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Anesthesia- Antiarrythmics > Pharmacology-Antiarrhythmic > Flashcards

Pharmacology-Antiarrhythmic Flashcards

1
Q

Anti-arrhythmic drugs are often used to treat

A

atrial arrhythmias

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2
Q

Anti-arrhythmic drugs have a potential to affect______ and may produce _______side effects

A

LV function
Pro-dysrhythmic

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3
Q

From Class 1-4, name the classes in order

A

Sodium
Beta
Potassium
Calcium
(shay better pass this class)

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4
Q

List subclass Sodium Channel Blockers in order from most potent to least

A

1C
1A
1B

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5
Q

Class 1 Sodium blockers are

A

negative Inotropes

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6
Q

MOA of Sodium Blockers

A

Bind to and block fast Na+ channels (keeps them in an inactive state)

decrease the slope of phase 0

decrease size of AP

decrease conduction velocity

cells have a harder time depolarizing

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7
Q

Negative Inotropes

A

decrease LV function

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8
Q

Some Na+ blockers act on _____channels

A

K+

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9
Q

With Na+channel blockers, class 1A prolongs phase_____, the refractory period

Class 1B shortens phase ____, the refractory period

A

3

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10
Q

Nodal cells are NOT dependent on

A

Fast Na+ channels

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11
Q

Class 1A drugs slows conduction velocity by prolonging _____ and __________

A

repolarization; duration of action potential

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12
Q

Class 1A often treats

A

Afib, Aflutter, SVT and VT

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13
Q

Class 1A have ______________effects, which can cause tachycardia

A

Anticholinergic

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14
Q

What are common Class 1A drugs

A

Quinidine
Procainamide
Disopyramide

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15
Q

Quinidine, a class 1A Na+ blocker slows the _____rate and is an ___________, which can cause vasodilation and HOTN

A

atrial rate; alpha 1 antagonist

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16
Q

What are the side effects of Quinidine, a class 1A Na+ blocker?

A

Anticholinergic
Torsades
Cinchonism (blurred vision, HA, tinnitus)
prolongs QT & QRS

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17
Q

Quinidine, a class 1A Na+ blocker is used to treat acute/chronic ______________ & ____________

A

SV arrhythmias
New onset Afib

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18
Q

Procainamide, a class 1A Na+ blocker slows __________rate and prolongs______

A

Ventricular; QRS

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19
Q

What are side effects of Procainamide?

A

HOTN

Myocardial depression

Vfib

SLE, leukopenia, thrombocytopenia (w/chronic administration)

Watch renal function

Drug fever/rash

N/V

Potential for Ventric asystole/fib

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20
Q

What is the metabolite of Procainamide?

A

NAPA metabolite

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21
Q

Disopyramide, a class 1A Na+ blocker slows_____&______ and can precipitate _____&______

A

atrial and ventricular rate;
CHF & HOTN

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22
Q

What are the side effects of disopyramide, a class 1A Na+ blocker?

A

Myocardial Depression
Anticholinergic
Prolong QT
Vtach
Dry Mouth
Urinary hesitancy
Blurred vision
Nausea

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23
Q

What are the medications that are 1B Na+ blockers

A

Lidocaine
Mexiletine
Tocainide
Phenytoin

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24
Q

When are class 1B drugs best used

A

work better in ischemic cells

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25
Q

Class 1B drugs have minimal effect on conduction velocity in normal cells and shortens _____&______

A

repolarization & AP duration

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26
Q

MOA of Class 1B Na+ blockers

A

bind inactivated Na+ channels in ischemic cells and maintain state

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27
Q

1B Na+ blockers treat

A

V-tachyarrhythmias associated w/MIs

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28
Q

All 1B Na+ blockers slow_________rate

A

Ventricular

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29
Q

What is the dose of Lidocaine?

A

2mg/kg IV
1-4mg/min IV

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30
Q

What are the side effects of Lidocaine?

