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Pharm Test 3 > Neuromuscular Blockers > Flashcards

Neuromuscular Blockers Flashcards

1
Q

What was the first NMB used?

A

d-tubocurarine

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2
Q

Characteristics of skeletal muscle?

A
  • Voluntary action
  • striated muscle
  • contains contractile filatments
  • multinucleated cells
  • Innervated by large, myelinated, alpha motor neuronts
    • cell bodies originate from ventral horns of spinal cord
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3
Q

As presynaptic motor nerve endings approach post-synaptic membrane of muscle cells, the muscle fiber motor neurons lose their ____ ____ and make contact with single muscle fiber.

A

myelin sheath

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4
Q

How does acetylcholine work at NMJ?

A
  • Synthesized in presynaptic neuron and stored in presynaptic vesicles
    • released in quanta
  • Released in quanta in response to action potential in presynaptic neuron
    • Ca dependent process
  • Diffuses across synaptic clef and reversibly binds to speicfic receptor sites on postsynaptic membrane with Na channels in trough
  • Postsynaptic membrane depolarizes and triggers AP that causes muscle contraction
  • ACh eliminated by acetylcholinesterase
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5
Q

What is ACh metabolized to by acetycholinesterase?

A

Acetate and choline

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6
Q

What forms Nicotinic Ach receptor?

A
  • ADULT receptor has two alpha subunits in association with single beta, delta, epsilon subunit
    • these form a channel (pore)
    • each alpha subunit has ACh binding site
    • alpha subunits are binding site for ACh and NMB!
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7
Q

What does binding of Ach on both subunits cause?

A
  • Channel opens
  • Na and Ca move into skeletal muscle and K leaves
  • AP propagate and results in muscle contraction
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8
Q

What is function of prejunctional nicotinic receptors?

A
  • Also activated by acetylcholine and function in positive feedback control system, which could mediate mobilization of the reserve storage of acetylcholine when high-frequency or tetanic stimulations occur.
  • This helps to mobilize acetylcholine when demand is high!
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9
Q

Which type of neuromuscular blocker tends to block prejunctional nicotinic receptors? What is the clinical impact?

A
  • Non delopolarizing NMBD
  • We will see “fade” on a TOF stimulation because there is not enough ACh available to sustain continuous contractions
  • With succinylcholine administration, you get either all 4 twictches, or no twitches. There is no fade exhibited
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10
Q

What are fetal nAch Receptors?

A
  • Immature, mostly extrajunctional receptors
  • Epsilon subunit is absent and replaced by the gamma subunit
    • all other subunits the same (two alpha, beta, delta)
  • these receptors proliferate in denervation (or immobility, trauma)
  • Resistant to non-depolarizing NMB and sensitive to succinylcholine
  • when activated, fetal receptors have prolonged open chennl time and this leads to exaggerated K efflux
    • causes extensive hyperkalemia in patients
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11
Q

What is the difference of sensitivity to NMB throughout various muscles of the body?

A
  • Muscle blood flow and receptor density difference is likely cause
  • The dose of non depolarizing NMB needed to block diaphragm is 1.5-2 times the dose needed to block the adductor pollicis
    • obicularis oculi** (reflects paralysis of laryngeal muscles) muscle twitch **will be lost first and regained first
  • Laryngeal adductors are resistant to NMB relative to adductor policis
    • high receptor density, greater release of acetylcholine, or less acetylcholinesterase activity
  • Onset of NMB is significantly faster at diaphragm and larngeal adductors than at adductor pollicis
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12
Q

What is odd thing about succinylcholine’s sensitivity to receptors?

A

Succinylcholine will give greater NMB at vocal cords than at adductor pollicis

No greater view than with succinylcholine!

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13
Q

NMB should not be administered just to ___ ___ ___

A

keep patient from moving.

Important to use other anesthetic agents to provide analgesic or amnestic properities. Otherwise, may have awareness during surgery

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14
Q

What are 4 positive outcomes of using NMB for intubation?

