Anti-Arrhythmics Flashcards

1
Q

Class 1B

A

VT

  • lidocaine - POST MI
  • mexiletine - LONG QT

UP K+ out = shorter AP duration

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2
Q

Class 1C

A

VT»>SVT

  • Flecainide =
  • IF NO HX OF ISCHEMIC DZ
  • RHYTHM CONTROL

STRONG Phase 0 block
NO POST MI
ATAXIA S.E>.

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3
Q

Class 1A

A

VT»>SVT (RHYTHM CONTROL)

  • Quinidine = SUPPRESS AFIB (W/ BB/CCB)
  • Procainamide
  • Disopyramide

DOWN K+ out = AP duration longer
S.E = anticholinergic (quinidine more), Torsades de Pointe (long QT), lupus-like syndr, IN HOSPITAL ONLY

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4
Q

Class 3

A

K+
VT + SVT
*amiodarone, dronedarone
*Sotalol, ibutalide

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5
Q

Class 4

A

Ca2+ block in AV node(L type) (rate control)
SVT
*verapamil
*Diltiazem

  • slow pacemaker current
  • slow conduction velocity
  • longer ERP

Careful CHF = less cardio muscle contract

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6
Q

Class 2

A

Beta (rate control)

SVT
*metoprolol

  • DOWN AV NODE conduction
  • DOWN excitability (ectopic pace)

Post MI reduce mortality

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7
Q

Other

A

SVT

  • digoxin
  • adenosine
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8
Q

Interfere with Na+ channels

Rx

A
  • lidocaine, Mexiletine
  • flecainide
  • quinidine, procainamide, disopyramide
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9
Q

Cause long QT

A
  • quinidine, procainamide, disopyramide

* Amiodarone, dronedarone, sotalol, ibutalide

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10
Q

Rhythm control

A
  • flecainide
  • quinidine, procainamide, disopyramide
  • amiodarone, dronedarone, sotalol, ibutalide
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11
Q

Rate control

A
  • Verapamil, diltaziem
  • Metoprolol
  • digoxin, adenosine
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12
Q

General concepts

A
  • antiarrythmics = possibly pro-arrythmic
  • dirty rx (synergistic, too many S.E.)
  • Tx of CHOICE = procedure (not Rx)
  • Tx tachs that are SYMPTOMATIC
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13
Q

Action potential duration

A

Start of AP to end

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14
Q

Refractory period duration =

A

Action potential duration

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15
Q

Sodium channels work best + recover quicker at

A

Depolarized (-) state

Explain why RPD has no APs

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16
Q

Phase 0 Na+ voltage channels depolarizing

A
  • Quick open/quick close

* Affect Velocity + ERP

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17
Q

Phase 2-3 Ca++ in channel depolarizing

A
  • slow open/close

* affects AP duration

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18
Q

Just VT

Rx

A

Lidocaine, mexiletine

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19
Q

VT»>SVT

Rx

A
  • Flecainide
  • Quinidine
  • Procainamide, disopyramide
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20
Q

VT + SVT

A
  • Amiodarone, dronedarone

* Sotalol, Ibutalide

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21
Q

SVT

Rx

A
  • Verapamil, Diltiazem
  • metoprolol
  • digoxin, adenosine
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22
Q

Phase 2-3 K+ (TEA) out channel repolarizing

A
  • delayed rectifier

* affects AP duration

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23
Q

Phase 4 Na+ in channels depolarizing

A
  • pacemaker

* affects heart rate (automaticity)

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24
Q

Phase 4 (3Na+ out/2K+ in) polarizing

A
  • Defines RMP

* indirectly affects Ca++ out

25
Q

Myocardium

What initatiates AP?

A

Na+ current starts AP

CCB doesnt’ affect

26
Q

Pacemaker

What channel during AP?

A

Only Ca+ channel during AP

CCB affects nodes

27
Q

QRS starts when

A

Depole ventricle starts (not purkinje)

28
Q

PR interval from

A

Atrial depole to start of apex ventricle depole

Index of conduction velocity + AV node delay

29
Q

QRS duration

A
  • index of conduction velocity

* Duration of ventricular AP

30
Q

Flutter

A

*organized tach (regular space b/w waves)

31
Q

Fibrillation

A

Disorganized tach (uneven spacing)

32
Q

CHD

What is

A
  • regional hypoxia

* less depole = UP refractory period

33
Q

Myocardium blood flow

A

Epi to endocardium

Endocardium MOST AT RISK for ischemia (ventricle, not for thin atria = less atrial reentry circuits)

34
Q

Requirements for Reentry

A
  • multiple conduction pathways
  • refractory (late) tissue
  • conduction time around circuit must be longer than late-refraction on late tissue
35
Q

