Neuromuscular Blockers Flashcards

1
Q

Commonalities of NMB’s

A
  • relaxation of skeletal muscle resulting in paralysis
  • all contain one or two quaternary nitrogens
  • related structurally to Ach
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2
Q

succinylcholine

A
  • depolarizing NMB
  • comprised of two Ach molecules
  • resistant to Achase
  • metabolized by butyrylcholinesterase
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3
Q

nondepolarzing NMBs

A
  • antagonize the mecahnism of Ach in a competitive manner
  • reduce the frequency of channel opening
  • do not effect the magnitude of conductance if the channel is opened
  • usually takes greater than a 70% blockade to see effects
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4
Q

phase 1 depolarizing block

A
  • succunyl choline is given
  • receptor is bound and stimulated
  • there is membrane depolarization, muscle fasciculation, followed by paralysis
  • Ach can not propogate a signal on an already depolarized end plate
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5
Q

phase 2 depolarizing block

A
  • end plate repolarizes, but succinylcholine is still bound to the nAchR
  • this acts similarly to a non-depolarizing NMB
  • occurs with prolonged use
  • we do not use it long enough to see this in medicine anymore
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6
Q

pre-junctional nAchR activity

A

-acts on prejunctional nicotinic receptors in a positive feedback manner to increase its own release during high frequency stimulation

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7
Q

non-depolarizing NMB and prejunctional nAchR activity

A

blocks prejunctional receptors resulting in failure of mobilization of Ach to keep pace with the demans of the high stimulation frequency
-this manifests clinically as the “fade phenomenon” which is a reduction in twitch height with successive stimuli

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8
Q

depolarizing NMB and prejunctional nAchR activity

A
  • does not cause the fade phenomenon

- this adds to the prejunctional depolarizing action leading to repetitive firing

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9
Q

general sequence of paralysis

A
  • larger muscles are more resistant to block
  • small, rapidly moving muscles > the limbs, neck, trunk, masseter and upper airway > intercostal muscles, larynx and face > diaphragm
  • offset occurs in reverse order
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10
Q

therapeutic uses of NMBs

A
  • endotracheal tube placement (succinylcholin, depolarizing)
  • skeletal muscle relaxation for surgical treatment, adjuvant anesthetic (non-depol)
  • facilitation or maintenance of mechanically ventialted patients (non-depol)
  • antishivering during hypothermia (non-depol)
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11
Q

characteristics of NMB

A
  • do not alter level of conciousness/pain
  • must be given IV
  • ionized and do not cross the BBB
  • time of action is how long it takes for the thumb to return to 25% of baseline
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12
Q

adverse effects of non-depolarizing NMB

A
  • tachycardia and hypertension due to vagolytic and sympathomimetic properties
  • histamine release potentially leading to hypotension, reflex tachycardia, flushing, urticarial bronchospasm
  • acute quadriplegic myopathy syndrome
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13
Q

depolarizing NMB adverse effects

A
  • hyperkalemia
  • masseter muscle rigidity
  • bradycardia
  • malignant hyperthermia
  • muscle pain
  • prolonged paralysis from butyrylcholinesterase deficiency
  • anaphylaxis
  • increased intragastric pressure
  • increased intra-ocular pressure
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14
Q

drugs that potentiate NMBs

A
  • inhalation anesthetics: reduction of post synaptic receptor sensitivity to Ach, reduced muscle contractility
  • antibiotics: decreased presynaptic Ach release
  • calcium channel blockers and anesthetics: decreased presynaptic release of Ach
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15
Q

monitoring blockade

A
  • done via transdermal stimulation to decrease unwanted effects of long term paralysis
  • used only for non-depolarizing NMBs
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16
Q

train of four

A
  • most commonly used technique for monitoring NMBs
  • supramaximal stimulus (0.2 ms pulses, 500 ms apart, 2Hz) ddelivered to the peripheral nerves
  • interpreted as a count in the number of contractions observed at the nerve being stimulated
  • number of contractions reflects the degree of blockade
17
Q

reversal of non-depolarizing NMB

A
  • AchE inhibitors (leaves more Ach in the synpase)

- these NMB antagonize Ach in a cometitive manner therefor adding more Ach to outcompete will reverse their effect

18
Q

reversal of depolarizing NMBs

A
  • not readily reversible
  • succinylcholine and Ach have the same mechanism of action
  • augmented but not reversed by Achase inhibitors
19
Q

classes of non-depolarizing NMBs

A
  • aminosteroid derivatives

- benzylisoquinolone derivatives

20
Q

effect of inhilation anesthetics on NMB

A
  • reduction of post synaptic receptor sensitivity to Ach, decreased muscle contractility
  • potentiation of blockade
21
Q

antibiotics on NMB’s

A
  • decreased pre-synaptic Ach release

- reduction of postsynaptic nAchR sensitivity, impairment of ion channels

22
Q

calcium channel blockers and local anesthetics

A

decreased pre-synaptic Ach release

  • decreased muscle contractility
  • potentiation of NMBs