A
  • Better view
  • decreased frequency of vocal cord lesions following intubation
  • decreased rate of postoperative hoarseness
  • reduces rate of adverse hymodynamic effects caused by deeper level of anesthesia
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15
Q

What type of patient might be suitable for intubation without need of NMB?

A

Younger, healthier patient can handle extra dose propofol (Etc) needed for intubation without NMB

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16
Q

What is MOA of NMB?

A
  • Quaternary ammonium compounds structurally related to ACh
    • do not cross BBB and are hydrophilic
  • NMB bind to alpha subunit on AChR
  • Non depolarizing bing to one or both alpha subunits and do not result in depolarization
    • competitive antagonist
    • binds to more post junctional than prejunctional
  • Depolarizing NMB bind to alpha subunit (one or both)and result in depolarization
    • results in membrane depolarization and hyperpolarization which prevents AP
    • partial agonism
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17
Q

What do NMB do to more centrall located neuromuscular units vs more peripherally located adductor pollicis muscles?

A

Blockade develops faster, lasts a shorter time, and recovers faster in more centrally located neuromuscular units

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18
Q

What are general characteristics of succinylcholine?

A
  • Structurally 2 molecules of acetylcholine bound together by methyl group
  • Partial agonist
  • Depolarizes AChR upon binding to one (or both) alpha subunits
    • also effects muscarinic autonomic receptors
  • NOT hydrolyzed by acetylcholinesterase
    • channel stays open and no further action potential can be transmitted
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19
Q

How does succinylcholine cause fasciculations?

A
  • When depolarizing NMJ, causes muscles to spasm
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20
Q

What can be done to prevent fasciculations with succinylcholine?

A
  • Small dose of differnet nondepolarizing NMBD administered before succ can prevent fasciculations.
    • The dose of nondepolarizing NMBD will have antagonistic effect to succ.
    • You will need to give a higher dose of succinylcholine after administering nondepolarizing NMBD
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21
Q

E 1/2 life of succinylcholine?

A

47 seconds

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22
Q

ED 95 and intubating dose of succinylcholine?

A

ED95= 0.3 mg/kg

intubating dose= 1.0 mg/kg (up to 1.5 mg/kg)

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23
Q

What is average time until intubating conditions for succinylcholine?

A

60 second (up to 30-60 seconds for 1.5 mg/kg)

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24
Q

What is the average time to 90% muscle strength recovery for succinylcholine?

A

9-13 minutes

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25
Q

What is metabolism and recovery from blockade for succinylcholine?

A
  • Metabolism: Hydrolyzed by butyrlcholinesterase (plasma cholinesterase)
    • ultrashort DOA of succinylcholine results from rapid hydrolysis by butrylcholinesterase into succinylmonocholine and choline
      • such an efficient enzyme that only 10% of succinylcholine reaches synaptic cleft
  • Recovery: diffusion away from NMJ down a concentration gradient
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26
Q

Which weight do use for succinylcholine dosing in obese patients?

A

total body weight

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27
Q

Where is butylcholinesterase synthesized? Where is it found?

A

Synthesized in liver

Found in plasma

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28
Q

When is butylcholinesterase reduced?

A
  • Advanced liver disease
  • Advanced age
  • Malnutrition
  • Pregnancy (but increase in Vd leads to no clinical effect in prolongation of DOA)
  • Burns
  • Oral contraceptives
  • use of MAOI’s
  • echothiophate (eye drop)
  • cytotoxic drugs
  • neoplastic disease
  • anticholinesterase drugs
  • metoclopramaide
  • bambuterol (prodrug of terbutaline)
  • esmolol
  • genetic variations of enzyme
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29
Q

What is the clinical implication in a decrease of butyrlcholinesterase activity?

A
  • When butyrlcholinesterase activity reduces by 20%, only prolongation of DOA of 3-9 min
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30
Q

Which drugs, commonly given around perioperative period, can inhibit butyrlcholinesterase?

