antirhythmics

Question 1

arrhythmia definition

Answer 1

Abnormalities in the electrical impulse generation or conduction through the heart.”
…too slow, too fast, irregular, wrong direction, wrong origin, etc.

Question 2

percentage of anesthetized patients with arrhythmias

Answer 2

> 50%

Question 3

percentage of MI patients with arrhythmias

Answer 3

80%

Question 4

percentage of CPB patients with arrhythmias

Answer 4

100%

Question 5

Virtually all antiarrhythmics work by

Answer 5

altering the ionic transmembrane balance (Na+, Ca++, K+) orthe sympathetic tone to the heart.

Question 6

1a

Answer 6

na channel blocker. slows phase 0 depol. in ven. muscle fibers

Question 7

1b

Answer 7

na channel blocker. slows phase 3 repol. in ven. muscle fibers

Question 8

1c

Answer 8

na channel blocker. markedly slows phase 0 depol. in ven. muscle fibers

Question 9

2

Answer 9

beta adrenoreceptor blocker. inhibits phase 4 depol. in SA and AV node

Question 10

3

Answer 10

K hannel blocker. prolongs phase 3 repol. in ven. muscle fibers

Question 11

4

Answer 11

ca channel blocker. inhibits action potential in SA and AV node

Question 12

Class I : Na+ Channel Blockers affect on qrs

Answer 12

Ia: PROLONG the action potential and affect QRS complexes Ib: Shorten the action potential without affecting QRS. Ic: Do not shorten the action potential

Question 13

class 1 drugs preferentially bind to

Answer 13

open Na+ channels rather than to fully repolarized Na+ channels.
-Consequently Class I drugs preferentially block conduction in tissues that are depolarizing more frequently. This is called “use-dependence” blockade. u

Question 14

how are class 1 drugs useful

Answer 14

useful because tissue that are causing arrythmias are getting blocked. they go where they need to go

Question 15

class 1a effect on AP

Answer 15

hift the action potential (AP) to the right by slowing Phase 0 depolarization (hence their nickname, “membrane stabilizers”).
- -Ia’s also inhibit some K+ channels (Class III activity) which widens the AP causing prolonged QT intervals.

Question 16

DOUBLE QUARTER POUNDER

Answer 16

Disopyramide
(Norpace)
•Quinidine (Quinidex)
•Procainamide (Pronestyl, Procan)

Question 17

QUINIDINE USED FOR

Answer 17

Been around forever. Given orally. • Used for various tachyarrhythmias:

Question 18

QUINIDINE SIDE EFFECTS

Answer 18

cinchonism(diarrhea,vertigo,vomiting,confusion), torsads de pointes

Question 19

torsades de pointes usually resolves

Answer 19

spontaneously but may devolve into v fib

Question 20

quinidine historically used for

Answer 20

malaria

Question 21

disopyramide

Answer 21

Like Quinidine, but more negative inotropic effects and SVR
– Do you want these effects with a sick heart?
No, of course not… they might precipitate HF!

Question 22

Procainamide only one you will see!!

Answer 22

Most widely used Ia
• Derived from procaine (a local anesthetic…hmmm…we might hear more about those later on…)
• Given orally, IV, IM

Question 23

procainamide side effects

Answer 23

Adverse effects similar to Quinidine (although less severe) but may cause reversible lupus erythematosus

Question 24

class 1b na channel blockers

Answer 24

Shift the action potential (AP) to the left by shortening Phase 3 repolarization.
-Ib’s have their greatest effect on heart cells with long action potentials like Purkinje fibers and ventricular myocytes.

Question 25

1b lettuce mayo tomato

Answer 25

•Lidocaine (Xylocaine) •Mexiletine (Mextil) •Tocainide (Tonocard)

Question 26

lidocaine

Answer 26

* Local anesthetic * Only given parenterally * Wide therapeutic index (what’s this mean?) safe * Major toxic side effect (at high doses) is cardiac depression * Extends refractory period further into diastole in depressed cardiomyocytes than in healthy ones. (What does THAT mean?) so sick heart cell cant fire as fast

Question 27

lidocaine DOC for

Answer 27

entricular arrhythmias, particularly those associated with “sick hearts” with arrhythmias like post-MI.***

Question 28

why is lidocaine in cardioplegia?

