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Pharmacology Exam 3 (Toy's) > Neuromuscular Blocking Drugs > Flashcards

Neuromuscular Blocking Drugs Flashcards

0
Q

Physio-chemical properties of muscle relaxants

A
  • Highly H20 soluble/ Relatively hydrophilic
  • Easily excreted in urine (and bile)-watch renal pts.
  • DOES NOT cross lipid membranes (BBB, most cells, placenta)
  • Small Vd
  • Relatively less actively metabolized by liver than lipophilic compounds
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1
Q

How are Neuromuscular Blocking Drugs classified

A
  • By Mechanism (Depolarizing, Non depolarizing)
  • By Duration (Short, intermediate, or long acting)
  • By structure (Aminosteroid, Benzylisoquinolinium)
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2
Q

***Depolarizing Muscle Relaxation

A
  • Depolarizing block-Action same as Ach, only longer r/t slower hydrolysis by plasma (pseudocholinesterase)
  • Reacts with nicotinic receptors to open channel & cause depolarization @ end plate
  • Phase 1 &2 blockade
  • Succinylcholine (Sux) is only one available in U.S
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3
Q

Phase 1 depolarizing MOA

A
  • accompanied by fasiculations

- desired/ expected block

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4
Q

How is phase 1 Neuromuscular Blockade reversed

A

hydrolysis

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5
Q

**Effect of anticholinesterase agent during phase 1 depolarizing block

A

-block is augmented (enhanced) not reversed. (Ach levels will increase which will cause depolarization therefor increasing the effect)

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6
Q

***Cause and characteristics of phase 2 block

A
  • From continued Sux exposure (high dose or inadequate hydrolysis)
  • Characteristic nearly identical to NDMB (r/t sux blocking receptors)
  • Reversible by anticholinesterase drugs (pt. gets better)
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7
Q

Cause of inadequate hydrolysis of Sux

A

Pseudocholinesterase deficiency

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8
Q

***How is Succinylcholine broken down. Any metabolites

A
  • Rapid hydrolysis in plasma (Pseudocholinesterase)

- weakly active metabolite: succinylmonocholine which is broken down to succinic acid and choline

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9
Q

Where is Pseudocholinesterase produce. What will effect its production? What can effect the degree of activity

A
  • Produced in liver
  • Advance liver disease will will effect production
  • Degree of activity may be effected by genetics (pts w/ atypical Pseudocholinesterase)
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10
Q
  • What is the most important genetic variation of pseudocholinesterase enzyme and why?
  • What is the effect of having this variant?
A

-Atypical pseudocholinesterase-Dibucaine-related variant
inhibits normal enzyme function by 80% and atypical by 20%
Prolong effects of Sux

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11
Q

***The dibucaine number effects______ of the enzyme not _____of available enzyme

A
  • quality

- not quanity

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12
Q

*****Dibucaine numbers r/t effects

A 
80= normal (96%)
60-79= slightly prolonged response (1:200-480)
20-45(59)= greatly prolonged response (1:20,000)
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13
Q

***Cardiac side effects of Sux

A
  • BRADYCARDIA, sinus arrest due to muscarinic stimulation (worst after subsequent doses); worst in pediatric pts.
  • Hyperkalemia (contraindication)
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14
Q

Possible causes for hyperkalemia

A
  • result of proliferation of extrajunctional cholinergic receptors in nerve damage or denervated states providing sites for K+ to leak from cell during depolarization
  • Pt. with muscular dystrophy, unhealed 3rd degree burns, denervation states, motor neuron lesions, severe skeletal muscle trauma
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15
Q

Succinylcholine is a trigger for this life-threatening state and its effects are also confused with this condition

A

Malignant hyperthermia

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16
Q

***Cause of Malignant hyperthermia (MH). How is it diagnosed

A
  • Autosomal dominant inherited skeletal muscle disorder

- Dx. by muscle biopsy

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17
Q

**2 biggest triggers of MH

A
  • Volatile agents

- Succinylcholine

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18
Q

signs of symptoms of MH crisis

A
  • Increased HR, ET CO2, Temperature (comes later)
  • Muscle rigidity (Masseter muscle may be 1st sign)
  • Decrease CO2
  • Hyperkalemia, acidosis
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19
Q

Safe anesthetic to give to pt. with hx. of MH

A
  • Regional
  • N2O
  • TIVA
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20
Q

Medication given to treat MH, action, and dose

A
  • Dantrolene (impairs Ca releasefrom sarcoplasmic reticulum causing relaxation)
  • 2.5mg/kg IV. Can add up to 9-10mg/ kg
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21
Q

Succinylcholine: How supplied? Dose?

