Antiarrhythmics Flashcards

1
Q

Class 1 drugs cause a longer time to get thru phase 0 and longer ERP means a longer time between depolarization. This causes a faster or slower HR?

A

slower

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2
Q

Class 1 drugs are good for what 2 SVTs? (AF, W)

A

A fib, WPW (reentry tachycardia)

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3
Q

Do class 1 work on cardiac or nodal APs?

A

cardiac

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4
Q

where in the heart do class 1C meds shorten the AP? (PF)

A

purkinje fibers

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5
Q

Class 2 drugs decrease the spontaneous rate of what phase in what cell’s AP?

A

phase 4 in nodal cells

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6
Q

Class 2: decreasing rise of phase 4 decreases the firing frequency of what and slows the conduction thru where?

A

SA node firing, conduction thru AV node

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7
Q

Is the DOA of the cardiac AP in ventricular myocardium (cardiac cells) altered by class 2 drugs?

A

no

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8
Q

class 2: slowing the conduction speed of the cardiac impulses thru atrial tissues results in prolongation of what interval?

A

PR interval

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9
Q

class 2 drugs are good for supraventricular and ventricular arrhythmias. Name the 2 SVTs and the 1 VT.

A

a fib, a flutter, V tach

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10
Q

sympathetic stimulation increases the slope of what phase, which hits threshold sooner causing more frequent depolarization and HR

A

nodal phase 4

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11
Q

by decreasing phase 4 slope, class 2 meds causes the nodal cell to reach what longer and thus decreases HR?

A

threshold

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12
Q

drug induced slowing of HR by class 2 meds results in a decrease in myocardial O2 requirements, which is desirable for pts with what?

A

CAD

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13
Q

class 2 meds may be important in suppressing ventricular arrhythmia during myocardial what and what? (I,R)

A

ischemia, reperfusion

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14
Q

class 2 drugs are effective in decreasing what 2 things related to arrhythmias? (M,M)

A

mortality, morbidity

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15
Q

class 3 meds block what phase in what cells?

A

phase 3 in cardiac cells

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16
Q

what 3 things do class 3s increase? (E, A, TBCD)

A

ERP, AP duration, and time between cardiac depolarization

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17
Q

class 3s prevent cardiac arrythmias by decreasing the portion of the cardiac cycle during which the myocardial cells are what? (E)

A

excitable

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18
Q

by decreasing the portion of the cardiac cycle that myocardial cells are excitable, class 3 meds make them less susceptible to what? (TE)

A

triggering event

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19
Q

phase 3 of the myocardial cells corresponds to what interval on the ECG

A

QT

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20
Q

class 3 meds slow HR by elongating what interval in the ECG and what period in the cardiac AP, thus creating more time between depolarizations

A

QT interval, effective refractory period

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21
Q

what type of tachycardias may class 3 drugs suppress if the AP duration becomes longer than the cycle length of the tachycardia circuit? (R)

A

reentrant tachycardias

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22
Q

by elongating the QT interval, class 3s put the heart at risk for what rhythm?

A

Torsade’s

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23
Q

why shouldn’t pts with prolonged QT intervals be given class 3 meds?

A

increases the risk of torsades

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24
Q

torsades can deteriorate to which rhythm?

A

V fib

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25
Q

class 4 meds are useful in the treatment of what 2 arrhythmia?

A

Supraventricular and idiopathic ventricular tachycardia

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26
Q

what channel does class 4 drugs block?

A

calcium

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27
Q

class 4 meds reduce the slope in what 2 phases in nodal cells?

A

phase 4 and phase 0

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28
Q

by reducing the slope of phase 4 in nodal cells, CCBs decrease the rate of what (SD), which reducing the rate of pacemaker what? (F)

A

spontaneous depolarization, firing

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29
Q

by delaying the slope of phase 0, CCBs decreasing the what in the SA node (F) and slow down the conduction where?

A

firing, av node

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30
Q

do nondihydropyridine or dihydrpyridine CCBs work on the SA and AV node?

A

nondihydropyridine

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31
Q

do nondihydropyridine or dihydrpyridine CCBs work on blood vessels?

A

dihydropyridine

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32
Q

do class 3 or class 4 drugs do a better job treating V tach?

A

class 3

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33
Q

do class 1 and 3 drugs work on cardiac or nodal APs?

A

cardiac

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34
Q

do class 2 and class 4 drugs work on cardiac or nodal APs?

A

nodal

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35
Q

proarrhythmic effects are bradyarrhythmias or tachyarrhythmias that represent a new cardiac arrhythmia associated with what therapy? (A)

A

antiarrhythmic therapy

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36
Q

what is the most common proarrhythmic effect rhythm?

A

Torsades

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37
Q

torsades is triggered by an early depolarization in a setting where what 2 things are delayed?

A

repolarization, ERP

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38
Q

what interval is prolonged for torsades to occur?

A

QTc interval

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39
Q

what two med classes increase the QTc interval and thus make the heart prone to torsades?

A

class 1A and class 3

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40
Q

incessant ventricular tachycardias (reentry arrythmias) are caused by meds that hasten or slow the conduction of cardiac impulses?

A

slow

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41
Q

what 2 med classes cause incessant ventricular tachycardias?

A

class 1A and 1C

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42
Q

class 1A and 1C can slow the conduction of cardiac impulses long enough to create a continuous what? (VTC)

A

ventricular tachycardia circuit

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43
Q

AKA for a continuous ventricular tachycardia circuit? (R)

A

reentry

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44
Q

what med class can cause wide complex ventricular rhythms in the setting of structural heart disease?

A

class 1c

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45
Q

wide complex ventricular rhythm reflects a what tachycardia and easily degenerates to what rhythm?

A

reentrant tachycardia, V fib

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46
Q

pts taking what drug class experience a higher incidence of sudden cardiac arrest d/t arrhythmic effects?

A

class 1c

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47
Q

what 2 drug classes increase mortality in pts with previous MI and ventricular arrhythmia?

A

class 1a and class 1c

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48
Q

what 1 drug and 1 drug class decrease mortality in pts with previous MI and ventricular arrhythmia?

A

amiodarone, beta blockers

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49
Q

what one drug and one class of med are not longer recommended in treatment of pts with early stages of acute MI?

A

lidocaine, class 4

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50
Q

what is the drug of choice for pts in torsades?

A

mg

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51
Q

what med can be sued solo or in adjunct with an ICD for the treatment of pts with arrythmias d/t heart failure?

A

amiodarone

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52
Q

what 1 med class and 3 drugs can be used to treat A fib after heart surgery? (B, A, S, M)

A

beta blockers, amiodarone, sotalol, magnesium

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53
Q

what med class is quinidine?

A

class 1a

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54
Q

quinidine is used for supraventricular or ventricular arrythmias?

A

supraventricular

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55
Q

quinidine prevents the recurrence of what tachyarrhythmia?

A

supraventricular

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56
Q

quinidine suppresses what ventricular contractions? (P)

A

premature ventricular conctractions

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57
Q

quinidine slows ventricular rate in the presence of what rhythm?

A

a fib

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58
Q

quinidine can possibly convert which rhythm to NSR?

A

a fib

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59
Q

quinidine can suppress SVTs associated with what syndrome?

A

Wolf-Parkinson-White

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60
Q

quinidine decreases the slope of what phase in nodal AP?

A

phase 4

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61
Q

quinidine increases fibrillation threshold in what 2 areas?

A

atria and ventricles

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62
Q

quinidine stops reentry arrythmias by doing what to the conduction of cardiac impulses in the area of injury? (P)

A

prolonging conduction of cardiac impulses

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63
Q

quinidine is eliminated by the liver how? (H)

A

hydroxylation

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64
Q

what 3 reasons is quinidine rarely used? (S, LTI, NA)

A

SEs, low TI, newer agents

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65
Q

quinidine do not use in pts with preexisting what 2 things?

A

heart block, prolonged QTc

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66
Q

quinidine may cause HR increase by what 2 actions? (AA, RSA)

A

anticholinergic action, reflex SNS activity increase

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67
Q

quinidine also has what blocking properties that can be an additive matter with vasodilating drugs?

A

alpha blocking

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68
Q

quinidine may increase or decrease the effects of NMBs?

A

increase

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69
Q

quinidine has a low TI with what 3 AEs? (HB, H, P?

A

heart block, hypotension, proarrythmic

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70
Q

what med class is procainamide?

