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UPR-RCM SRNA PHARM I > Chapter 12: NMBD and Reversal agents > Flashcards

Chapter 12: NMBD and Reversal agents Flashcards

1
Q

What is the state of the acetylcholine receptor in its resting state?

A
  • Is closed when in its resting state​
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2
Q

How is the acetylcholine receptor channel opened?

A
  • Simultaneous binding of two acetylcholine molecules to the receptor alpha subunits.
  • Causes a conformational change to open the channel​
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3
Q

How do Nondepolarizing muscle blockers work?

A
  • They produce competitive antagonism by binding a single molecule
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4
Q

What is the action of Succinylcholine on the neuromuscular endplate?

A
  • Produces prolonged depolarization of the endplate region
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5
Q

Where is acetylcholinesterase found and what is its role?

A
  • Acetylcholinesterase (true cholinesterase) is present at the neuromuscular junction
  • Responsible for the hydrolysis of released acetylcholine to acetic acid and choline.
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6
Q

What is the role of Butyrylcholinesterase?

A
  • Butyrylcholinesterase (plasma cholinesterase, pseudocholinesterase), synthesized in the liver, catalyzes the hydrolysis of succinylcholine mainly in the plasma
  • Metabolizes :mivacurium, cocaine, procaine, and chloroprocaine.
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7
Q

What are the characteristics of a Depolarizing block?

A
  • Also known as phase I block
  • The only type of depolarizing neuromuscular blocking drug (NMBD) in clinical use.
  • Often preceded by muscle fasciculations resulting from antidromic action potentials
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8
Q

What is the purpose of precurarization in depolarizing blocks?

A
  • Administration of a small dose of nondepolarizing neuromuscular blocker (precurarization)
  • Helps prevent fasciculations
  • Increases intraocular pressure
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9
Q

Is masseter spasm consistently associated with malignant hyperthermia (MH)?

A
  • May be an early indicator of MH but is NOT consistently associated with it
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10
Q

How are nondepolarizing neuromuscular-blocking drugs (NMBDs) classified?

A

Nondepolarizing NMBDs are classified based on:
1. Chemical class (steroidal or benzylisoquinolinium)
2. Duration of action

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11
Q

How is Atracurium metabolized and what are its characteristics?

A
  • Metabolized by Hofmann elimination and ester hydrolysis.
  • Atracurium is a racemic mixture of 10 stereoisomers.
  • It is eliminated 70% in bile and the remainder in urine.
  • Elimination impaired by biliary obstruction.
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12
Q

What are the key properties of Cisatracurium?

A
  • Cisatracurium is a more potent isomer of atracurium.
  • Metabolized by Hofmann elimination,
  • Produce less laudanosine
  • Does not cause histamine release​
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13
Q

How is Mivacurium metabolized?

A
  • Metabolized by butyrylcholinesterase at a rate similar to succinylcholine.
  • Consit of three (3) stereoisomers.
  • May produce histamine release if administered rapidly.
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14
Q

What are the key characteristics of Pancuronium?

A
  • Is a potent, long-acting NMBD.
  • Has vagolytic properties
  • Blocks Norepinephrine reuptake
  • Blocks Butyrylcholinesterase-inhibiting properties.
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15
Q

What is the significance of ED95 in the context of neuromuscular blockade?

A
  • ED95 is the dose resulting in 95% depression of twitch height.
  • It is used to determine the appropriate dose for tracheal intubation and to maintain neuromuscular blockade​.
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16
Q

What is the difference between steroidal and benzylisoquinolinium NMBDs?

A
  • Steroidal NMBDs are generally monoquaternary compounds.
  • Benzylisoquinolinium NMBDs, like curare derivatives, are bisquaternary ammonium compounds.
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17
Q

Which steroidal neuromuscular-blocking drugs (NMBDs) does Sugammadex work best with?

A
  • Sugammadex is most effective with Rocuronium.
  • followed by Vecuronium.
  • Least effective with Pancuronium.
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18
Q

What is the primary action of Acetylcholinesterase Inhibitors in the context of NMBDs?

A
  • They antagonize the residual effects of nondepolarizing NMBDs.
  • Causes acetylcholine to accumulate at the neuromuscular junction and compete for available sites.
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19
Q

What is the effective dose range for neostigmine?

A
  • The effective dose range is 60 – 80 mcg/kg
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20
Q

What is the effective dose range for Edrophonium?

A
  • The effective dose range is 1 – 1.5 mg/kg
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21
Q

What are the common side effects associated with acetylcholinesterase inhibitors?

A
  • Bronchoconstriction.
  • Increased airway resistance.
  • Increased salivation.
  • Increased bowel motility.

Muscarinic effects must be blocked by Atropine or Glycopyrrolate.

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22
Q

Describe the chemical structure of Sugammadex.

A
  • Is a modified γ-cyclodextrin compound.
  • With a structure resembling a hollow truncated cone or doughnut.
  • Has a hydrophobic cavity and a hydrophilic exterior.
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23
Q

How does Sugammadex work to reverse neuromuscular blockade?

