Antidysrhythmics ppt Flashcards Preview

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Flashcards in Antidysrhythmics ppt Deck (66):
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

31

Lidocaine
class?
treats what?

-IB
-primarily reentry
--------Ventricular dysrhythmias
-------- PVC, V-tach

32

Lidocaine
MOA

decreases the rate of phase 4 repolarization by diminishing the decrease in K+ permeability
-Decreases AV node and HIS conduction in high doses

33

Lidocaine
metabolism

hepatic- active metabolites

34

Lidocaine
SE:

-Toxic plasma concentration= vasodilation and myocardial depression
-SZ @ plasma levels > 5 mcg/ml
- CNS depression/apnea/arrest at plasma concentration > 10 mcg/ml

35

Lidocaine
Dose? both load and infusion

load- 1-2 mg/kg
Infuse- 1-4 mg/min

36

Phenytoin
class?
treats what?
effects are similar to what other drug?

-IB
-reentry and automaticity
-lidocaine

37

Phenytoin
treats Ventricular Dysrhythmias associated with _____ toxicity

digitalis

38

Phenytoin
1) Shortens QT more than_______
2) Hypotension occurs with ______
3) may depress ___ node activity, improves ___ node activity

1) any other
2) rapid administration
3) SA node / AV node

39

Phenytoin
metabolism
half time

hepatic
24 hours

40

Phenytoin
SE

-Ataxia
-nystagmus
-vertigo
- slurred speech
- Sedation
- mental confusion ( >18mcg/ml blood level)
- inhibits insulin secretion (hyperglycemia)
-Leukopenia
-agranulocytosis
-thrombocytopenia
-BM ( not poop, bone marrow) suppression

41

Beta Blockers
class?
actions?

-II
- decreased conduction velocity
- Increased refractory period
- Increased PR duration
- Decreased QT duration

42

Carvedilol
also blocks what?
Modestly prolong ______
chronic administration causes what?

-K+, Ca++, Na+
- APD ???? (action potential depolarization)
-increased # of Ca++ channel numbers

43

Class III
MOA?

- Block inhibitory K+ channels
-Prolong action potential, repolarization and refractory period

44

Amiodarone
class?
treat what?

-III
- reentry and automaticity
-----SVT, VT, and A-fib

45

Amiodarone
suppresses tachydysrhythmias associated with what d/o?

WPW

46

Amiodarone
may decrease mortality after what?

MI

47

Amiodarone
decreases conduction in the __1__ __1__, and the __2__ __2__.

1)- AV node
2)- bypass tracts

48

Amiodarone
prolongs ______ ______ in all cardiac tissues?

Refractory period

49

Amiodarone
is made up of 37% what?

iodine
(cool fact)

50

Amiodarone
the antiadrenergic effect is due to blockade of what?

alpha and beta
- K+ and Ca++ channel blocking effects

51

Amiodarone
had minor __1__ inotropic effects, and potent __2__ properties

1) negative
2) vasodilating

52

Amiodarone
dilates _____ arteries, leading to questionable antianginal effects

Coronary arteries

53

Amiodarone
T 1/2 ?
metabolism?

29 days
hepatic

54

Amiodarone
SE?

-Pulm alveolities (5-15%) (acute or insidious)
-QT prolonged (brady, block, low CO)
-Antiadrenergic- accenuated under GA
-Depress Vit K factors
- corneal microdeposits, photosensitivity
-rash
-Cyanotic discoloration
-peripheral neuropathy
-weakness
- increased DIG levels (70%)
-thyroid abnormalities

55

Amiodarone
dose

150mg/100 mg over 10 min
gtt 900 mg/500 ml mix
1 mg/min x 6 hours
0.5 mg/min x 18 hours

56

Sotalol
Class

II and III

57

Sotalol
why is it 2 classes

- nonselective Beta antagonist (low doses) II
-prolongs action potentials of all tissues (high doses) III

58

Sotalol
excretion

Renal

59

Sotalol
Main SE

Torsade de pointes!!!!!

60

Digoxin
Class?
treats what?

Unclassified
- Atrial tachydysrythmias and Cardiac failure

61

Digoxin
MOA (basic)

positive inotrope- through inhibition of the NA-K ATPase ion transport system
-SLOWS CONDUCTION THROUGH AV NODE
-thus increase SV and decreases LVEDP

62

Digoxin
Bc we just learned that dig is positive inotrope- through inhibition of the NA-K ATPase ion transport system
-SLOWS CONDUCTION THROUGH AV NODE, what does this mean?????? only 2 correct answers!!!!! not 300 don't try it

thus increase SV and decreases LVEDP

63

Digoxin
positive __1__
Negative __2__

Lusitrope (myocardial relaxation)
Chronotrope (speed on contraction)

64

Digoxin
narrow or wide therapeutic index (range)

Narrow
this was a gimme if you missed it stand up drop your pants, put on golf cleats and donkey kick yourself in your pathetic little nut sac that hangs off your little NP vagina full of crayons and feces, you dumb dumb dumb fucktard bastard

65

Digoxin
Hypokalemia is induced by what?
What occurs during this dig toxicity and hypokalemia?

-dig toxicity
-HypoK+- increased myocardial binding
- hyperventilation
-hyperCa++
-hypoMg
impaired renal function

66

Digoxin
symptoms of dig toxicity

--Early signs
Anorexia/ N/V/ pain stimulating trigeminal neuralgia

- other signs
- Prolonged PR
-degrading block
- atrial tachy with block
-V-fib- arrest