Anti-arrhythmic drugs Flashcards

1
Q

Flecanide

A
known to increase pacing thresholds
1c drugs (flecanide, proprafenone) need pacing lead threshold increased
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2
Q

Steroids

A

reduce pacing thresholds (on tips of some leads)

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3
Q

Class I drugs

A

Sodium channel blockers

Use dependent - Block enhanced at higher HR

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4
Q

Class III drugs

A

K channel blockers
Reverse use dependence - block at slower HR (keep in SR) - also causes inc’d QT prolongation - > causes torsades - tx with Mg,K+, if unstable DCCV (or temp overdrive pacing and IV isoproterenol - inc HR, dec QTc) - NO AMIO (inc’s QT)
Dronedarone
Dofetilide (not with HF or perm AF) - renally excreted
Sotolol - renally excreted

DO NOT USE WITH HF patients

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5
Q

Amiodarone

A

blocks P-450
- raises coumadin and NOAC levels in serum (blocks breakdown)
- raises INR of those on coumadin
better than lidocain survival of patient with out of hospital VF arrest vs vidocaine to hospital admission

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6
Q

Class Ic

A

Flecande - do not give with CAD/HF/structural heart dz
Propraneone
Contraindicated in HF/CAD

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7
Q

Dronedarone

A

contraindicated in severe HF(NYHA III/IV) or permanent afib

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8
Q

Class IV CCB

A

Non-dihydropyramines - verapamil, diltiazem

reduce contractility so DO NOT USE IN HF

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9
Q

Nifedipine

A

DO NOT USE IN STEMI

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10
Q

Dofetilide

A

inc’d QT when given with HCTZ,

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11
Q

Class 1a

A

Quinidine
Disopyramide
Procainamide - for pre-excited AF, unmask brugada - can cause lupus like syndrome

Use dependent - more effective at faster HR

Block mainly Na but also K+ (prolong QT)
Contraindicated in HF 2/2 neg ionotropy

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12
Q

Class 1c

A
Flecanide
Proprafenone
Na channel blockade
Prolong PR and QRS but no effect on QT
Use dependent - more effective at faster HR

Neg ionotropy - do not use with HFrEF or recent MI

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13
Q

Pill in pocket

A

Pharm cardioversion of recent onset AF <48hrs

  • initial rate control
  • single bolus of Class Ic antiarrythmic (flecanide 300 or proprafenone 450-600)
  • Class Ic drugs contraindicated with structural heart disease or conduction system dz (BBB)
  • or Class III (ibutilide, dofetide) - need to do in hospital because of QT prolong/TdP risk
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14
Q

Amiodarone

A

need loading because of large volume of distribution

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15
Q

Increased automaticity

A

abnormal phase 4 depolarization - initiates AP that can be provoked by ischemia, catechola, hypoxia

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16
Q

Triggered activity - happens after AP is triggered

A

afterdepolarization - secondary depolarizations after onset of AP
EAD - before membrane repolarizes - occur at slow rates when AP is prolonged (drugs cause AP prolongation?)
DAD - after membrane repolarizes - occurs at fast rates with rapid stimulation (ie catecholamines,excercise, dig tox, ischemia in RVOT VT/PVCs

initation of AP by after depolarization either at plateau of depolarization (early after depolariz) or when membrane repolarized (delayed after depolariza)

EAD - drugs that prolong AP - ie Ic/III, LQTS, drugs (more time for time and voltage dep recovery and opening of L type Ca channels to carry added depolarizing current) - phase 2 AP

DAD - intracellular Ca+ overload - dig tox, ischemia RVOT VT/VPCs/dig tox

17
Q

Re-entry

A

slow conduction and unidirectional conduction block
-AVNRT, AVRT, VT from scar (prior MI)
Fast circuit - Na+
Slow circuit Ca only or Na/Ca blend

18
Q

Decreased impulse formation

A

1) hyperpolarization of PPm cells - take longer to reach threshold to initiate AP (ie vagal tone hyperpolarizes SA node cells slowing rate of depolarization)
2) Reducing rate at which PPM cells depolarize and fire (hyperkalemia depolarizes SA node so it won’t fire)
3) Failure of PPM mechanism

19
Q

Abnormal impulse conduction

A

insufficient current reaching next cell to depolarize
1) uncoupled or poorly coupled gap junctions ie from MI or bad deploarizing mech - ie Na+/Ca2+ channels from MI
too much repolarizing current to overcome (adenosine)

Depression at SA node causes SA node exit block
at AV node causes 1st deg, 2nd deg, CHB
at prox purkinje AV block, BBB, hemiblock

20
Q

Dig toxicity

A

bidirectional VT - when dig combined with dronedarone - increases dig level - tx with digibind

21
Q

Class 1a Use dep

A

Quinidine, Disopyramide, Procainamide
Na+, IKr
Prolong QT
DO NOT USE IN HF (neg ionotropes)

Procainamide - tx of pre-excited WPW AF
Unmask brugada
s/e lupus like

22
Q

Class 1b Use dep

A

Lidocaine and mexilitene
Treat VT/VF
Lido - CNS tox
Lidocaine - affinity for ischemic myocardium

23
Q

Class 1c Use dep

A
Flecanide, Proprafenone
Prolong AP (PR/QRS)
little QT prolong
When treating AF - can organize into flutter -> 1:1 flutter -> need BB too
Widen QRS at high HR 2/2 Use dep - looks like VT

DO NOT USE WITH HF (neg ionotrope)

24
Q

Class III

A

Prolong QT by prolonging repolarization - susceptible to EAD (cell already kinda depolarized so ectopic beats can put over threshold -> TdP
r/o torsades

Sotolol - renally cleared - more QT prolonging in CKD - inc’d r/o torsades
Dofetilide
Dronedarone

25
Q

Things that decrease levels of NOACs/coumadin

A
P450 inducers (inc breakdown)
Phenytoin
St Johns wart
rifampin
carbamazepine
26
Q

Things that increase levels of NOACs/coumadin

A

protease inhibitor
amiodarone, dronedarone, verapamil
azoles
clarithromycin

27
Q

Warfarin levels high

A

NO BLEEDING
INR 4-10 - hold 1-2 doses
>10 - oral vit K

Bleeding
PCC
FFP
Plts

28
Q

Dronedarone

A

DO NOT USE with persistent AF or CHF

29
Q

Dofetilide

A

ONLY use with persistent AF