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23 spring anesthesia > Test 3: 43 neuromuscular > Flashcards

Test 3: 43 neuromuscular Flashcards

1
Q

why use neuromuscular blocking agents

A

make tracheal intubation easier
reduced skeletal muscle tone at lighter anesthetic planes
prevention of patient movement
keeps eyes in place
control respiration

does not provide analgesia, may need to ventilate if diaphragm is affected, does not affect consciousness

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2
Q

ACh binds to — receptor on the muscle cell

A

nicotinic cholinergic receptors

2 ACh binds to ion channel that lets Na, Ca in and K out

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3
Q

what breaksdown ACh

A

Acetylcholinesterase (AChE) rapidly hydrolyzes ACh

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4
Q

how does NMJ work

A

Action potential arrives at the pre-junctional motor nerve ending → nerve terminal depolarizes → adenylate cyclase converts ATP to cyclic AMP → Ca2+ enters into the nerve terminal → causes release of ACh into the synaptic cleft → ACh binds to the post-junctional receptor → Ion channels open; sodium, calcium influx, potassium effluxes → post-junctional muscle cell is depolarized → ACh is hydrolyzed by acetylcholinesterase, removed from the receptor, and
repolarization occurs

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5
Q

how do depolarizing agents work

A

mimic ACh- cause prolonged depolarization and activation of channels

Phase 1: bind and cause fasciculations

Phase II: Ach receptors become desensitized → flaccid paralysis

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6
Q

how do non-depolarizing agent work

A

bind ACh but cannot induce the conformational
change needed to open the ion channel

  • No phase 1 block- no AP is made
  • NMB can occur even even if only one a-subunit is blocked- decouples AP transmission and muscular contraction, causing paralysis
  • Function as ACh receptor competitive antagonists, outcompete ACh based on concentration
  • Success of NMB depends on the concentration of NMBA vs concentration of ACh
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7
Q

— is a depolarizing NMBA

A

succinylcholine

only small amount gets to NMJ, because it is apidly hydrolyzed by the enzyme pseudocholinesterase (plasma cholinesterase) that are made by the liver

causes transient paralysis as drug diffuses away

Greater dose administered= faster onse

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8
Q

pancuronium

A

aminosteroid non depolarizing NMBA

  • Onset is about 5 mins, duration of action 40-50 mins
  • Also blocks cardiac muscarinic receptors, causing ↑HR
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9
Q

atracurium is a — NMDA

A

short acting non depolarizing NMDA
(Benzylisoquinolones)

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10
Q

what is hofmann elimination

A

spontaneous degradation without enzymes; temperature and pH- dependent

Atracurium- short-acting non-depolarizing NMBA

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11
Q

how is atracurium broken down

A

Hofman elimination- spontaneous degradation without enzymes; temperature and pH-dependent

Can give to patients with hepatic or renal insufficiency without increasing duration of action

Atracurium- short-acting non-depolarizing NMBA

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12
Q

Cisatracurium

A

4x potency of atracurium and even further reduced histamine release compared to atracurium though has similar onset and duration of action, 5 mins and duration is about 30 min

Also undergoes Hofmann elimination

short-acting non-depolarizing NMBA

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13
Q

vecuronium

A

devoid of cardiovascular effects (no tachycardia, no histamine release)

More than half of the drug undergoes hepatic metabolism with the remaining portion undergoing renal excretion

Both rocuronium and vecuronium have the advantage of being reversed by suggamadex

short-acting non-depolarizing NMBA

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14
Q

rocuronium

A

derivative of vecuronium with 1/8th potency

Administered as a larger dose and thus has a faster onset though still not as fast as succinylcholine; duration of action around 40 mins

Both rocuronium and vecuronium have the advantage of being reversed by suggamadex

short-acting non-depolarizing NMBA

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15
Q

Guaifenesin

A

Disrupts nerve impulse transmission at the level of the interneurons of the
spinal cord, brainstem, and subcortical areas

  • Relaxation of skeletal muscle with little effect on respiratory muscles/diaphragm at therapeutic doses
  • Produces neither analgesia nor unconsciousness
  • Cannot antagonize
  • 10% concentration can cause hemolysis, hemoglobinuria, or venous thrombosis; 5% concentration ‘safe’
  • Damaging to tissues if extravasates
  • Crosses blood-placenta barrier
  • Most commonly used in field anesthesia as part of a ‘triple drip’
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16
Q

