Lecture 4-Antiarrhythmics

Question 1

What are the phases of the cardiac action potential?

Answer 1

• Phase 0
• Phase 1
• Phase 2
• Phase 3
• Phase 4

Question 2

Phase 0 = ___

Answer 2

rapid depolarization

mostly d/t sodium entering the cell

Question 3

Phase 1 = ___

Answer 3

early rapid repolarization

mostly d/t potassium leaving the cell; sodium channels inactivated

Question 4

Phase 2 = ___

Answer 4

plateau

mostly d/t calcium slowly entering the cell and potassium slowly leaving the cell

Question 5

Phase 3 = ___

Answer 5

rapid repolarization

mostly d/t potassium leaving the cell; no significant movement of sodium or calcium during this phase

Question 6

Phase 4 = ___

Answer 6

spontaneous depolarization

d/t inward/outward movement of calcium and potassium; ATP-dependent pumps move ions to restore balance

Question 7

Phase 0 rapid depolarization–increase in ___ (what electrolyte?) conductance through ion-specific fast channels; start out at ___ mV; ___ contraction; ___ channels change from “closed” to “open”; ends with ___ channels becoming “inactive” at ___ mV

Answer 7

Phase 0 rapid depolarization–increase in sodium conductance through ion-specific fast channels; start out at -70 mV; ventricular contraction; sodium channels change from “closed” to “open”; ends with sodium channels becoming “inactive” at +65 mV

Question 8

What is the resting membrane potential? ___ mV

Answer 8

-70 mV

Question 9

Phase 1 early rapid repolarization–___ permeability is rapidly inactivated; the cell starts to ___; ___ channels open, begin transient efflux, rapidly inactivated

Answer 9

Phase 1 early rapid repolarization–sodium permeability is rapidly inactivated; the cell starts to repolarize; potassium channels open, begin transient efflux, rapidly inactivated

Question 10

Phase 2 plateau–repolarization is delayed by an increase in conductance of ___ (what electrolyte?) influx through slow channels; ___ channels open and maintain plateau through ___ efflux (delayed rectifier); maintains voltage at ___ to ___ mV

Answer 10

Phase 2 plateau–repolarization is delayed by an increase in conductance of calcium influx through slow channels; potassium channels open and maintain plateau through potassium efflux (delayed rectifier; maintains voltage at +10 to -20 mV

Question 11

Phase 3 rapid repolarization–complete repolarization due to inactivation of ___ conductance and an increase in ___ permeability; no significant movement of ___ or ___

Answer 11

Phase 3 rapid repolarization–complete repolarization due to inactivation of calcium conductance and an increase in potassium permeability; no significant movement of calcium or sodium

Question 12

Phase 4 spontaneous depolarization–slow depolarization characteristic of all pacemaker cells; results from a complex interaction between inward and outward currents of ___ and ___ during ___ (systole/diastole); ___-dependent pumps move ions to regain balance

Answer 12

Phase 4 spontaneous depolarization–slow depolarization characteristic of all pacemaker cells; results from a complex interaction between inward and outward currents of calcium and potassium during diastole; ATP-dependent pumps move ions to regain balance

Question 13

Comparison of action potentials–in ventricular muscle cells, ___ (sodium/calcium) is responsible for initial depolarization

Answer 13

sodium

Muscle cells are more sodium dependent for initial depolarization; calcium accounts for the plateau phase in these cells

Question 14

Comparison of action potentials–in SA/AV node cells, ___ (sodium/calcium) is responsible for initial depolarization

Answer 14

calcium

Automatic cells in the SA/AV node are calcium dependent

Question 15

Slow, calcium mediated channels are responsible for phase ___ in SA/AV nodes and phase ___ in ventricular contractile cells

Answer 15

phase 0 in SA/AV nodes (slow conduction velocity) and phase 2 (prolongs refractory period) in ventricular contractile cells

Question 16

What other phase do slow, calcium mediated channels affect?

Answer 16

Phase 4 spontaneous depolarization

Question 17

Slow, calcium mediated channels are facilitated by ___

Answer 17

catecholamines–they can affect the movement of calcium through cyclic AMP

Question 18

Calcium mediated channels are ___ (fast/slow)

Answer 18

slow

Question 19

Sodium mediated channels are ___ (fast/slow)

Answer 19

fast

Question 20

Sodium mediated channels are responsible for phase ___ and have a ___ (slow/rapid) conduction velocity

Answer 20

phase 0 and have a rapid conduction velocity

Question 21

Mechanism of arrhythmias = impulse generation or ___

Answer 21

automaticity

Question 22

Cells that undergo spontaneous phase 4 depolarization are automatic and capable of impulse generation–T/F?

Answer 22

True

Question 23

Factors that reduce automaticity at higher pacemaker sites will ___ (actively/passively) favor the movement of the pacemaker to ___ (higher/lower) sites

Answer 23

passively favor the movement of the pacemaker to lower sites

Question 24

___ influences passively favor the movement of the pacemaker to lower sites–i.e.: ___ drugs; ___ drugs; ___ (what induction agent?)

Answer 24

Vagal influences–i.e.: digitalis drugs; parasympathomimetic drugs; halothane

Question 25

___ result from enhanced automaticity at a site outside the SA node

Answer 25

Ectopic foci

Question 26

What arrhythmia do we commonly see ectopic foci/ectopic pacemaker?

Answer 26

A-Fib

Question 27

These factors increase the chance of ectopic foci–___ influences; ___carbia; ___oxia; ___ toxicity

Answer 27

sympathomimetic influences; hypercarbia; hypoxia; dig toxicity

Question 28

Mechanism of arrhythmias–re-entry–for re-entry to occur, you must have unidirectional block of impulse conduction (area of injury) and slow conduction via an alternate pathway–T/F?

Answer 28

True

Question 29

Re-entry can occur at many sites, including ___ node, ___, ___ node, ___

Answer 29

SA node, atrium, AV node, ventricle

Question 30

Re-entry at atrium occurs in atrial ___ or ___

Answer 30

atrial tachycardia or flutter

Question 31

Re-entry at ventricle occurs in ___

Answer 31

V-tach

Question 32

Pharmacologic arrhythmia management relies upon the ___ responsible for impulse generation in the atria and ventricles versus the SA and AV nodes

Answer 32

different ion channels

Question 33

Sodium channels are responsible for impulse management in the ___ and ___

Answer 33

atria and ventricles

Question 34

Calcium channels are responsible for impulse management in the ___ and ___

Answer 34

SA node and AV node

Question 35

This class of antiarrhythmics slows conduction and prolongs the QRS complexes in the atria and ventricles

Answer 35

Sodium channel blockers (Type I)

Question 36

This class of antiarrhythmics slows the atrial rate (SA node effect) and slows conduction through the AV node (prolonging the PR interval)

Answer 36

Calcium channel blockers (Type IV)

Question 37

This class of antiarrhythmics interrupts reentry by slowing conduction or increasing the refractory period; they prolong the QT interval and induce triggered activity in the ventricle causing polymorphic VT (Torsades de Pointes)

Answer 37

Potassium channel blockade (Type III)

Question 38

Class I antiarrhythmics inhibit fast ___ channels

Answer 38

inhibit fast sodium channels

Question 39

Class ___ = quinidine, procainamide, disopyramide, moricizine

Answer 39

Class IA

Question 40

Class ___ = lidocaine, mexilitine

Answer 40

Class IB

Question 41

Class ___ = flecainide, propafenone

Answer 41

Class IC

Question 42

Class II antiarrhythmics decrease the rate of ___

Answer 42

depolarization

Question 43

What medication class is considered a class II anti arrhythmic?

Answer 43

Beta blockers

Question 44

Class III antiarrhythmics inhibit ___ ion channels

Answer 44

potassium ion channels

Question 45

Amiodarone is a class ___ anti arrhythmic

Answer 45

class III

Question 46

What beta blocker is considered a class III antiarrhythmic? Why?

Answer 46

Sotalol because it inhibits potassium channels

Question 47

Class IV antiarrhythmics inhibit slow ___ channels

Answer 47

inhibit slow calcium channels

Question 48

What two medications are considered class IV antiarrhythmics?

Answer 48

Diltiazem and verapamil (nondihydropyridine CCBs)

Question 49

Effects of antiarrhythmics on the action potential–type IA slows phase ___, prolongs phase ___

Answer 49

slows phase 0, prolongs phase 3

Question 50

Effects of antiarrhythmics on the action potential–type IB slows phase ___, shortens phase ___

Answer 50

slows phase 0, shortens phase 3

Question 51

Effects of antiarrhythmics on the action potential–type IC very slow phase ___, no phase ___ effects

Answer 51

very slow phase 0, no phase 3 effects

Question 52

Effects of antiarrhythmics on the action potential–type II reduces slope of phase ___

Answer 52

reduces slope of phase 4

Question 53

Effects of antiarrhythmics on the action potential–type III prolongs phase ___

Answer 53

prolongs phase 3

Question 54

Effects of antiarrhythmics on the action potential–type IV reduces slope of phase ___

Answer 54

reduces slope of phase 4

Question 55

Which type of antiarrhythmic has the most significant effect on phase 0?

Answer 55

Type IC–very slow phase 0

Question 56

Procainamide is type ___ antiarrhythmic; it is a ___ and ___ channel blocker; it depresses automaticity by decreasing the slope of phase ___, and increases ___

Answer 56

Procainamide is a type IA antiarrhythmic; it is a sodium and potassium channel blocker; it depresses automaticity by decreasing the slope of phase 0 depolarization, and increases refractoriness

Question 57

Procainamide prevents reentry by converting ___ to ___ block

Answer 57

converting unidirectional to bidirectional block

Question 58

Indications for procainamide include ventricular ___dysrhythmias and atrial ___ in the presence of accessory pathways

Answer 58

ventricular tachydysrhythmias and atrial tachycardia in the presence of accessory pathways

Question 59

What are 4 dysrhythmias that can be treated with procainamide?

Answer 59

• SVT
• A-Fib
• PVCs
• VT

Question 60

Procainamide toxicity–myocardial ___; profound ___tension; QRS complex/QT ___ leads to ___, complete ___, and ventricular ___

Answer 60

myocardial depression; profound hypotension; QRS complex/QT prolongation leads to Torsades, complete heart block, and ventricular ectopy

Question 61

Chronic procaindamide administration can lead to a ___-like syndrome

Answer 61

systemic lupus erythematous-like syndrome

this can also occur with hydralazine; 50-80% of people had positive titers for SLE; lots of GI upset

Question 62

Half-life of procainamide is ___-___ hours

Answer 62

3-4 hours

Question 63

Does procainamide have an active metabolite?

Answer 63

Yes–N-acetyl procainamide (NAPA)

Question 64

Half-life of N-acetyl procainamide is ___-___ hours; it is eliminated by the ___

Answer 64

6-10 hours; it is eliminated by the kidneys

Question 65

Increased risk of ___ and ___ when procainamide is administered to patients with poor kidney function

Answer 65

Increased risk of side effects and QT prolongation/Torsades when procainamide is administered to patients with poor kidney function

Question 66

Caution giving procainamide to patients with ___ dysfunction

Answer 66

renal dysfunction

Question 67

Quinidine is a class ___ antiarrhythmic; it produces ___ and ___ blockade; ___ (increased/decreased) threshold for excitability, ___ (increased/decreased) automaticity; prolongs action potential, prolongs refractoriness

Answer 67

Quinidine is a class IA antiarrhythmic; it produces sodium and potassium blockade; increased threshold for excitability, decreased automaticity; prolongs action potential, prolongs refractoriness

Question 68

There has been some evidence of ___ blockade and ___ inhibition with quinidine; this causes ___tension, ___cardia, atrial ___arrhythmias

Answer 68

some evidence of alpha 1 blockade and vagal inhibition with quinidine; this causes hypotension, tachycardia, atrial tachyarrhythmias

Question 69

Quinidine can be used to treat what 4 arrhythmias? atrial ___, atrial ___, ventricular ___, and ventricular ___

Answer 69

atrial flutter, atrial fibrillation, ventricular tachycardia, and ventricular fibrillation

Question 70

Quinidine toxicity results in QT ___, which can lead to ___ and ___; loose ___; ___penia; and ___ism

Answer 70

QT prolongation, which can lead to torsades and VTach; loose stools; thrombocytopenia; and cinchonism (includes headache and tinnitus)

Question 71

Quinidine pharmacokinetics–it is a potent CYP2D6 ___; PGP ___; half-life ___-___ hours

Answer 71

it is a potent CYP2D6 inhibitor; PGP inhibition; half-life 6-8 hours

Because it inhibits the metabolism of other medications, this can lead to toxicity

Question 72

Disopyramide is a class ___ antiarrhythmic; it is similar to quinidine without the ___ effects; it has some ___ effects; used to treat atrial and ventricular ___arrhythmias

Answer 72

disopyramide is a class IA antiarrhythmic; it is similar to quinidine without the alpha effects; it has some anticholinergic effects (dries you out, agitation in children/elderly, delirium); used to treat atrial and ventricular tachyarrhythmias

Question 73

Disopyramide toxicity results in ___ side effects; ___ exacerbation; ___ prolongation; ___penia

Answer 73

anticholinergic side effects; heart failure exacerbation; QT prolongation; thrombocytopenia

Question 74

Procainamide, quinidine, and disopyramide (all class IA antiarrhythmics) can be used to treat any arrhythmia (atrial or ventricular), but they come with a lot of complications and thus have fallen out of favor–T/F?

Answer 74

True

Question 75

Disopyramide is ___ eliminated; half-life is ___ hours

Answer 75

renally eliminated; half-life is 6.7 hours

Question 76

Lidocaine is a class ___ antiarrhythmic

Answer 76

class IB

Question 77

Lidocaine is a ___ channel blocker–the channel is ___ and ___; it decreases the slope of phase ___, reduces ___

Answer 77

Lidocaine is a sodium channel blocker–the channel is open and inactivated; it decreases the slope of phase 4 depolarization, reduces automaticity

Question 78

Lidocaine indications = ___ arrhythmias, particularly ___ dysrhythmias

Answer 78

ventricular arrhythmias, particularly reentry dysrhythmias

Question 79

Lidocaine is ineffective against ___ arrhythmias

Answer 79

supraventricular arrhythmias (atrial beats)