A

class 1a

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71
Q

procainamide effective at treating what type of tachyarrhythmias, but less effective at treating what type of tachyarrhythmias?

A

ventricular, atrial

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72
Q

procainamide effective at treating what 2 rhythms?

A

PVCs, paroxysmal VT

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73
Q

procainamide is the analogue of which LA?

A

procaine

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74
Q

does procainamide or quinidine prolong the QTc interval more?

A

quinidine

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75
Q

does procainamide have vaoglytic effects?

A

no

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76
Q

since no vagolytic effects procainamide can be used in pts with A fib to suppress ventricular irritability without increasing what? (VR)

A

ventricular rate

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77
Q

what is procainamide’s cardio active metabolite? (N)

A

N-acetyl-procainamide (NAPA)

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78
Q

N-acetyl-procainamide (NAPA) can build up and reach dangerous levels in what pts?

A

renal failure pts

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79
Q

procainamide not used as much because of what profile?

A

SE profile

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80
Q

SE of procainamide: causes what d/t direct myocardial depression? (H)

A

hypotension

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81
Q

SE of procainamide: causes what in the presence of a heart block?

A

V fib and asystole

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82
Q

SE of procainamide: causes a syndrome that resembles what with chronic use?

A

SLE

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83
Q

Procainamide may prolong what and cause what wave changes?

A

prolong QRS, ST-T wave changes

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84
Q

what class of med is disopyramide

A

class 1a

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85
Q

disopyramide is comparable to what other med in effectively suppressing atrial and ventricular tachyarrhythmias

A

quinidine

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86
Q

disopyramide’s elimination is prolonged if what organ is dysfunctioning

A

kidneys

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87
Q

disopyramide has what SEs from its anticholinergic activity (DM, UH)

A

dry mouth, urinary hesitancy

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88
Q

what med class is moricizine

A

class 1a

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89
Q

what class 1 drug is reserved for treatment of life-threatening ventricular arrhythmias when other meds are not available? (M)

A

moricizine

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90
Q

what class is lidocaine?

A

class 1b

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91
Q

Does lidocaine principally suppress ventricular or supraventricular arrhythmias?

A

ventricular

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92
Q

in one word, how does lidocaine effect supraventricular arrhythmias? (M)

A

minimally

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93
Q

lidocaine delays the rate of spontaneous depolarization of what phase in ventricular cardiac cells?

A

phase 4

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94
Q

lidocaine delays the rate of spontaneous depolarization in ventricular cardiac cells by preventing the decrease of what ion permeability?

A

potassium

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95
Q

lidocaine is effective at suppressing what type of cardiac arrhythmias such as PVCs and VT?

A

reentry cardiac arrhythmias

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96
Q

What is bolus dose of lidocaine (mg/kg)? What is continuous infusion after the bolus (mg/min)?

A

2 mg/kg; 1-4 mg/min

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97
Q

What are the 4 advantages of lidocaine over quinidine and procainamide? (RO, RO, GTI, LSE)

A

rapid onset, rapid offset, greater TI, less SEs

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98
Q

where is lidocaine metabolized?

A

liver

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99
Q

lidocaine’s metabolites may possess what type of cardiac activity? (A)

A

antiarrhythmic

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100
Q

lidocaine may also block ATP-dependent channels preventing ischemia-mediated shortening of ventricular what? (D)

A

depolarization

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101
Q

decrease lidocaine dose in pts with what 2 heart conditions?

A

acute MI, CHF

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102
Q

decrease lidocaine dose in pts with decreases in what two blood flows situations?

A

decreased CO, decrease hepatic BF

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103
Q

At therapeutic levels, lidocaine has no significant effects on what 2 parts of the heart rhythm and conduction where?

A

QRS, QTc interval; AV node conduction

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104
Q

at hi doses, lidocaine can decrease conduction in what 2 places?

A

AV node, purkinje fibers

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105
Q

Unlike quinidine and procainamide, lidocaine does not alter the duration of what or the activity of what system?

A

QRS complex, SNS

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106
Q

At what plasma concentration does lidocaine not have effects on ECG, CV system or CNS?

