Flashcards in Antidysrhythmics ppt Deck (66)
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1
what are 2 major physiologic mechanisms that cause ectopic cardiac dysrhythmias are what?
-reentry
-enhanced automaticity
2
What factors can cause cardiac dysrhythmias? This is a huge card don't get overwhelmed look it through very important he and the book make a big deal about it.
-Arterial hypoxemia
-Electrolyte abnormality (hypokalemia or hypomagnesemia from diuretics predispose to ventricular dysrhythmias )
-Acid-base abnormalities (alkalosis more likely than acidosis to trigger cardiac dysrhythmia {i dunno I found that cool})
-Altered autonomic nervous system activity (increased activity predisposes to ventricular fibrillation)
-Bradycardia (predisposes to ventricular dysrhythmias)
-drugs (prolong QT-congenital or acquired) acquired (drugs)- hypoK, HypoMg, hypoCa, quinidine, amiodarone, metoclopramide, CCB, droperidol, haloperidol, R on T phenomenon
-Myocardial ischemia
-altered sympathetic activity (lowers fibrillatory threshold)
-Dilated cardiomyopathy (cells stretch)
All on pg 336 Nag
3
When to treat dysrythmias during anesthesia?
trick question...
the majority of cardiac dysrhythmias that occur during anesthesia DO NOT REQUIRE TREATMENT.
Treat only if
-can't fix cause
-hemodynamic compromise
-can degrade to a more serious dysrythmia
4
classes of antidysrhythmics
I-IV
for a bonus there is a class A B C for class I
5
Class I:
what group are they?
They work by inhibiting what?
-SODIUM CHANNEL BLOCKERS
- inhibit fast Na+ channels
6
MOA for ALL class I drugs (sodium channel blockers)
-Block fast inward Na+ current and can decrease the rate of phase 0 depolarization
-ALL CLASS I DRUGS-
1) depress automaticity
2) depress conduction in bypass tracts
3) have a depressant effect on phase 0 depolarization @ rapid heart rates
7
Class IA MOA
(4)
-depress phase 0 depolarization
**prolong the action potential duration
- slow conduction velocity
- intermediate binding and dissociation from receptor
8
Class IB MOA
(4)
**shorten the action potential duration
** little effect on phase 0 depolarization
**** most rapid binding and dissociation
**** bind in the inactive state- more effective for tachy
9
What is the main difference b/t Class IA and IB
- IA prolongs action potential duration
- IB shorten action potential duration
10
Class IC MOA
(5)
-Marked depress Phase 0 depolarization
**** Minimal effect on the action potential duration
Profoundly slow conduction velocity
-slowest binding and dissociation
-Use dependent CV and QRS duration
11
If for every class I drug, you had to pick 4 main characteristics to differentiate them what are they? and then differentiate them
1) phase 0 depol
2) action potential
3) binding and dissociation
4) conduction velocity
1) phase 0 depol
-- IA -depresses
-- IB- little effect
-- IC- Marked depress
2) action potentials
--IA- prolongs
--IB- shortens
--IC- minimally effects
3) binding and dissociation
--IA- intermediate
--IB- most rapid
--IC- slowest
4) Conduction Velocity
--IA-slow
--IB-n/a
--IC- profoundly
12
What is the most familiar class I group?
IB
13
which Class IA drug is very bad b/c it has active metabolites?
procainamide
14
Class IA drugs
Quinidine
Pocainamide
Disopyramide
The book adds -Moricizine
15
Class IB drugs
Lidocaine
Mexiletine
phenytoin
additional
Tocainide
16
Class IC drugs
Flecainide
Propafenone
additional
Lorainide
His chart has moricizine here??
17
Class II down and dirty MOA
decrease rate of depolarization
18
Class III down and dirty MOA
inhibit K+ channels
19
Class IV down and dirty MOA
inhibits slow Ca++ channels
20
Which Class IA drug increases SVR
Disopryamide
21
Class II drugs
remember they decrease the RATE of depolarization
- Propanolol
- Esmolol
Book also adds
Acebutolol
22
Class III drugs
-Amiodarone
-Ibutilide
-Sotalol (II and III)
book adds
Dofetilide
bretylium
23
Which drug is both class II and III
Sotalol
24
Class IV drugs
remember inhibits slow Ca++ channels
- verapamil
-Diltiazem
25
what are 2 unclassified antidysrhythmic drugs
Digoxin (lanoxin)
Adenosine (adenocard)
26
Procainamide
class?
analog of what LA?
treats what?
-IA
-Procaine
-Reentry and automaticity
-------Atrial and Ventricular tachydysrhythmias
27
Procainamide
SE?
Active metabolite?
-Prolonged QT, QRS, ST-T changes (can develop heartblock) and Profound HYPOTENSION
-N-acetyl procainamide (NAPA)-contributes to antidyrhythmic effects (K+ channel blockade)
28
Procainamide
Metabolism
Renal 40%
hepatic 60%
--hepatic metabolism obviously causes active metabolites
29
Procainamide
odd or unique SE besides the HYPOTENSION
Lupus like syndrome
30
