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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

Procainamide
dose???
initial then titration

-100 mg Q5 min until dysrhythmia controlled or total dose reaches 15mg/kg
-once controlled infuse 2-6mg/min