Question 80

Lidocaine toxicity–CNS changes range from ___ to ___

Answer 80

depression to seizure

Question 81

Lidocaine toxicity CNS–early signs = ___, ___ changes

Answer 81

early signs = nystagmus, speech changes

Question 82

Lidocaine toxicity CV–may depress ___ performance in pre-existing ___ dysfunction; rarely cause further slowing in patients with sinus ___cardia; almost no effect on ___ interval

Answer 82

May depress LV performance in pre-existing LV dysfunction; rarely cause further slowing in patients with sinus bradycardia; almost no effect on QT interval

Question 83

Lidocaine does not prolong the QT interval, so the risk of Torsades is practically non-existent–T/F?

Answer 83

True

Question 84

Lidocaine pharmacokinetics–significant ___ metabolism; half-life ~___ minutes (longer with ___)

Answer 84

significant first pass metabolism; half-life ~8 minutes (longer with continuous infusions)

Question 85

Lidocaine dose should be reduced in patients with ___ or ___ disease; half-life could be up to ___ hours in these patient populations

Answer 85

dose should be reduced in patients with CHF or liver disease; half-life could be up to 8 hours in these patient populations

Question 86

Lidocaine may accumulate with infusions > ___ hours

Answer 86

> 36 hours

Question 87

Lidocaine can be used for atrial and ventricular arrhythmias–T/F?

Answer 87

FALSE–lidocaine can only be used to treat ventricular arrhythmias

Question 88

Phenytoin is a class ___ antiarrhythmic

Answer 88

class IB

Question 89

Phenytoin is a ___ channel blocker; depresses phase ___ diastolic ___

Answer 89

phenytoin is a sodium channel blocker; depresses phase 4 diastolic depolarization

Question 90

Phenytoin indications–it is useful in the suppression of ___ dysrhythmias associated with ___ toxicity; it is also useful in paradoxical ___ or ___ that is associated with prolonged QTc interval

Answer 90

it is useful in the suppression of ventricular dysrhythmias associated with digitalis toxicity; it is also useful in paradoxical VTach or Torsades de pointes that is associated with prolonged QTc interval

Question 91

Rapid phenytoin administration is associated with respiratory ___, severe ___tension, ventricular ___, and ___

Answer 91

respiratory arrest, severe hypotension, ventricular ectopy, and death

Question 92

Phenytoin toxicity CNS effects–___ness, ___mus, ___ea, ___go

Answer 92

drowsiness, nystagmus, nausea, vertigo

Question 93

Phenytoin ___ (is/is not) a first choice antiarrhythmic

Answer 93

is not–it is more commonly used as an antiseizure medication

Question 94

Flecainide is a class ___ antiarrhythmic

Answer 94

class IC

Question 95

Flecainide blocks ___, ___, and ___ channels; it depresses action potential phase ___; prolongs ___ and to a lesser extent ___ interval; may suppress ___ node like beta blockers and calcium channel blockers; delays conduction in ___ tracts

Answer 95

blocks sodium, potassium, and calcium channels; it depresses action potential phase 0; prolongs QRS and to a lesser extent PR interval; may suppress SA node like beta blockers and calcium channel blockers; delays conduction in bypass tracts

Question 96

Flecainide is an ___ medication also known as ___

Answer 96

oral medication also known as tambocor

Question 97

Flecainide is given to patients in a-fib who can’t tolerate ___

Answer 97

amiodarone

Question 98

Flecainide is very pro-arrhythmic–T/F?

Answer 98

True

Question 99

Flecainide indications–it is effective in suppressing ___; can be used to treat atrial ___dysrhythmias including ___ syndrome because it delays conduction in bypass tracts

Answer 99

it is effective in suppressing PVCs; can be used to treat atrial tachydysrhythmias including Wolff-Parkinson White syndrome because it delays conduction in bypass tracts

Question 100

Flecainide side effects–moderate negative ___ effect; ___go; difficulty in visual ___

Answer 100

moderate negative inotropic effect (beta blocking effect); vertigo; difficulty in visual accommodation

Question 101

Do not administer flecainide to patients with ___, ___ failure, ventricular ___ because of its ___ effects

Answer 101

CAD, LV failure, ventricular tachycardia because of its negative inotropic (beta blocking) effects

It will worsen ischemia!!!

Question 102

Beta blockers are class ___ antiarrhythmics

Answer 102

class II

Question 103

Beta blockers lead to slowing of the ___ node, decreased slope of phase ___ depolarization; slow the rate of depolarization of ___ pacemakers; prolonged ___ nodal conduction; ___ (increased/decreased) refractoriness of AV node

Answer 103

beta blockers lead to slowing of the SA node, decreased slope of phase 4 depolarization; slow the rate of depolarization of ectopic pacemakers; prolonged AV nodal conduction; increased refractoriness of AV node

Question 104

Indications for beta blockers–control of ___; convert atrial tachyarrhythmias to ___ rhythm; slow ventricular response to atrial ___ and ___

Answer 104

control of SVT; convert atrial tachyarrhythmias to sinus rhythm; slow ventricular response to atrial fib and flutter

Question 105

Beta blockers are good for ___ (atrial/ventricular) arrhythmias only

Answer 105

ATRIAL arrhythmias only

Any arrhythmia originating distal to the AV node, beta blocker will not help

Question 106

Beta blocker toxicity–profound ___cardia or ___; ___ failure; acute broncho___

Answer 106

profound bradycardia or asystole; LV failure; acute bronchospasm

Question 107

Which (3) beta blockers can cause bronchospasm?

Answer 107

• propranolol
• carvedilol
• labetalol

^ because they are nonselective and block both beta 1 and beta 2 receptors (beta 2 activation usually causes bronchodilation)

Question 108

Treatment of beta blocker toxicity = ___, ___, ___

Answer 108

atropine, glucagon, pacemaker

Question 109

Amiodarone is a class ___ antiarrhythmic

Answer 109

class III

Question 110

Amiodarone is a potent inhibitor of abnormal ___; it prolongs the effective ___ period and action potential duration in all cardiac tissues, including accessory bypass tracts

Answer 110

potent inhibitor of abnormal automaticity; it prolongs the effective refractory period and action potential duration in all cardiac tissues, including accessory bypass tracts

Question 111

Amiodarone blocks inactivated ___ channels and ___ movement; has an anti___ effect–noncompetitive blockade of ___ and ___ receptors; prolongs ___, ___, and ___ intervals

Answer 111

amiodarone blocks inactivated sodium channels and potassium movement; has an antiadrenergic effect–noncompetitive blockade of alpha and beta receptors; prolongs PR, QRS, and QT intervals

Question 112

Amiodarone may potentiate slowing of the SA node and AV conduction–T/F?

Answer 112

True

Question 113

Amiodarone may potentiate what (2) medication classes?

Answer 113

beta blockers and calcium channel blockers

Question 114

Amiodarone indications–IV for the acute termination of ___ and ___ arrhythmias

Answer 114

ventricular and supraventricular arrhythmias

Question 115

Amiodarone indications–recurrent V ___ or recurrent unstable V ___ in patients unresponsive to or unable to tolerate other agents

Answer 115

recurrent V Fib or recurrent unstable V Tach in patients unresponsive to or unable to tolerate other agents

Question 116

Amiodarone is effective in maintaining sinus rhythm in patients with ___

Answer 116

Amiodarone is effective in maintaining sinus rhythm in patients with a fib

Question 117

Amiodarone can effectively suppress tachydysrhythmias associated with ___ syndrome

Answer 117

amiodarone can effectively suppress tachydysrhythmias associated with Wolff Parkinson White (WPW) syndrome

Question 118

Half-life of amiodarone in patients on the oral agent for several years can be prolonged for ___ to ___

Answer 118

can be prolonged for weeks to months

Question 119

Because the half-life can be prolonged in patients on amiodarone for several years, omission of 1 or 2 doses is unlikely to result in recurrence of arrhythmia–T/F?

Answer 119

True

Question 120

Amiodarone drug interactions–CYP3A4 substrate; CYP3A4, CYP2C9, and PGP ___ (inducer/inhibitor)

Answer 120

inhibitor

Question 121

Amiodarone drug interactions–when given with anticoagulants (i.e.: rivaroxaban, warfarin, apixaban), ___ (increased/decreased) bleeding risk, ___ (increased/decreased) INR

Answer 121

increased bleeding risk, increased INR

Question 122

Amiodarone drug interactions–when given with medications that prolong QT interval, can lead to ___

Answer 122

torsades de pointes

Question 123

Amiodarone drug interactions–when given with digoxin, increases risk of ___

Answer 123

digoxin toxicity

Question 124

Amiodarone drug interactions–when given with lidocaine, increases risk of ___

Answer 124

lidocaine toxicity

Question 125

Amiodarone drug interactions–when given with statins (i.e.: simvastatin, lovastatin), increases risk of ___

Answer 125

myalgias

Question 126

Amiodarone drug interactions–when given with versed, results in prolonged ___ effect, increased risk of respiratory ___

Answer 126

results in prolonged sedative effect, increased risk of respiratory depression

Question 127

Amiodarone drug interactions–when given with suggamadex, increased risk of ___cardia (additive effects)

Answer 127

increased risk of bradycardia

Question 128

Amiodarone drug interactions–when given with AV nodal blockers (i.e.: beta blockers), increased risk of ___cardia, sinus ___, and AV ___

