Anti-arrhythmic drugs

Question 1

Flecanide

Answer 1

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

Question 2

Steroids

Answer 2

reduce pacing thresholds (on tips of some leads)

Question 3

Class I drugs

Answer 3

Sodium channel blockers

Use dependent - Block enhanced at higher HR

Question 4

Class III drugs

Answer 4

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

Question 5

Amiodarone

Answer 5

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

Question 6

Class Ic

Answer 6

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

Question 7

Dronedarone

Answer 7

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

Question 8

Class IV CCB

Answer 8

Non-dihydropyramines - verapamil, diltiazem

reduce contractility so DO NOT USE IN HF

Question 9

Nifedipine

Answer 9

DO NOT USE IN STEMI

Question 10

Dofetilide

Answer 10

inc’d QT when given with HCTZ,

Question 11

Class 1a

Answer 11

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

Question 12

Class 1c

Answer 12

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

Question 13

Pill in pocket

Answer 13

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

Question 14

Amiodarone

Answer 14

need loading because of large volume of distribution

Question 15

Increased automaticity

Answer 15

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

Question 16

Triggered activity - happens after AP is triggered

Answer 16

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

Question 17

Re-entry

Answer 17

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

Question 18

Decreased impulse formation

Answer 18

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

Question 19

Abnormal impulse conduction

Answer 19

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

Question 20

Dig toxicity

Answer 20

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

Question 21

Class 1a Use dep

Answer 21

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

Question 22

Class 1b Use dep

Answer 22

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

Question 23

Class 1c Use dep

Answer 23

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)

Question 24

Class III

Answer 24

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

Question 25

Things that decrease levels of NOACs/coumadin

Answer 25

``` P450 inducers (inc breakdown) Phenytoin St Johns wart rifampin carbamazepine ```

Question 26

Things that increase levels of NOACs/coumadin

Answer 26

protease inhibitor amiodarone, dronedarone, verapamil azoles clarithromycin

Question 27

Warfarin levels high

Answer 27

NO BLEEDING INR 4-10 - hold 1-2 doses >10 - oral vit K Bleeding PCC FFP Plts

Question 28

Dronedarone

Answer 28

DO NOT USE with persistent AF or CHF

Question 29

Dofetilide

Answer 29

ONLY use with persistent AF