Cardio Lecture 10--Pharmacology Of Ant-Arrythmics

Front 1

What class of drug is procainamide and what is its mechanism? What does it do to the ECG? What is it used for?

Back 1

Class IA--sodium channel blocker(also blocks K channels)--Prolongs the QT interval--Used for atrial or ventricular arrhythmias but not much anymore because it depresses LV function and causes arrhythmias

Front 2

What class of drug is Lidocaine and what is its mechanism? What does it do to the ECG? What is it used for?

Back 2

Class IB--sodium channel blocker that blocks the inactivated channels--DECREASE QT interval--used for emergency treatment of ventricular arrhythmias and has no effect on the atria

Front 3

What are some bad effects of
flecanide and when is it never used?

Back 3

depresses LV function so it is never used in systolic dysfunction or any SHD

Front 4

What are some side effects of lidocaine?

Back 4

Neurotoxicity in high doses

Front 5

What class of drug is Flecanide and what is its mechanism? What does it do to the ECG? What is it used for?

Back 5

Class IC--sodium channel blockers that are the MOST POTENT--no effect on the QT interval--used for atrial and rarely ventricular arrhythmia

Front 6

What class of drug is propanolol or atenolol and what is its mechanism? What does it do to the QT interval? What is it used for?

Back 6

Class II--Beta receptor blockers--no effect--Used to decrease the conduction rate and automaticity so primary use is for atrial arrhythmias and indirectly for ventricular ischemic arrhythmias

Front 7

Beta blockers can have what negative effects?

Back 7

May slow down the heart too much in old people and also cause bronchospasm through the blocking of Beta 2 receptors that work to keep the bronchioles dilated

Front 8

What class of drugs are potassium channel blockers? What is an example and what is it used for? What does it do to the ECG?

Back 8

Class III drugs--amniodarone(commonly used)--used for ventricular and atrial arrhythmias--PROLONGS THE QT interval

Front 9

What are Class IV drugs and what are some examples? What do they do?

Back 9

Calcium channel blockers that have no effect on the QT interval--verapamil and diltiazem--these act like beta blockers(they are just further down in the process than the receptors)

Front 10

What class of drug is Adenosine? What condition is it ALWAYS used for? What does it do?

Back 10

Class 5--always used for AVRT's--can break arrhythmias by slowing conduction through the AV node

Front 11

What are the class IA drugs?

Back 11

Quinidine, procainamide, disopyramide

Front 12

What are the class IB drugs?

Back 12

Lidocaine, mexiletine, tocainide, and phenytoin

Front 13

What are the class IC drugs?

Back 13

Flecainide and propafenone

Front 14

What are the Class II drugs?

Back 14

Amniodarone, sotalol, dofetilide, and ibutilide

Front 15

A problem in the AV node will present as what?

Back 15

prolongation of the PR interval

Front 16

What is the most effective way to prolong the QT interval?

Back 16

By blocking the potassium channels with a Class III antiarrhythmic

Front 17

What are the three ways you can change the automaticity of pacemaker cells?

Back 17

Change the slope of Phase4/0, change the depolarization potential, or change the threshold potential

Front 18

How is the slope of the depolarization changed?

Back 18

CLASS 2 and 4 AA's DECREASE THE SLOPE--Calcium channel blockers decrease the slope; catecholamines stimulate cAMP production which increases the slope

Front 19

How can the depolarization potential be changed?

Back 19

Ach can hyperpolarize the ligand gated K+ channels to make it more negative and less likely to fire--blocking Ach with an anti-cholinergic will induce faster firing

Front 20

What can increase the threshold potential to make it more difficult to induce an AP?

Back 20

Blocking sodium or calcium channels

Front 21

What can trigger DAD's? When do they occur?

Back 21

Cardiac glycosides and catecholamines--they occur after full repolarization is completed

Front 22

What causes EAD's and when do they occur?

Back 22

They are caused by a secondary slow inward sodium current--they occur during the plateau phase and cause Torsade

Front 23

Which has a faster upstroke, the AV/SA nodes or the bundle of His? How?

Back 23

Bundle of His because it has a lot of sodium rushing in during Phase 0

Front 24

Reentry ultimately leads to what if it is ventricular?

Back 24

Premature Ventricular Contractions

Front 25

What are two ways of treating ventricular reentry?

Back 25

Prolong the AP with a Class II calcium blocker so the second stimulus will create a bidirectional block--or you can shorten the AP by using Lidocaine, a Type IB antiarrhythmic

Front 26

Why are Anti-arrhythmics toxic?

Back 26

Because they slow down conduction--this encourages reentry

Front 27

What classes of drugs decrease membrane responsiveness and conductive velocity? What is the effect?

Back 27

Class IA, IC, and III--converts to a bidirectional block

Front 28

What classes of drugs increase the membrane responsiveness and conductive velocity? What is the effect?