Answer 28

reduces irritibility minimizes ven. arrhythmias

Question 29

Mexiletine

Answer 29

Like an oral lidocaine | • Used in treatment of WHAT? v tach

Question 30

tocainamide why?

Answer 30

ike lidocaine...blah, blah, blah. • Given orally • Used in patients resistant to &/or sensitive to lidocaine/mexiletine. • *Pulmonary toxicity fairly common—can cause pulmonary fibrosis rendering Tonocard a 2nd or 3rd line treatment!

Question 31

Class Ic : Na+ Channel Blockers

Answer 31

Does not shift the action potential. -Ic’s even have profound effects on normal hearts. Recent studies indicate some are very dangerous and are not used when better/safer alternatives exist.

Question 32

1C FRIES PLEASE

Answer 32

•Flecainide (Tambocor) •Propafenone (Rhythmol)

Question 33

Flecainide

Answer 33

Tambocor. Given orally • Suppresses Phase 0 upstroke in Purkinje fibers and cardiomyocytes. • Dramatically slows conduction and automaticity is decreased via an increase in the threshold potential (explain this). • Used for refractory ventricular arrhythmias (particularly PVCs). • Negative inotropic effects worsen CHF. • Recent studies suggest FlecainIDE is more likely to harm than help in the long-run.

Question 34

PROPAFENONE

Answer 34

Rhythmol. Similar uses as quinidine • Given orally • Considered to be a “broad spectrum” antiarrhythmic but used mostly for supraventricular tachyarrhythmias

Question 35

Class II :β-Adrenoceptor Blockers how they work on AP

Answer 35

β1-blockers are cardioselective but many/most have other adrenergic blocker activity. Some have partial adrenergic agonist activity. -Work by diminishing Phase 4 depolarization = DECREASE automaticity, prolonged AV conduction, negative chronotrope, negative inotrope.

Question 36

WHAT ARRHYTHMIAS ARE BETA BLOCKERS USED FOR

Answer 36

Atrial tachyarrhythmias: ...including AV nodal re-entrant tachyarrythmias (the most common type, particularly in women.)Also extensively used post-MI for those nasty ventricular arrhythmias (you know, the ones that kill.)

Question 37

PROPRANOLOL

Answer 37

INDERAL. non selective beta blocker Extensively used for decades. *Has been proven to decrease incidence of mortality within the first year of an MI.

Question 38

metoprolol

Answer 38

lopressor,toprol-XL. less B2 than inderal. most common beta blocker for arrythmias

Question 39

esmolol

Answer 39

brevibloc. very short acting. IV used during surgery/ emergencies

Question 40

class 3 potassium channel blocker effect on ap

Answer 40

- Block K+ channels with little effect on Na+ channels - By blocking the outward flow of K+ during repolarization they prolong the action potential without affecting Phase 0 (depolarization). - increase refractory period and “refractoriness”.

Question 41

class 3 potassium blocker blocks reentrant arrythmia

Answer 41

by increasing refractory period. if that wave comes back it will do nothing

Question 42

class 3 potassium channel blocker negative side effect

Answer 42

reverse use- dependence blockade” (remember “use- dependence blockade with Class I’s?) which can contribute to arrhythmias. (Please describe)BLOCK TISSUE THAT ARE NOT CAUSING MI prolong QT

Question 43

AMIODARONE EFFECTS ALL___ AND IS DOC for

Answer 43

CORDARONE. CLASS 3 K BLOCKER. It’s an “iodinated benzofuran” which means it looks a little like thyroxine. * Effects all cardiac tissues, so it has a broad- spectrum of antiarrhythmic activity. * Often the D.O.C. for A-fib

Question 44

amiodarone used for___. half life for

Answer 44

sed as a 2nd-line Rx for lots of refractory arrhythmias. • Very long half-life (20-100 days!) combined with high ability to interact with other drugs and a boat-load of side-effects (particularly with long-term use) limit its use. • Often D.O.C. for A-Fib

Question 45

amiodarone toxicity

Answer 45

Less toxicity at lower dosages (100- 200 mg/day)... • BUT at lower dosage it takes weeks to months to get to therapeutic levels (because of long half-life... • So you have to give high loading doses (800-1600 mg/day).