A
  • 20mg/ ml (also 500mg powder for infusion)
  • 0.7-1mg/ kg IV (1.5 if pre-treated); 2.5-4mg/ kg IM
  • Infusion: 0.5-10mg/ min titrated (<5mg/kg avoids phase 2 block)
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22
Q

Nondepolarizer MOA

A
  • Competitive antagonist @ nicotinic receptors, no intrinsic activity
  • Competes with Ach @ post junctional receptor. At high doses may block ion receptor channel
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23
Q

**How much of receptors can be occupied by a NMBD before evidence of a blockade will show on blockade monitor

A

***Up to 70% can be occupied before it shows on monitor.

(0-70% will look the same on monitor/ train of four. Up to 70% of drug can still be in symptom and pt. appears reversed on monitor)

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24
Q

Cardiovascular effects of NDMB drugs. Why

A

-Decrease B/P r/t histamine release and other vasoactive substances

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25
Q

**Only NDMB drug that increases HR. Why?

A
  • Pavulon

- May block cardiac muscarinic receptors. (atropine-like efects)

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26
Q

Other physiology that can enhance effect of NMBD

A
  • **hypothermia
  • hypotension
  • hypokalemia
  • acidosis
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27
Q

How is the speed of onset and duration of neuromuscular blockade measured

A

monitoring response to skeletal muscle to an electrical stimulus (peripheral nerve stimulator, PNS)

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28
Q

What muscle is usually monitored by PNS (peripheral nerve stimulator) and by what nerve?

A

adductor pollicis muscle via ulnar nerve

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29
Q

***How are potency comparisons of neuromuscular blocking drugs made?

A

The amount of drug needed to produce a 95% block when given with the barbiturate, opiate, and N2O (ED95)

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30
Q

**What type of muscles are effected by NMBD before the diaphragm

A

small, rapidly moving muscles (diaphragm may take 2x the dose)
9ex. onset rapid to the vocal cords)

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31
Q

Body muscles sensitivity to NDMR from most resistant to least.

A

Diaphragm> Face> larynx> peripheral limb> abdomen> masseter> upper airway muscles

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32
Q

Why monitor NMBD?

A
  • **Assessment of reversal readiness
  • Wide inter-patient variability in dose requirement
  • Differentiate block type (Depolarizing phase 1 vs. 2, Non-depolarizing)
  • Careful titration to effect
  • Assessment of reversal adequacy
33
Q

Which nerve/ muscles are better to asses cord paralysis, why?

A
  • Orbicularis oculi muscle (facial nerve)

- Effects are short acting and can be minimum by the time drugs reaches the ulna ( adductor Pollicis)

34
Q

(5)Types of stimulation patterns (monitors)

A
  • Single Impulse/ twitch
  • Train of Four (TOF)
  • Tetany
  • Double burst Simulation (DBS)
  • Post Tetanic Count (PTC) after tetany
35
Q

Tetanus monitoring facts, including amount of frequency

A 
***50 Hz, fade with NDMR's
100 Hz w/out NDMR's
-sensitive indicator of residual block
-PAINFUL
-can't repeat too soon (underestimates block)
36
Q

ST (single twitch) PNS characteristics

A
  • Single impulse/ twitch 1Hz lasting 0.1-0.2 mSec
  • Onset depends on frequency recovery
  • Twitch magnitude decreases @ 75% block until gone @ 100%
  • Control REQUIRED, may still have residual paralysis
37
Q

Tetanus PNS

A
  • 50 Hz fade with NDMR (100Hz w/out NDMR)
  • **sensitive indicator of residual block
  • Painful
  • Can’t repeat to soon r/t underestimates block (receptors flooded)
38
Q

***Train of Four

A
  • 2 Hz x4
  • Measures continued relaxation
  • Identifies phase 2 block
  • No control required (no need to know what pt. looked like before)
  • Tolerable in awake pts.
  • Questionable visual reliability
  • allows good titration
39
Q

***Double Burst Stimulation

A
  • ** 2 burst of 50 Hz, separated by 750mSec
  • each burst has 3, 0.3mSec duration pulses
  • Measured fade correlates with TOF
  • Tactile&visual evaluation response superior to TOF
40
Q