A

Neostigmine and pyridostigmine

  • If succinylcholine is given after antagonism of residual neuromuscular block, (as in postextubation laryngospasm) the effect of succinylcholine will be pronounced and significantly prolonged, (by 11-35 minutes in some studies)

-Even 90 minutes after neostigmine administration, butrylcholinesterase activity will have returned to less than 50% of baseline!!

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31
Q

____ also inhibit butyrlcholinesterase and may augment the ffects of succinylcholine and mivacurium by decreasing hydrolysis by the enzyme.

A

Procaine

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32
Q

What is a dibucaine number?

A
  • Amide local anesthetic that can be used in lab to test for genetic variation in plasma cholinsterase
  • Dibucaine number reflects quality, not the quantity of enzyme
  • 1:3500 homozygous for varient; will prolong NMB with Sch for 4-8 hours
  • 1:480 heterozygous for variant; prolongs NMB 50-100%
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33
Q

Does dibucaine inhibit the normal enzyme or abnormal enzyme?

A

Has prefernce for inhibiting NORMAL enzyme

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34
Q

What is a normal dibucaine number? Abnormal values and what they signify?

A
  • Homozygous normal = 70-80= normal response SCh
  • Heterozygous atypical 50-60= lengthened by 50-100%
  • Homozygous atypical 20-30= prolonged 4-8 hours

Dibucaine number indicates the percentage of enzyme inhibited

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35
Q

What will occur during TOF testing after administration of Sch to someone with a butylcholinesterase deficiency?

A

You will see fade.

Normally, you will not see fade with a depolarizing NMB. If you see fade after administration succinylcholine, something is off

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36
Q

What conditions can cause nAchR upregulation?

A
  • Spinal cord injury
  • Stroke
  • Burns
  • Prolonged immobility
  • Prolonged exposure to NMB
  • Multiple sclerosis
  • Guillain Barre syndrome
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37
Q

What conditions can lead to nAChR downregulation?

A
  • Myasthenia gravis
  • Anticholinesterase poisoning
  • organophosphate poisoning
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38
Q

What happens when succinylcholine given to denervated muscle?

A
  • Muscle has upregulated nad extrajuncitonal AChRs
  • Sch comes in contact with all the AChRs throughout the membrane
  • massive efflux of K into extracellular fluid with potentially lethal hyperkalemia
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39
Q

What is malignant hyperthermia?

A
  • Calcium ion channel defent in ryanodine receptor leads to failure of Ca ion active transport pump following muscle contraction
    • this leads to sustained muscle contraction and heat production
  • First sign of malignant hyperthermia is sudden, acute increase in ETCO2 from increased body metabolism
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40
Q

What can trigger malignant hyperthermia?

A
  • Succinylcholine and volatile anesthetics
  • Triggers are avoided in patients with susceptibility
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41
Q

What are the cardiovascular side effects of SCh?

A
  • Action at cardiac muscarinic cholinergic receptors can cause bradycardia
    • increased likelihood with children and when 2nd dose is given within 5 minutes of first dose
    • seen in low doses (both negative inotropic and chronotropic)
    • this can cause cardiac arrest in kids!
  • ANS ganglion can also cause increased HR and BP
    • autnomic stimuli can cause ventricular dysrhythmia during laryngoscopy
    • seen in large doses of Sch
42
Q

How does succinylcholine cause hyperkalemia?

A
  • In normal, healthy patient, Sch will cause 0.5mEq/L increase in K level
  • severe, life threatening hyperkalemia can occur in burn patient, pt with severe abdominal infections, sever metabolic acidosis, closed head injury, or any condition leading to upregulation of extrajunctional Ach receptors
  • SCh is NOT recommended in children d/t potential for massive rhabdomyolysis, hyperkalemia and death d/t undiagnosed muscle dx
    • may only be used in emergency tracheal intubation
43
Q

If you give succinylcholine, and begin to see sudden increased PVCs, what could you suspect?