A

<5 mcg/mL

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107
Q

What 6 lidocaine toxicity effects are seen at plasma concentrations of 5-10 mcg/mL? (PV, MD, B, PPRI, WQC, S)

A

peripheral vasodilation, myocardial depression, bradycardia, prolonged PR interval, wide QRS complex, seizures

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108
Q

what 3 lidocaine toxicity effects are seen at plasma concentrations of >10 mcg/mL? (CD, A, CA)

A

CNS depression, apnea, cardiac arrest

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109
Q

Decreased convulsion threshold related to lidocaine toxicity in what 3 conditions? (H, H, A)

A

hypoxemia, hyperkalemia, acidosis

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110
Q

Mexiletine is what class of drug?

A

class 1b

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111
Q

Mexiletine and tocainide are oral analogues of what drug?

A

lidocaine

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112
Q

Mexiletine is used for chronic suppression of ventricular or supraventricular tachyarrhythmias?

A

ventricular

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113
Q

Mexiletine should be used in combo with beta blockers or other antiarrhythmic drugs for synergistic effect to decrease incidence of what at higher doses?

A

side effects

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114
Q

Mexiletine has an amine side group allowing it to avoid significant what? (part of metabolism)

A

liver first pass effect

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115
Q

does lidocaine have this amine side group that Mexiletine has to avoid a significant first pass effect?

A

no

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116
Q

what class is phenytoin?

A

class 1b

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117
Q

phenytoin is useful in treating VT or torsades that is associated with what type of heart rhythm?

A

prolonged QTc interval

118
Q

is phenytoin effective at treating atrial tachyarrhythmias?

A

no

119
Q

what is the dose of IV phenytoin that is administered every 5 minutes until the arrhythmia is controlled? (mg/kg)

A

1.5 mg/kg

120
Q

phenytoin is administered at a dose of 1.5 mg/kg every 5 minutes until what dose range is administered? (mg/kg)

A

10-15 mg/kg

121
Q

phenytoin’s effects on automaticity and conduction velocity of cardiac impulses resembles what other drug?

A

lidocaine

122
Q

what does phenytoin shorten more than any other antiarrhythmic drug?

A

QTc interval

123
Q

what 2 parts of the heart rhythm does phenytoin not effet?

A

QRS complex, ST-T waves

124
Q

Does phenytoin depress the myocardium?

A

no

125
Q

phenytoin improved conduction in what node?

A

AV node

126
Q

phenytoin depresses activity in what node?

A

SA node

127
Q

phenytoin metabolism: phenytoin is what (H) and then conjugated with what (GA) for excretion in the urine

A

hydroxylated, glucuronic acid

128
Q

phenytoin blood levels may be increased in what organ dysfunction?

A

liver

129
Q

what are the 3 phenytoin SEs? (H, BMD, PIIS)

A

hypotension, bone marrow depression, partially inhibits insulin secretion

130
Q

with its effect on the pancreas, does phenytoin increase or decrease blood glucose?

A

increases blood glucose

131
Q

phenytoin toxicity manifests as what disturbances and especially in what area?

A

CNS disturbances; especially cerebellar

132
Q

what are the 6 CNS disturbances of phenytoin toxicity? (A, N, V, SS, MS, C)

A

ataxia, nystagmus, vertigo, slurred speech, mental sedation, confusion

133
Q

what does phenytoin suppress with digitalis toxicity?

A

ventricular arrhythmias

134
Q

do you use D5W or NS with phenytoin?

A

NS

135
Q

what class of med is flecainide?

A

class 1c

136
Q

flecainide is a fluorinated LA analogue of what med? (P)

A

procainamide

137
Q

flecainide is more effective than quinidine and disopyramide at suppressing what 2 rhythms?

A

PVCs, VT

138
Q

flecainide is effective in treating what type of tachyarrhythmias?

A

atrial tachyarrhythmias

139
Q

Because flecainide delays conduction in the bypass tracts, flecainide can treat what mechanism of arrhythmias? (R)

A

reentry mechanism arrhythmias

140
Q

flecainide can treat the reentry mechanism of what syndrome?

A

Wolff-Parkinson-White syndrome

141
Q

flecainide is reserved for treatment of what arrhythmias? (LT)

A

life-threatening arrhythmias

142
Q

flecainide elimination is decreased in pts with what 2 conditions?