Answer 128

increased risk of bradycardia, sinus arrest, AV block

Question 129

Amiodarone toxicity–respiratory effects = ___, pulmonary ___

Answer 129

ARDS, pulmonary fibrosis

Question 130

Amiodarone toxicity–CV effects = ___cardia, ___tension, dys___, heart ___, heart ___, sinus ___

Answer 130

bradycardia, hypotension, dysrhythmias, heart failure, heart block, sinus arrest

Question 131

Amiodarone toxicity–hematologic effects = coagulation ___–prolongs ___, increased risk of ___

Answer 131

coagulation abnormalities–prolongs INR, increased risk of bleeding

Question 132

Amiodarone toxicity–hepatic effects = increased ___, liver ___

Answer 132

increased LFTs, liver failure

Question 133

Amiodarone toxicity–endocrine effects = ___ or ___thyroidism

Answer 133

hypo- or hyperthyroidism

Amiodarone molecule has an iodine component to it, which leads to hypothyroidism in most patients; most patients will be on Synthroid with amiodarone

Question 134

Amiodarone toxicity–other effects = peripheral ___, muscle ___/___

Answer 134

peripheral neuropathy, muscle pain/weakness

Question 135

Dronedarone (MULTAQ) indication is ONLY for ___

Answer 135

atrial fibrillation to maintain NSR

It only comes in 400 mg tablets, no injectable form

Question 136

Dronedarone contraindications–increased risk of death, stroke, and heart failure for patients with decompensated ___ or permanent ___

Answer 136

decompensated heart failure or permanent a-fib

Question 137

Dronedarone is also contraindicated in patients with ___/___ degree heart block, HR < ___ bpm; medications that ___ (induce/inhibit) CYP3A4, prolong ___; ___; significant ___ disease

Answer 137

Dronedarone is also contraindicated in patients with second/third degree heart block, HR < 50 bpm; medications that inhibit CYP3A4, prolong QTc interval; pregnancy; significant liver disease

Question 138

One benefit of dronedarone over amiodarone is that is does not have effects on the ___

Answer 138

thyroid

Question 139

Ibutilide = ___ formulation; dofetilide = ___ form

Answer 139

ibutilide = IV formulation; dofetilide = oral form

Question 140

Ibutilide/dofetilide is a class ___ antiarrhythmic

Answer 140

class III

Question 141

Ibutilide/dofetilide is used for conversion of ___ to ___

Answer 141

atrial fibrillation to NSR

Question 142

Ibutilide/dofetilide has high incidence of ___ and ___

Answer 142

torsades and ventricular tachyarrhythmias

Question 143

How is ibutilide/dofetilide typically given?

Answer 143

It has to be started in a hospital under direct observation

Question 144

Verapamil is a class ___ antiarrhythmic

Answer 144

class IV antiarrhythmic

Question 145

Verapamil selectively blocks slow channels by inhibiting the normal ___ influx into the cell

Answer 145

calcium influx

Question 146

Verapamil’s effect on slow channel activity is most important in ___ and ___

Answer 146

SA and AV nodes

It prolongs AV nodal conduction/refractoriness and depresses the rate of SA node discharge

Question 147

Verapamil indications–treat ___, slow ventricular rate in ___ and ___

Answer 147

treat SVT, slow ventricular rate in A-fib and flutter

Question 148

Verapamil has no effect on ___

Answer 148

accessory tracts

Question 149

Verapamil toxicity–___ is a major side effect, most common; it is a very potent ___ compared to ___ and ___

Answer 149

hypotension is a major side effect, most common; it is a very potent vasodilator compared to cardizem and beta blockers

Question 150

Verapamil toxicity–___cardia, ___, and ___ block have been seen

Answer 150

bradycardia, asystole, and AV block have been seen

Question 151

Myocardial depression with verapamil is common in patients with reasonable LV function–T/F?

Answer 151

False–is Uncommon in patients with reasonable LV function

Question 152

Diltiazem is a class ___ antiarrhythmic

Answer 152

class IV

Question 153

Diltiazem MOA–slow channel blocking prolongs ___ nodal conduction and refractoriness

Answer 153

prolongs AV nodal conduction and refractoriness

Question 154

Diltiazem indications–ventricular rate control in ___ or ___

Answer 154

a fib or a flutter

Question 155

Diltiazem is a potent CYP3A4 ___ (inducer/inhibitor)

Answer 155

inhibitor–many drug interactions

Question 156

Diltiazem toxicity–___cardia, ___tension, lower extremity ___, ___ation

Answer 156

bradycardia, hypotension, lower extremity edema, constipation

Question 157

Digoxin MOA–inhibits ___

Answer 157

Na+/K+ ATPase

Question 158

Digoxin directly prolongs the effective refractory period in the ___ node

Answer 158

AV node

Question 159

Digoxin slows the ventricular response rate in ___ but enhances conduction through ___

Answer 159

slows the ventricular response rate in a fib but enhances conduction through accessory pathways

Question 160

Because digoxin enhances conduction through accessory pathways, it can increase the ventricular response in what condition?