A

Might have increased K, need to give membrane stabilizers (Ca, insulin, glucose combo) in order to prevent severe hyperkalemia

44
Q

What drugs can you give if you suspect hyperkalemia?

A
  • 500-1000 mg Calcium chloride or calcium gluconate over 3 minutes IV
  • 10 units regular insulin in 50mL of 50% glucose for adults
    • children 0.15 units/kg of regular insulin in 1.0 mL/kg of 50% glucose IV
  • Also hyperventilate patient
45
Q

What other side effects can Sch cause?

A
  • Myoglobinuria- usually seen only after administration to pt with malignant hyperthermia or muscular dystophy
  • Increased IOP- attneuated with pretreatment small dose NDNMB
  • Increased intragastric pressure: evidnce of clnical harm unclear
  • Increased IOP- peaks 2-4 min, subsides in 6 min
  • Myalgias: increased in women and ambulatory pt
  • Masseter spasm
    • can be early sign of MH
    • Does not always herald MH
  • ANlaphylaxis 0.06%- mainly european/australian
46
Q

Is it ok to use succinylcholine for eye operations?

A

Not contraindicated unless anterior chamber is open.

  • Administering NDNMD beforehand can diminish increased IOP
  • Weighed with fact that bucking and coughing also causes increased IOP. This will cause IOP 3-4 times greater than with SCh administration
47
Q

What are SCh black box warnings?

A
  • Administration in children carries risk of cardiac arrest and sudden death
  • risk due to undiagnosed skeletal muscle myopathy
  • X-linked, recessive Duchenne’s muscular dystrophy is most common
    • absence of dystrophin
48
Q

What are the classes of non-depolarizing NMB?

A

Steroidal

Benzyliosquinolinium

other blockers

49
Q

What drug is out long-acting, steroidal compound?

A

Pancuronium

50
Q

What drugs are intermeidate(20-50 min) steroidal compounds?

A

Vecuronium, Rocuronium

51
Q

What drug is long acting benzylisoquinolinium compound?

A

d-Tubocurarine

52
Q

What drugs are intermediate acting benzylisoquinoliniums?

A

Atracurium

Cisatracurium

53
Q

What drug is short acting benzylisoquinolinium?

A

Mivacurium

54
Q

The speed of onset is _____ proportional to potency of nondepolarizing neuromuscular blocking drugs.

A

inversely

the more potent, fewer molecules needed, longer onset time

55
Q

What does ED 95 mean? ED 50?

A

Dose required to have a 95% or 50% decrease in baseline twitch height.

Defines drugs potency

56
Q

Unlike SCh, non depolarizing NMBDs should be given to obses patients on basis of ____

A

IBW (ideal body weight)

57
Q

How many receptors must be occupied before appearnace of neuromuscular block?

A

90% of receptors must be occupied before block is complete at adductor pollicis

58
Q

Which drug is exception to rule of inverse relationship betwen potency and onset?

A

Atracurium. ED 95 is 0.21mg/kg, but onset is 3.2 min

(which longer than vecuronium, and vec’s ed95 is 0.043mg/kg)

59
Q

What is buffered diffusion?

A
  • Buffered diffusion causes reptitive binding and unbinding to receptors, thus keeping potent drugs in neighborhood of effector sites and potentially lenghtening the duration of effect
  • Seen in high potency, but not low potency drugs
  • Contributes to slower onset time for cisatracurium than atracurium.
60
Q

What determines time to maximum blockade?

A
  • Intensity of maximum glockade is affected directly by administered dose
    • subparalyzing range, time to reach maximum effect is dose independent
    • when dose is sufficient to effect complete disappearnce of neuromuscular response, time to maximum blockade is dose-dependent
61
Q

What causes potentiation of NMB?

A

N2O and anesthetic vapors increase action of NMB

Of all the volatile agents, desflurance has most potentiation

62
Q

What are the autonomic effects of succinylcholine?

