Neuromuscular Blockers Flashcards

1
Q

Where is the best place to measure onset of blockade?

A
  • muscle = orbicularis occult (closes lid) or corrugator supercilii (eyebrow twitch)
  • nerve = facial nerve
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2
Q

Where is the best place to measure recovery of blockade?

A
  • muscle = adductor pollicis (thumb adduction) or flexor hallicus (big toe flexion)
  • nerve = ulnar nerve or post tibial nerve
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3
Q

How does succs cause bradycardia?

A

stimulates the M2 receptor on the SA node

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4
Q

Does succs cause tachycardia?

A
  • yes
  • it mimics action Ach at the sympathetic ganglia
  • can cause tachycardia and HTN
  • causes tachycardia in adults more than bradycardia
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5
Q

How does succs affect intraocular pressure?

A

it increases intraocular pressure by 5-15 mmHg for up to 15 min.

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6
Q

How does succs affect intracranial pressure?

A
  • it temporarily increases intracranial pressure

- minimized or prevented by a defasciculating dose

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7
Q

How does succs affect intragastric pressure?

A
  • causes contraction of abdominal contents
  • increases lower esophageal sphincter tone
  • these 2 cancel each other out and therefore the pressure is unchanged
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8
Q

Do you cancel the case if the pt has a masseter spasm after succs?

A
  • No, not if it happens in the absence of other s/sx of MH

- succs is a trigger of MH

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9
Q

What metabolizes acetylcholine?

A
  • Type 1 cholinesterase
  • Acetylcholinesterase
  • True cholinesterase
  • Specific cholinesterase
  • Genuine cholinesterase
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10
Q

What metabolizes succs, mivacurium, and ester LAs?

A
  • Type 2 cholinesterase
  • Butyrylcholinesterase
  • False cholinesterase
  • Plasma cholinesterase
  • Pseudocholinesterase
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11
Q

What are drugs that reduce Pseudocholinesterase activity?

A
  • Metoclopramide
  • Esmolol
  • Neostigmine (NOT edrophonium)
  • Echothiophate
  • Oral contraceptives / estrogen
  • Cyclophosphamide
  • Monoamine Oxidase Inhibitors
  • Nitrogen mustard
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12
Q

What are co-existing conditions that reduce Pseudocholinesterase activity?

A
  • Atypical PChE
  • Severe liver disease
  • Chronic renal disease
  • Organophosphate poisoning
  • Burns
  • Neoplasm
  • Advanced age
  • Malnutrition
  • Pregnancy (late stage)
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13
Q

Who is at risk for post-op myalgia with Succs?

A
  • young adults undergoing adulatory surgery (women > men)

- those who do not engage in routine strenuous activity

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14
Q

How can post-op myalgia from Succs be reduced?

A
  • it may be reduced by pretreatment with a NDNMB
  • on tenth of the ED95 of a NDNMB can reduce fasciculations
  • should be administered 3-5 min before succs
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15
Q

What is Hoffman Elimination dependent upon?

A
  • normal blood pH and temperature
  • rxn is faster w/ alkalosis and hyperthermia
  • rxn is slower w/ acidosis and hypothermia
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16
Q

Does mivacurium produce an active metabolite?

A

No

17
Q

What drugs potentiate NMBs?

A
  • volatile anesthetics (Des>Sevo>Iso>N2O>Propofol)
  • Antibiotics (Aminoglycosides, Polymyxins, Clindamycin, Lincomycin, Tetracycline)
  • Antidysrhythmics (verapamil, amlodipine, lidocaine, quinidine)
  • local anesthetics (probably all of them)
  • Diuretics (furosemide)
  • dantrolene, cyclosporine, tamoxifen
18
Q

What electrolyte imbalances potentiate NMBs?

A
  • inc lithium (activates K+ channels)
  • inc Mg (dec Ach release from presynaptic nerve)
  • dec Ca+2 (dec Ach release from presynaptic nerve)
  • dec K+ (dec resting membrane potential)
19
Q

What patient factors potentiate NMBs?

A
  • hypothermia (dec metabolism and clearance)

- women (women are more sensitive to the effects of NMBs compared to men)

20
Q

A patient with what type of condition should not receive pancuronium?

A
  • hypertrophic cardiomyopathy
21
Q

What is the order of highest to lowest likelihood of NMBs that produce anaphylaxis?

A

succs > atracurium > cisatracurium > rocuronium > vec