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C & R II - wk1 > antiarrhythmic therapy > Flashcards

antiarrhythmic therapy Flashcards

1
Q

what are the goals of antiarrhythmic therapy

A
  • restore normal sinus rhythm and conduction
  • prevent more serious/lethal arrhythmias (AADs are no guarantee to prevent arrhythmic sudden death)
  • decrease clinical signs
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2
Q

what are the clinical signs of arrhythmias

A
  • syncope
  • weakness
  • poor performance
  • congestive heart failure
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3
Q

what causes arrhythmias

A
  • scars in myocardium from ischemia, cardiomyopathy
  • drugs, stress (adrenaline)
  • genetic defects in ion channels or myocardial ultrastructure -> disturbance of ionic homeostasis in myocytes can trigger arrhythmias
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4
Q

what type of channels control the ionic balance and are good targets for antiarrhythmic drugs

A

ion channels

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5
Q

what makes up the supraventricular conduction system

A
  • sino-atrial node
  • atrial myocardium
  • atrio-ventricular node
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6
Q

what makes up the ventricular conduction system

A
  • purkinje fibers
  • ventricular myocardium
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7
Q

what type of channel are nodal cells

A

Ca channel

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8
Q

what type of channel are atrial myocardium, purkinje fibers, and ventricular myocardium

A

Na channel

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9
Q

what is the drug target with atrial/ventricular myocardial cells and purkinje fibers

A
  • block sodium channel
  • block potassium channel
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10
Q

what is the drug target in the SA and AV nodal cells

A
  • block calcium channel
  • block k channel
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11
Q

what is the basic classification of antiarrthythmic agents based on predominant electrophysiologic properties

A
  • class I: Na channel blockers
  • class II: beta blockers
  • class III: K channel blockers
  • class IV: Ca channel blockers
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12
Q

how are these drugs antiarrhythmic

A

alter the conduction velocity of the cardiac conduction system

  • decrease rate of spontaneous depolarization (blocking entry of Ca, Na ions)
  • increase length of repolarization (increase AP duration, make refractory period of all cells uniform)

change balance of autonomic tone
* sympathetic - parasympathetic

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13
Q

what do Na channel blockers do

A

slow conduction velocity in myocytes and purkinje

  • decrease slope of phase 0
  • prolong repolarization (slope of phase 4 (Ia)
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14
Q

what are the subtypes of Na channel blockers

A
  • IA, IB, IC
  • degree of blockage and effect on refractory period
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15
Q

what are the IA Na channel blockers

A

quinidine, procainamide

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16
Q

what are the IB Na channel blockers

A

lidocaine, mexiletine

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17
Q

what are the IC Na channel blockers

A

flecainide, propafenone

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18
Q

what is the clinical use of Na channel blocker: IA - quinidine

A
  • IV and per os (nasogastric tube)
  • HORSE: conversion of AF to sinus rhythm
  • does NOT work for AF in dogs/cats
19
Q

what are the side effects of of Na channel blocker: IA - quinidine

A
  • GI disturbances
  • hypotension
  • seizures
  • pro-arrhythmia: bc it also blocks K channels
  • vagolytic
  • negative inotrope
20
Q

what is the clinical use of Na channel blocker - Class IA: procainamide

A
  • relatively poor efficacy - works occasionally
  • IV
  • life threatening ventricular tachycardia (second line agent if lidocaine - class IB, doesnt work)
  • supraventricular tachycardia
  • per os: short half-life (3-5hr), makes oral dosing impractical
21
Q

what are the side effects of Na channel blocker - Class IA: procainamide

A
  • reduced contractility (neg ionotrope)
  • hypotension
22
Q

what is lidocaine

A

Na channel blocker - class IB

  • IV only: ER situation
  • 1st choice for life-threatening ventricular tachycardia
  • not effective for supraventricular arrhythmias
  • lower efficacy if hypokalemia
  • works well
23
Q

what are the side effects of lidocaine

A
  • minimal myocardial depressant effects
  • vomiting, depression, seizures
24
Q

what is mexiletine

A

Na channel blocker - IB

  • oral (less effective) analogue of liodcaine
  • long-term tx of VT associated with myocardial dysfunction (not effective for supraventricular arrhythmias)
  • weak monotherapy
25
Q

what are the side effects of mexiletine

A

common

GI: anorexia, vomiting

26
Q

how do beta blockers work (class II)