A
  • Autnomic ganglia- stimulates
  • Cardiac muscarinic receptors- stimulate (drop in HR)
  • Histamin release- slight
63
Q

What are autonomic effects of mivacurium?

A
  • Autonomic ganglia- none
  • cardiac mscarinic receptors- none
  • histamine release- slight
64
Q

What are autonomic effects of atracurium?

A
  • Autonomic ganglia- none
  • cardiac mscarinic receptors- none
  • histamine release- slight
65
Q

What are autonomic effects cisatracurium?

A
  • Autonomic ganglia- none
  • cardiac mscarinic receptors- none
  • histamine release- none
66
Q

What are autnomic effect tubocurarine?

A
  • Autonomic ganglia- blocks
  • cardiac mscarinic receptors- none
  • histamine release- moderate
67
Q

What are autnomic effects vecuronium?

A
  • Autonomic ganglia- none
  • cardiac mscarinic receptors- none
  • histamine release- none
68
Q

What are autonomic effect rocuronium?

A
  • Autonomic ganglia- none
  • cardiac mscarinic receptors- blocks weakly
  • histamine release- none
69
Q

What are autonomic effects pancuronium?

A
  • Autonomic ganglia- none
  • cardiac muscarinic receptors- blocks moderatly
  • histamine release- none
70
Q

What is d-Tubocurarine?

A
  • Benzylisoquinolone; monoquarternary, long acting
  • no active metabolism
  • excreted uncahnged in urine; hepatic secondary rout
  • not indicated in renal or hepatic failure
  • onset: slow
  • DOA: long
  • HISTAMINE RELEASE
71
Q

What is atracurium?

Intubating Dose, onset, class, characteristics?

A

Benzylisoquinolone; intermediate acting

  • Dose: 0.5 mg/kg (intubating dose)
  • Onset 2-2.5 minutes, max NMB 3-5 min
  • Racemic mixture of 10 steroisomers
  • Hofmann elimination: spontaneous degradation at physiologic temp and pH and ester hydrolyis (60-90%)
    • 10-40% KIDNEY
  • INACTIVE METABOLITE: Laudanosin, CNS stimulant, is metabolite and can cross BBB (seizures)
    • 70% in bile, remainder in urine
    • excretion impaired in biliary obsturciton
  • HISTAMINE RELEAE
72
Q

Cisatracurium?

Class, intubating Dose, DOA, Metabolism?

A

Benzylisoquinlolone; intermediate acting

  • Dose- 0.1mg/kg (4-5x more potent than atracurium)
  • 1R cis- 1’R cis isomer of atracurium
  • Hofmann elimination (77%) renal clearance (16%)
    • NO ester hydrolysis
  • Laudanosine is also produced but at much lower amounts (1/5th of atracurium)
  • NO HISTAMINE RELEASE
73
Q

Mivacurium

Class, dose, DOA, characteristics

A

Benzylisoquinolone; short acting

  • intubating dose: 0.15 mg/kg
  • Only short acting NDNMB
    • reintroduced in US in dec 2016
  • Metabolized by plasma cholinesterase
    • Butyrlcholinesterase–> monoester and dicarboxylic acid at 70-88% of the rate at which succ is metabolized by same enzyme
  • HISTAMINE release- reason why many people don’t use it
74
Q

Pancuronium?

Dose, class, DOA, metabolism, characteristics

A

Steroidal non-depolarizing NMB; LONG ACTING

  • Intubating dose: 0.08 mg/kg
  • Direct vagolytic and sympathomimetic activity
    • causes tachycardia
  • Renal clearance 40-60%- cannot give in renal failure
  • 3-OH metabolite accumulation leads to prolongation of NMB- ACTIVE METABOLITE
    • half as potent as pancuronium
    • largely excreted by kidney, small liver pathway
    • total clearance is delayed, DOA significantly lenghtened by renal or hepatic dx
    • E 1/2 t increased 500% in pt with renal failure
75
Q

Vecuronium?

Class, dose, doa, metabolism, characteristics?