Post Tetanic Count (PTC)

A
  • 50Hz for 5 sec, followed in 3 sec by ST @ 1-2Hz
  • Shouldn’t repeat more frequently than 6 minute
  • ***used to MONITOR INTENSE BLOCK
  • predicts optimal time for reversal
41
Q

***Percentage of block with 4 TOF twitches & clinical significance

A

0-75%blocked

May be able to move with weakness. Can be reversed (may not need it)

42
Q

***Percentage of block with 3 TOF twitches & clinical significance

A

75%
May need additional drug to prolong relaxation. Short or intermediate acting agents may be reversed (pt. doesn’t have good relaxation)

43
Q

***Percentage of block with 2 TOF twitches & clinical significance

A

80%

Suitable short term relaxation as well as LONG TERM MECHANICAL VENTILATION

44
Q

***Percentage of block with 1 TOF twitches & clinical significance

A

90%

  • Condition for short term procedures like INTUBATION and long term MECHANICAL VENTILATION
  • Can reverse, but 2 twitches better
45
Q

***Percentage of block with 0 TOF twitches & clinical significance

A

100%

  • Intubation conditions. long term saturation may lead to prolonged effects
  • CAN NOT REVERSE
46
Q

How many twitches on TOF is optimal for reversal

A

2

47
Q

Neuromuscular function extubation criteria(5)

A
  • Head lift >5 sec
  • Sustained hand grips
  • NIP -50cm H20 ADULTS (-30 PEDS)
  • Vital capacity 15ml/ kg
  • Absence of nystagmus/ diplopia
48
Q

PNS (peripheral nerve stimulator) Criteria for extubation

A

1-2 twitches prior to reversal
sustained tetany to 50 Hz
No fade on DBS

49
Q

Anticholinergic only offset_____receptors

A

Muscarinic (Not nicotinic)

50
Q

When are NDMR used

A
  • Intubation
  • Bolus dose after Sux
  • Intermittent boluses
  • Continuous infusion
51
Q

Prototype of NDMR

A

Curare

52
Q

What is a defasiculating dose and when is it given

A

small dose of NDMR given before Sux

53
Q

Drug structure of Curare

A

Isoquinolinium

54
Q

***Pancuronium structure, length of action, cardiac effects, histamine release, where it’s metabolized

A
  • Bi-isquarternary aminosteroid
  • long acting
  • Increases HR (selective vagal blockade)L slight increase in B/P
  • 55-70% unchanged in urine, remainder in Hepatic metabolism to active metabolites (PROLONGED ELIMINATION)
  • Rare histamine release
55
Q

Atracurium (Tracrium)

Structure, length of action, metabolism/ metabolite, heart effects, histamine release

A
  • Benzylisoquinolinium
  • intermediate acting (on shorter side)
  • Hoffman & Plasma (ester) hydrolysis
  • Metabolite= LAUDANOSINE, CNS stimulate excreted via kidney
  • Histamine release
56
Q

Cisatracurium (Nimbex)

Structure, length of action, metabolism/ metabolite, heart effects, histamine release

A
  • Benzylisoquinolinium
  • Intermediate (slower onset than atracurium)
  • Hoffman metabolism; some ester hydrolysis
  • ? metabolite (none mentioned) though Atracurium isomer
  • Cardiac stable
  • Little/ no histamine release
57
Q

Vecuronium (Norcuron) Structure, length of action, metabolism/ metabolite, heart effects, histamine release

A

-Monoquaternary aminosteroid
-Intermediate acting
-Hepatic metabolism
-Active Metabolite (1/2 of parent drug activity)
-30% renal excretion, 40-70% biliary (Considered safe for renal7 liver pts.)
-Cardiac stable w/ some bradycardia
No signif. histamine release
-Doesn’t significantly cross placenta
-No change in IOP

58
Q

Rocuronium (Zemron)

Structure, length of action, metabolism/ metabolite, heart effects, histamine release

A
  • Monoquaternary Amine
  • Intermediate acting (faster onset, less potent than vecuronium)
  • Recommended for RSI
  • Liver metabolism to inactive metabolites (safe in renal pts)
  • Prolonged effects in liver pts.
  • Cardiac stable
  • Rare, if any histamine release
  • Large bile excretion
59
Q

Mivacurium (Mivacron)

