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Julie Pharm > antiarrhythmics > Flashcards

antiarrhythmics Flashcards

1
Q

All arrhythmias result for 2 things

A
  1. disturbances in impulse formation ( ectopic pacemakers)

2. disturbances in impulse conduction ( nodal block or reentry)

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2
Q

Goal of antiarrhythmic therapy

A
  1. reduce ectopic pacemaker activity ( decrease phase 4 depolarization or increase threshold for action potential firing)
  2. modify conduction or refractoriness in re-entry circuits
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3
Q

major mechanism of antiarrhythmic therapy

A
  • sodium channel blockade ( phase 0; atrial muscle, ventricle muscle and his purkinje - effects threshold and firing potential.)
  • blockade of sympathetic autonomic effects on the heart (increasing of decreasing SA node pacemaking and AV node conduction)
  • prolong effective refractory period ( K+ channel blockers- refractory pd starts once repolarizing starts)
  • calcium channel blockade (SA nodal pacing and AV nodal conduction)

GOAL PROTECT VENTRICULAR FUNCTION

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4
Q

Vaughn williams classifications

A

based on dominant electrophysiological action
Class 1 - Na channel blockers (Ia, IB IC)
Class 2- beta blockers
Class 3 - K+ channel blockers
Class 4 - Ca++ channel blockers

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5
Q

Class IA

A

quinidine, procainamide,-> moderate Na blockers
disopyramide
- dont reduce mortality
-increase action potential duration
-slow down phase 0
-increase QT interval
-weak K+ channel blocker -> ^ AP duration / QT
-adverse effects- refractory heterogeneity -> same parts of the heart come out of their refractory pd at different times and lose coordination ( can cause arrhythmias - torsades de pointes) aka quinidine syncope -> lightheadedness

  • used for atrial flutter/ fib and v tachy
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6
Q

CLass IA - side effects

A

quinidine - antimuscarinic activity -> increase AV conduction and SA pacing and can lead to tachy and arrhythmia

-adverse effects- refractory heterogeneity -> same parts of the heart come out of their refractory pd at different times and lose coordination ( can cause arrhythmias - torsades de pointes) aka quinidine syncope -> lightheadedness

drug interaction: quinidine/ digoxin drug interaction - digoxin stays around longer and sides of toxicity is increased

procainamide - pt develop lupus like symptoms (1/3)

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7
Q

Class IB

A

lidocaine, mexiletine, tocainide, phenytoin

  • weak Na+ channel blockers
  • decrease phase 0
  • little effect on action potential duration
  • not effective on normal tissue
  • effects depolarized arrhythmic tissue since many of the channels are inactivated and class IB prefers to effect those channels
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8
Q

Class IB - side effects,drug interactions indications

A
  • side effects: CNS-> tremor , lightheadedness, nausea
  • drug interactions- B blockers decrease clearance of lidocaine so should monitor lidocaine levels in patients who are taking b blockers

indications: acute suppression of ventricular arrhythmias esp after MI/cardioversion

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9
Q

Class IC

A

inhibit fast NA+ channels and Ito K+currents

  • effective in his-purkinje system
  • may slightly prolong AP duration
  • PRO ARRHYTHMIC - kill people
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10
Q

CLass IC - indications

A

life-threatening ventricular arrhythmias-
atrial fibrillation in pts without left vent disease or coronary disease
-paroxysmal supraventricular tachy

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11
Q

Class II

A

beta blockers - propranolol, sotalol, acebutolol

blocks sympathetic effects
- effects SA and AV nodes
-decrease automaticity and AV nodal conduction
-slight prolongation of AV node AP due to blocking sympathetic effects on K+ channels ( symp slightly increases K currents)
-bronchoconstriction - AVOID WITH ASTHMATICS
-sudden withdrawal-> rebound hypersensitivity
-reduce arrhythmia-associated mortality
-

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12
Q

Class II - indications

A
  • supraventricular arrhythmias
  • control ventricular rate in atrial flutter and fibrillation
  • ventricular arrhythmias associated with re-entry circuits
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13
Q

Class III

A 
K+ channel blocker 
amiodarone, dronedarone bretylium, sotalol, ibutilide, dofetilide 
- prolong AP duration, by blocking K+ channels , prolonged repolarization. 
- conduction velocity is unaffected
-ibutilide and dofetilide - pure class III agents 
- amiodarone - has class I, II and IV activity
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14
Q

amiodarone - side effects

A

cardio - decrease AV or Sa node function and cardiac contractility, hypotension
pulmonary - pneumonitis leading to pulmonary fibrosis
thyroid- hyperthyroidism or hypothyroidism
hepatic - hyperthyroidism or hypothyroidism
neurological - peripheral neuropathy, headache, ataxia, tremors
other: corneal microdeposits, testicular dysfunction, skin discoloration

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15
Q

amiodarone - indications

A

ventricular arrhythmias, recurrent atrial fibrillation or flutter

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16
Q

Class IV

A

verapamil, diltiazem

  • Ca++ channel blockers, so their effects are mostly on SA and AV nodes
  • reduce SA node automaticity
  • reduce AV nodal conduction
  • avoid with b-blockers use
  • systemic effects can lead to hypotension
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17
Q