A

Steroidal non-depolarizing NMB; Intermediate acting

  • Intubating dose: 0.1 mg/kg
  • CHemical structure similar to pancuronium
  • Primarily hepatic metabolism
    • elimination 40-50% liver, 30% renal
  • ACTIVE METABOLITE: 3-OH metabolite can accumulate
    • also 3- desacetylvecuronium is active metabolite and has 80% potency of vecuronium
      • has slower plasma clearance and longer DOA than vec.
  • Must be stored in powdered form
76
Q

Rocuronium?

Class, intubating dose, doa, metabolism, characteristics?

A

Steroidal non depolarizing NMB; intermediate acting

  • Intubating dose:0.6 mg/kg
  • “Gloden child”
  • 6 times less potent than pancuronium and vecuronium d/t change allyl group attachded to quaternary nitrogen
  • Primarily eliminated in liver (>70%), renal 10-25%
  • Shortest onset of the NDNMB <– pretty close to succ.
  • Can be used for RSI in high doses (1.2 mg/kg)
  • only good for 60 days on shelf d/t terminal sterilization that degrades drug
77
Q

Mivacurium

ED95

Intubation dose

time to max block (onset)

time to return to 25% control (duration)

A

ED 95= 0.067 mg/kg

Intubating dose= 0.15 mg/kg

Time to block= 3.3 min

time to return- 16.8 min

78
Q

Cisatracurium

ED95

Intubation dose

time to max block (onset)

time to return to 25% control (duration)

A

ED95= 0.04

Intubation dose 0.1 mg/kg

time to max block (onset)= 5.2 min

time to return to 25% control (duration)= 45 min

79
Q

Vecuronium

ED95

Intubation dose

time to max block (onset)

time to return to 25% control (duration)

A

ED95= 0.043 mg/kg

Intubation dose: 0.1

time to max block (onset)= 2.4

time to return to 25% control (duration): 45 min

80
Q

ATRACURIUM

ED95

Intubation dose

time to max block (onset)

time to return to 25% control (duration)

A

ED95= 0.21 mg/kg

Intubation dose: 0.21 mg/kg

time to max block (onset): 3.2 min (outlier)

time to return to 25% control (duration): 45 min

81
Q

Rocuroinum

ED95

Intubation dose

time to max block (onset)

time to return to 25% control (duration)

A

ED95= 0.305

Intubation dose: 0.6 mg/kg

time to max block (onset)= 1.7 min

time to return to 25% control (duration)= 35 min

82
Q

Pancuronium

ED95

Intubation dose

time to max block (onset)

time to return to 25% control (duration)

A

ED95= 0.067 mg/kg

Intubation dose= 0.08 mg/kg

time to max block (onset)= 2.9 min

time to return to 25% control (duration)= 85 min

83
Q

What increases potency of non-depolarizin NMB?

A
  • Inhaled anesthetics
    • desflurance> sevo>iso>halo>nitrous/barb/opioid or propofol
  • Aminoglycoside antibiotics, polymyxins, lincomycin, clindamycin, tetracyclines
  • Hypothermia
  • Magneium sulfate
  • Local anesthetics
  • Some antidysrhythmics
84
Q

What decreases potency of nondepolarizing NMB?

A

Chronic anticonvulsant therapy: increases dose and frequency

Hypercalcemia

85
Q

Relationship with antibiotics and NMBD?

A
  • under normal conditions, most antibiotics can cause meuromuscular blockade in absence of NMBDs
    • The aminoglycosides include gentamicin, amikacin, tobramycin, neomycin, and streptomycin
  • Can exhibit combo of pre/post synaptic inhibition of ACh
  • antagonism of NMB with neostigmine has been reported to be more difficult after administration of aminoglycosides, you should let NMB terminate spontaneously
  • antagonism is not sustained and may prevent effect of antibiotics
86
Q

How can Ca decrase effectiveness of NMBD?