— Interferes with excitation-contraction coupling of actin and myosin by decreasing
the amount of calcium used in the sarcoplasmic reticulum

A

dantrolene

17
Q

— Disrupts nerve impulse transmission at the level of the interneurons of the
spinal cord, brainstem, and subcortical areas

A

guaifenesin

18
Q

dantrolene is used to treat

A

Interferes with excitation-contraction coupling of actin and myosin by decreasing the amount of calcium used in the sarcoplasmic reticulum

Used in malignant hyperthermia (MH) treatment

May cause severe myocardial depression if used with calcium channel blockers

19
Q

besides the NMJ NMBA can cause

A
  • older agents may decrease BP by blocking the action of ACh at the sympathetic ganglia and decreasing vasomotor tone or via histamine release
  • Pancuronium may increase HR via cardiac muscarinic receptor blockade and decreased parasympathetic activity, or via stimulating release of
    norepinephrine

For modern NMBA, histamine release dose is higher than relaxant dose, and less likely with steroid relaxants than benzylisoquinolones

20
Q

side effects of succinylcholine

A

↑ potassium- in already sick pts with i ncreased number of extrajunctional ACh receptors such as in burn patients, muscle trauma, or nerve
damage

↑ intraocular pressure

↑ intragastric pressure → worsens regurgitation and bad for GDV

post- anesthetic myalgia from phase 1 block

21
Q

respiratory acidosis — intensity of muscle blockade while respiratory alkalosis — its effect

A

increases
decreases

Metabolic acidosis and alkalosis may both potentiate NMBA effects and make antagonism more difficult and may need to return patient to closer to physiological pH

22
Q

Decreases in ECF potassium result in — of endplate

A

hyperpolarization

23
Q

Increases in ECF potassium — the resting membrane potential (opposing relaxant effect)

A

lowers

24
Q

Increased calcium will likely require — doses of NMBA to achieve effects

A

higher

25
Q

— patients may be resistant to Phase I succinylcholine blockade
but extremely sensitive to non-depolarizing NMBA and Phase II blockade because of
a decreased number of ACh receptors

A

Myasthenia gravis

26
Q

what are antibiotics that interfere with NMBA

A
  • Polymyxin may depress post-synaptic sensitivity of ACh and enhance channel block
  • Aminoglycosides depress ACh release

When an antibiotic is given to a patient receiving a NMBA, an enhanced block or residual
paralysis is possible

27
Q

electrical stimulus hould be — to ensure that all nerve fibers in the nerve bundle are depolarized

A

supramaximal

28
Q

single twitch compare with — response

A

pre-relaxant

  • Delivered every 7-10 seconds
  • Not depressed until 75-80% of receptors are blocked and abolished with 90-95% of receptors are blocked
29
Q

train of four

A

ratio of intensity of the fourth twitch to the first (T4:T1 ratio)

Absence of block= 1.0; a ratio of 0.7 or greater is considered adequately
recovered (0.9 for some sources)

  • When 70% of the receptors are occupied, the twitches will fade (4th, 3rd, 2nd, then 1st) and reappear in reverse order
30
Q

— stimulation is used for detecting if there is residual blockade

A

Tetanic stimulation

31
Q

how to reverse NMB

A

cholinesterase-inhibitors/anticholinesterases, such as Neostigmine,Pyridostigmine, Edrophonium

Suggamadex- a ‘selective relaxant binding agent’; selectively with antagonize rocuronium or
vecuronium

Work by enabling ACh to be in higher concentration than the NMBA at the NMJ; but as consequence ACh is also at higher concentrations than usual elsewhere (muscarinic receptor stimulation)

32
Q

side effects of reversal of NMB

A

↑parasympathetic - bradycardia, bronchoconstrictions

33
Q

what drugs go through hofmann elimination

A

atracurium and cisatracurium

not based on enzymes

34
Q

Anticholinesterases will prevent breakdown on ACh; this will have effects (—) throughout the body, not just at the NMJ and should be paired with an anticholinergic (atropine or glycopyrrolate)

A

bradycardia, SLUD signs

target is the nicotinic receptors as the NMJ, but we also affect the muscarinic receptors causing these (clinically) negative effects

23 spring anesthesia (40 decks)

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