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Pharmo for medic school > Antidysrhythmics > Flashcards

Antidysrhythmics Flashcards

1
Q

Vaughn Williams 5 classes of antidysrhythmic

A 
Class I - Sodium channel
Class II - Beta blockers
Class III - Potassium channel blockers
Class IV - Calcium channel blockers
Class V - Other
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2
Q

Class I

A

Sodium channel blockers, decrease conduction velocity in atria, ventricles, perkinje

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3
Q

2 subtypes of class I agents

A

IA - Quinidine - delays repol
IB - lido - accelerates repol
(plus flecainide) IC - delays repol

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4
Q

Quinidine

A 
Class IA is the oldest and best studied class IA agent
Blocks sodium channels in heart, slows impulse conduction in AVH
Used for long term suppression of SVT, a-fib/flutter
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5
Q

AVP for this is

A

Atria ventricles and His/purkinje

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6
Q

Procainamide

A

Class IA, similar to quinidine, useful against broad spectrum of dysrhythmias
Used prehospital for stable Vtach

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7
Q

Drug slides

A

Put them all into one

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8
Q

Class IB

A

Differ from IA in 2 ways
Class IB accelerate repol
Class IB have little or no effect on the ECG

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9
Q

Lidocaine

A

IB, for ventricular dysrhythmias, not useful for SVTs at all

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10
Q

3 main effects of lido on the heart

A

Lido is IB
Slows conduction through AVH
Reduces automaticity in the ventricles and his-purkinje
Accelerates repol in ventricles

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11
Q

Class IC

A

Flecainide and propafenone, rarely used

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12
Q

Beta blockers

A

Class II
Reduces calcium influx into myocardial cells
Good for afib/flutter

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13
Q

Class III Potassium Channel Blockers

A

Delay repol of fast potentials, therefore the prolong action potential
Can also prolong QT

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14
Q

Ami

A

Class III (K+ blocker)
Main antidysrhythmic for VT/VF in a cardiac arrest
Delays repol, therefore QRS widening and prolongation of PR and QT are possible
May also produce dilation of coronary and peripheral blood vessels

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15
Q

Class IV

A 
Calcium Channel Blockers
Similar MOA to betablockers
Reduction in calcium influx into myocardial cells causes:
Slowing of SA node firing
Delay of AV node conduction
Reduction of myocardial contractility
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16
Q

Class IV (CCBs) on ECG

A 
Prolonged PRI
Rapid effects (within 2 minutes)
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17
Q

Class V

A

Others. Includes Adenosine which is drug of choice for terminating PSVT
2-10 second half life so give close to heart
Decreases automaticity in SA node and slows conduction through AV node as well

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18
Q

Class V more info

A

Doesn’t work on a fib, flutter or ventricular dysrhythmias

Only to be used in PSVT, including WPW

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19
Q

Sides of class V

A 
Bradycardia
Dyspnea
Hypotension
Facial flushing
Chest discomfort
Feeling like they're going to die
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20
Q

Dig

A

Class V, known as a cardiac glycoside
Derived from purple foxglove plant (digitalis purpurea)
Main uses are for heart failure pts and control of VF/VT and PSVT

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21
Q

Dig MOA

A

Suppresses dysrhythmias by decreasing conduction through AV and decreasing SA automaticity
Increases automaticity in purkinje fibers and has positive inotropic action
This drug can slow the heart rate and terminate dysrhymthias and improve myocardial contractility

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22
Q

Beta receptor MOA

A

B1 couple to calcium channels
B1 activates G protein and alpha subunit dissociates and activates adenylyl cyclase which converts ATP to cAMP
cAMP activates protein kinase which phosphorylates (in this case) calcium channel (enhances calcium entry)

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23
Q

Calcium by location

A

SA node increases rate
AV node increase conduction velocity
Myocardium increases force of contraction

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24
Q

Phase 0

A

Rapid depol. Influx of sodium

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25
Q

Fast action potentials go through

A

Muscle, and His-purkinje

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26
Q

Phase 1

A

Rapid (partial) repol. No relevance to antidysrhytmics

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27
Q

Phase 2

A

Prolonged plateau, membrane remains stable and calcium enters
Drugs that inhibit calcium do not effect cardiac rhythm, but do reduce contractility

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28
Q

Phase 3

A

Rapid repol. K+ leaves. Delay of repol prolongs action potential and prolongs effective refractory period (absolute) So delaying this extends minimal interval between responses
K+ channel blockers hit here

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29
Q

Phase 4

A

Membrane may remain stable or undergo spontaneous depol

Phase 4 gives cardiac cells automaticity. Makes potential pacemakers of all cells.

