Cardio-Antiarrythmics

Question 1

Class I Anti-arrythmics MOA

Answer 1

block fast inward Na channels

in conductive tissues of the heart

Question 2

Class 1A agents (3)

Answer 2

Quinidine
Procainamide
Disopyramide

Question 3

Class 1B agents (2)

Answer 3

Lidocaine

Mexiletine

Question 4

Class 1C agents (2)

Answer 4

Propanefone

Flecainamide

Question 5

Class I Anti-Arrythmics Uses

Answer 5

Ventricular dysrhythmias and/or digitalis or MI-induced arrythmia

Question 6

Clinical applications of quinidine

Answer 6

refractory patients

to convert AFib or FLutter, Prevent recurrences of AFib, treat life-threatining ventricular arrythmias

Question 7

Procainamide MOA

Physiolgical effects

Answer 7

blocks Na channels

blocks K channels

Slowed conduction, automaticity, excitability

Prolongs APD and refractoriness

Question 8

Procainamide clinical uses

Answer 8

Acute treatment of:
reentrant SVT
A-Fib
Atrial flutter associated with WPW Syndrome

Life-threatening ventricular arrythmias

HAS TO BE DELIVERED SLOWLY OVER TIME

Question 9

Procainamide Adverse Effects

Answer 9

Cardiac - arrythmia aggravation, torsades, long QT syndrome

Non-cardiac: SLE-like syndrome, GI nausea and vomiting

Question 10

Lidocaine Clinical Uses

Pharmacologic implications

Answer 10

second choice for life-threatening/sympotmatic arrythmias

Extensive 1st pass metabolism - needs IV use with multiple loading doses and a maintenance infusion

Question 11

Propafenone MOA

Physiological effects

Answer 11

strong inhibitor of Na channels

strong effects on phase 0 depolarization

lengthened QRS and APD, PR as well

Question 12

Propanefone clinical uses

Answer 12

atrial arrythmias, PSVT

ventricular arrythmias in patient with no or minimal heart disease and PRESERVED VENTRICULAR FUNCTION

Question 13

Flecainide MOA

Clinical use

Answer 13

strong Na inhibitor

severely slows ventricular conduction

REFRACTORY life-threatening ectopic ventricular arrythmia

Question 14

Class II Anti-arrythmics MOA

Answer 14

Beta-adrenergic antagonists

Decreased SA node automaticity, Decreased AV node conduction, Decreased Ventricular contractility

Question 15

Class II Anti-arrythmics Clinical uses

only drugs found to what?

Answer 15

supra-ventricular tachycardias d/t increased sympathetic activity

preventing sudden death in patients with prior MI

Question 16

Class III Agents MOA

Answer 16

Potassium (HIGHEST EFFECT), Calcium, and Na channels

Beta-receptor blockers

Main effect = Prolong phase 3 repolarization = increased QT interval

Question 17

Class III Anti-arrythmics (5)

Answer 17

Dronedarone
Amiodarone
Sotalol
Ibutilide
Defetilide

Question 18

Class III Anti-arrythmics Clinical uses

Answer 18

wide range of different arrythmias

Question 19

Amiodarone MOA and Effects

Answer 19

Blocks K+ channels - prolongs refractoriness and APD

Blocks Na+ channels that are in the inactivated state

Block Ca2+ channels - slows SA node phase 4

Slows conduction through the AV node

Question 20

Amiodarone important clinical use

Answer 20

acute termination of V-tac or V-fib

Question 21

Important Clinical Pharmacology Points for Amiodarone

Answer 21

highly lipid-soluble (high Vd)

Metabolized to DEA - has even higher anti-arrythmic potency than amiodarone

Wide range of half life

rapidly redistributed out of myocardium until all tissues are saturated

Question 22

Amiodarone adverse effects (only 3-4% of people)

Answer 22

High dose IV can decrease cardiac contractility and hypotension

Interstitial pneumonitis (MAJOR SIDE EFFECT)

Hyper or hypothyroidism

Question 23

Class IV Anti-arrythmics

Answer 23

Verapamil

Diltiazem

Question 24

Major Cardiovascular sites of Class IV MOA

Answer 24

Vascular smooth muscle
Cardiac myocytes
SA and AV nodes

Question 25

Do CCB's bind to all pores of the L-type Calcium channels?

Answer 25

No, only Motif IV

Question 26

Two Classes of CCB's

Answer 26

Dihydropyridine - Nifedipine Non-dihydropyridine - Verapamil, Diltiazem

Question 27

Dihydropyridinemainly effects? Non-dihydropyridine mainly effects?

Answer 27

vasculature heart

Question 28

Major Cardiovascular Actions of CCB's

Answer 28

more marked vasodilation in arterial/arteriolar vessels - DECREASES AFTERLOAD Negative chronotropic/dromotropic - NDHP agents only

Question 29

Main Clinical Applications of CCB's

Answer 29

Systemic HTN Angina Pectoris SVT Post-Infarct protection

Question 30

Verapamil Clinical application

Answer 30

Supraventricular tachycarida Rate control in A-Fib

Question 31

Verapamil Adverse effects (2) Contraindications

Answer 31

Constipation EXACERBATE CHF WPW syndrome with A-Fib V-Tac

Question 32

Miscellaneous Anti-arrythmics

Answer 32

Adenosine, digoxin, ....

Question 33

Adenosine MOA

Answer 33

activates A1 receptor in SA and AV nodes increases cAMP-independent, ACh/Adosensitive K channels Activates A2 receptors in vasculature - potassium channel - vasodilation

Question 34

Adenosine physiological effect

Answer 34

SA node hyperpolarization Decreased firing rate Shortened AP duration of atrial cells Depression of AV Conduction

Question 35

Adenosine clinical applications Clinical pharmacology

Answer 35

Conversion of paroxysmal SVT caused by re-entry Must use IV Bolus to a central vein 10-15 second half-life

Question 36

Sinus tachycardia, PSVT -treatment

Answer 36

vagal stimulation through carotid sinus massage or valsalva maneuver