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Anesthesia Pharm II-Josh > Antidysrhythmics ppt > Flashcards

Antidysrhythmics ppt Flashcards

Due to Mr. Boyd's inability to transpire his knowledge to the brains of the new and uprising stars study this to pass his section

1
Q

what are 2 major physiologic mechanisms that cause ectopic cardiac dysrhythmias are what?

A
  • reentry

- enhanced automaticity

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2
Q

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.

A
  • 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

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3
Q

When to treat dysrythmias during anesthesia?

A

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

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4
Q

classes of antidysrhythmics

A 
I-IV
for a bonus there is a class A B C for class I
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5
Q

Class I:
what group are they?
They work by inhibiting what?

A
  • SODIUM CHANNEL BLOCKERS

- inhibit fast Na+ channels

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6
Q

MOA for ALL class I drugs (sodium channel blockers)

A
  • 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
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7
Q

Class IA MOA

4

A
  • depress phase 0 depolarization
  • *prolong the action potential duration
  • slow conduction velocity
  • intermediate binding and dissociation from receptor
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8
Q

Class IB MOA

4

A
  • *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
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9
Q

What is the main difference b/t Class IA and IB

A
  • IA prolongs action potential duration

- IB shorten action potential duration

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10
Q

Class IC MOA

5

A

-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

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11
Q

If for every class I drug, you had to pick 4 main characteristics to differentiate them what are they? and then differentiate them

A

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

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12
Q

What is the most familiar class I group?

A

IB

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13
Q

which Class IA drug is very bad b/c it has active metabolites?

A

procainamide

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14
Q

Class IA drugs

A

Quinidine
Pocainamide
Disopyramide

The book adds -Moricizine

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15
Q

Class IB drugs

A

Lidocaine
Mexiletine
phenytoin

additional
Tocainide

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16
Q

Class IC drugs

A

Flecainide
Propafenone

additional
Lorainide
His chart has moricizine here??

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17
Q

Class II down and dirty MOA

A

decrease rate of depolarization

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18
Q

Class III down and dirty MOA

A

inhibit K+ channels

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19
Q

Class IV down and dirty MOA

A

inhibits slow Ca++ channels

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20
Q

Which Class IA drug increases SVR

A

Disopryamide

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21
Q

Class II drugs

A

remember they decrease the RATE of depolarization

  • Propanolol
  • Esmolol

Book also adds
Acebutolol

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22
Q

Class III drugs

A
  • Amiodarone
  • Ibutilide
  • Sotalol (II and III)

book adds
Dofetilide
bretylium

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23
Q

Which drug is both class II and III

A

Sotalol

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24
Q

Class IV drugs

A

remember inhibits slow Ca++ channels

  • verapamil
  • Diltiazem
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25
Q

what are 2 unclassified antidysrhythmic drugs

A

Digoxin (lanoxin)

Adenosine (adenocard)

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26
Q

Procainamide
class?
analog of what LA?
treats what?

A
  • IA
  • Procaine
  • Reentry and automaticity
  • ——Atrial and Ventricular tachydysrhythmias
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27
Q

Procainamide
SE?
Active metabolite?

A
  • Prolonged QT, QRS, ST-T changes (can develop heartblock) and Profound HYPOTENSION
  • N-acetyl procainamide (NAPA)-contributes to antidyrhythmic effects (K+ channel blockade)
28
Q

Procainamide

Metabolism

A

Renal 40%
hepatic 60%
–hepatic metabolism obviously causes active metabolites

29
Q

Procainamide

odd or unique SE besides the HYPOTENSION

A

Lupus like syndrome

30
Q

Procainamide
dose???
initial then titration

A
  • 100 mg Q5 min until dysrhythmia controlled or total dose reaches 15mg/kg
  • once controlled infuse 2-6mg/min
31
Q

Lidocaine
class?
treats what?

A
  • IB
  • primarily reentry
  • ——-Ventricular dysrhythmias
  • ——- PVC, V-tach
32
Q

Lidocaine

MOA

A

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

33
Q

Lidocaine

metabolism

A

hepatic- active metabolites

34
Q

Lidocaine

SE:

A
  • Toxic plasma concentration= vasodilation and myocardial depression
  • SZ @ plasma levels > 5 mcg/ml
  • CNS depression/apnea/arrest at plasma concentration > 10 mcg/ml
35
Q

Lidocaine

Dose? both load and infusion

A

load- 1-2 mg/kg

Infuse- 1-4 mg/min

36
Q

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

A
  • IB
  • reentry and automaticity
  • lidocaine
37
Q

Phenytoin

treats Ventricular Dysrhythmias associated with _____ toxicity

A

digitalis

38
Q

Phenytoin

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

A

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

39
Q

Phenytoin
metabolism
half time

A

hepatic

24 hours

40
Q

Phenytoin

SE

A
  • 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
Q

Beta Blockers
class?
actions?

A
  • II
  • decreased conduction velocity
  • Increased refractory period
  • Increased PR duration
  • Decreased QT duration
42
Q

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

A
  • K+, Ca++, Na+
  • APD ???? (action potential depolarization)
  • increased # of Ca++ channel numbers
43
Q

Class III

MOA?

A
  • Block inhibitory K+ channels

- Prolong action potential, repolarization and refractory period

44
Q

Amiodarone
class?
treat what?

A
  • III
  • reentry and automaticity
  • —-SVT, VT, and A-fib
45
Q

Amiodarone

suppresses tachydysrhythmias associated with what d/o?

A

WPW

46
Q

Amiodarone

may decrease mortality after what?

A

MI

47
Q

Amiodarone

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

A

1) - AV node

2) - bypass tracts

48
Q

Amiodarone

prolongs ______ ______ in all cardiac tissues?

A

Refractory period

49
Q

Amiodarone

is made up of 37% what?

A

iodine

cool fact

50
Q

Amiodarone

the antiadrenergic effect is due to blockade of what?

A

alpha and beta

- K+ and Ca++ channel blocking effects

51
Q

Amiodarone

had minor __1__ inotropic effects, and potent __2__ properties

A

1) negative

2) vasodilating

52
Q

Amiodarone

dilates _____ arteries, leading to questionable antianginal effects

A

Coronary arteries

53
Q

Amiodarone
T 1/2 ?
metabolism?

A

29 days

hepatic

54
Q

Amiodarone

SE?

A
  • 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
Q

Amiodarone

dose

A

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
Q

Sotalol

Class

A

II and III

57
Q

Sotalol

why is it 2 classes

A
  • nonselective Beta antagonist (low doses) II

- prolongs action potentials of all tissues (high doses) III

58
Q

Sotalol

excretion

A

Renal

59
Q

Sotalol

Main SE

A

Torsade de pointes!!!!!

60
Q

Digoxin
Class?
treats what?

A

Unclassified

- Atrial tachydysrythmias and Cardiac failure

61
Q

Digoxin

MOA (basic)

A

positive inotrope- through inhibition of the NA-K ATPase ion transport system

  • SLOWS CONDUCTION THROUGH AV NODE
  • thus increase SV and decreases LVEDP
62
Q

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

A

thus increase SV and decreases LVEDP

63
Q

Digoxin
positive __1__
Negative __2__

A

Lusitrope (myocardial relaxation)

Chronotrope (speed on contraction)

64
Q

Digoxin

narrow or wide therapeutic index (range)

A

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
Q

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

A

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

66
Q

Digoxin

symptoms of dig toxicity

A

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

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

Anesthesia Pharm II-Josh (8 decks)

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