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30
Q

Slow potentials

A 
SA and AV node. 
Three distinct features
1) Phase 0 - depol is slow and mediated by calcium
2) these potentials conduct slowly
3) Phase 4 determines SA node rate
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31
Q

Phase 0 in slow action potentials

A

Differs significantly from fast. Caused by slow influx of calcium instead of rapid influx of sodium.
Drugs that inhibit calcium can slop or stop AV conduction

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32
Q

Phase 2 and 3 slow potentials

A

Lack a phase 1. Not significantly different in regard to antidysrhythmics

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33
Q

Phase 4 slow

A

Beta blocks and CCBs can suppress depol in phase 4 and decrease automaticity of SA node

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34
Q

Reentry

A

One way conduction block of purkinje fiber so impulse can travel back up as it didn’t depol (doesn’t enter an absolute refractory state)

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35
Q

Two way drugs can stop a reentry

A

Can improve conduction in a sick branch eliminating block or suppress conduction creating a two way block

36
Q

Class I

A

Sodium channel blockers

Slows impulse in atria, ventricles, and His-Purkinje system

37
Q

Class II

A

Beta blockers, reduce calcium entry
Reduce SA automaticity
Slow AV conduction
Reduce atrial and ventricluar contractility

38
Q

Class III

A

K+ blockers delay repol of fast potentials. Prolong action potential and effective refractory period

39
Q

Class IV

A 
Calcium channel blockers
Only verapamil and Diltiazem
Nearly identical effects to class II
40
Q

Class V

A

Adenosine and dig

41
Q

QT prolonging drugs are

A

Class IA and class III

42
Q

PVCs

A

Benign, in presense of acute MI, betablocker is drug of choice

43
Q

SVT tx

A

Valsalva, beta blockers or CCB

Amiodarone

44
Q

V tach

A

Amiodarone, lido, procainamide

45
Q

Class I

A 
All block sodium
IA delay repol
IB accelerate repol
IC have pronounced prodysrhytmic actions
Similar in action and structure to local anesthetics (and lido is both)
46
Q

IA

A

Delay repol (plus Na+ block)

47
Q

Class IB

A

Accelerate repol (plus block Na+)

48
Q

Quinidine is a class

A

IA

49
Q

Quinidine

A

Slows impulse to atria ventricles and His-purkinje. Delays repol by blocking K+ as well
Strongly anticholinergic and blocks vagal input to heart
Pts usually given dig, verapamil or beta blockers too

50
Q

Quinidine and the ECG

A 
Slows depol so widens QRS
Prolongs QT (by delaying repol)
51
Q

Quinidine is used for

A

SVT and ventricular dysrhytmias. Usually used for long term tx of SVT, a fib/flutter and sustained ventricular tachycardias
Usually need AV blocker with it
Also treats malaria (and has antipyretic properties)

52
Q

Quinidine adverse effects

A

Diarrhea
Cinchonism (tinnitus, headache, nausea, vertigo, disturbed vision)
Cardiotoxicity (sinus arrest, AV block, vtach/fib, asystole) secondary to increased automaticity of purkinje fibers and reduce conduction
Alpa blockade (hypotension)

53
Q

Procainamide

A

Class IA
Blocks sodium channels decreasing conduction velocity in atria, ventricles and His-purkinje and delays repol
Less antichol
Widening of QRS and prolongs QT as well
Can’t use long term as 70% get lupus like symptoms (antibodies that attack their own nucleotides)

54
Q

Class IB

A

Block sodium AND accerlarate repol. Have little to no effect on ECG
Lido

55
Q

Lidocaine

A

Class IB
Only for ventricular dysrhythmias
Slows conduction in atria, ventricles and His-purk
Reduces automaticty in ventricles and His-purk
Shortens action potential and ERP (absolute refract)
No antichol properties
No QRS widening, possibly small reduction in QT interval
Used only against ventricular dysrhytmias
Drowsiness, paresthesias, seziures and resp arrest

56
Q

Phenytoin for the heart (dilantin)

A

Reduces automaticity in ventricles. No effect on ECG. INCREASES AV node conduction (unique)
Sedation, ataxia, gingival hyperplasia

57
Q

Phenytoin in the heart is used for

A

Dig induced dysrhythmias and acute or chronic supppresion of ventricular dysrhythmias

58
Q

Class IC

A

Flecainine, propafenone
Block sodium channels in atria ventricles His-purk. Delay repol and small increase in refract period. Can exacerbate or cause new dysrhythmias