A
  • Forms tight complexes with steroidal NMBDs.
  • Particularly Rocuronium, independent of the depth of the neuromuscular block.
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24
Q

What are the key pharmacokinetic properties of Sugammadex?

A
  • Sugammadex is biologically inactive.
  • Does not bind to plasma proteins.
  • Primarily eliminated through the urine (75%).
  • 59%-80% excreted in urine within 24 hrs post administration
  • In patients with renal impairment, clearance of Sugammadex and rocuronium is affected.
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25
Q

What are the primary purposes of monitoring neuromuscular function?

A
  • Allows for appropriate dosing,
  • Ensures adequate recovery (TOFR ≥ 0.9).
  • Helps avoid risks of residual paralysis (upper airway obstruction, aspiration, and hypoxemia).
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26
Q

What does subjective evaluation of neuromuscular blockade involve?

A
  • Includes visual and tactile assessment of evoked responses.
  • Assessing the degree of blockade, but is considered unreliable.
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27
Q

What is electromyography (EMG) and how is it used in neuromuscular monitoring?

A
  • EMG involves stimulating a peripheral nerve and measuring the muscle action potential.
  • It is the oldest form of neuromuscular monitoring but is subject to electrical interference.
  • Does not analyze muscle movement.
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28
Q

Why is Mechanomyography considered the gold standard in neuromuscular blockade monitoring?

A
  • It measures the force of muscle contraction in response to electrical stimuli.
  • Is the GOLD STANDARD due to its accuracy.
  • Its clinical use is limited by stringent preparation requirements.
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29
Q

What is the principle behind Acceleromyography in neuromuscular monitoring?

A
  • Is based on Newton’s second law (force = mass x acceleration).
  • Measures the acceleration of a muscle, usually the adductor pollicis.
  • Its use may be limited by surgical positioning
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30
Q

How does a Kinemyographic device function in neuromuscular monitoring?

A
  • Uses a mechanosensor strip that generates an electrical signal proportional to the magnitude of bending.
  • The results may not consistently correlate with the gold standard MMG
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31
Q

How do Depolarizing and Nondepolarizing blockades differ in response to peripheral nerve stimulation (PNS)?

A
  • Depolarizing block shows absence of fade and posttetanic potentiation.
  • Nondepolarizing block shows fade after repeated stimulation and can cause posttetanic potentiation​
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32
Q

What are the characteristics of a Depolarizing (Phase I) Block?

A
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32
Q

How do different muscle groups respond to NMBDs?

A
  • Vessel-rich central muscle groups like the diaphragm are more susceptible to NMBDs, become paralyzed before peripheral muscles, and recover faster.
  • The adductor pollicis is one of the last muscles to recover from NMBD-induced paralysis
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33
Q

What are the characteristics of a Non-Depolarizing (Phase II) Block?

A
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34
Q

What is Suggamadex’s affinity in numbers for Rocuronium?

A
  • 4,723 more affinity to Rocuronium than Atracurium.
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35
Q

What are the doses of Suggamdex?

A
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36
Q

Sugammadex should be avoided in patients with Creatinine clearance of:

A

< 30 mL/min

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37
Q

What are the common clinical signs of Recovery from a Neuromuscular Blockade?

A
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38
Q

What discovery refuted the electrical theory of neuromuscular transmission?

A
  • The discovery of the role of acetylcholine in neuromuscular transmission refuted the electrical theory, leading to Dale and Loewi’s Nobel Prize in 1936 for this discovery.
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39
Q

When and by whom was curare first successfully administered for surgical relaxation?

A
  • The first successful administration of curare was in 1912 by Arthur Läwen, who used a partially purified preparation for surgical relaxation.
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40
Q

When was a significant milestone in the use of NMBDs in clinical anesthesia, and what happened?

A
  • A significant milestone was on January 23, 1942, when Enid Johnson, under Harold Griffith’s instructions, administered curare intravenously for an appendectomy, marking a turning point in the use of NMBDs in anesthesia.
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41
Q

What are the two chemical classifications of neuromuscular-blocking drugs?

A
  • Depolarizing NMBDs which act as agonists at nicotinic acetylcholine receptors causing prolonged membrane depolarization.
  • Nondepolarizing NMBDs, which compete with acetylcholine at the receptors and are competitive antagonists.
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42
Q

What is an example of a depolarizing NMBD currently in clinical use?

A
  • Succinylcholine is the only depolarizing NMBD currently used in clinical practice.
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43
Q

What is the state of the acetylcholine receptor ion channel in the resting state?

A
  • The ion channel of the acetylcholine receptor is closed.
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44
Q

How is the acetylcholine receptor ion channel activated?

A
  • Activation occurs when two acetylcholine molecules bind to the α subunits.
  • Causing conformational changes that open the channel.
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45
Q

How do nondepolarizing neuromuscular-blocking drugs (NMBDs) work?

A
  • Nondepolarizing NMBDs bind to one α subunit of the acetylcholine receptor, sufficient to produce neuromuscular block as competitive antagonists.
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46
Q

What is the mechanism of action of succinylcholine at the neuromuscular junction?