Class IV indications

A

supraventricular tachyarrhythmias

control ventricular rate in atrial flutter and fibrillation

18
Q

Adenosine

A

acts via adenosine receptor -> opens K+ channels and indirectly inhibits Ca++ channels

  • mostly affects nodal tissue , esp AV nodal conduction
  • brief duration
  • effects reduced in presence of adenosine receptor blockers, including caffeine and theophylline
  • indications : drug of choice for paroxysmal supraventricular tachycardia
19
Q

IV magnesium

A

weakly blocks Ica and inhibits INa and Ik

  • can be used to slow ventricular rate, but not used for PSVT
  • useful in treating torsades des pointes
20
Q

Which antiarrhythmic do I use : paroxysmal supraventricular tachycardia

A

acute : either IV adenosine, verapamil or diltiazem will work. Carotid massage is also effective in many cases

chronic: not very common. oral verapamil, diltiazem or beta-blockers are effective

21
Q

Which antiarrhythmic do I use: atrial fibrillation

A

rate control vs rhythm control: two potential ways to deal with AFib.

rhythm control: restore proper sinus rhythm by correcting aberrant atrial electrical activity with either a class III or a class IC agent

rate control: no attempt is made to control atrial activity ; rather the ventricular rate is controlled by limiting the rate of impulse propagation through the AV node with either b-blockers or class IV agents

try rate control first

22
Q

Which antiarrhythmic do I use: ventricular arrhythmias

A

IV lidocaine is usually the drug of choice, although flecanide and amiodarone are also be used

23
Q

quinidine

A 
IA 
blocks Na channel 
prolongs Repolarization time 
atrial fib and flutter 
Paroxysmal supraventricular tachy 
ventricular tachy
24
Q

procainamide

A 
IA 
blocks Na channel 
prolongs Repolarization time 
atrial fib and flutter 
Paroxysmal supraventricular tachy 
ventricular tachy
25
Q

disopyramide

A 
IA 
blocks Na channel 
prolongs Repolarization time 
atrial fib and flutter 
Paroxysmal supraventricular tachy 
ventricular tachy
26
Q

lidocaine

A 
IB
blocks Na channel 
SHORTENS Repolarization time 
digitalis-induced arrhythmias  
ventricular tachy
27
Q

phenytoin

A 
IB
blocks Na channel 
SHORTENS Repolarization time 
digitalis-induced arrhythmias  
ventricular tachy
28
Q

mexiletine

A 
IB
blocks Na channel 
SHORTENS Repolarization time 
digitalis-induced arrhythmias  
ventricular tachy
29
Q

tocaninide

A 
IB
blocks Na channel 
SHORTENS Repolarization time 
digitalis-induced arrhythmias  
ventricular tachy
30
Q

flecainide

A 
IC
blocks Na channel 
unchanged Repolarization time 
atrial fib 
Paroxysmal supraventricular tachy
ventricular tachy
31
Q

propafenone

A 
IC
blocks Na channel 
unchanged Repolarization time 
atrial fib 
Paroxysmal supraventricular tachy
ventricular tachy
32
Q

B-blockers

A

II
inhibits phase IV
aV AP prolonged Repolarization time

atrial fib and flutter
Paroxysmal supraventricular tach
ischemia-related ventricular tachy
atrial or ventricular premature beats

33
Q

amiodarone

A

III
blocks K+ current
prolonged Repolarization time

atrial fib and flutter
bypass tract mediated Paroxysmal supraventricular tachy
ventricular tachy

34
Q

ibutilide

A

III
blocks K+ current
prolonged Repolarization time

atrial fib and flutter
bypass tract mediated Paroxysmal supraventricular tachy
ventricular tachy

35
Q

sotalol

A

III
blocks K+ current
prolonged Repolarization time

atrial fib and flutter
bypass tract mediated Paroxysmal supraventricular tachy
ventricular tachy

36
Q

bretylium

A

III
blocks K+ current
prolonged Repolarization time

atrial fib and flutter
bypass tract mediated Paroxysmal supraventricular tachy
ventricular tachy

37
Q

verapamil

A

IV
blocks Ca2+ channels
unchanged Repolarization time

atrial fib and flutter ( to reduce ventricular rate)
Paroxysmal supraventricular tachy
multifocal atrial tachy ( to reduce ventricular rate)

38
Q

diltiazem

A

IV
blocks Ca2+ channels
unchanged Repolarization time

atrial fib and flutter ( to reduce ventricular rate)
Paroxysmal supraventricular tachy
multifocal atrial tachy ( to reduce ventricular rate)

39
Q

adenosine

A

IV-like

opens K+ channels ( decreases SA nodal firing, decrease I ca2+ and reduces AV conduction)
unchanged RT
PSVT **
- diagnostic to find where the vent tachy is coming from

40
Q

Afib - rate control

rhythm control

A

rate : b blockers, CCBs

rhythm: amiodarone, doraniodarone, propafenone

41
Q

V tach

A

IV Amiodarone

Julie Pharm (14 decks)

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