Answer 160

Wolff-Parkinson-White syndrome

Question 161

Digoxin indirectly ___ (increases/decreases) vagal activity and ___ (increases/decreases) sympathetic activity

Answer 161

indirectly increases vagal activity and decreases sympathetic activity

Question 162

Digoxin is indicated for ventricular rate control in ___, ___, and ___

Answer 162

a fib, a flutter, and SVT

Ventricular rates are easier to control in a fib than a flutter

Question 163

Digoxin’s alterations in cardiac rate and rhythm may stimulate almost every known rhythm disturbance–T/F?

Answer 163

True

Question 164

What is the most common arrhythmia caused by digoxin?

Answer 164

PVCs

Question 165

What is the most fatal arrhythmia caused by digoxin?

Answer 165

VFib

Question 166

Cardiac toxicity from digoxin is enhanced by what electrolyte disturbance?

Answer 166

Hypokalemia

Question 167

Adenosine MOA–activates ___ channels that hyperpolarize nodal tissue, causing a transient ___

Answer 167

activates potassium channels that hyperpolarize nodal tissue, causing a transient third degree AV block

Question 168

Adenosine has less effect in he atrium because it is already hyperpolarized–T/F?

Answer 168

True

Question 169

Adenosine causes depression of the action potential in the SA and AV nodes–T/F?

Answer 169

True

Question 170

Adenosine inhibits the effects of increased ___, reduces ___ currents to increase AV node refractoriness

Answer 170

inhibits the effects of increased cAMP, reduces calcium currents

Question 171

Bolus dose of adenosine may induce transient ___ (sympathetic/parasympathetic) activation via ___

Answer 171

may induce transient sympathetic activation via carotid baroreceptors

Question 172

Continuous adenosine infusion causes ___tension

Answer 172

hypotension

Question 173

Review–adenosine works through ___ channel activation

Answer 173

potassium channel activation–opens up the channels and lets them leak

Question 174

Review–adenosine makes it more difficult for the heart to initiate the next beat; it’s so severe, the heart goes down to a ___, EKG ___, heart ___

Answer 174

heart goes down to a third degree heart block, EKG stops, heart resets

Question 175

Review–adenosine is effective for treatment of ___

Answer 175

PSVTs–paroxysmal SVTs

Question 176

Adenosine affects the atria–T/F?

Answer 176

False–does not affect anything in the atria

Question 177

There are several subtypes of adenosine receptors, two particular ones = ___ and ___

Answer 177

A1 and A3 receptors

Question 178

A1 receptor is a negative ___ (Inotrope, chronotrope, dromotrope), beta ___ (sympatholytic/sympathomimetic) activity

Answer 178

A1 receptor is a negative dromotrope [slows down conduction through cardiac pathway], beta sympatholytic [beta blocking] activity

Question 179

A3 receptor is a negative ___, negative ___

Answer 179

negative Inotrope [weakens strength of contraction], negative dromotrope [slows down conduction through cardiac pathway]

Question 180

Adenosine indications–treatment of ___, including those that involve accessory pathways

Answer 180

treatment of PSVTs–paroxysmal SVTs, including those that involve accessory pathways

Question 181

Adenosine is effective in treating arrhythmias originating distal to the AV node–T/F?

Answer 181

False–NOT effective in treating arrhythmias distal to the AV node

Question 182

Adenosine ___ (is/is not) effective in the treatment of a. fib or a. flutter

Answer 182

is not effective in the treatment of a. fib or a. flutter

Question 183

Adenosine is contraindicated in patients who had a ___ transplant; patients who already have ___ or ___ degree AV block; ___ syndrome; ___cardia

Answer 183

Adenosine is contraindicated in patients who had a heart transplant; patients who already have second or third degree AV block; sick sinus syndrome; bradycardia

Question 184

Adenosine is administered by rapid bolus followed by a saline flush–T/F?

Answer 184

True

Question 185

Adenosine starting dose is ___ mg; adenosine second dose is ___ mg if first dose is ineffective

Answer 185

starting dose is 6 mg; second dose is 12 mg if first dose is ineffective

Question 186

Adenosine pediatric dosing–incremental doses starting at ___ mcg/kg

Answer 186

50 mcg/kg

Question 187

Adenosine half-life is ___ seconds

Answer 187

1.5 seconds

Question 188

Adenosine is inactivated by ___

Answer 188

cellular uptake

Question 189

Adenosine toxicity–facial ___, ___nea, and ___ pressure are most common side effects, but usually subside in < ___ seconds

Answer 189

facial flushing, dyspnea, and chest pressure are most common side effects, but usually subside in < 60 seconds