59
Q

Propranolol

A

Non-selective beta adrenergic blocker (also effects bronchi)
Decreased automaticity of SA node
Decreased velocity through AV node
Decreased myocardial contractility
Reduction in AV conduction translates to prolonged PRI

60
Q

Propranolol used for

A

Excessive sympathetic stim. Sinus tach, severe recurrent ventricular tach, excerise-induced tach and paroxysmal atrial tach from emotional or exercise
It both slows SA and reduces ventricular rate through decreased AV node impulses

61
Q

Adverse effects of propranolol

A

Heart failure, sinus arrest, AV block, hypotension secondary to decreased CO, worsening of asthma

62
Q

Class III

A 
Amio
Dronedarone
Dofeltiide
ibultitide
SOlatol (also a BB)
63
Q

Amiodarone

A

Good for atrial and ventricular dysrhythmias
Lung damage and visual impairment are common so only for life threatening
Works on afib, vtach, vfib

64
Q

Ami ECG

A

Delays repol, prolongs action potential
Reduces automaticity in SA node, reduces contractility, reduced velocity in AV node and His-purk secondary to block of sodium calcium and beta receptors

65
Q

Ami adverse effects

A

Half life of 25-110 days
Pulmonary tox
Cardiotox - dysrhytmias plus SA and AV blocks and HF
Thyroid tox
Liver tox
Eye effects
Dermatologic tox - UV rays can turn skin bluish grey

66
Q

Ami ECG

A

Primarily effects AV if given IV. Probably from antiandrenergic reactions

67
Q

Class IV

A 
Only verapamil and Diltiazem block calcium channels in the heart
Slows SA node automaticity
Delay AV conduction
Reduces myocardial contractiltiy
Identical effects to beta blockers
68
Q

Adenosine

A

For PSVT
Decreases automaticity in SA node and greatly slows conduction in AV. Prolongs PRI
Inhibits cAMP induced calcium influx

69
Q

Adenosine for

A

PSVT including WPW. Does nothing against afib/flutter or ventricular dysrhythmias
1.5-10 second half life
Since methylxanthines block adenosine receptors people on them may need bigger doses and it may not work

70
Q

Dig on the heart

A

Decreases conduction through AV node and decreases automaticity of SA node.
Increases vagal impulse to AV node.
Decreases sympa to SA and increases parasympa to SA
Can increase automaticity in purkinje fibers, partly the reason it causes dysrhythmias
Prolong PRI
Shortened QT
ST depression T wave depressed or inverted

71
Q

Procainamide used for

A

Long term suppression of SVT a fib a flutter

Or stable V tach

72
Q

Contras to procain

A

hypersens
2nd/3rd degree block
Torsades

73
Q

Procainamide dose

A

20-50mg/min max 17mg/kg

74
Q

Stop use of procain

A

Hypotension
QRS widening 50%
Arrythmia resolves
Hit max dose (17mg/kg)

75
Q

Lido (xylocaine) indications

A

Stable V tach
V tach
V fib

76
Q

Contras to lido

A

Hypersens

Any type of AV block

77
Q

Lido dose

A

VF/VT 1.0-1.5mg/kg IVP repeat at 0.5-0.75mg/kg max 3mg/kg

Stable v tach same dose but SIVP instead, repeat in 10-15 minutes

78
Q

Ami (cordarone) indications

A

VF/Pulselss VT

VT with a pulse

79
Q

Ami contras

A

Hypersense
2nd/3rd degree block
Acute hepatitis (not cardiac arrest)
Thyroid dysfunction (not cardiac arrest)

80
Q

Ami dose

A

300mg IV 1 5 max 450

If a pulse 150mg in 250 of D5W over 10 minutes with a 10gtt at 4 drops/second

81
Q

Class 5 expect

A

Bradycardia, dyspnea, hypotension, facial flushing, chest discomfort.

82
Q

Adenosine indications

A

PSVT with WPW

83
Q

Contras to adenosine

A 
Hypersens
2nd/3rd degree AV block
Sick sinus
bradycardia
Afib/flutter
Bronchospasm 
Pts taking carbmazepine, dipyridamole
84
Q

Dig indications

A

Rapid afib/flutter or PSVT

Contras are hypersens or dig tox

85
Q

Dig dose

A

10-15mcg/kg SIVP

86
Q

Mag contras

A

Heart block/renal failure

87
Q

Mag dose

A

2G IV

2G IV over 5 min in PMVT

Pharmo for medic school (26 decks)

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