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Pharmo for medic school > Antidysrhythmics > Flashcards

Antidysrhythmics Flashcards

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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
Fast action potentials go through
Muscle, and His-purkinje
26
Phase 1
Rapid (partial) repol. No relevance to antidysrhytmics
27
Phase 2
Prolonged plateau, membrane remains stable and calcium enters Drugs that inhibit calcium do not effect cardiac rhythm, but do reduce contractility
28
Phase 3
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
29
Phase 4
Membrane may remain stable or undergo spontaneous depol | Phase 4 gives cardiac cells automaticity. Makes potential pacemakers of all cells.
30
Slow potentials
``` 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 ```
31
Phase 0 in slow action potentials
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
32
Phase 2 and 3 slow potentials
Lack a phase 1. Not significantly different in regard to antidysrhythmics
33
Phase 4 slow
Beta blocks and CCBs can suppress depol in phase 4 and decrease automaticity of SA node
34
Reentry
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)
35
Two way drugs can stop a reentry
Can improve conduction in a sick branch eliminating block or suppress conduction creating a two way block
36
Class I
Sodium channel blockers | Slows impulse in atria, ventricles, and His-Purkinje system
37
Class II
Beta blockers, reduce calcium entry Reduce SA automaticity Slow AV conduction Reduce atrial and ventricluar contractility
38
Class III
K+ blockers delay repol of fast potentials. Prolong action potential and effective refractory period
39
Class IV
``` Calcium channel blockers Only verapamil and Diltiazem Nearly identical effects to class II ```
40
Class V
Adenosine and dig
41
QT prolonging drugs are
Class IA and class III
42
PVCs
Benign, in presense of acute MI, betablocker is drug of choice
43
SVT tx
Valsalva, beta blockers or CCB | Amiodarone
44
V tach
Amiodarone, lido, procainamide
45
Class I
``` 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
IA
Delay repol (plus Na+ block)
47
Class IB
Accelerate repol (plus block Na+)
48
Quinidine is a class
IA
49
Quinidine
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
Quinidine and the ECG
``` Slows depol so widens QRS Prolongs QT (by delaying repol) ```
51
Quinidine is used for
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
Quinidine adverse effects
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
Procainamide
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
Class IB
Block sodium AND accerlarate repol. Have little to no effect on ECG Lido
55
Lidocaine
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
Phenytoin for the heart (dilantin)
Reduces automaticity in ventricles. No effect on ECG. INCREASES AV node conduction (unique) Sedation, ataxia, gingival hyperplasia
57
Phenytoin in the heart is used for
Dig induced dysrhythmias and acute or chronic supppresion of ventricular dysrhythmias
58
Class IC
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
Propranolol
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
Propranolol used for
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
Adverse effects of propranolol
Heart failure, sinus arrest, AV block, hypotension secondary to decreased CO, worsening of asthma
62
Class III
``` Amio Dronedarone Dofeltiide ibultitide SOlatol (also a BB) ```
63
Amiodarone
Good for atrial and ventricular dysrhythmias Lung damage and visual impairment are common so only for life threatening Works on afib, vtach, vfib
64
Ami ECG
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
Ami adverse effects
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
Ami ECG
Primarily effects AV if given IV. Probably from antiandrenergic reactions
67
Class IV
``` 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
Adenosine
For PSVT Decreases automaticity in SA node and greatly slows conduction in AV. Prolongs PRI Inhibits cAMP induced calcium influx
69
Adenosine for
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
Dig on the heart
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
Procainamide used for
Long term suppression of SVT a fib a flutter | Or stable V tach
72
Contras to procain
hypersens 2nd/3rd degree block Torsades
73
Procainamide dose
20-50mg/min max 17mg/kg
74
Stop use of procain
Hypotension QRS widening 50% Arrythmia resolves Hit max dose (17mg/kg)
75
Lido (xylocaine) indications
Stable V tach V tach V fib
76
Contras to lido
Hypersens | Any type of AV block
77
Lido dose
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
Ami (cordarone) indications
VF/Pulselss VT | VT with a pulse
79
Ami contras
Hypersense 2nd/3rd degree block Acute hepatitis (not cardiac arrest) Thyroid dysfunction (not cardiac arrest)
80
Ami dose
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
Class 5 expect
Bradycardia, dyspnea, hypotension, facial flushing, chest discomfort.
82
Adenosine indications
PSVT with WPW
83
Contras to adenosine
``` Hypersens 2nd/3rd degree AV block Sick sinus bradycardia Afib/flutter Bronchospasm Pts taking carbmazepine, dipyridamole ```
84
Dig indications
Rapid afib/flutter or PSVT | Contras are hypersens or dig tox
85
Dig dose
10-15mcg/kg SIVP
86
Mag contras
Heart block/renal failure
87
Mag dose
2G IV | 2G IV over 5 min in PMVT

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