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Flashcards in Muscle Relaxants Deck (20):
1

Neuromuscular junction and Ach receptor

-binding of 2 Ach molecules to the paired alpha (not beta) subunits results in Na and Ca to flow down their [ ] gradients into the cell and K to flow down its [ ] gradient out of the cell
-movement of cations leads to end-plate potential and depolarizes perijunctional membrane, leading to opening of voltage-gated Na channels-->action potential
-action potential activates Na channel receptors on T-tubule system and Ca is released by sarcoplasmic reticulum-->contraction

2

Myasthenia Gravis and effect on neuromuscular blockade

-autoimmune or congenital, antibodies to AchR

*decreased sensitivity to sux: increased dosage of a depolarizing agent is required to achieve Phase 1 blockage because you must active enough Ach receptors

*increased sensitivity to non-depolarizers: reduced dose of nondepolarizer needed because there are fewer Ach receptors (fewer receptors to occupy for a given effect)

3

Eaton-Lambert Syndrome (ELS)

aka myasthenic syndrome
-reduced amount of presynaptic Ach-->up-regulation of AchR at NMJ
-increased sensitivity to both NDNMB and sux
*sux: more receptors=easier to depolarize=smaller dose needed
*non-depolarizers (competitive inhibition w/Ach): less Ach=less competition=smaller dose needed

4

Meaning of fade on TOF

1. non-depolarizing muscle relaxants
or
2. phase II block w/sux

5

Phase II block

-prolonged depolarization of the perijunctional muscle endplate results in conformational changes to the Ach-R, such that it resembles the block of a nondepolarizer

6

TOF=% blockade

1/4=90%
2/4=80%
3/4=75%

7

Succinylcholine and fasciculations

-increased ICP and abdominal pressure (strongest correlation)
-diffuse myalgia (strong association, but not 100%)
-increased abdominal pressure offset by increase in LES tone (no change in aspiration risk)
-intraocular pressure increases w/sux independent of fasciculations

8

Most common side effect of muscle relaxants
-Benzylisoquinolones (-curium)
-Steroidals (-curonium)

-Benzylisoquinolones (-curium): histamine release-->flushing, vasodilation, and bronchospasm
*mivacurium and atracurium most likely

-Steroids (-curonium): vagolytic-->tachycardia and HTN

9

Effect of giving neostigmine before succinylcholine

Prolonged duration of action of sux
-neostigmine inhibits pseudocholinesterase

10

Causes of muscle blockage prolongation

-Volatiles
-Magnesium
-Hypocalcemia
-Hypokalemia
-Acidosis
-Hypothermia
*Neonates (more sensitive than adults)

11

Anti cholinesterase drugs and effect on succinylcholine
-neostigmine
-physostigmine
-edrophonium

-neostigmine: inhibits pseudocholinesterase-->prolongs sux duration
-physostigmine: inhibits pseudocholinesterase (less than neostigmine)-->slightly prolongs sux duration
-edophonium: no effect on pseudocholinesterase-->no change in sux duration

12

Cerebral Palsy effect on muscle relaxants

-normal response to sux: no increased risk of hyperkalemia, even in setting of contractures, as there is no proliferation of exntrajunctional nicotinic AchR

-resistant to nondepolarizers

13

Extensive burns and effect on muscle relaxants

-resistance to nondepolarizers (increased receptors)

-hyperkalemia w/sux (extrajunctional proliferation)

14

SLE and effect on muscle relaxants

Sensitivity to nondepolarizers AND depolarizers
*autoimmune disorders in general have hypersensitivity to all muscle relaxants (likely only true for those disorders with rheumatologically derived weakness)

15

Cisatracurium Metabolism

1. Hoffman elimination- organ-independent, occurs in plasma, slowed by hypothermia
2. Laudanosine- byproduct metabolized in liver and excreted by kidneys, CNS excitation at high levels (no intrinsic neuromuscular blockade)
3. Atracurium also produces laudanoside: atra is less potent than cis, so greater dose required and thus increased levels of laudanosine w/atra compared to cis

*cisatricurium not associated w/histamine release (atracurium is)

16

Prolonged vecuronium gtt side effect

Prolonged polyneuropathy w/muscle weakness lasting months, especially in setting of steroid use
*does not occur in the OR, even with longs cases and steroids (nor w/roc or panc)

17

Metabolism of NDNMBDs
-pancuronium
-vecuronium
-rocuronium

Liver failure?

Spectrum: panc-->vec-->roc
-Pancuronium: most metabolism (liver), greatest amount of renal excretion (40%), and least amount of bile excretion (10%)
-Vecuronium: minimal metabolism, 25% renal excretion, and 75% bile excretion
-Rocuronium: no metabolism (essentially) and thus no metabolites, least renal excretion (10% excreted in urine unchanged), and most bile excretion

Liver failure w/poor bile excretion: rocuronium is not excreted-->prolongs blockade

18

Extubation criteria

-TV >5 cc/kg
-VC >10 cc/kg
-NIF 5 seconds
-Head lift >5 seconds
-RSBI <105

19

RSBI

RR/TV
*low = slow, large breaths

20

Neostigmine:
-onset, peak, duration
-Crosses placenta?
-Crosses BBB?

-Onset 5 min, peak effect 10 min, duration 1 hour
-Crosses the placenta (glycopyrolate does not, so use atropine!)
-Does NOT cross BBB (physostigmine does- used to "reverse" scopolamine induced central anticholinergic syndrome)