A
  • Succinylcholine causes prolonged depolarization of the endplate, resulting in desensitization of nicotinic acetylcholine receptors.
  • Inactivation of voltage-gated sodium channels.
  • Increased potassium permeability.
  • Hyperpolarization
  • Neuromuscular transmission blockade.
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47
Q

What enzymes hydrolyze Choline Esters and where are they found?

A
  • Acetylcholinesterase (true cholinesterase) is at the neuromuscular junction and hydrolyzes acetylcholine.
  • Butyrylcholinesterase (plasma cholinesterase) is in the plasma, hydrolyzing succinylcholine and other substances like mivacurium and local anesthetics.

Butyrylcholinesterase : Succinylcholine, Mivacurium, Cocaine, Procaine,

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48
Q

What distinguishes succinylcholine in clinical use?

A
  • Succinylcholine, also known as suxamethonium
  • Is the only depolarizing neuromuscular-blocking drug (NMBD) used in clinical practice.
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49
Q

What causes muscle fasciculations after succinylcholine administration?

A
  • May result from antidromic conduction of action potentials activating parts of the motor unit, leading to variable fasciculations among patients.
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50
Q

What is the purpose of precurarization before administering succinylcholine?

A
  • Precurarization, using a small dose of nondepolarizing neuromuscular blocker.
  • is intended to prevent succinylcholine-induced side effects.
  • Its effectiveness is inconsistent across studies.
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51
Q

Describe the structure of succinylcholine.

A
  • Succinylcholine is a long, thin, flexible molecule.
  • Made up of two acetylcholine molecules linked through the acetate methyl groups.
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52
Q

How does succinylcholine act on cholinergic receptors?

A
  • Succinylcholine stimulates cholinergic receptors at the neuromuscular junction and at nicotinic and muscarinic autonomic sites.
    Causes side effects like:
    1. Increased intraocular
    2. Increased intragastric pressure.
    3. cardiac arrhythmias by opening the ionic channel in the acetylcholine receptor.
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53
Q

What is the elimination half-life of succinylcholine?

A
  • 47 seconds and follows first-order kinetics.
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54
Q

What is the usual dose of succinylcholine for tracheal intubation, and what are its effects?

A
  • Is 1.0 mg/kg. This dose results in complete suppression of neuromuscular response in about 60 seconds.
  • Recovery to 90% muscle strength in 9 to 13 minutes in those with normal butyrylcholinesterase activity.
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55
Q

How does the dose of succinylcholine influence intubating conditions?

A
  • Doses larger than 1.5 mg/kg do not provide significant advantages.
  • A dose of 2.0 mg/kg does not guarantee excellent intubating conditions in all patients.
  • Intubating conditions depend on the depth of anesthesia, airway anatomy, and the anesthesiologist’s experience.
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56
Q

How is succinylcholine metabolized?

A
  • Is rapidly hydrolyzed by butyrylcholinesterase to succinylmonocholine (a weaker agent) and choline.
  • Only 10% of the administered drug reaching the neuromuscular junction.
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57
Q

What is the role of butyrylcholinesterase in the action of succinylcholine?

A
  • Butyrylcholinesterase controls the onset and duration of succinylcholine’s action by hydrolyzing the drug in plasma before it reaches and after it leaves the neuromuscular junction.
  • Recovery occurs as the drug diffuses away from the junction.
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58
Q

Where is butyrylcholinesterase synthesized and what is its function?

A
  • Is synthesized by the liver
  • It’s found in the plasma, and is responsible for metabolizing drugs like:
    1. succinylcholine
    2. mivacurium
    3. several local anesthetics
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59
Q

What factors can decrease butyrylcholinesterase activity?

A
  • Factors include:
    1. Liver disease
    2. Aging
    3. Malnutrition
    4. Pregnancy
    5. Burns
    6. Certain medications
    7. Neoplastic disease
    8. High estrogen levels.
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60
Q

How does butyrylcholinesterase activity affect neuromuscular block induced by succinylcholine?

A
  • A reduction in butyrylcholinesterase activity prolongs the neuromuscular block induced by succinylcholine or mivacurium.
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61
Q

What is the effect of esmolol on butyrylcholinesterase activity?

A
  • Esmolol inhibits butyrylcholinesterase, causing only a minor prolongation of succinylcholine block.
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62
Q

How does liver disease affect butyrylcholinesterase activity?

A
  • In severe liver disease, plasma cholinesterase activity can be reduced to 20% of normal.
  • Significantly increasing the duration of succinylcholine-induced apnea.
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63
Q

How do anticholinesterase drugs like neostigmine affect butyrylcholinesterase activity?

A
  • Neostigmine and similar drugs can cause a profound decrease in butyrylcholinesterase activity.
  • Leading to prolonged neuromuscular blockade after succinylcholine administration.
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64
Q

What effect does pregnancy have on butyrylcholinesterase activity?

A
  • High estrogen levels in pregnancy can decrease butyrylcholinesterase activity by up to 40%,
  • This does not typically prolong the action of succinylcholine-induced paralysis.
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65
Q

How do genetic variants of butyrylcholinesterase affect neuromuscular block induced by succinylcholine or mivacurium?