A

CHF, renal failure

143
Q

flecainide increases the plasma concentration of what 2 drugs? (D, P)

A

digoxin, propranolol

144
Q

flecainide SEs: in one word, describe its negative inotropic effects. (M)

A

moderate

145
Q

does flecainide increase or decrease pacemaker capture threshold?

A

increase

146
Q

flecainide depresses what nodes function?

A

SA node

147
Q

does flecainide have proarrhythmic effects?

A

yes

148
Q

what drug class is propafenone?

A

class 1c

149
Q

Is propafenone an effective oral antiarrhythmic for suppression of ventricular tachyarrhythmias, atrial tachyarrhythmias or both?

A

both

150
Q

propafenone possesses weak blocking of what other channels?

A

beta, calcium

151
Q

where is propafenone extensively metabolized?

A

liver

152
Q

Does propafenone have principally active metabolites?

A

yes

153
Q

how potent is propafenone’s active metabolites?

A

equal potent to the parent drug

154
Q

what are the 2 slowing SEs of propafenone? (MD, SANS)

A

myocardial depression, SA node slowing

155
Q

what are the 2 blocking SEs of propafenone involving the heart?

A

AV node block, BBB

156
Q

propafenone interferes with the metabolism of what 3 meds causing their plasma concentrations to increase? (P, M, W)

A

propranolol, metoprolol, warfarin

157
Q

propafenone is especially a proarrhythmic in pts in what sustained rhythm and with what condition?

A

sustained VT, poor LV function

158
Q

Beta blockers are what class?

A

class 2

159
Q

Class 2 meds are effective at treating cardiac arrhythmias related to enhanced activity of what?

A

SNS

160
Q

class 2 meds can be used control ventricular response in what 2 rhythms?

A

a fib, a flutter

161
Q

what are the 4 class 2 meds? (MAPE)

A

metoprolol, acebutolol, propranolol, esmolol

162
Q

what is the mg range of IV metoprolol to give over 20 minutes?

A

5-15 mg

163
Q

how many hours (range) does 5-15 mg of IV metoprolol given over 20 minutes?

A

5-7 hours

164
Q

what class 2 med is effective in treating frequent PVCs?

A

acebutolol

165
Q

what class 2 med may be effective in controlling torsades in pts with a prolonged QTc interval?

A

propanolol

166
Q

what 3 class 2 meds are approved for preventing of sudden death following MI?

A

metoprolol, acebutolol, propranolol

167
Q

class 2 meds decrease the depolarization rate in what phase in nodal cells?

A

phase 4

168
Q

class 2 meds decrease conduction in what 2 sites of the heart?

A

SA node, AV node

169
Q

Do class 2 meds shorten or prolong the PR interval?

A

prolong

170
Q

do class 2 meds have a lot or little effect on the ST-T wave?

A

little

171
Q

do class 2 meds shorten or prolong overall QTc interval?

A

shorten

172
Q

what are the 4 SEs of class 2 drugs related to inhibiting SNS? (B, H, MD, B)

A

bradycardia, hypotension, myocardial depression, bronchospasm

173
Q

What are the 2 most common CNS SEs of class 2 meds? (MD, F)

A

mental depression, fatigue

174
Q

class 2 meds make what disease worse?

A

raynaud disease

175
Q

do class 2 meds make extremities warm or cold?

A

cold extremities

176
Q

class 2 meds interfere with glucose metabolism resulting in hyperglycemia or hypoglycemia in DM pts?

A

hypoglycemia

177
Q

Chronic use of class 2 meds cause a downregulation or upregulation of beta receptors?

A

upregulation of receptors

178
Q

pts taking class 2 meds will be unresponsive to what med that is used to treat low HR or BP? (E)

A

ephedrine

179
Q

Upregulation of beta receptors with chronic class 2 med use can lead to what type of rhythm with abrupt discontinuation?

A

supraventricular tachycardias

180
Q

class 2 meds have depressant effects on myocardium d/t what blockade and what direct effects on the cardiac muscle

A

beta blockade, depressant effects

181
Q

what drug class is amiodarone?

A

class 3

182
Q

what 4 places does amiodarone block?

A

potassium channels, calcium channels, beta receptors, sodium channels

183
Q

amiodarone potent against what 2 tachyarrhythmias? (RS, V)

A

refractory supraventricular tachyarrhythmias, ventricular tachyarrhythmias

184
Q

what is the IV dose (mg) of amiodarone for VT or V fib resistant to defibrillation?

A

300 mg

185
Q

amiodarone is effective in suppressing tachyarrhythmias associated with what?

A

WPW syndrome

186
Q

what is the PO maintenance dose (mg) of amiodarone of ventricular tachyarrhythmias?

A

400 mg

187
Q

what is the PO maintenance dose (mg) of amiodarone for suppression of supraventricular tachyarrhythmias?

A

200 mg

188
Q

what is the IV dose (mg/kg) of amiodarone that is administered over 2-5 min?

A

5 mg/kg

189
Q

amiodarone decreases mortality after what similar to beta blockers?

A

MI

190
Q

preop oral amiodarone decreases the incidence of what rhythm after cardiac surgery?

A

A fib

191
Q

after initiation of oral therapy, amiodarone decreases in ventricular tachyarrhythmias within how many hours?

A

72 hours

192
Q

amiodarone prolongs what in all cardiac tissues?

A

ERP

193
Q

is amiodarone a major or minor negative inotrope?

A

minor

194
Q

amiodarone is a minor negative inotrope that may be offset by its potent what properties?

A

vasodilating

195
Q

amiodarone: competitive or noncompetitive blockade of alpha/beta receptors?

A

noncompetitive blockade

196
Q

amiodarone: constricts or dilates coronary arteries and increases or decreases coronary BF

A

dilates, increases

197
Q

amiodarone: small or large Vd?

A

large

198
Q

amiodarone: elimination half-life is how many days?

A

29 days

199
Q

amiodarone: chronic oral therapy results in effects up to how many days after discontinuation?

A

60 days

200
Q

amiodarone: minimal or extensive protein binding?

A

extensive

201
Q

amiodarone has extensive protein binding making it not easily removed by what?

A

HD

202
Q

amiodarone displaces what drug from protein-binding sites?

A

digoxin

203
Q

what is the active metabolite of amiodarone that accumulates with chronic therapy? (D)

A

desethylamiodarone

204
Q

Desethylamiodarone is active or inactive and has a shorter or longer elimination half life than amiodarone?

A

active; longer elimination half life

205
Q

amiodarone inhibits P450 resulting in increased plasma concentrations of what 6 drugs? (D, P, Q, W, P, C)

A

digoxin, procainamide, quinidine, warfarin, phenytoin, cyclosporine

206
Q

amiodarone potentiates warfarin by depressing clotting factors dependent on what?

A

vitamin K

207
Q

amiodarone SEs are especially seen if daily maintenance dose is > how many mg?

A

> 400 mg

208
Q

what is the most serious SE of amiodarone?

A

pulmonary toxicity (alveolitis)

209
Q

what can you consider restricting in pts who are on amiodarone?

A

oxygen

210
Q

how does restricting oxygen in pts on amiodarone help with pulmonary toxicity?

A

decreases production of free oxygen radicals

211
Q

what 2 tests a pt a on amiodarone have before GA?

A

PFTs, chest x ray

212
Q

pts with preexisting amiodarone induced pum toxicity are at an increased risk of developing what postop?

A

ARDS

213
Q

acute onset of pulm toxicity is manifested as how postop?

A

pulm edema

214
Q

what other test is recommended for pts on amiodarone?

A

liver function tests

215
Q

amiodarone increases what enzyme concentration and what liver infiltration?

A

transaminase, fatty liver infiltration

216
Q

where can microdeposits occur in pts on amiodarone?

A

cornea

217
Q

amiodarone can cause neuropathy where resulting in a mild degree of visual loss?

A

optic neuropathy

218
Q

amiodarone can cause neurologic toxicity resulting in what 5 symptoms? (PN, T, SD, HA, PSMW)

A

peripheral neuropathy, tremors, sleep disturbances, HA, proximal skeletal muscle weakness

219
Q

what does amiodarone contain that can affect thyroid metabolism?

A

iodine

220
Q

what level should be checked to ensure amiodarone hasn’t caused hypo or hyperthyroidism?

A

TSH

221
Q

amiodarone causes a block at what node?

A

AV node

222
Q

amiodarone prolongs what interval?