A
  • Ca stimulates ACh release from nerve terminals, and enhances excitation-contraction coupling
  • Increased Ca concentration decreased sensitivity to dTc and pancuronium
  • hypercalcemia associated with decreased sensitivity to atracurium and thus shortened time course for NM blockade
87
Q

Which drugs can you give for RSI?

A
  • Rapid onset: Sch and Roc
  • Roc in high dose (0.9-1.2 mg/kg) or succ 1.5 mg/g can be used interchangeably for rapid tracheal intubation beacuse they provide adequate intubating conditions within 60-90 seconds
    • if succ is undesirable or contraindicated, high dose roc can be used

Increasing roc doubles the clinical DOA from 37-73 minutes!

88
Q

What can we do to prevent defasciulation?

A
  • 10% of intubating dose of NDNMB to prevent SCh induced fasciulation
  • Fasiculations increase risk of hyperkalemia, myalgias, increases intra-gastric pressure and aspiration
  • Can temporize increase in ICP when SCh used in increased ICP
  • Dose of defasciulation
    • Roc= 0.06-1.0 mg/kg (usually 5-10 mg)
89
Q

Relationship between NMBD and histamine release?

A
  • When large doses of certain NMBD are administered too rapidly
    • erythema of face, neck, upper torso
    • brief hypotension and slight to moderate increase in HR
    • Bronchospasm rare
  • Effect involve chemical displacemnet of the contents of mast cell granules containing histamine, prostaglandin, and other vasoactives
  • Most often noted following admin of benzylisoquinolinium class of muscle relaxants
  • Short duration 1-5 min, dose related and clinically insignificant
90
Q

Relationship between NMB and anaphylaxis?

A
  • Largest proportion of allergic reactions under anesthesia are attributable to muscle relaxants
  • cross reactivity b/w NMBD, food, cosmetics, disinfectant and industrial materials
  • IgE response/mast cell degranulation
91
Q

What to do if you suspect allergic reaction to NMB?

A
  • Stop giving drug,
  • Give 100% o2
  • small dose IV epi (10-20mcg)
  • give crystalloid
  • consider need to intubation
  • antihistamine/steroids?
92
Q

How do we redose NMB for continues paralysis?

A
  • Clinical managmenet of patient should be guided by monitoring of NMB, with objective NM monitoring technique
  • Supplemental doses should be 1/10 (LONG ACTING) 1/4 of intubating dose (intermediate/short)
    • should not be given until quantitative evidence of beginning recovery is present
  • Infusion dose is decreased 30-50% in presence of potent volatile anesthetics
93
Q

Combining NMBD will either be additvie or synergistic

Drugs in same class are usually _____

drugs in different classes are ______

A

Additive

Synergistic

94
Q

Which NMB exhibit histamine release?

A

Succinylcholine (slight)

Mivacurium (slight)

Atracurium (slight)

Tubocurarin(moderate)

(spells MAST!!)

Benzylisoquinolones tend to have more histamine release

95
Q

Which NMB have active metabolites?

A

Atracurium (laudanosin. Not ACTIVE in drug sense, but increases sz risk. )

Cisatracurium (laudanosin- lower than atracurium)

Vecuronium (3-OH- 80% potency of vec)

Pancuronium (3-OH)

Rocuronium- 17-desacetylrocuronium

96
Q

Suffix - curium= what class?

A

Benzylisoquinolinum

97
Q

Suffix -ronium = what class?

A

Steroidal

98
Q

Mneumonic to remember DOA of non-depolarizing NMB?

A

Many Can Ventilate A Really Poor Trach

Mipivacurium, cisatracurium, vecuronium, atracurium, rocuronium, pancuronium, d-Tubocaine

99
Q

Mneumonic to remember histamine relasers?

A

MAST

Mipivacurium

Astracurium

Succinylcholine

(T) -D-tubocraine

100
Q

What should you give patient with metabolic acidosis or hypvolemia before succinylcholine administration?

A

NaHCO3 (sodium bicarb) and hyperventilation

Pharm Test 3 (5 decks)

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