antirhythmics Flashcards
arrhythmia definition
Abnormalities in the electrical impulse generation or conduction through the heart.”
…too slow, too fast, irregular, wrong direction, wrong origin, etc.
percentage of anesthetized patients with arrhythmias
> 50%
percentage of MI patients with arrhythmias
80%
percentage of CPB patients with arrhythmias
100%
Virtually all antiarrhythmics work by
altering the ionic transmembrane balance (Na+, Ca++, K+) orthe sympathetic tone to the heart.
1a
na channel blocker. slows phase 0 depol. in ven. muscle fibers
1b
na channel blocker. slows phase 3 repol. in ven. muscle fibers
1c
na channel blocker. markedly slows phase 0 depol. in ven. muscle fibers
2
beta adrenoreceptor blocker. inhibits phase 4 depol. in SA and AV node
3
K hannel blocker. prolongs phase 3 repol. in ven. muscle fibers
4
ca channel blocker. inhibits action potential in SA and AV node
Class I : Na+ Channel Blockers affect on qrs
Ia: PROLONG the action potential and affect QRS complexes Ib: Shorten the action potential without affecting QRS. Ic: Do not shorten the action potential
class 1 drugs preferentially bind to
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 are class 1 drugs useful
useful because tissue that are causing arrythmias are getting blocked. they go where they need to go
class 1a effect on AP
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.
DOUBLE QUARTER POUNDER
Disopyramide
(Norpace)
•Quinidine (Quinidex)
•Procainamide (Pronestyl, Procan)
QUINIDINE USED FOR
Been around forever. Given orally. • Used for various tachyarrhythmias:
QUINIDINE SIDE EFFECTS
cinchonism(diarrhea,vertigo,vomiting,confusion), torsads de pointes
torsades de pointes usually resolves
spontaneously but may devolve into v fib
quinidine historically used for
malaria
disopyramide
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!
Procainamide only one you will see!!
Most widely used Ia
• Derived from procaine (a local anesthetic…hmmm…we might hear more about those later on…)
• Given orally, IV, IM
procainamide side effects
Adverse effects similar to Quinidine (although less severe) but may cause reversible lupus erythematosus
class 1b na channel blockers
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.
1b lettuce mayo tomato
•Lidocaine
(Xylocaine)
•Mexiletine (Mextil)
•Tocainide (Tonocard)
lidocaine
- 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
lidocaine DOC for
entricular arrhythmias, particularly those associated with “sick hearts” with arrhythmias like post-MI.***
why is lidocaine in cardioplegia?
reduces irritibility minimizes ven. arrhythmias
Mexiletine
Like an oral lidocaine
• Used in treatment of WHAT? v tach
tocainamide why?
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!
Class Ic : Na+ Channel Blockers
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.
1C FRIES PLEASE
•Flecainide
(Tambocor)
•Propafenone (Rhythmol)
Flecainide
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.
PROPAFENONE
Rhythmol. Similar uses as quinidine
• Given orally
• Considered to be a “broad spectrum” antiarrhythmic but used mostly for supraventricular tachyarrhythmias
Class II :β-Adrenoceptor Blockers how they work on AP
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.
WHAT ARRHYTHMIAS ARE BETA BLOCKERS USED FOR
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.)
PROPRANOLOL
INDERAL. non selective beta blocker Extensively used for decades.
*Has been proven to decrease incidence of mortality within the first year of an MI.
metoprolol
lopressor,toprol-XL. less B2 than inderal. most common beta blocker for arrythmias
esmolol
brevibloc. very short acting. IV used during surgery/ emergencies
class 3 potassium channel blocker effect on ap
- 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”.
class 3 potassium blocker blocks reentrant arrythmia
by increasing refractory period. if that wave comes back it will do nothing
class 3 potassium channel blocker negative side effect
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
AMIODARONE EFFECTS ALL___ AND IS DOC for
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
amiodarone used for___. half life for
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
amiodarone toxicity
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).
potential problems with amiadorone
really complex and has a lot of drug interaction
amiodarone side effects
hypotension, bradycardia, ards,pulmonary fibrosis, vomiting,jaundice,blueskin
dronedarone half life side effects
( 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
sotalol
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
sotalol reduces
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.
dofetilide doc for
tikosyn. CLASS 3 K BLOCKER. Often the D.O.C. for a-fib in patients with HF or EF’s.
ibutilide doc amd properties
corvert class 3 k blocker. Ibutilide has both Class III and IA antiarrhythmic properties • D.O.C. for : atrial flutter
class 3 are more prone to causing what type of arrythmia
torsades de pointes
Class IV: Ca++ Channel Blockers
-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
which calcium blockers do we use?
Verapamail > Cardizem > Nifedipine
why not nifedipene for arrythmias
Nifedipene is more vascular affects and causes more arrythmias
VERAPAMIL AND CARDIZEM
Used almost interchangeably for arrhythmias
, ANGINA,HYERTENSION, AV NODALREENTRANT TACHYCARDIA, ATRIAL FLUTTER
VERAPAMIL AND CARDIZEM AVOID IN
HF
VERAPAMIL CARDIZEM ARE USE DEPENDENT MEANING
(preferring to block channels on tissues depolarizing too fast) and block
Ca++ channels most effectively on the AV and SA nodes
classless antiarrythmics
Digoxin, Adenosine, and Magnesium sulfate(and they probably have fewer side-effects!)
digoxin slows down ven response rates in a fib and a flutter how?
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
adenosine doc for
adenocard. used for abolishing SVT on bypass cuz you have to give fast IV push
adenosine moa and half life
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
Magnesium Sulfate MOA and DOC
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