A

QTc

223
Q

because amiodarone prolongs QTc, there is an increased risk of what type of tachyarrhythmias?

A

VTs (including torsades)

224
Q

amiodarone decreases HR with a resistance to what med? (A)

A

atropine

225
Q

amiodarone causes a decrease responsiveness to SNS d/t blocking what 2 receptors?

A

alpha and beta

226
Q

amiodarone’s negative inotropic effects enhanced by what 3 types of meds? (G, B, C)

A

GA, beta blockers, CCBs

227
Q

amiodarone can accentuate the effects of lidocaine which can increase the likelihood of what condition?

A

sinus arrest

228
Q

chronic amiodarone pts may need what intervention and/or what medication intraop? (TAP, I)

A

temporary artificial pacemaker; isoproterenol

229
Q

what class is dronedarone?

A

class 3

230
Q

dronedarone is a derivative of what med?

A

amiodarone

231
Q

dronedarone is recommended for treatment of A fib/flutter in pts who will be undergoing drug therapy/cardioversion to get them back to what rhythm or in pts who are already in what rhythm?

A

NSR; NSR

232
Q

dronedarone is contraindicated for pts with what 2 conditions? (AHF, PAF)

A

advanced heart failure, permanent atrial fibrillation

233
Q

dronedarone blocks multiple sites like amiodarone, but is stronger at blocking which 2?

A

Na channels, adrenergic receptors

234
Q

dronedarone is a moderate inhibitor of CYP3A4 so avoid with what 3 meds? (A, MA, PIs)

A

antifungals, macrolide abx, protease inhibitors

235
Q

lower dose of dronedarone with verapamil and diltiazem to avoid what 2 things? (SB, CB)

A

severe bradycardia, conduction block

236
Q

what are the 2 most common SEs of dronedarone? (N, D)

A

nausea, diarrhea

237
Q

in the ATHENA trial, pts on dronedarone did not have increased rates of what 3 things? (ILD, H, H)

A

interstitial lung disease, hypothyroidism, hyperthyroidism

238
Q

what drug class is sotalol?

A

class 3

239
Q

what type of blocker is sotalol? (acting, selectivity, receptor)

A

long-acting, noncardioselective beta blocker

240
Q

how does sotalol act at low dosages?

A

like a nonselective beta blocker

241
Q

at higher dosages, sotalol prolongs the cardiac AP in what 3 areas of the heart? (A, V, ABT)

A

atria, ventricles, accessory bypass tract

242
Q

sotalol can treat what 2 sustained rhythms as well as what type of rhythm after cardiac surgery?

A

V Tach, V Fib; atrial tachyarrhythmia (A fib)

243
Q

sotalol is not recommended in pts with what 3 conditions? (A, LVD, CCA)

A

asthma, LV dysfunction, cardiac conduction abnormalities (including prolonged QTc)

244
Q

what is the most dangerous SE of sotalol?

A

Torsades

245
Q

what organ excretes sotalol?

A

kidneys

246
Q

should sotalol dose be adjusted for renal disease?

A

yes

247
Q

which sotalol isomer is the beta antagonist?

A

L isomer

248
Q

which sotalol isomer may increase mortality in pts with ventricular dysfunction and recent MI?

A

D isomer

249
Q

What drug class is ibutilide, dofetilide and bretylium?

A

class 3

250
Q

ibutilide is able to convert a recent onset of what 2 rhythms to NSR?

A

a fib, a flutter

251
Q

what is rhythm SE of ibutilide?

A

polymorphic VT

252
Q

Dofetilide is a potent, pure blocker of what channel?

A

potassium

253
Q

Dofetilide prolongs the AP duration increasing what interval?

A

QT interval

254
Q

Dofetilide is effective in converting pts to NSR who recently onset into what 2 rhythms?

A

A fib, A flutter

255
Q

Dofetilide is also effective at maintaining NSR in pts who have been successfully what?

A

cardioverted

256
Q

Dofetilide’s dose should be adjusted if which organ isn’t functioning?

A

kidneys

257
Q

proarrhythmic effects occur if Dofetilide is administered with which other drug type?

A

CCBs

258
Q

Dofetilide can cause dose-related Torsades in pts with preexisting what dysfunction?