A
  • Genetic variants can significantly prolong the neuromuscular block induced by succinylcholine or mivacurium.
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66
Q

How is butyrylcholinesterase phenotype determined?

A
  • Is determined using specific enzyme inhibitors like Dibucaine or Fluoride.
  • Which produce phenotype-specific dibucaine or fluoride numbers.
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67
Q

What do different dibucaine numbers indicate about butyrylcholinesterase genotypes?

A
  • A Dibucaine number of 70 or higher indicates the usual genotype (E1uE1u).
  • Numbers less than 30 indicate homozygous atypical genes (E1aE1a).
  • Heterozygous atypical variants (E1uE1a) have Dibucaine numbers between 40 to 60.
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68
Q

How does butyrylcholinesterase genotype affect the duration of neuromuscular block?

A
  • In Homozygous atypical genotypes (E1aE1a), the block can last 4 to 8 hours.
  • In Heterozygous atypical genotypes (E1uE1a), it can be 1.5 to 2 times longer than in individuals with the usual genotype.
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69
Q

What is the recommended treatment for a prolonged neuromuscular block?

A
  • Keep the patient sedated.
  • Maintaining artificial ventilation until the train-of-four ratio (TOFR) recovers to 0.9 or more.
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70
Q

What does measuring butyrylcholinesterase activity reveal?

A
  • Shows the efficiency of the enzyme in hydrolyzing succinylcholine or mivacurium
  • Which can be influenced by genotype.
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71
Q

How do certain butyrylcholinesterase variants affect enzyme activity?

A
  • Some rare variants are associated with increased enzyme activity, leading to resistance to succinylcholine and mivacurium.
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72
Q

What cardiac effects can succinylcholine cause?

A
  • Sinus bradycardia
  • Junctional rhythm
  • Sinus arrest

Reflecting its action on cardiac muscarinic cholinergic receptors.

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73
Q

When are cardiac dysrhythmias most likely to occur with succinylcholine administration?

A
  • More likely when a second dose of succinylcholine is given.
  • About 5 minutes after the first dose.

Children will have dysrhythmias at the first dose.

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74
Q

In whom is sinus bradycardia frequently seen following succinylcholine administration?

A
  • Is common in children and adults after a repeated dose of succinylcholine.

Due to stimulation of cardiac muscarinic receptors.

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75
Q

How is succinylcholine-induced bradycardia treated or prevented?

A
  • Atropine is effective in treating or preventing succinylcholine-induced bradycardia.
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76
Q

What contrasting effects does succinylcholine have on the autonomic nervous system?

A

Succinylcholine can cause Ganglionic stimulation, leading to increases in:

  1. Heart rate
  2. Systemic blood pressure

Similar to acetylcholine’s physiologic effect at autonomic ganglia.

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77
Q

What can cause ventricular dysrhythmias after succinylcholine administration?

A
  • May be due to autonomic stimuli associated with laryngoscopy and tracheal intubation.
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78
Q

How does succinylcholine administration affect plasma potassium levels?

A
  • Potassium Increase of 0.5 mEq/dL in plasma concentration in healthy individuals.
  • Usually without causing dysrhythmias.
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79
Q

Are patients with renal failure more susceptible to hyperkalemia from succinylcholine?

A
  • Patients with renal failure are not more susceptible to an exaggerated hyperkalemic response to succinylcholine than those with normal renal function.
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80
Q

Which patients are at risk of severe hyperkalemia from succinylcholine?

A

Patients at risk of severe hyperkalemia:

  1. Burns
  2. Severe abdominal infections
  3. Severe Metabolic acidosis
  4. Closed head injuries
  5. Conditions causing upregulation of extrajunctional acetylcholine receptors.
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81
Q

Is succinylcholine recommended for use in children?

A

Is not recommended except for emergency tracheal intubation, due to the risk of:

  • Rhabdomyolysis
  • Hyperkalemia
  • Death

In children with undiagnosed muscle disease, succinylcholine.

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82
Q

What does the occurrence of myoglobinuria indicate after succinylcholine administration?

A
  • Suggests skeletal muscle damage.
  • Especially in pediatric patients
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83
Q

What conditions are often found in patients with Rhabdomyolysis and Myoglobinuria after succinylcholine administration?

A

Are often found to have:

  1. Malignant Hyperthermia.
  2. Occult Muscular Dystrophy.
84
Q

How does succinylcholine affect intraocular pressure?

A
  • Usually causes an increase in intraocular pressure.
  • peaking at 2 to 4 minutes post-administration
  • Returning to normal by 6 minutes.
85
Q

Is succinylcholine recommended for use in open eye injuries?

A
  • The use is controversial
  • It was shown to cause no adverse events in a study of patients with penetrating eye injuries.
86
Q

What is the efficacy of precurarization in attenuating increases in intraocular pressure following succinylcholine administration?

A
  • In reducing succinylcholine-induced increases in Intraocular pressure is controversial.
87
Q

How does succinylcholine affect intragastric pressure?

A
  • Succinylcholine causes a variable increase in intragastric and lower esophageal sphincter pressures.
  • Related to the intensity of fasciculations of abdominal skeletal muscle and an increase in vagal tone.
88
Q

Does succinylcholine predispose patients to regurgitation?

