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Cardiology M2 > 11 14 2014 Anti- Arrhythmetics > Flashcards

11 14 2014 Anti- Arrhythmetics Flashcards

1
Q

Goal of anti-arrhythmic therapy?

A
  1. decrease automaticity of pacemaker and non-pacemaker cells
  2. disrupt reentrant pathways
  3. Eliminate trigger activity
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2
Q

Who are the Class I drugs (in general?

Who are Class II drugs (in general)?

Who are Class III drugs (in general)?

Who are Class IV drugs ( in general)?

What are other agents that can be used?

A
  1. Sodium Channel blockade
  2. Sympathetic autonomic blockade (Beta blockers and also some calcium channel blockers)
  3. Potassum channel blockate – prolong the effective refractory period
  4. Calcium channel blockade
  5. Magnesium, digitalis, Digibind (antibodies against digitalis), adenosine
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3
Q

What are the two types of anti-arrhythmetic drugs that can be used to decrease automaticity of pacemaker cells?

A
  1. Beta blockers ( slow condution of AV node)
  2. Ca2+ channel blockers ( L-type) because the decrease the upslope of AV node .

This slow rise in action poential = prolonged repolarization at AV node

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4
Q

How would you disrupt reentry pathways and what class of durgs are the most useful?

A

Reentrant loops form when a pathway has time to repolarize.

–> Prolong refractory period so that the returning impulse finds unexcitable tissue

* Class III drugs : K+ channel blockers will increase the duration of an action potential.

~ aka elongates refractory period

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5
Q

How would you eliminate trigger activity?

  1. Early afterpolarization

vs.

  1. Delayed afterpolarization
A
  1. Early polarizaiton is caused by a prolonged aciton potential. Therapeutic goal = decrease AP.

= Lidocane

  1. DAD are caused by high states of intracellular calcium
    - usually due to digitalis toxicity or excessive catecholamine stimulation
    - you want to blunt Ca2+ actions
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6
Q

Who are the Class IA drugs?

What is their mechanism?

What are some of th Extracardiac effects of this drug?

A

Procainamide, Quinidine, disopyramide

Block the upstroke of action potetenial by binding to open/inactivated Na+ channels. May also bind to K+ channels with intermediate kinetcis and moderate affiinity (Quinidine)

Extracardiac effects: Procainamide reduces peripheral vascular resistance =Hypotension

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7
Q

What are some toxicities associated with Class 1 A drugs?

  1. overall
  2. Procainamide
  3. Quinidine
A

They can slow conduction and action potential prolongation – increase risk of induction of torsade de pointes, syncompe, and early afterdepolarizations.

Procainamide can also cause : syndrome resembling lupus erythematosus and parenchymal pulmonary disease, pericaditis, pleuritis

Quinidine and Disopyramide ahve antimuscarinic effects: urinary retention, dry mouth, blurred vision, constipaiton, worsening of glaucoma.

Quinidine also causes cinchoism ( tinnitus, headache, GI disturbance) and thrombocytopenia

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8
Q

Pharmacokinetics of Procainamide

A

Well absorbed orally

Short half-life (2-3 hrs)

Elimiated by hepatic metbolism

Accumulation of metabolite (NAPA) = torsade de pointes

Dose must be decreased in someone with renal failure

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9
Q

What Arrhythmias can be treated with Class 1a Drugs?

A

Atrial and ventricular arrhythmias (especially after myocardial infarction)

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10
Q

Mechanism of action of Class 1b Drugs?

Who are the Class 1b drugs?

Clinical uses for Class 1b drugs?

A

Lidocaine, Mexiletine

highly selecive use- and state-dependent Na+ block : block open or inactivated Na+

Shorten phase 3 repolarizaiton in ventriular myoctes

* rapidly associate and disassociate from Na+ channels!

VENTRICULAR ARRHYTHMIAS!!! espeically during an myocardial ischemia (MI).

Drug does not slow condution so it does not have an effect on Atrial or AV junction arrhytmias.

ALSO used for DIGITALIS- induced Arrhythmias

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11
Q

Pharmacokinetics of Lidocaine/ Mexiletine

A

Lidocaine:

Administred: IV or IM (intramuscular)due to high pass metabolism by liver

  • almost entirely excreted by liver
  • durtaion: 1-2hrs

Mexiletine:

Administration is oral and longer duratin of action than lidocaine.

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12
Q

Toxicity/ Adverse effects of Lidocaine

A

Lidocaine:

  • CNS: drowsiness, slurred speech, paresthia, agitation, confusion, convulsion, sedation, arrhythmias (rarer)
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13
Q

What is the prototype of Class IC drugs.

Describe mechanism

What type of arrhythmia can Class IC drug be used for?

A
  1. Flecainide
  2. slowly dissociates from RESTING Na+ channels
    - blockes Na+ in purkinje and myocardial fibers

* slows conduction velocity and pacemaker activity

*minor effect on action potential duration/ refraction — just decreases automaticity due to an increase in threshold

  • has negative ionotropic effect and can aggravate congestive heart failure
    3. Refractory arrhythmias

( Ventricular arrhythmias and paroxysmal supraventricular tachycardias)

  • also blocks premature ventricular contraction
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14
Q

Pharmacokinetics of Flecainide?

Adverse Effects?

A

Class IC drug:

Pharmacokinetic:

  • oral – undegoes minimal biotransformation
  • long duration ( 20hrs)

Toxicity:

  • CNS: dizziness, blurriness, headache, nausea
  • can aggrevate pre-existing arrhythmias or induce ventricular tachycardia
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15
Q

Who are the Class II drugs and their main mechanism of action?

A

Beta- blockers: propanol, metroprolol, Esmolol

Deminish phase 4 depolarization in AV and SA node condution = thus depressing automaticity, prolongue AV conduction, decrease heart rate and contractility

used mostly for: tachycardias caused by increase SNS. Can also be used for atrial flutter/fibrillation and AV-nodal reentry tachycardia

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16
Q

Propanolol

  1. mechanism
  2. clinical use
  3. pharmacology
  4. adverse effects
A
  1. non-selective block of Beta receptors = slowed pacemaker activity
  2. Reduces incidence of sudden arrhytmic death after MI
  3. oral/ parenteral

Duraiton 4-6 hrs

  1. toxicities: Bronchospasm, cardiac depression, AV block, hypotension
17
Q

Metroprolol – difference agaisnt Propanolol?

Esmolol– difference from Propanolol?

A

Mesoprolol: similar to propranolol but is Beta- 1 selective ANd reduces the risk of bronchospasm

Esmolol: selective beta-1 receptor blockade. Can only be delivered via IV, and 10 minute duration. use in perioperative and throtoxicosis arrhythmias

18
Q

Class III drugs

Who are they?

Mechanism and effect?

A

sotalol, Ibutilide, Amiodarone, Dronedarone, Vernakalant, Ranolazine

* Amiodarone is a beta blocker but it is put in this class because it markedly prolongs AP duration and blocks some sodium channels.

K+ channel blockers – elongated refractory period

OR enhancing inward current.

= reduces heart to responsd to rapid tachycardias. Have little effect onphase 0 or conduction velocity.

19
Q

Sotalol

  1. mechanism
  2. therapeutic use
  3. pharmacokinetics
  4. adverse effects
A
  1. nonselective beta-blcoker but has stronger K+ blocking activities (blocks outward K+ current

(Class III)

  1. life-threatening ventricular arrhythmias and maintains sinus rhythm in patients with atrial fibrillation. Suppress ectopic beats
  2. Oral, duration 7 hrs
  3. Dose-related incidence of long QT interval.

Torsade de pointes

20
Q

Amiodarone

  1. mechanism
  2. therapeutic use
  3. pharmacokinetics
  4. adverse effects
A
  1. Ik block = prolongation of AP and refractory period.

Group 1 = activity slows conduction

Group 2 and 4 = additional antiarrhythic activity

(Class III drug)

  1. Refractory arrhythmias: supraventricular and ventricular tachycardias
  2. Oral/parenternal ; 1/2 life and duration of action of 1-10 weeks
  3. Thyroid abnormalities (because of the iodine in structure), skin depositions, cornea depositions, pulmonary fibrosis, optic neuritis
21
Q

Dronedarone

  1. structure/ therapeutic use
  2. Pharmacokinetics
  3. Adverse effects
A
  1. Class III drug that is a structural analog of amiodarone (lacks the iodine)

First line arrhythmetic for patients with perisitant atrial fibrillaion

  1. 1/2 life = 24 hours
  2. Lacks major side effects of Amiodarone.

Toxicities: diarrhea, nausea, vomiting, abdonmial pain, photosensitivity, QT prolongation

22
Q

Ibutilide

  1. mechanism
  2. Clinical application
  3. Pharmacokinetics
  4. Adverse effects
A
  1. Class III – selective Ik block

Prolonged action potential and QT interval

  1. Treatment of acute atrial ibrillation
  2. only IV administration; Duration = 6 hrs
  3. Torsades de pointes
23
Q

Dofetilide

  1. mechanism
  2. Clinical application
  3. Pharmacokinetics
  4. Adverse effects
A
  1. Selective Ik block.

= prolongued AP and QT interval

  1. prophylaxis for atrial fibrillation
  2. oral; duration = 7 hrs
  3. torsades de pointes
24
Q

Class IV drugs overall mechanism

A

L-type Ca2+ blockers = decrease spontaneous phase 4 depolarization in AV node

Can also affect vascular smooth muscle

25
Q

Verapamil

  1. mechanism
  2. Clinical application
  3. Pharmacokinetics
  4. Adverse effects
A
  1. binds to open Ca2+ channels, slows AV node conduction and slows pacemaker activity. PR interval prolongation

(Class IV)

  1. AV nodal arrhythmias (especially in prophylaxis)
  2. Oral, parental; duration = 7 hrs
  3. Adverse effects: Cardiac depression , constipation, hypotension
26
Q

Diltiazem

  1. mechanism
  2. Clinical application
  3. Pharmacokinetics
  4. Adverse effects
A
  1. Blocks open Ca2+ L-type channels; slow conduction via AV node and pacemaker activity. Cause an enlongated PR interval

(Class IV – negative ionotropes)

  1. Rate control in Atrial fibrillation
  2. Oral, parenteral; duraton = 6h
  3. Adverse effects: Cardiac depression, constipation, hypoptension
27
Q

Adenosine

  1. mechanism
  2. Clinical application
  3. pharmacokinetics
  4. adverse effects
A
  1. (Miscellaneous) : Increase diastolic Ik of AV node = hyperpolarization and condutionc block. Causes a reduction in ICa2+ and If currents
  2. Acute nodal tachycardias
  3. IV administration ONLY; short duration time : 15 seconds
  4. Flushing, bronchospasm, chest pain, headache
28
Q

Potassium Ion

  1. mechanism
  2. Clinical application
  3. pharmacokinetics
  4. adverse effects
A
  1. increase in all K+ currents = decrease automaticity; decrease digitalis toxicity
  2. Digitalis toxicity, other arrhythmias if serium is K+ low
  3. Oral or IV
  4. hypokalemia and hyperkalemia associated with arrhythmogenesis. Severe hyperkalemia = cardiac arrest
29
Q

Magnesium ion

  1. mechanism
  2. Clinical application
  3. pharmacokinetics
  4. adverse effects
A
  1. poorly understood, possible increase in Na/K+ ATPase activity
  2. Digitalis arrhythmias or other arrhythimas in serum Mg is low
  3. IV
  4. Muscle wekaness, respiratory paralysis
30
Q

Digoxin:

Why is it used?

What happens during toxic dose?

A
  1. used in adjunct therapy to help control ventricular resposne in atrial fibrillation or flutter and may terminate some paroxysmal (reentrant) supraventricular arrhythmias by slowing AV conduction.

Shortens the refractory period in atrial and ventricular myocytes = diminishing conduction velocity in AV node.

Toxicity: causes ectopic ventricular beats that may result in ventricular tachycardia and fibrillation.

Cardiology M2 (25 decks)

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