Ectopic pacemakers

A
  • usually atrial
  • faster than Sa node
  • pulm vein
  • fastest ectopic takes over rhythm
  • AV node brakes signal (max 250bpm)
36
Q

Rate control in Afib

A
  • screw p wave = won’t be normal
  • A-fib remains, a-fib conduction slowed
  • metoprolol
  • verapamil
  • digoxin
37
Q

Rhythm control in A-fib

A

Want normal P wave, abolish a-fib
*Rx/cardioversion

*amiodarone, flecainide

38
Q

A-fib

Rate vs. Rhythm control

A

Either acceptable

39
Q

A-fib

Anti-coag therapy

A

NOT ESSENTIAL IN EVERYONE

2+ CHA2DS2-VASc = high stroke risk, consider anti-coag

40
Q

Goals of tachyarrythmia Rx therapy

A
  • DOWN automaticity
  • DOWN conduction velocity AV node (PR interval, QRS duration UP)
  • UP AP duration (UP QT duration)
  • interfere w/ Sympa regulation of HR at SA/AV nodes
41
Q

Class 1 Na+ channel Rx

A

VT
*lidocaine, mexiletine

VT»>SVT

  • Flecainide
  • Quinidine, Procainamide, disopyramide
42
Q

Class 1 Na+ channel drugs

Selectivity

A
  • only block fraction of Na+ channels
  • Channel must be open
  • more selective for “diseased” tissue (unactivated state)
43
Q

Class 1 Na+ channel Rx

Mech + ECG

A
  • LESS activated channel
  • LESS Na+ in
  • LESS conduction velocity
  • UP ERP (refractory period) = longer than AP, longer to reset

ECG: Longer PR + QRS
(Use to monitor efficacy/toxicity)

44
Q

Class 1 Na channel Rx

Ectopic pacemakers

A

Make less excitable

45
Q

Class 1 Na+ channel Rx

Reentry

A

Up ERP

  • ERP now longer than conduction time around circuit = stops reentry
  • reentries are predominantly ventricular
46
Q

Class 1 Na+ effects

A
  • block Open (activated) states
  • UP ERP/recovery
  • Ectopic pacemakers
  • block reentry (UP erp)
47
Q

Class 1 Na+ channel blocker

Prolongation of ERP comparison

A

1C > 1A > 1B

48
Q

Inherited Long QT syndrome

A

Class 1A contraindicated
= Torsades de Pointes tach

Mutations:

  • Rectifying K+ channel = tx metoprolol
  • Na+ channel = mexiletine (1B)

WATCH giving RX with long qt side effect

49
Q

Amiodarone

A

Class 3

*block K+ efflux (phase 3), LONG AP DURATION + REFRACTORY PERIOD

  • Low dose = A-fib (rhythm control)
  • High dose = VT (structurally abnormal hearts (post-MI))
50
Q

Amiodarone

S.E.

A

Rhabdomyolysis, long qt, pulm fibrosis

BITCH

  • B radycardia/Blue Man
  • I nterstitial Lung Dz
  • T hyroid (hyper/hypo)
  • C orneal/Cutaneous (blue)
  • H epatic/Hypotension (IV-solvents)
51
Q

Sotalol

A

Class 3 = SVT + VT

  • Block K+ Phase 3
  • Longer AP Duration

Reduce repeated arrythmia (now amiodarone)

52
Q

Ibutalide (semi-not important)

A

Class 3

Block K+ efflux, Long AP duration

ACUTE CARDIOVERSION SVT

53
Q

Vtach after MI

Acute
Chronic

A

Acute = amiodarone, DC cardioversion

Chronic = ICD w/ or w/o amiodarone

54
Q

Vfib

Acute crhonic

A

Acute= Defib

Chronic = ICD w/ or w/o amiodarone

55
Q

Contraindicated in WPW

A

Rate control Rx. (Down AV conduction)

56
Q

DIgoxin

A

Good choice w/ CHF

  • Up vagal activity
  • Long refractory period
  • Down AV conduction
57
Q

Adenosine

A

Down AV node conduction

IV
T1/2 = seconds

AV-node dependent narrow complex tach (TX + DX acute)

58
Q

Afib / A tach

Acute
Chronic

A
CONTROL V RATE
ACUTE/CHRONIC= 
*Verapamil/diltiazem
*BBlocker
*digoxin
RESTORE SINUS RHYTHM:
ACUTE=
*Defib
*ibutilide
CHRONIC=
*Amiodarone
59
Q

A flutter

Acute
Chronic

A
CONTROL V RATE
ACUTE:
*Verapamil/diltiazem
*Beta-blocker
*Digoxin
CHRONIC: 
*ablation

RESTORE SINUS RHYTHM
*Defib/Ibutilide