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Cardio 2 > anti-arrythmics > Flashcards

anti-arrythmics Flashcards

1
Q

class Ia NaCh Blockers

A

Double Quarter Pounder
disopyramide
quinidine
procainamide

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2
Q

class Ib NaCh blockers

A

lettuce, tomato, mayo
lidocaine
tocainide
mexiletine

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3
Q

class Ic NaCh blockers

A

more fries please
moricizine
Flecainide
propafenone

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4
Q

class II beta blockers

A

esmolol
metoprolol
propranolol

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5
Q

class III KCh blockers

A 
a big dog is scary 
amidarone
bretylium
dofetilide
ibutilide
sotalol
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6
Q

class IV CCBs

A

verapamil

diltiazem

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7
Q

other ACLS drugs

A 
adenosine
atropine
MgSO4
anticoagluants
digoxin
naloxone
vasopressors
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8
Q

vassopressors

A

Epi
NE
vasopressin
dopamine

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9
Q

Na concentrations

A

intracellular 5-15

extracellular 135-142

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10
Q

K concentrations

A

intracelluarl 135-140

extracellular 3-5

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11
Q

factors which may precipitate or exacerbate an arrythmia

A

ischemia, hypoxia, acidosis, alkalosis, electrolyte abnormalities, excessive catecholamine exposure, autonomic influences, durg toxicity, over stretching of cardiac fiber

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12
Q

duration of diastolic interval

A

determined by slope of phase 4

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13
Q

early after depolarizations

A

transient deplarization that interrupts phase 3

exacerbated at slow heart rates contributes to long QT

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14
Q

delayed afterdepolarization

A

interrupts phase 4
often occurs when intracellular Ca is increased
exacerbated by fast HR
responsible for some arrhytmias related to excess digitalis, catecholamines, and myocardial ischemia

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15
Q

abnormal impulse conduction: severe depressed conduction

A

may result in simple block (AV, bundle branch)

b/c parasympathetic control of AC conduction is significant partial AV block sometimes relieved by atropine

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16
Q

abnormal impulse conduction: reentry

A

impulse reenters and excited areas of heart more then once
3 conditions:
-must be obstacle, thus establishing a circuit
-must be unidirectional
-conduction time must be long enough that retrograde impluse does not encounter refractory period

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17
Q

depress autonomic properties of abnormal pacemaker cell

A

decrease slope of phase 4 and/or elevate threshold potential

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18
Q

alter conduction characteristics of pathways of reentry - facilitate conduction

A

(shorten refractoriness) of area of unidirectional block -> anterograde conduction can proceed

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19
Q

-depress conduction

A

(prolong refractoriness) in area of unidirectional block or in pathway w/slowed conduction and short refractory period -> retrograde propagation of impluse no permitted causing bidirectional block

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20
Q

type I

A

NaCh Blockers

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21
Q

Ia

A

prolong action potential duration, dissociate from channel w/intermediate kinetics

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22
Q

Ia effects

A
  • decrease conduction velocity
  • increase refractoriness
  • decrease autonomic properties of Na dependent conduction
  • unidirectional block transformed to bidirectional
  • some K blocking properties
  • effective in supraventricular and ventricular arrhythmias
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23
Q

Ib

A

shorten AP duration in some tissues in heart and dissociate rapidly

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24
Q

Ib effects

A

decrease refractoriness w/no effect on conduction velocity -> improces anterograde conduction, eliminating area of unidirectional block
in diseased tissue refractoriness prolonged leading to bidirectional block
clinically effective in ventricular arrhythmias > suprventricular