A
  • Succinylcholine does not typically predispose to regurgitation in patients with an intact lower esophageal sphincter
  • As the increase in intragastric pressure usually doesn’t exceed the “barrier pressure.”
89
Q

What is the effect of succinylcholine on intracranial pressure?

A
  • It can increase intracranial pressure.
  • This increase can be attenuated or prevented by pretreatment with a nondepolarizing NMBD.
90
Q

What are the characteristics of postoperative myalgias induced by succinylcholine?

Think “NBA”

A

Can cause postoperative skeletal muscle myalgia, especially in the:
1. Neck
2. Back
3. Abdomen

It occurs more frequently in:

  • Young adults undergoing minor surgeries
  • Ambulatory patients
  • Particularly women > men
91
Q

How common is succinylcholine-induced myalgia, and what might cause it?

A
  • The incidence varies widely, from 0.2% to 89%.
  • The cause is not fully understood
  • May be related to muscle damage from fasciculations or involve prostaglandins and cyclooxygenases.
92
Q

How can succinylcholine-induced myalgias be prevented?

A
  • Using muscle relaxants
  • Lidocaine
  • Nonsteroidal anti-inflammatory drugs.
  • Prostaglandin inhibitors like Lysine acetyl salicylate or Diclofenac.
93
Q

What is the relationship between succinylcholine, masseter spasm, and malignant hyperthermia?

A
  • While succinylcholine can trigger malignant hyperthermia,
  • Masseter spasm may be an early indicator but is not consistently associated with this condition.
94
Q

Why might masseter spasm be more common in children given succinylcholine?

A
  • Might be due to inadequate dosing of succinylcholine.
95
Q

How do Nondepolarizing Neuromuscular-Blocking Drugs (NMBDs) work?

A
  • Act as competitive antagonists by binding to the α subunits of the nicotinic acetylcholine receptor.
96
Q

What are the bases for classifying nondepolarizing NMBDs?

A

Are classified based on:

  1. Chemical class (steroidal, Benzylisoquinolinium)
  2. Duration of action (long-acting, intermediate-acting, or short-acting).
97
Q

What are the general characteristics of nondepolarizing NMBDs?

A
  • Nondepolarizing NMBDs are positively charged
  • And relatively large molecules.
98
Q

What are the typical dosing strategies for nondepolarizing NMBDs?

A
  • Generally, a dose of 2 to 3 times the ED95 is used for tracheal intubation.
  • 10% of the ED95 is used to maintain neuromuscular blockade.
99
Q

What inspired the development of Benzylisoquinoline-type relaxants?

A
  • The arrow poisons used by South American Indians.
  • Known as curare, served as the basis for developing benzylisoquinoline-type relaxants like Tubocurarine.
100
Q

Why is Tubocurarine, a benzylisoquinolinium compound, no longer in use?

A
  • Is not currently used anymore due to its side effects
  • Tubocurarine was initially introduced as an NMBD for surgical anesthesia.
101
Q

What is the composition of Atracurium?

A
  • Is a racemic mixture of 10 stereoisomers,
  • Divided into cis-cis, cis-trans, and trans-trans isomer groups
  • In a ratio of approximately 10:6:1.
102
Q

How does Atracurium degrade in the body?

A
  • Undergoes spontaneous degradation through Hofmann elimination
  • Produce Laudanosine monoquaternary acrylate
  • Can also undergo Ester Hydrolysis.
103
Q

What is Hofmann elimination, and what are the metabolites of atracurium?

A
  • Hofmann elimination is a chemical process that degrades atracurium into laudanosine and a monoquaternary acrylate.
  • Both metabolites of atracurium.
104
Q

How is Laudanosine cleared from the body, and what are its effects?

A
  • About 70% of laudanosine is excreted in the bile and the remainder in urine.
  • It crosses the blood-brain barrier
  • Has CNS stimulating properties
  • Its seizure threshold in humans is unknown.
105
Q

Are high blood levels of laudanosine a concern for patients in intensive care?

A
  • In intensive care patients, blood levels of laudanosine can reach 5.0 to 6.0 μg/mL.
  • However, there is no evidence that prolonged administration of atracurium leads to concentrations capable of causing convulsions.
106
Q

What is the plasma elimination half-life of laudanosine in patients with normal and impaired renal function?

A
  • Is similar in patients with normal and impaired renal function
  • 197 ± 38 min normal renal function
  • 234 ± 81 min impaired renal function
107
Q

What is Cisatracurium and how potent is it compared to Atracurium?

A
  • Cisatracurium is the 1R cis–1’R cis isomer of Atracurium.
  • Comprising 15% of the atracurium mixture by weight but over 50% in terms of neuromuscular-blocking activity.
108
Q

How is Cisatracurium metabolized?

A
  • Is metabolized by Hofmann elimination to laudanosine and a monoquaternary alcohol metabolite, without undergoing ester hydrolysis.
109
Q

What are the clinical advantages of Cisatracurium over Atracurium?

A
  • Cisatracurium, being more potent, produces less laudanosine.
  • Does not cause histamine release, unlike Atracurium.
110
Q

What is Mivacurium, and how is it metabolized?