Question 190

Adenosine may exacerbate broncho___ in asthmatic patients

Answer 190

bronchoconstriction

Question 191

pro___ effects of antiarrhythmic medications = Brady or tachydysrhythmias that represent new cardiac dysrhythmias associated with chronic antidysrhythmic drug treatment

Answer 191

prodysrhythmic effects of antiarrhythmic medications

Question 192

What are (3) common dysrhythmias associated with chronic antidysrhythmic drug treatment? ___, increased ventricular ___, ___ ventricular rhythm

Answer 192

• Torsades de pointes
• Increased ventricular tachycardias
• Wide complex ventricular rhythm

Question 193

Torsades de Pointes may result from ___ channel blockade and prolonged ___ interval

Answer 193

potassium channel blockade and prolonged QT interval

Question 194

Class ___ and class ___ antiarrhythmic drugs block potassium channels and prolong the QTc interval (and thus can lead to torsades)

Answer 194

Class IA and III antiarrhythmic drugs

Question 195

Torsades occurs in 1-8% of patients who receive QT prolonging drugs–T/F?

Answer 195

True

Question 196

What (2) antipsychotics prolong the QT interval?

Answer 196

Haldol, risperidone (risperdal)

Question 197

Diuretics can prolong the QT interval d/t ___ abnormalities

Answer 197

electrolyte abnormalities

Question 198

What antifungals can prolong the QT interval?

Answer 198

-azole antifungals (i.e.: fluconazole)

Question 199

What (2) classes of antibiotics can cause QT prolongation?

Answer 199

• Macrolides (i.e.: azithromycin, clarithromycin, erythromycin, roxithromycin)
• Fluoroquinolones (i.e.: ciprofloxacin, levofloxacin)

Question 200

What (2) classes of antidepressants prolong the QT interval?

Answer 200

• Celexa/Lexapro (SSRIs)

- TCAs (i.e.: amitriptyline)

Question 201

What (3) antiemetics cause QT prolongation?

Answer 201

• 5HT3A inhibitors (i.e.: zofran)
• chlorpomazine (thorazine)–this is also an antipsychotic medication
• cisapride

Question 202

(2) other medications that can prolong QT interval

Answer 202

• methadone

- aricept (donepezil–used to treat dementia in Alzheimer’s disease)

Question 203

Volatile anesthetics ___ (do/do not) prolong QT interval

Answer 203

do prolong QT interval

Question 204

Other QT prolongation risk factors–older than ___ years of age; ___cardia; congenital ___; electrolyte abnormalities–i.e.: ___kalemia, ___magnesemia, ___calcemia; ___ (male/female gender); ___ disease; ___ drug metabolism impairment

Answer 204

older than 65 years of age; bradycardia; congenital long QT syndrome; electrolyte abnormalities–i.e.: hypokalemia, hypomagnesemia, hypocalcemia; female gender; heart disease–MI, CHF, LV failure, HF with reduced EF; hepatic drug metabolism impairment

Question 205

QT prolongation risk factors–increased QTc interval > ___ ms compared to the pretreatment value

Answer 205

> 60 ms compared to the pretreatment value

Question 206

QT prolongation risk factors–QTc > ___ ms

Answer 206

QTc > 500 ms

Question 207

QT prolongation risk factors–recent cardio___

Answer 207

recent cardioversion

Question 208

QT prolongation risk factors–___etes, ___thyroidism, ___thermia

Answer 208

diabetes, hypothyroidism, hypothermia

Question 209

Incessant ventricular tachycardia is precipitated by class ___ and class ___ drugs that slow conduction of cardiac impulses sufficiently to create a continuous ventricular tachycardia circuit (reentry)

Answer 209

class IA and class IC drugs

Question 210

Incessant ventricular tachycardia is rarely associated with class ___ with a weaker blocking effect on sodium channels

Answer 210

class IB

Question 211

Incessant ventricular tachycardia is more likely to occur with ___ (low/high) doses and in patients with a prior history of sustained ___ and poor ___ function

Answer 211

more likely to occur with high doses and in patients with a prior history of sustained V. tach and poor LV function

Question 212

Incessant ventricular tachycardia is generally ___ (faster/slower) due to drug effect, but may be resistant to ___ or ___

Answer 212

generally slower d/t drug effect, but may be resistant to drugs or countershocks

Question 213

Wide complex ventricular rhythm is usually associated with class ___ drugs in the setting of ___

Answer 213

usually associated with class IC drugs in the setting of structural heart disease

Question 214

Excessive ___ concentrations of drug or an abrupt change in the ___ may result in wide complex ventricular rhythm

Answer 214

excessive plasma concentrations of drug or an abrupt change in the dose may result in wide complex ventricular rhythm

Question 215

Wide complex ventricular rhythm is thought to reflect a ___ tachycardia and easily degenerates to ___

Answer 215

thought to reflect a reentrant tachycardia and easily degenerates to V. Fib