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25
Ic
minimal effects on AP duration and dissociate slowly
26
Ic effects
profoundly decreased conduction velocity while leaving refractoriness theroretically eliminate reentry by slowing conduction to point where impulse is extinguished clinically effective in supraventricular and ventricular arrhythmias, but ventricular limited due to risk of proarrhythmias
27
II
``` sympatholytic beta blockers decrease conduction velocity increase refractoriness decrease automaticity in nodal tissues anti-adrenergic actions ```
28
III
KCh blockers prolong AP duration prolong refractoriness in atrial and ventricular tissues delay repolarization by blocking KChs
29
IV
CCBs slows conduction where AP dependent on Ca (SA and AV nodes) decreases conduction, increases refractoriness, decreases automacity in Ca dependent tissues
30
procainamide
Ia slows upstroke of AP, slows conduction, prolongs QRS, prolongs APD (due to some KCh block), direct depressant effects on SA and AV nodes
31
procainamide extracardiac effects
ganglion blocking -> decreased TPR -> hypotension
32
procainamide toxicity
``` excessive prolongation induction of TdP new arrythmias reversible lupus like syndrome nausea, diarrhea rash, fever, hepatits, agranulocytosis ```
33
procainamide dosage
IV, IM, PO | reduction required in renal failure
34
NAPA
``` metabolite of procainamide had class III activity associated w/ TdP especially in renal failure ```
35
uses of procainamide
atrial and ventricular arrythmias | long term therapy avoided
36
quinidine
Ia like procainamide can cause GI issues, headache, dizziness, tinnitus, rare immunologic rxns rarely used
37
disopyramide
Ia much more pronounced antimuscarinic effects, (should beadministered w/drug that slows AV conduction) precipitates HF, urinary retention, dry mouth, blurred vision, constipation
38
lidocaine
blocks activated and inactivated NaChs w/rapid kinetics
39
lidocaine toxicity
least cardiotoxic of NaCh blockers SA node arrest, worsening of imparied conduction, ventricular arrhythmias uncommon large does -> hypotension most common- neurologic (parasthesias, tremors, nausea, hearing, speech, convulsions) dose related
40
use of lidocaine
termination of ventircular tachycardia and prevention of V fib after cardioversion in setting of acute ischemia
41
mexiletine
orally active congener of lidocaine also has neuro side effects used for ventirucalr arrythmias, off label use for chronic pain
42
flecainide
potent blocker of Na and KChs but does not prolong AP or OT interval
43
flecainide toxicity
severe exacerbation of arrhythmia in patients w/preexisting Vtach or previous MI
44
flecainide uses
supraventricular arrythmias
45
propafenone
similar to Flecainide, but wea beta-blocking activity, does not porlong AP
46
propafenone toxicity
metallic taste, constipation, arrhythmia exacerbation
47
propafenone uses
supraventircular arrythmias
48
amiodarone
markedly prolongs AP and OT interval by blocking Ikr chronic uses -> Iks blockage also blocks NaChs, weak adrenergic and CCB activity
49
amiodarone extracardiac effects
peripheral vasodilation
50
amiodarone toxicity
symptomatic bradycardia heart block in preexisting sinus of AV node disease accumulates in heart, lung, liver, skin, and concentrates in tears pulmonary toxicity, fetal pulmonary fibrosis, skin and corneal lesions, may cause hypo or hyperthyroidism
51
amiodarone PK
after discontinuation affects may last 1-3 months | many drugs interactions ) increases statins, digoxin, and warfarin levels)
52
use of amiodarone
Afib, prevention of recurrent Vtach, not associated w/increased mortality in CAD or HF, used as adjunct w/ICD
53
dronedarone
analog of amiodarone w/iodine removed to eliminate thyroid adverse effects works on Ikr, Iks, Ica, Ina, and beta Rs
54
dronedarone toxicity
black box warning against use in acute decompensated or advanced (class IV) HF
55
dronedarone uses
Afib
56
sotalol
both beat blocking and AP prolonging actions L-isomer- beta blocker (not cardioselective) D and L isomers prolong AP
57
sotalol toxicity
dose related incidence of TdP | further depression of LV function in patients w/HF
58
uses of sotalol
life-threatening ventricualr arrhythmias, maintenance of sinus rythem in Afib, supraventriuclar and ventriucalr arrhythmias in peds
59
dofetilide
dose-dependent blockage of rapid component of delayed rectifier K current increasing hypokalemia slow recovery from blockade
60
dofetilide toxicity
OT prolongation and risk of ventricular arrythmias
61
dofetilide relative contraaindications
OTc> 450ms bradycardia <50bpm hypokalemia
62
uses of dofetilide
maintencance of NSR is Afib and restoring NSR in Afib
63
verapamil
blocks both activated and inactivated L-type CaChs effect more marked in tissues that fire frequently, those that are less completely polarized at rest, and those in which actiation depends exclusively on Ca current (SA&AV nodes) AV node conduction and effective refractory period prolonges SA node conduction dlowed, but hypotensive action may result in reflex increase in SA node suppresses both early and delayed after depolarizations
64
extracardiac effects of verapamil
peripheral vasodilation
65
verapamil toxicity
hypotension and Vfib if IV in Vtach misdiagnosed as supraventricular tachycardia can induce AV blcok constipation, lassitude, nervousness, peripheral edema
66
verapamil uses
supraventricular tachycardia, Afib, Aflutter angina, HTN
67
diltiazem toxicity
edema and headache | AV block, bradycardia, hypotension
68
uses of diltiazem
supraventricualr tachycardia, angina, HTN
69
adenosine
activates inward rectifying K current and blocks Ca current -> marked hyperpolarization inhibits AV node conduction and increases refractory period
70
adenosine toxicity
``` flushing SOB chest burnign high grade AV block Afib headache hypotension nausea paresthesias ```
71
uses of adenosine
drug of choice for conversion of paroxysmal supraventricular tachycardia
72
atropine
blocks actions of Ach at parasympathetic sites increasing CO
73
atropine toxicity
arrhythmias, tachycardia, dizziness, constipation, urinary retention
74
atropine uses
bradycardia, neuromucular blockade reversal, cholinergic poisoning
75
magnesium
may influence Na/K ATPase, NaChs, KChs, CaChs, | anti-arrhythmic effects in patients w/normal Mg levels
76
uses of Mg
digitalis induced arrhythmias if hypomagnesemia present | TdP even in Mg normal

Cardio 2 (17 decks)

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