A
  • Is a mixture of three (3) stereoisomers
  • Metabolized by Butyrylcholinesterase to a Monoester and a Dicarboxylic acid
  • Similar to succinylcholine.
111
Q

Does Mivacurium cause histamine release?

A
  • Mivacurium may produce histamine release, especially when administered rapidly.
112
Q

What is significant about the structure of steroidal neuromuscular-blocking drugs?

A
  • Steroidal compounds possess onium centers
  • It is essential for one of the nitrogen atoms in the molecule to be quaternized for effective interaction with nicotinic acetylcholine receptors.
113
Q

What role does the acetyl ester play in steroidal compounds?

A
  • Facilitates the interaction of steroidal compounds with nicotinic acetylcholine receptors at the postsynaptic muscle membrane.

The acetyl ester, resembling an acetylcholine-like moiety

114
Q

What are the key properties of Pancuronium?

A
  • Is a potent long-acting NMBD with vagolytic, direct sympathomimetic stimulation
  • Blocks Norepinephrine reuptake
  • Butyrylcholinesterase-inhibiting properties.
  • 40-60% cleared by the kidney
  • 11% is excreted in the bile
  • 15%-20% is metabolized, mainly by deacetylation in the liver.
  • The metabolites 3-OH, 17-OH, and 3,7-di-OH
115
Q

How is Pancuronium metabolized and excreted?

A
  • About 40% to 60% of pancuronium is cleared by the kidneys
  • 11% excreted in bile
  • 15%-20% metabolized, mainly by deacetylation in the liver
  • Its metabolites are less potent NMBDs and excreted in urine.
116
Q

Why might clinicians opt for other NMBDs over Pancuronium?

A
  • Due to its prolonged effect
  • The risk of postoperative residual paralysis
  • Associated morbidity

clinicians often prefer other NMBDs for achieving neuromuscular blockade.

117
Q

What are the key characteristics of vecuronium?

A
  • Vecuronium is a monoquarternary NMBD with intermediate action duration
  • Less potent than pancuronium
  • With virtually no vagolytic properties
  • Increased lipid solubility leading to greater biliary elimination.
118
Q

How does vecuronium differ from pancuronium?

A
  • Vecuronium lacks the quaternizing methyl group present in pancuronium
  • Leading to a slight decrease in potency
  • Loss of vagolytic properties
  • Molecular instability in solution
  • Increased lipid solubility.
119
Q

How is Vecuronium metabolized and excreted?

A
  • Vecuronium is metabolized in the liver into metabolites like 3-OH vecuronium,
  • Around 30%- 40% excreted in bile as the parent compound
  • 30% excreted in urine. (Renal)
  • Its Neuromuscular block duration depends mainly on hepatic function.
120
Q

How stable is vecuronium in solution?

A
  • Vecuronium is less stable in solution
  • Prepared as a lyophilized powder
  • Cannot be prepared as a ready-to-use solution with a long shelf life.
121
Q

What are the properties of Rocuronium?

A
  • Rocuronium is an intermediate-acting monoquarternary NMBD with a
  • Faster onset than vecuronium or pancuronium
  • Is about 6 times less potent than vecuronium.
122
Q

How is Rocuronium eliminated and how stable is it?

A
  • Primarily eliminated by the liver
  • Excreted in bile
  • 30% is excreted unchanged in urine.
  • It is stable at room temperature for 60 days.
  • Pancuronium is stable for 6 months.
123
Q

How is the potency of nondepolarizing NMBDs expressed?

A
  • Is expressed as ED50 and ED95
  • indicating the doses required for 50% or 95% depression of twitch height, respectively.
124
Q

How does the potency of nondepolarizing NMBDs affect their speed of onset?

A
  • The speed of onset of nondepolarizing NMBDs is inversely proportional to their potency.
  • Low-potency drugs have a rapid onset
  • High-potency drugs have a slow onset.
125
Q

What is the relationship between molar potency and onset time in NMBDs?

A
  • Molar potency (ED50 or ED95 in μM/kg) is predictive of the time to onset of effect
  • Lower molar potency drugs like rocuronium having a rapid onset compared to higher potency drugs.
126
Q

Why do low-potency drugs have a faster onset than high-potency drugs?

A
  • Low-potency drugs have a higher number of molecules for an equipotent dose
  • Creating a greater diffusion gradient to the neuromuscular junction and a faster transfer rate from plasma to biophase.
127
Q

What is “buffered diffusion,” and how does it affect NMBD recovery?

A
  • Buffered diffusion, seen in high-potency drugs,
  • Is where drug diffusion is impeded due to binding to high-density receptors within a restricted space.
  • It causes repetitive binding and unbinding from receptors, lengthening the duration of effect.
128
Q

How do inhalational anesthetics affect the potency of nondepolarizing NMBDs?

A
  • Inhalational anesthetics potentiate the neuromuscular-blocking effect of nondepolarizing NMBDs
  • Reduce the required dosage
  • Prolongs both action duration and recovery time.
129
Q

What factors influence the potentiation of NMBDs by inhalational anesthetics?