Structure, length of action, metabolism/ metabolite, heart effects, histamine release

A
  • Benzylisoquinolinium
  • Short acting (? availability/ discontinuance)
  • Plasma hydrolysis (cholinesterase). Effects can prolong with atypical pseudocholinesterase
  • Histamine release
  • Minimal cardiac effects
  • Increased doses has less impact on DOA r/t rapid hydrolysis
60
Q

***Pharmokinetic rational for choosing drug (muscle relaxant)

A
  • **METABOLISM & ELIMINATION
  • Vd
  • Clearance
  • Elimination 1/2 life
61
Q

Pharmacodynamic rational for choosing drug (muscle relaxant)

A

dose- response
plasma level- response
effect compartment- response

62
Q

***Considerations for choosing a Muscle relaxant

A
  • onset time
  • DOA
  • Pharmacokinetic profile
  • Cardiovascular effects
  • need for reversal
  • Disease states (Liver, Cardiac, Renal)
  • Elimination route
63
Q

How blood flow and cardiac output effects onset

A
  • Increased blood flow (& increase dose)= faster onset

- Decrease CO = slower onset

64
Q

Cardiac stable muscle relaxants

A
  • Cisatracurium (Nimbex)
  • Vecuronium (Norcuron)
  • Rocuronium (Zemuron)
  • Mivacurium (Mivacron)
65
Q

Dugs that release histamine

A
  • Mivacurium (Mivacron)
  • Atracurium
  • Pancurium (Rarely)
  • D-Tubocurarine (Curare)
66
Q

Drugs that aren’t cardiac stable

A
  • Succinylcholine (Bradycardia/ sinus arrest)
  • Pancurium (Pavulon): Increase HR, Increase B/P (r/t HR)
  • Atracurium (Tracurium): hypotension r/t histamine release
  • Vecuronium (Some incidence of bradycardia, but cardiac stable)
67
Q

Drugs that don’t release histamine

A
  • Pancuronium (Pavulon): rare histamine release
  • Vecuronium (Norcuron)
  • Rocuronium (Zemuron): rare, if any
  • Cisatracurium (Nimbex): little to no
68
Q

Pt. population to monitor when using NMBD and why?

A

Renal patients. Drug easily excreted through urine (and bile). Relatively hydrophilic & highly water soluble.

69
Q

What are the 2 structures of NMBD

A
  • Aminosteroid

- Benzylisoquinolinium

70
Q

Patient populations to use caution/ avoid with Succinylcholine

A
  • Neuro pts.
  • Eye injury
  • Increased ICP
71
Q

Causes of altered response to NDMR (decreased effect)

A
  • Hyperkalemia (Resistance to NDMR)
  • Burn injury (Resistance to NDMR)
  • Paresis (may cause resistance r/t proliferatiom of extrajunctional receptors)
  • Men> resistant than women
72
Q

Mnemonic for sensitivity to NDMR resistance (Toy’s made up) from Greatest resistance to least.

A

Down For Long Periods And Moving Up

Diaphragm>Face(muscles)> Larynx (muscles)> Peripheral limbs> Abdominal muscles> Masseter> Upper airway

73
Q

Benzylquinolinium Structured NDMR

A

*-Atracurium (Tracrium)
*-Cisatracurium (Nimbex)
*-Mivacurium (Mivacron
(Doxacurium)

74
Q

Biisoquaternary aminosteroid structured Drugs

A
  • Pancuronium (Pavulon)

- (Pipercurion)

75
Q

Monoquaternary Aminosteroid sructured NDMR

A
  • Rocuronium (Zemron)

- Vecuronium (Norcuron)

76
Q

NMBD that release histamine (M.A.D.S)

A
  • Mivacurium (Mivacron)
  • Atracurium (Tracrium)
  • DTC/D-Tubocurarine (Curare)
  • Succinylcholine
77
Q

Major metabolite of Atracurium and where its excreted

A
  • Laudanosine

- Kidney excretion (Not good for renal Pts)

78
Q

Best reversal to use with Mivacurium (Mivacron)

A

-Edrophonium (Enlon)

Neostigmine, theoretically, increases effects

79
Q

Which muscle relaxant has the fastest onset?

A

Succinylcholine

80
Q

What is the “self-taming” technique to administering a NDMR

A

20% of planned Sux dose given first followed by the rest later. (after propofol)

Pharmacology Exam 3 (Toy's) (5 decks)

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