Dd&t2 Antiarrhythmic Agents

Front 1

What is the biggest issue with antiarrhythmic drugs?

Back 1

Narrow therapeutic range

Front 2

What is the most common mechanism for antiarhythmic drugs?

Back 2

Reducing the rate of spontaneous discharge in automatic tissues

Front 3

What are the four goals of antiarrhythmic drugs?

Back 3

Suppress the initiating mechanism (often premature beats), alter/terminate a reentrant circuit by blocking propagation of the action potential, slow automatic rhythms, abolish triggered activity

Front 4

Na channel blocking drugs: depend on?

Back 4

heart rate and membrane potential

Front 5

Na channel blocking drugs: 3 general effects?

Back 5

Slowed conduction in fast response tissue (increased QRS duration), increased refractoriness (to terminate reentry and allow less room for premature beats), increased threshold (reduces phase 4 automaticity)

Front 6

What are the affects of Na channel blocking drugs on the EKG?

Back 6

Decreased automaticity, increased QRS duration, little effect on APD/QT interval, drugs with long trecovery (most potent blockers) can also increase the PR interval

Front 7

What are the proarrhythmic effects of Na channel blocking drugs?

Back 7

Conduction slowing could actually enhanced the conditions for reentry and worse arrhythmias. Drugs with a long t-recovery are prone to 1:1 atrial flutter with fast ventricular rate.

Front 8

What are the 4 effects of beta-adrenergic receptor stimulation?

Back 8

Increases magnitude of Ca current (decreased PR inteval), increases repolarizing current (K and CL) - decreased QT interval, increased pacemaker current, can increased triggered arrhythmias

Front 9

What are the 2 effects of beta-adrenergic receptor blockade?

Back 9

Suppressed SA nodal automaticity (slows sinus rate), inhibits Ca current in slow response tissue (increased PR interval and slow AV nodal conduction)

Front 10

What are the side effects of beta blockers?

Back 10

Bradycardia, heart block, fatigue, bronchospasm, impotence, aggravation of heart failure; good one - reduced mortality after MI

Front 11

What drug causes action potential prolongation?

Back 11

K channel block

Front 12

What are the effects of K channel blockers?

Back 12

Reduced normal automaticity, prologned APD and refractoriness (increased QT interval),

Front 13

What are the side effects of K channel blockers?

Back 13

Can cause proarrhythmia (torsades de Pointes)

Front 14

What are the effects of Ca channel blockers?

Back 14

Slows conduction/increases refractoriness in slow response tissue - slows sinus rate, increased PR interval, slows AV nodal conduction

Front 15

How do beta blockers and Ca channel blockers differ clinically?

Back 15

Ca channel blockers do not reduce mortality in patients after an acute MI

Front 16

What are the side effects of Ca channel blockers?

Back 16

Severe sinus bradycardia or heart block, depression of cardiac contractility

Front 17

What are the 4 classes of antiarrhythmic drugs?

Back 17

I (Na channel blockers), II (beta adrenergic receptor blockers), III (APD prolongation - K channel blockers), IV (Ca channel blockers)

Front 18

What are the 3 subtypes of Na channel blockers?

Back 18

I (intermediate time course of recovery from Na block), II (fast recovery from Na block), III (very slow recovery from Na block)

Front 19

Class Ia

Back 19

Quinidine, procainamide

Front 20

Class Ib

Back 20

Lidocaine

Front 21

Class Ic

Back 21

Flecainide

Front 22

Class II

Back 22

Sotalol, esmolol

Front 23

Class III

Back 23

amiodarone, sotalol

Front 24

Class IV

Back 24

Verapamil, Diltiazem, adenosine

Front 25

Which group of Na channel blockers doesn't work in the atrium?

Back 25

Ib

Front 26

EKG changes of Ia

Back 26

Increased QRS (especially at high rates or high conc.), increased QT

Front 27

EKG changes of Ib

Back 27

no major changes

Front 28

EKG changes of Ic

Back 28

Increased PR, increased QRS

Front 29

When is DC cardioversion the treatment of choice?