Back 28

Class IB--eliminate the block

Front 29

What do class I drugs do? What are they used against?

Back 29

Fast Sodium Channel Blockers (Phase 0) and also block potassium channels - broad spectrum of atrial and ventricular arrhythmias

Front 30

What do class II drugs do? What are they used against?

Back 30

Beta Blockers--used against atrial and excessive catcholamine arrhythmias

Front 31

What do class III drugs do? What are they used against?

Back 31

Potassium channel blockers--reentry arrhythmias

Front 32

What do class IV drugs do? What are they used against?

Back 32

Calcium channel blockers--atrial and AMI arrhythmias

Front 33

What are the unclassified drugs?

Back 33

Cardiac glycosides, adenosine, magnesium sulfate, atropine, and phenylephrine

Front 34

What are the Class IA drugs?

Back 34

Quinidine, procainamide, disopyramide, moricizine

Front 35

How can Torsades be caused by antiarrhythmics?

Back 35

Blockage of potassium channels

Front 36

What causes Torsades?

Back 36

Increase in ion movement within myocytes due to decreased efflux(mutation in sodium channel gene causing inactivation) or increased influx(potassium channel mutation or blockage from drugs)

Front 37

What drug class is procainamide? What phase does it effect and what can continue its action? What are the adverse effects?

Back 37

Class IA--it effects Phase 0 primarily and continues its action through acetylation--Adverse effects include systemic lupus like symptoms

Front 38

What drug class is Disopyramide and what is it for?

Back 38

Class IA--mostly related to Anticholinergic actions

Front 39

What do Class IB drugs do?

Back 39

They BLOCK FAST Sodium channels that are in the inactive state--they don't change QRS and don't cause Torsade, but they do depress conduction slightly, decrease AP duration, and DO DECREASE QT INTERVAL

Front 40

What drug should be given for digoxin toxicity?

Back 40

Lidocaine

Front 41

What is tocainide?

Back 41

Orally effect lidocaine analog(Class IB)

Front 42

What are the side effects of procainamide?

Back 42

Systemic lupus like syndrome, agranulocytosis, and torsade

Front 43

True/False: Lidocaine causes Torsade

Back 43

FALSE

Front 44

Are Class IB drugs useful against atrial arrhythmias?

Back 44

NO

Front 45

What are the class IC drugs?

Back 45

Flecainide, Propefenone, and Moricizine

Front 46

What do Class IC drugs do and what are some adverse side effects?

Back 46

Block fast Na channels, severely depress conduction, broaden the QRS, and cause no change in QT--Drug interactions, proarrhythmic

Front 47

What are Class IC drugs used for?

Back 47

For chronic stable ventricular arrhythmias that do not respond to conventional anti-arrhythmics

Front 48

What do Class II drugs do?

Back 48

They block Phase 4 spontaneous depolarization of the pacemaker cells--so they inhibit sympathetic modulation of the SA node and decrease AV node transmission

Front 49

What are the Class II drugs and what are they useful for?

Back 49

Propanolol, Metoprolol, Sotalol, Acebutolol, Esmolol--used for supraventricular arrhythmias and ventricular arrhythmias associated with too many catecholamines

Front 50

What are the adverse effects associated with beta blockers?

Back 50

exercise intolerance, BRONCHOSPASM, and bradycardia

Front 51

What are the several Class III drugs?

Back 51

Amniodarone, Sotalol, Dofetilide, and Ibutilide

Front 52

Why are class III drugs dirty?

Back 52

Because they prolong ERP by BLOCKING EVERYTHING--Na, beta receptors, and calcium channels

Front 53

What do Class III drugs do to the heart AP?

Back 53

They block the iK channel and slow phase 3 down--so they increase AP duration and increase QT interval

Front 54

If a patient already has thyroid problems, then what drug should be used to correct their reentry arrythmia?

Back 54

Dronedarone

Front 55

Amniodarone is used to correct what conditions?

Back 55

Reentry and ventricular arrythmias as well as atrial arrythmias

Front 56

What class of drugs is good at prolonging the ERP without affecting conduction?

Back 56

Class III anti-arrhythmics

Front 57

Sotalol is good for ______ arrhythmias, while Dofetilide and Ibutilide are good for _____ arrhythmias.

Back 57

Ventricular--Atrial flutter and fibrillation

Front 58

Class IV drugs do what to the AP?

Back 58

Block slow Calcium channels and so decrease Phase 0 and Phase 4 of pacemaker cells

Front 59

What are Class IV drugs really good for and what are some toxicities?

Back 59

Supraventricular arrhythmias and ventricular arrythmias associated with AMI--can cause HF from negative inotropy, hypotension from excessive vasodilation, heart block, and constipation