A

Assess for LAST

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31
Q

What are side effects of Tocainide & Mexiletine, class 1B Na+ blockers

A

synergistic effects w/BB

Pulmonary fibrosis w/toc

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32
Q

Phenytoin act similar to

A

Lidocaine

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33
Q

What are side effects of Phenytoin

A

CNS related (vertigo, sedation, confusion, nystagmus, and ataxia)

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34
Q

Class 1C Na+ blockers slows conduction velocity and treats

A

life-threatening ventricular & SVT

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35
Q

Class 1C Na+ blockers can cause

A

other dysrhythmias
pro-dysrhythmic effects

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36
Q

Examples of 1C Na+ blockers

A

Flecainide
Propafenone
Moricizine

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37
Q

Flecainide, 1C Na+ blocker, slows______ and treats________

A

atrial; PVCs and SVT

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38
Q

What are side effects of Flecainide, a class 1C Na+ blocker

A

Negative Inotrope
Depressed SA node
Vtach
Blurred Vision

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39
Q

Propafenone and Moricizine, class 1C Na+ blockers, slow_______

A

Ventricular rates

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40
Q

What are side effects of Propafenone

A

Dysrhythmias
CHF exacerbation
Blurred Vision

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41
Q

Side effects of Moricizine

A

Increased mortality post-MI
Dysrhythmias

42
Q

Na+ channel blockers slow_______, effect __________Na+channels, and some have effects on phase ______

A

tachyarrythmias
fast
3 repolarization

43
Q

What are the 2 common Class II beta blockers in the OR

A

Metoprolol
Esmolol

44
Q

Class II Beta Blockers work on the _______action potential and slows down the ______cells

A

nodal
pacemaker

45
Q

MOA of Class II Beta Blockers

A

Bind to and block Beta-1 receptors

Decreases conduction velocity, cAMP, Ca+ currents and slope of phase 4

Slows spontaneous depolarization

Prolonged repolarization/refractory period at AV node

46
Q

Class II Beta Blockers slows_____&_____ and treats_______,_______and_______

A

atrial & ventricular rate

treats SNS induced arrhythmias
ectopic beats
tachyarrhythmias

Non-nodal: prolongs AP duration and refractory period

47
Q

What are side effects of Class II BETA BLOCKERS

A

Myocardial Depression
HOTN,bradycardia, AV block
Increased airway resistance
Depression
Fatigue
Upregulation of beta receptors in
chronic therapy

Non-selective: Hypoglycemia, hyperkalemia, bronochoconstriction

48
Q

Class III potassium blockers prolong

49
Q

MOA of Class III Potassium blockers

A

bind to and block K+ channels
decrease K+ currents
slows repolarization
increases effective refractory
period

50
Q

Class III potassium blockers prolongs cardiac __________, action potential _________, and effective ________period

A

depolarization
duration
refractory

51
Q

What is the prodrug of Class III potassium blockers

A

Amiodarone

52
Q

Amiodarone exhibits what blockades

A

Na+, BB, and Ca+

53
Q

Amio has anti-anginal effects by ______coronary arteries and ______coronary blood flow

A

dilating; increasing

54
Q

Amio affects what classes

A

Class I, II, III, IV

55
Q

Amio treats

A

ventricular and atrial tachyarrhythmias

56
Q

Amio has both _____&____receptoor blockade, making it a negative ______& ______

A

alpha & beta (anti-adrenergic effects)
inotrope & vasodilation

prolongs QT

57
Q

Amio is ______, which is why it often needs a loading dose

A

lipophilic
(PO may take days to week)

58
Q

What is the active metabolite of Amio

A

Desmethylamiodarone
(slow effects and lingers)

59
Q

Dosage of Amio

A

Loading 150mg over 10min
Maintenance 1mg/min over 6hrs
0.5mg/min over 18hrs

60
Q

What are the side effects of Amio

A

Alveolar Pneumonitis
Pulm Edema
ARDS
HOTN
AV/SA node block
Decreased response to
catecholamines
Increases free O2 radicals=cellular destruction
Inhibits CYP450
Photosensitivity

61
Q

What are other Class III drugs

A

Sotalol
Ibutilide
Dofetilide

62
Q

Class III Potassium blockers Ibutilide and Dofetilide treat Afib/flutter with these side effects

A

Prolonged QT
Life-threatening V-arrhythmias
Torsades

63
Q

Sotalol, a Class III Potassium blocker treats_____&_____ tachyarrhythmias and is a _______beta blocker at low doses

A

Atrial & Ventricular

Non-selective

64
Q

Sotalol, a Class III potassium blocker has what side effects

A

Prolonged QT
Bradycardia
Torsades
Decreased MI Contractility
Delayed Conduction

65
Q

Class IV CCB MOA

A

Bind to and block Ca+ channels

Maintains inactivate/closed states

Inhibits slow inward Ca+ currents

Decreases/flatten slope of phase 0 and 4

slows conduction velocity

Prolongs repolarization in AV node

66
Q

Class IV CCB can be subdivided into

A

Dihydropyridines and non Dihydropyridines

67
Q

Non-dihydropyridines are

A

cardiac selective

68
Q

Non-dihydropyridines medications are

A

Diltiazem
Verapamil

69
Q

Non-dihydropyridines treat

A

SVT, VTs (reentry)
early/delayed afterdepolarizations

70
Q

CCB and BB should

A

NOT be administered together due too exaggerated effects

71
Q

What are the side effects of Class IV Non-dihydropyridines

A

negative inotropy (MI depression and decreased CO)