A

LV dysfunction

259
Q

does Dofetilide depress myocardial contractility?

A

no

260
Q

Verapamil is effective at treating what 2 arrhythmias? (PST, RT)

A

paroxysmal SVT, reentry tachycardia (usually including the AV node)

261
Q

What med effective controls ventricular rate in pts who develop A fib or A flutter?

A

Verapamil

262
Q

Will Verapamil slow the ventricular response with WPW syndrome?

A

no

263
Q

does Verapamil depress accessory tracts?

A

no

264
Q

does Verapamil have some, little, or large efficacy in ventricular ectopic beats?

A

little

265
Q

what is the IV dose range (mg or mcg/kg) of Verapamil given over 1-3 min followed by a continuous infusion of what rate (mcg/kg/min)?

A

5-10 mg or 75-150 mcg/kg; 5mcg/kg/min

266
Q

What is the antiarrhythmic IV dose (mg) of diltiazem?

A

20 mg

267
Q

Digoxin plays a role in what pt population? (CLOCHF)

A

chronic, low output CHF

268
Q

Digoxin is a positive inotrope by increasing what intracellularly?

A

Ca

269
Q

what does Digoxin inhibit to increase intracellular Na?

A

Na/K ATPase pump

270
Q

what does this increased intracellular Na that Digoxin caused block which increases intracellular Ca?

A

Na/Ca exchanger

271
Q

Digoxin decreases what 4 things in the failing heart without increasing what 1 thing? (LVP, A, WT, OC; H)

A

LV preload, afterload, wall tension, oxygen consumption; HR

272
Q

in the absence of HF, Digoxin increases myocardial what?

A

contractility

273
Q

Digoxin stabilizes what atrial activity thus preventing/treating atrial tachyarrhythmias?

A

electrical activity

274
Q

What is Digoxin’s vagolytic effect on the heart?

A

slowing impulse thru AV node

275
Q

Digoxin’s vagolytic effect causes what effect on ventricular response rate to a fib?

A

decreases it

276
Q

What is the PO dose range (mg) of Digoxin that is divided over 12-24 hrs?

A

0.5 - 1 mg

277
Q

why shouldn’t Digoxin be used in WPW syndrome?

A

enhances conduction impulses thru accessory tracts and increases ventricular response rate

278
Q

Digoxin toxicity can be any cardiac arrhythmia, however what is the most common one? (ATWB)

A

atrial tachycardia with block

279
Q

Digoxin toxicity can be partially reversed giving what?

A

potassium

280
Q

what 5 things contribute to Digoxin toxicity? (H, H, D, DSMM, RD)

A

hypercalcemia, hypomagnesemia, diuretics, decrease skeletal muscle mass, renal dysfunction

281
Q

does an increased SNS from hypoxemia contribute to digoxin toxicity?

A

Yes

282
Q

Adenosine slows conduction impulse thru where?

A

AV node

283
Q

Adenosine is an effective alternative to CCBs for what rhythm?

A

paroxysmal supraventricular tachycardia (including WPW)

284
Q

What is IV dose (mg) of Adenosine and if necessary repeat with what dose range (mg) 3 minutes later?

A

6 mg; 6-12 mg

285
Q

By stimulating cardiac adenosine 1 receptors, Adenosine has what 3 effects? (increases what, shortens what, hyperpolarizes what)

A

increases K currents, shortens AP duration, hyperpolarizes cardiac cells

286
Q

Adenosine decreases concentration of what, thus inhibiting L-type calcium channels?

A

cAMP

287
Q

what are the 4 steps of Adenosine causing negative dromotropy?

A
  1. decrease cAmp
  2. inhibit L-type Ca channels
  3. decrease Ca entry into cell
  4. decrease conduction velocity in SA & AV node
288
Q

what are the 3 steps of Adenosine causing negative chronotropy

A
  1. inhibit pacemaker current
  2. decrease slope of nodal cell phase 4
  3. decrease rate of spontaneous firing
289
Q

What is Adenosine’s elimination half-time (seconds)?

A

10 seconds

290
Q

What are 3 SEs of Adenosine? (FF, TAVB, B)

A

facial flush, transient AV block, bronchospasm

291
Q

Adenosine is not effective in what 3 rhythms?

A

A fib, A flutter, VT