A
  • The potentiation depends on the duration of inhalational anesthesia
  • The specific anesthetic used, and
  • Its concentration.

Des > Sevo > Iso > Halothane> N2O

Nitrous oxide have varying degrees of potentiation.

130
Q

How do certain antibiotics potentiate neuromuscular blockade?

A
  • Aminoglycoside antibiotics, polymyxins, lincomycin, and clindamycin inhibit acetylcholine release and depress receptor sensitivity
  • Tetracyclines exhibit postjunctional activity.

Aminoglycosides = Gentamicin, Amikacin, Trobamycin, Neomycin, Streptomycin

131
Q

How do hypothermia and magnesium sulfate affect neuromuscular blockade?

A
  • They potentiate the blockade
  • Hypothermia increasing recovery time
  • Hypermagnesemia inhibits calcium channels at presynaptic nerve terminals.
132
Q

What effect do local anesthetics and antidysrhythmic drugs have on neuromuscular block?

A
  • Large doses of local anesthetics and antidysrhythmic drugs like quinidine potentiate neuromuscular block
  • Smaller doses of local anesthetics have no significant effect.
133
Q

How does chronic anticonvulsant therapy affect resistance to nondepolarizing NMBDs?

A
  • Chronic anticonvulsant therapy can lead to resistance to nondepolarizing NMBDs (except mivacurium and atracurium)
  • Requiring increased doses for complete neuromuscular blockade and resulting in accelerated recovery.
134
Q

What are the possible causes of resistance to nondepolarizing NMBDs?

A
  • May be due to increased clearance
  • Increased binding to α1-acid glycoproteins
  • Upregulation of neuromuscular acetylcholine receptors.
135
Q

How does hyperparathyroidism affect the sensitivity to nondepolarizing NMBDs?

A
  • In hyperparathyroidism, hypercalcemia decreases sensitivity to NMBDs like atracurium, tubocurarine, and pancuronium,
  • leading to a shorter duration of neuromuscular blockade.

THINK: Hyperthyroidism = Decreases A-T-P

136
Q

What is the significance of NMBDs in adverse reactions during anesthesia?

A
  • NMBDs are responsible for a significant proportion of adverse drug reactions
  • Deaths during anesthesia, with 10.8% of adverse reactions and 7.3% of deaths attributable to them.
137
Q

How do neuromuscular-blocking agents affect the autonomic nervous system?

A

NMBDs interact with nicotinic and muscarinic cholinergic receptors in the sympathetic and parasympathetic systems causing effects like:

  • Ganglion blockade
  • Hypotension
  • Reflex tachycardia
  • Bronchospasm.
138
Q

What are the specific autonomic effects of tubocurarine?

A
  • Causes ganglion blockade leading to hypotension
  • Can trigger histamine release, resulting in flushing, reflex tachycardia, and bronchospasm.
139
Q

What is the vagolytic effect of pancuronium?

A
  • Pancuronium has a direct vagolytic effect
  • can block muscarinic receptors on sympathetic postganglionic nerve terminals
  • affecting catecholamine release modulation.
140
Q

How does pancuronium influence catecholamine release?

A
  • May stimulate catecholamine release from adrenergic nerve terminals
  • Influences the sympathetic nervous system.
141
Q

Which neuromuscular-blocking compounds cause histamine release and what are the effects?

A

Benzylisoquinolinium compounds like Mivacurium, Atracurium, and Tubocurarine can cause histamine release, leading to:

  • Skin flushing
  • Decreases in blood pressure
  • Increased pulse rate
  • Systemic vascular resistance changes
142
Q

Do steroidal NMBDs cause histamine release?

A
  • In typical clinical doses, are not associated with histamine release.

Steroidal compounds: P-V-R

143
Q

What are the clinical effects and duration of histamine release from NMBDs?

A
  • The effects of histamine release, such as skin flushing and hypotension, occur with rapid drug administration, usually last 1-5 minutes
  • Are dose-related.
  • They can be clinically insignificant in healthy patients but
  • May cause bronchospasm in those with hyperactive airway disease.
144
Q

How does histamine affect the cardiovascular system?

A
  • Can cause peripheral vasodilatation,
  • Leading to hypotension and reflex responses
  • Has positive inotropic and chronotropic effects on myocardial H2 receptors.
145
Q

What considerations should be made when choosing NMBDs for hemodynamically compromised patients?

A
  • In such patients, it’s better to use drugs with less or no histamine release, like cisatracurium, vecuronium, or rocuronium
  • Administer benzylisoquinolinium NMBDs slowly or with prophylactic histamine H1- and H2-receptor antagonists.
146
Q

How often do life-threatening anaphylactic reactions occur during anesthesia?

A
  • Anaphylactic reactions occur in approximately 1 in 1,000 to 1 in 25,000 anesthesia administrations,
  • With a mortality rate of about 5%.
147
Q

What are the most common causes of anaphylaxis during anesthesia?

A
  1. NMBDs (58.2%)
  2. Latex (16.7%)
  3. Antibiotics (15.1%).
148
Q

What is the difference between anaphylactic and anaphylactoid reactions?