bradycardia

AV nodal block

Vasoodilation and HOTN

72
Q

Class I Na+ channel blockade can cause

A

reentry mechanism
v-tachyarrhythmias, wide-complex
common w/1C

73
Q

Class III Potassium can

A

Prolong repolarization, refractory, and QT interval

Torsades is Common!!

Exacerbated by hypokalemia/magnesemia

74
Q

Adenosine is made by our bodies by

A

breakdown of ATP

75
Q

Adenosine MOA

A

Stimulates cardiac A1 (adenosine) receptors, which increases K+ conductance (hyperpolarization) & inhibits L-type Ca+ influx in nodal cell

Decreases slope of phase 0 & 4

Decreases conduction velocity & automaticity

76
Q

Adenosine can treat

A

acute PSVT, WPW

77
Q

Additional actions of adenosine include

A

Stimulates vascular A2 adenosine receptors, which increases cAMP in smooth muscle and causes vasodilation

Also blocks NE release from presynaptic SNS terminals

increased cAMP has a negative effect on kinase

78
Q

What is the dosage of Adenosine

A

6mg IV initial
6mg or 12 mg IV after 3min
rapid flush 10-20 mL NS due to rapid transport into RBC (give close to heart)

79
Q

What are side effects of Adenosine

A

AV block (pause common)
Vasodilation (rapid arterial HOTN, flushing, HA)

80
Q

Digitalis Glycosides (Digoxin) is used to

A

Slow down atria arrythmias

81
Q

What is the MOA of Digoxin

A

Na/K/ATPase potent inhibitor

Reduced activity of Na/Ca+ exchanger

82
Q

Digoxin _____slope of phase 4 and _______slope of phase 0

Increases __________&__________

positive inotropy

A

increases; decreases

depolarization & automaticity

83
Q

Digoxin is used to treat_______inotropy in _______patient

A

increased; HF

84
Q

Digoxin treats_________ and is known to be a________

A

atrial tachyarrhythmias and HF

parasympathomimetic, which increases vagal activity, decreases SA firing and AV conduction (prolongs PR) and suppresses ectopic PMs

85
Q

Digoxin will show these ECG changes

A

ST depression
Shorter QT
Inverted T waves

86
Q

What are the therapeutic levels of digoxin

A

0.5-2ng/mL

87
Q

Digoxin uses what as a resivoir

A

muscle
may be floating around in the elderly

cleared by the kidney

88
Q

What are the toxic levels of digoxin

A

> 2-3 ng/mL
3.5ng/mL in PEDS

89
Q

What are the causes of dig toxicity

A

*Hypokalemia
Hypomagnesemia
Impaired renal function
Decreased muscle mass

90
Q

What are the early manifestation of digitalis toxicity

A

anorexia
N/V
trigeminal neuralgia

91
Q

What are the cardiac effects of digitalis toxicity

A

atrial & ventricular dysrhythmias
delayed AV conduction
*AT w/block
*VF most common cause of death

92
Q

What is the treatment of digitalis toxicity

A

treat underlying cause
lidocaine or class I for ventricular
atropine for excess vagal activity
propranolol or class II to
suppress increased
automaticity

93
Q

When would a patient need a pacemaker

94
Q

What is the ultimate treatment for digitalis toxicity

A

Digibind and Digifab: which decreases plasma concentration (antigen binding abx)

95
Q

What are the H&Ts of arrhythmias

A

HYPO/HYPERthermia
Hypovolemia
Tension PTX
Tamponade
Toxins/Drugs
Thromboembolism

96
Q

Atropine dose

97
Q

How to treat AFIB (ABCD)

A

Anticoag
BB
CCB/cardiovert
Digoxin

prevent w/procainamide

98
Q

How to treat SVT (ABC)

A

Adenosine
BB
CCB

(Mg sulfate, Class 1A or 1C III)

99
Q

How to treat PVCs

A

BB
Non-dihydropyridine CCB
Class I
Mg
Lidocaine

100
Q

How to treat Vtach/fib

A

Lidocaine
Amio
Mg
BB

tx polymorphic w/Mg

prevention w/amio and lidocaine

Anesthesia- Antiarrythmics (4 decks)

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