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anti arrhythmic Flashcards

1
Q

two gradients that influence energy requiring pumps

A

130-140 Na (high outside)

3.5-5 K

gradient

also creates electrical differential

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2
Q

two types of gates in the sodium channel

A

activation M

and inactivation h

inactivation contributes to the early repolorization of phase 1

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3
Q

inactivation gate is closed at what resting potential

A

-75– -55
but the activation gates are opened

this is important because during the activation

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4
Q

which nodes are more Ca dependent

A

SA and AV
more Ca dependent because of funny channel

no the non-dihydropyridine work here

(CLASS IV)

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5
Q

CLASS I arrhythmicss are

A

Na channel blockers

characterized by their ability to block these entry potins into the cell during depolarization

and decrease the rise of phase 0

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6
Q

no phase 1 or 2 in what AP

A

OF the pacemaker cells

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7
Q

how do cardiac muscle cells differ

A

resting membrane potential is at -90 due to constant leak of K

Na rushese in causing rapid depolarization

then K channels open (voltage gated)
leading to small dip that is phase 1

positive K ions leave and Ca go in
cause plateau of phase 2

then rapid depolarization of phase 3 of K leaving

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8
Q

abnormal automaticity

A

increased permeability to Na in phase 4

triggered activity
normal leakage of Ca ions that causes after dopolorization

and

rentry

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9
Q

This class of drugs slow the rate of rise of phase 0 and prolong the effective refractory period of the ventricle

A

Class 1a

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10
Q

these drugs shorten action potential duration and refractory period of purkinje fibers

A

1B

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11
Q

IC drugs work by

A

having the greates effect on the early depolarization and have less of an effect on the refractory period of ventricle

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12
Q

Class 1A 1B and 1C drugs

A

Class IA = Disopyramide, Quinidine, and Procainamide

Class IB = Lidocaine and Mexiletine

Class IC = Flecainide and Propafenone

Double Quarter Pounder
Lettece Mayo
Fries Please

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13
Q

class II drugs

A

LOL

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14
Q

class III drugs

A 
AIDS
A = amiodarone
 I = ibutilide
 D = dofetilide
 S = Sotalol
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15
Q

Class IV

A

• Class IV Antiarrhythmics are the

calcium channel blockers verapamil and diltiazem.

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16
Q

hyperkalemia effects

A

increases in serum K can depolarize the resting membrane potential

can inactivate Na channels resulting in increased refractory period duration and slowed impulse propagation

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17
Q

elevated potassium

A

slows a pacemaker

euthanasia
high doses dead

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18
Q

hypokalemia

A

make a pacemaker worse

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19
Q

inactivation gates close

A

-75 and -55
-55
and stimulation will have less Na here

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20
Q

what exacerbates arrhythmia

A 
ischemia
hypoxia
acidosis
electrolyte abnormalities 
excessive catecholamine
drug toxicity 
overstretching of cardiac tissue
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21
Q