A

block sympathetic tone to heart

  • decrease SA node discharge rate: HR goes down - neg chronotrop
  • slow AV node conduction: neg dromotrop
  • but also decrease contractility: neg inotrop = side effect
27
Q

what are the indications to use beta blockers

A
  • arrhythmias caused by increased catecholamines (exercise, thyroid, stress)
  • sinus tachycardia, ventricular arrhythmias
  • second line agent, combined with class I or class III drugs
28
Q

what are 1st generation beta blockers

A

non-selective B1 and B2 receptor

  • propanolol: IV and PO (B2 effect: bronchocontriction)
29
Q

what are 2nd generation beta blockers

A

cardiac - selective for B1

  • PO: atenolol, metroprolol
  • IV: esmolol
30
Q

what do class III K channel blockers do

A
  • prolong repolarization (phase 3)
  • lengthens AP duration: QT interval increased (pro-arrhythmia)
31
Q

what are the indications to use sotalol

A
  • PO
  • class III: K channel blocker
  • first line oral drug for tx of life-threatening VT
  • also effective for suppression of some atrial arrhythmias
  • works well
32
Q

what are the side effects of sotalol

A
  • rare
  • neg inotrope bc of mild class II effects
33
Q

what is amiodarone (route & side effects)

A

PO and IV - **class III: K channel blocker **

  • class I, class II, and class IV effects (less neg inotrope compared to sotalol)
  • side effects: reversible elevation of liver enzymes and neutropenia, hypothyroidism
34
Q

what is benzothiazepines (diltiazem)

A
  • class IV: Ca channel blocker
35
Q

what is the primary effect of diltiazem

A
  • to slow the conduction through the AV node
  • depress slope of depolarization
36
Q

what are the indications to use diltiazem PO and IV

A
  • slow the ventricular response rate in atrial fibrillation
  • terminate supraventricular reentrant arrhythmias which rely on the AV node
  • no benefits for ventricular arrhythmias
37
Q

what are the side effects of diltiaxem

A
  • anorexia
  • if overdosed: bradycardia, hypotension
38
Q

what is amlodipine

A
  • different class of Ca-channel blocker
  • anti-hypertensive: relax vascular smooth muscle (no effect on cardiac conduction)
39
Q

what are class IV drugs: Ca channel blockers great for

heart problems

A
  • atrial tachycardias
  • atrial fibrillation
40
Q

what are the side effects of using diltiazem PO

A
  • mild neg inotrope
  • 2nd or 3rd degree AV block/bradycardia: dose-depenent
  • cats: anorexia
  • can be added to sotalol or digoxin to slow AVN conduction even more (monitor HR)
41
Q

what are the side effects of using diltiazem IV

A
  • horse and dog: hypotension - but dose -dependent
  • sinus arrest, 2nd or 3rd degree AV block/bradycardia: dose-depenent (monitor BP and ECG during infusion)
42
Q

what are cardiac glycosides

A
  • digoxin: PO
  • indirect antiarrhythmic effect: vagomimetic
  • slows AV node conduction by prolonging AV nodal refractoriness
  • works for AFib only
43
Q

cardiac glycosides - use

A
  • weak as monotherapy
  • only antiarrhythmic infication: AFib
  • goal: slowing of ventricular response
  • best rate control if combined with a Ca channel blocker
44
Q

what are the adverse effects of digoxin

A

narrow therapeutic window and eady to cause toxicity

  • GI: anorexia, vomiting, diarrhea
  • cardiac arrhythmias (intracellular Ca overload -> ventricular arrhythmias)
  • neurological (depression)

bc of high individual variablility, serum digoxin concentrations must be checked 5-7 days after starting digoxin

C & R II - wk1 (13 decks)

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