Back 29

For any unstable rhythm causing hemodynamic compromise

Front 30

Quinidine MOA

Back 30

Blocks Na and multiple K currents, with an alpha receptor block and vagal inhibition

Front 31

Quinidine clinical use

Back 31

Chronic oral therapy of atrial fib/flutter (and VT in patients with ICDs)

Front 32

Quinidine Aes

Back 32

Diarrhea/GI, may increase mortality in patients with a fib/flutter, torsades de pointes, cinchonism

Front 33

Procainamide uses

Back 33

effective IV for supraventricular and ventricular arrhythmias

Front 34

What do you watch for with procainamide usage?

Back 34

Hypotension, marked slowing of conduction, QRS prolongation

Front 35

Describe the metabolism of procainamide.

Back 35

Metabolized in NAPA which blocks K channels only, must dose adjust in renal disease

Front 36

What is the side effect of procainamide?

Back 36

Lupus syndrome during chronic oral therapy

Front 37

Lidocaine uses

Back 37

Decreases incidence of ventricular fibrillation in coronary care unit (but increases mortality)

Front 38

Describe the pharmacokinetics for lidocaine.

Back 38

Rapid distribution to plasma (8 min T1/2) with slower elimination (108 min) mandates a complex loading scheme. An increased infusion rate will just get you to a different steady state, not help you get there faster.

Front 39

Flecainide clinical use

Back 39

Suppresses isolated ventricular premature beats and reentrant supraventricular tachycardia; approved for supraventricular arrhythmias

Front 40

What is the main side effect of flecainide.

Back 40

Increased mortality in patients following an MI, aggravation of heart failure

Front 41

esmolol general description

Back 41

ultra-short-acting Beta1 selective IV beta blocker

Front 42

When is esmolol useful?

Back 42

When you'd like to try a beta blocker but are worried that they patient might develop severe side effects

Front 43

What is amiodarone used for?

Back 43

Refractor VT/VF, prominent in ACLS protocols, also used for prevention of atrial fibrillation/flutter

Front 44

Describe the actions of amiodarone

Back 44

Classes I, II, III, and IV

Front 45

What is the problem with amiodarone?

Back 45

Very effective for most arrhythmias, but can't be used as first line therapy due to multiple toxicities (lungs, eyes, liver, skin, thyroid during chronic treatment)

Front 46

How must amiodarone be dosed and why?

Back 46

Loading regiment used due to extraordinarily long elimination half life - need a slow accumulation to steady state

Front 47

How does amiodarone interact with other drugs?

Back 47

Potently inhibits the hepatic metabolism/renal elimination of many compounds - warfarin, digoxin

Front 48

Sotalol MOA

Back 48

Non-selective beta blocker and K channel blocker

Front 49

Sotalol uses

Back 49

Supraventricular and ventricular arrhythmias (wide variety)

Front 50

Sotalol side effects

Back 50

Dose-related incidence of Torsades de Pointes, beta-blocker side effects

Front 51

Verapamil MOA

Back 51

Ca channel blocker having the most potent AV nodal blocking properties

Front 52

Verapamil administration

Back 52

IV - may cause hypotension, limiting its use (especially if other vasodilators or with left ventricular dysfunction)

Front 53

When do you avoid using verapamil?

Back 53

Undiagnosed wide complex tachycardia, WPW, heart failure, AV block, sinus node dysfunction

Front 54

Dilatiazem usage, administration

Back 54

IV form, preferred AV nodal blocker usually without hypotension

Front 55

Adenosine affects

Back 55

AV nodal blocker, very short acting

Front 56

What is adenosine the DOC for?

Back 56

Supraventricular tachycardias, undiagnosed wide-complex tachycardia

Front 57

How is adenosine administered?

Back 57

Rapid intravenous push

Front 58

Side effects of adenosine

Back 58

Chest pain, shortness of breath (patient SHOULD feel this)