Question 46

potential problems with amiadorone

Answer 46

really complex and has a lot of drug interaction

Question 47

amiodarone side effects

Answer 47

hypotension, bradycardia, ards,pulmonary fibrosis, vomiting,jaundice,blueskin

Question 48

dronedarone half life side effects

Answer 48

( multaq) CLASS 3 K BLOCKER Like amiodarone without the iodine (whew, no thyroid dysfunction or blue skin!) • Much shorter half-life (24 hours) than amiodarone which means what? • Less effective than amiodarone for a-fib but has fewer of those side effects except increases stroke and death

Question 49

sotalol

Answer 49

betaspace,sorine CLASS 3 K BLOCKER wait, we’ve seen this before! • Yep, it’s a non-selective β-blocker. *Not only does it reduce post-MI mortality (as do most β-blockers) but it also has Class III activity (lengthening of refractory period

Question 50

sotalol reduces

Answer 50

CLASS 3 K BLOCKER myO2cardial consumption and acts as a powerful antiarrhythmic. *Helps prevent fibrillation and makes defibrillating patients easier so it’s ideal for post-MI patients.

Question 51

dofetilide doc for

Answer 51

tikosyn. CLASS 3 K BLOCKER. Often the D.O.C. for a-fib in patients with HF or EF’s.

Question 52

ibutilide doc amd properties

Answer 52

``` corvert class 3 k blocker. Ibutilide has both Class III and IA antiarrhythmic properties • D.O.C. for : atrial flutter ```

Question 53

class 3 are more prone to causing what type of arrythmia

Answer 53

torsades de pointes

Question 54

Class IV: Ca++ Channel Blockers

Answer 54

-Decrease the rate of Phase 4 spontaneous depolarization. -Class IV’s also preferentially slow the rate of conduction in tissues dependent on calcium currents for depolarization

Question 55

which calcium blockers do we use?

Answer 55

Verapamail > Cardizem > Nifedipine

Question 56

why not nifedipene for arrythmias

Answer 56

Nifedipene is more vascular affects and causes more arrythmias

Question 57

VERAPAMIL AND CARDIZEM

Answer 57

Used almost interchangeably for arrhythmias | , ANGINA,HYERTENSION, AV NODALREENTRANT TACHYCARDIA, ATRIAL FLUTTER

Question 58

VERAPAMIL AND CARDIZEM AVOID IN

Answer 58

HF

Question 59

VERAPAMIL CARDIZEM ARE USE DEPENDENT MEANING

Answer 59

(preferring to block channels on tissues depolarizing too fast) and block Ca++ channels most effectively on the AV and SA nodes

Question 60

classless antiarrythmics

Answer 60

Digoxin, Adenosine, and Magnesium sulfate(and they probably have fewer side-effects!)

Question 61

digoxin slows down ven response rates in a fib and a flutter how?

Answer 61

atria are peppering ventricles. as fast as they get through refractory period they fire. if you increase refractory period doesnt matter how fast atria are going

Question 62

adenosine doc for

Answer 62

adenocard. used for abolishing SVT on bypass cuz you have to give fast IV push

Question 63

adenosine moa and half life

Answer 63

it decreases AV node automaticity and cardiac conduction velocity and automaticity. • Has a very short half-life (~10-15 seconds!) and causes transient hypotension *First dose is 6 mg fast IV push *If that doesn’t convert the SVT give 12 mg fast IV push. GIVE THROUGH MANIFOLD. used for coming off bypass

Question 64

Magnesium Sulfate MOA and DOC

Answer 64

Among other things, it slows the rate of SA node impulse formation and the rate at which the impulse travels through myocardium • D.O.C.fordigoxin-inducedarrhythmias: • Must be given IV to be effective as an antiarrhythmic