MOA of procaniamide

A

blocks Na
prolongs QRS
increases refractory period
slow upstroke

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22
Q

procainamide can only be given ___ for

A

IV
WBW
VT

Afibb with others to slow HR

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23
Q

these drugs are used for rate control

A

digoxin
BB
CCB

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24
Q

when we talk about rhythm control

A

we are talking about turning quivering into normal depolarization

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25
why can't you use CCB with HFrEF
increase contractility can only use BB or digoxin
26
anticholinergic effect of 1a is concerning
because it can increase the rate has vagolytic effects this is why they need to be used in conjunction with rate control
27
AE of procainamide
``` hypotension lupus like depression agranulocytosis PROLONGS QT ```
28
quinidine SE
tinnitius | HA
29
disopyramide ADE
very strong anticholinergic effects can cause sxs like urinary retention can worsen HF
30
lidocaine is used for these three events
VENTRICULAR ARRHYTHMIAS ONLY: PVC VT VF or post MI binds to both activated and inactivated greater suppression in the tissues and long acting
31
need to reduce lidocaine in
liver failure and HF
32
lidocaine SE
seizures | CNS effects: drowsiness or aggitation
33
mexiletine is used
orally instead of topically or IV like lidocaine more GI
34
propafenone SE
also has some BB effect so you need to be worried about bronchospasms CAN'T USE IN HF
35
main effect of amiodarone
increasing APD (prolongs re-polorization through Na channel blockade) BB and Ca channel blockade so can be used for rate and rhythm
36
what do we need to monitor with amiodarone
TSH can cause hypo hyperthyriod CXR: pulmonary fibrosis hepatotox: LFTs
37
like procainamide (except no ganglion blockade
quinidine
38
SE of quinidine
``` •cinchonism: HA, vertigo, tinnitus (can decrease hearing) altered color >5mcg •hypotension •hypersensitivity, diarrhea, nausea •Prolongs QT (Torsades risk) ```
39
quinidine adjustments needed with
Liver (80%) and renal. Reduce dose renal failure, liver dysfunction, HF.
40
* shortens AP, shortens refractory period * blocks activated and inactivated Na channels w/ rapid kinetics (the inactivated Na channel block ensures greater effect on Purkinje cells)
lidocaine
41
Active ventric AR only. Can use in HF but high dose may cause hypotension.
lidocaine
42
need normal heart inorder to take these medications
1C | think baby needs normal heart
43
how to BB (propanolol, atenolol, metoprolol) Work to slow HR
decrease phase 4 and increase PR
44
why can BB cause AV block
prolonged PR
45
SE of BB
bronchospasm, masks hypoglycemia in DM
46
when would you use a BB
rate control afib SVT ST OF VT Post MI!!!! post-op afib rate control
47
why can't you use propafenone in HF
negative inotropic effect will increase mortality in pts who have HF or MI
48
propafenone DDI
DI ritonovir and digoxin as well as other drugs that prolong QT
49
IV BB that is short acting
esmolol
50
amidarone PK
good oral absorption binds to a lot of tissues absorption is anywhere from 22-86% gigantic Vd 1/2life is 40-113 days steady state 200 days
51
most troubling SE of amiodarone
pulmonary fibrosis and inflammation will start with cough and shortness of breath need CXR at baseline
52
other than pulmonary fibrosis what do we worry about SE wise with amiodarone
photosens, blue-grey skin (permanent) * corneal microdeposits (halos around lights at night) * hypo/er thyroid: monitor TSHq6mos. HAS IODINE * hepatotoxic: monitor LFTs q6mos (dc or dec dose if LFTs 3x ULN or 2x baseline). Risk of fulminant liver failure. * pulm inflamm and fibrosis: do CXR and PFTs d6mos. Inquire about any new cough/dyspnea. Mortality 10%. May need steroids * Severe brady (CCB and BB effect) * Exacerbation ventricular ar (not as common as Class I agents) * Hypotension, phlebitis (IV >3mg/mL) neurological: paresthesias, tremor, ataxia, HA
53
DDI withamiodarone
increase dig levels warfarin: need to reduce dose increased risk of torsades with other prolonged QT: phenothiazines, FQ ritonavir: large increases in serum amiodarone concentrations
54
how often do you need to check LFTs for amiodarone
every 6 months don't forget to check TSH too
55
dronedarone used
limited nonpermanent afib and flutter as well as rhythm control in structural heart dz does not help with permanent HF or afib
56
SE of dronedarone
similar to amiodarone but with less risls still prolongs QTs brady arrhythmias
57
Betablocker with class III properties
sotolol
58
Sotolol compare anc contrast to regular BB as far as SE go
pro arrythmic effect but ortherwise same SE will lower bP
59
ibutilide is different that the other class III
does not affect K
60
ibutilide would be seen
in hosp
61
dofetilide mOA
block k current conversion and maintenance of NSR
62
dofetilide
HA main one can also be seen with dyspnea
63
can use this K blocking drug in HF
doetilide
64
You can not use these antiarrythmics in HF
disopyramide (1a) properafone (Ia) flecainaid (Ia) dronedarone (III) sotalol (III) Verapamil (IV) dilitiazem (IV)
65
which class III can you use in HF
amiodarone dofetilide maybe ibutilide but that is used in the hospital
66
adenosine receptors are in the
AV node
67
digoxin works by
inhibiting Na/k pump | positive inotrope
68
adenosine use
emergency rate controls SVT reentry not good for converting afibb or a flutter SUPER SHORT HALF LIFE
69
adenosine AE
facial flushing SOB can mimic angina
70
Mg is used for
torssades and digoxin arrythmias
71
Vasopressin
potent vasoconstrictor
72
atropine
anticholinergic so it is used for bradycardia
73
dopamine
can increase HR and positive inotropic effect
74
isoproterenol
B1 and B2 agonist may cause tachycardia
75
POST MI these two drugs have been shown to reduce arrhythmic death and improve survival
amiodarone and BB
76
HF seen as sudden cardiac arrest or sustain VT is best treated with
ICD amiodarone sotalol or mexilitine
77
AFIBB Rate control tx
for most casses can use BB or CCB except in LV dysfunction or HF then use BB or dig "][p-09
78
negative inotropic
1c AND SOTALOL
79
which classes are proarrythmis
1B 1c III
80
which drugs are CI in ptrs w/ prolonged QT
phase 3

Pharm II (16 decks)

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