Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

pharmocology > antirhythmics > Flashcards

antirhythmics Flashcards

1
Q

arrhythmia definition

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

percentage of anesthetized patients with arrhythmias

A

> 50%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

percentage of MI patients with arrhythmias

A

80%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

percentage of CPB patients with arrhythmias

A

100%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Virtually all antiarrhythmics work by

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

1a

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

1b

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

1c

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

2

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

3

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

4

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Class I : Na+ Channel Blockers affect on qrs

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

class 1 drugs preferentially bind to

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

how are class 1 drugs useful

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

class 1a effect on AP

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

DOUBLE QUARTER POUNDER

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

QUINIDINE USED FOR

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

QUINIDINE SIDE EFFECTS

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

torsades de pointes usually resolves

A

spontaneously but may devolve into v fib

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

quinidine historically used for

A

malaria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

disopyramide

A

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!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Procainamide only one you will see!!

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

procainamide side effects

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

class 1b na channel blockers

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

1b lettuce mayo tomato

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

lidocaine

A
  • 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
27
Q

lidocaine DOC for

A

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

28
Q

why is lidocaine in cardioplegia?

A

reduces irritibility minimizes ven. arrhythmias

29
Q

Mexiletine

A

Like an oral lidocaine

• Used in treatment of WHAT? v tach

30
Q

tocainamide why?

A

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!

31
Q

Class Ic : Na+ Channel Blockers

A

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.

32
Q

1C FRIES PLEASE

A

•Flecainide
(Tambocor)
•Propafenone (Rhythmol)

33
Q

Flecainide

A

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.

34
Q

PROPAFENONE

A

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

35
Q

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

A

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.

36
Q

WHAT ARRHYTHMIAS ARE BETA BLOCKERS USED FOR

A

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.)

37
Q

PROPRANOLOL

A

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

38
Q

metoprolol

A

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

39
Q

esmolol

A

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

40
Q

class 3 potassium channel blocker effect on ap

A
  • 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”.
41
Q

class 3 potassium blocker blocks reentrant arrythmia

A

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

42
Q

class 3 potassium channel blocker negative side effect

A

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

43
Q

AMIODARONE EFFECTS ALL___ AND IS DOC for

A

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
44
Q

amiodarone used for___. half life for

A

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

45
Q

amiodarone toxicity

A

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).

46
Q

potential problems with amiadorone

A

really complex and has a lot of drug interaction

47
Q

amiodarone side effects

A

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

48
Q

dronedarone half life side effects

A

( 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

49
Q

sotalol

A

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

50
Q

sotalol reduces

A

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.

51
Q

dofetilide doc for

A

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

52
Q

ibutilide doc amd properties

A 
corvert class 3 k blocker. Ibutilide has both Class III and IA antiarrhythmic properties
• D.O.C. for : atrial flutter
53
Q

class 3 are more prone to causing what type of arrythmia

A

torsades de pointes

54
Q

Class IV: Ca++ Channel Blockers

A

-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

55
Q

which calcium blockers do we use?

A

Verapamail > Cardizem > Nifedipine

56
Q

why not nifedipene for arrythmias

A

Nifedipene is more vascular affects and causes more arrythmias

57
Q

VERAPAMIL AND CARDIZEM

A

Used almost interchangeably for arrhythmias

, ANGINA,HYERTENSION, AV NODALREENTRANT TACHYCARDIA, ATRIAL FLUTTER

58
Q

VERAPAMIL AND CARDIZEM AVOID IN

A

HF

59
Q

VERAPAMIL CARDIZEM ARE USE DEPENDENT MEANING

A

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

60
Q

classless antiarrythmics

A

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

61
Q

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

A

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

62
Q

adenosine doc for

A

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

63
Q

adenosine moa and half life

A

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

64
Q

Magnesium Sulfate MOA and DOC

A

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

pharmocology (20 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions