized excreted unchanged by kidneys (lower with renal failure)
98
Ibutilide is a class III antidysrhythmic that is indicated for
a-fib a-flutter *slows repolarization and prolongs APD
99
Name the three Class IV antidysrthmics and their MOA
Verapamil Diltiazem Nefedipine *calcium channel blocker
100
Phenylalkylamines and benzothiazepines are calcium channel blockers that are selective for
AV node
101
Dihydropyridines are CCB taht are selective for
arteriolar beds
102
What is the MOA of
selectively blocks the inward transfer of calcium through slow calcium channels in heart and vasculature
103
What is the effect of CCB on the heart
decreased HR decreased contractility decreased SA/AV nodal conduction * prevents recurrent SVT * reduces the ventricular rate in a. fib
104
What is the effect of CCB on the vascular smooth muscles
vasodilation>>relaxation
105
Verapamil and diltiazem also block
fast sodium channels
106
Verapamil is a
phenylalkylamine
107
Verapamil binds to which portion of the L-type calcium channel
intracellular portion when the channel is in an OPEN state (occludes the channel)
108
What are two isomer of verapamil and their MOA
dextro-isomer act upon fast sodium channels levo-isomer acts upon the calcium channels
109
What effect does verapamil have on the SA node
direct depressant
110
What is verapamil effective in treating
SVT (a fib, a-flutter with RVR)
111
Nifedipine is a
dihydropyridine calcium antagonist
112
Nifedipne binds to which side on the calcium channel
outer gate of the slow calcium channel
113
Nefedipine primarily acts on the
arterial smooth muscles
114
Nefedipine is used to tx what four conditions
prinzmetal's angina raynaud's phenomenon essential HTN pulmonary HTN
115
Nifedipine is rapidly oxidized by
light *must be given immediately if drawn into a syringe
116
What is the MOA of digoxin
inhibition of sodium-potassium ATPase pumpe
117
What is the effect of blocking the NA/K+ atpase pump
increases intracelluar sodium decreases extrusion of calcium leading to greater intracellular calcium availability>>>greater contractility (INOTROPISM)
118
What effect does digoxin have on phase 0
decreased d/t inhibition of outward transport of sodium
119
What effect does digoxin have on the APD
decreases it d/t shortened phase 2
120
By enhancing PSNS tone, digoxin has what three effects on the heart
decreased SA node activity prolongs absolute (effective) refractory suppresses conduction across AV node
121
What percentage of digoxin is excreted unchanged by the kidneys
75%
122
Digoxin competes with what electrolyte
potassium *with low level of potassium, digoxin activity increases
123
What are the three main body systems effected by digoxin toxicity
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
Name four methods of correcting digoxin toxicity
d/c digoxin correct hypoxemia/hypokalemia treat dysrhythmias Give DIGIBIND
125
What is the three MOA of adenosine
slows conduction through AV node interrupts re-entry pathways through AV node restores SR in SVT and WPW patients
126
What is the initial dose of adenosine and the repeat dose
6 mg IV RAPID (1-2 seconds) 12 mg repeat dose with refractory dysrhythmia

Pharmacology (27 decks)

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