A
  • Anaphylactic reactions are immune-mediated involving IgE antibodies
  • Anaphylactoid reactions are exaggerated pharmacologic responses, not immune-mediated.
149
Q

What can nondepolarizing NMBDs cross-react with?

A
  • Food
  • Cosmetics
  • Disinfectants
  • Industrial materials
150
Q

Do steroidal NMBDs cause significant histamine release?

A
  • Steroidal NMBDs (e.g., rocuronium, vecuronium) do not cause significant histamine release but still can cause anaphylaxis.
151
Q

What is the recommended treatment for anaphylactic reactions during anesthesia?

A
  • 100% oxygen
  • Intravenous epinephrine (10-20 mcg/kg)
  • Early tracheal intubation (Angioedema)
  • Fluids (crytalloids/colloids)
  • potentially norepinephrine or a sympathomimetic drug like Phynelephrine
  • Treatment for dysrhythmias.

The use of antihistamines and steroids is controversial.

152
Q

What is the function of acetylcholinesterase at the neuromuscular junction?

A
  • Acetylcholinesterase rapidly hydrolyzes released acetylcholine at the neuromuscular junction
  • About 50% hydrolyzed before reaching nicotinic receptors.
153
Q

How do acetylcholinesterase inhibitors work to reverse nondepolarizing neuromuscular blockade?

A
  • Increase acetylcholine concentration at the neuromuscular junction,
  • Compete with nondepolarizing NMBDs for receptor sites and accelerating recovery.
154
Q

What is the ceiling effect of acetylcholinesterase inhibitors?

A
  • Once maximum inhibition of acetylcholinesterase is reached additional doses won’t increase acetylcholine concentration further.
155
Q

What are the maximum effective doses of neostigmine and edrophonium?

A
  • The maximum effective dose for neostigmine is 60 to 80 μg/kg
  • Edrophonium, it is 1.0 to 1.5 mg/kg.
156
Q

How widely used is neostigmine in clinical practice?

A
  • Neostigmine is the most widely used anticholinesterase agent by anesthesiologists worldwide.
157
Q

When should neostigmine be administered for optimal effect?

A
  • It should ideally be administered when there is partial spontaneous recovery from a nondepolarizing NMBD,
  • Using a small dose if fade cannot be detected on TOF stimulation.
158
Q

What are the elimination half-lives and routes of excretion for edrophonium, neostigmine, and pyridostigmine?

A
  • Edrophonium, neostigmine, and pyridostigmine have similar elimination half-lives,
  • With renal excretion
  • Accounting for 50% for neostigmine
  • About 75% for pyridostigmine and edrophonium.
  • Renal failure decreases their plasma clearance.
159
Q

What are the general side effects of acetylcholinesterase inhibitors?

A
  • Increases acetylcholine concentration at all synapses,
  • Affecting both nicotinic and muscarinic receptors.
160
Q

How are the cardiovascular side effects of acetylcholinesterase inhibitors managed?

A
  • Anticholinergic agents like atropine or glycopyrrolate are coadministered to block muscarinic effects.
  • Atropine matches the action of edrophonium
  • Glycopyrrolate matches that of neostigmine and pyridostigmine.
161
Q

What are the pulmonary and alimentary side effects of acetylcholinesterase inhibitors?

A

These inhibitors can cause:

  • Bronchoconstriction
  • Increased airway resistance
  • Increased salivation
  • Increased bowel motility

Anticholinergics help reduce these effects.

162
Q

Does neostigmine increase the incidence of postoperative nausea and vomiting?

A
  • There is no evidence that neostigmine increases postoperative nausea and vomiting.
  • It may have antiemetic properties or no effect on the incidence of these conditions.
163
Q

What is a common postanesthetic issue associated with acetylcholinesterase inhibitors?

A
  • Incomplete reversal and residual postoperative weakness are frequent
  • With studies reporting a high incidence of postoperative residual neuromuscular blockade
164
Q

What was the reported incidence of postoperative residual neuromuscular blockade in a 2003 study?

A
  • In 2003, Debaene and colleagues reported a 45% incidence of this condition in patients arriving in the postanesthesia care unit.
165
Q

How does practitioner overconfidence affect the management of NMBDs?

A
  • Most practitioners are overconfident in their knowledge and ability to manage NMBDs,
  • often not knowing what constitutes adequate recovery from neuromuscular blockade
166
Q

What are the limitations of using nerve stimulators and reversal agents for NMBDs?

A
  • Lack of routine use of quantitative nerve stimulators and the ceiling effect of reversal agents when administered at a deep level of neuromuscular blockade.
167
Q

Does the use of reversal agents and nerve stimulators eliminate critical respiratory events postoperatively?

A
  • Despite using nerve stimulators and neostigmine, critical respiratory events in the postoperative care unit remain significant, indicating a need for changes in clinical care.
168
Q

What are cyclodextrins and their natural forms?

A
  • Cyclodextrins are cyclic dextrose units from starch, with natural forms being α-, β-, or γ-cyclodextrin, comprising 6-, 7-, or 8-cyclic oligosaccharides, respectively.
  • They have a hydrophobic cavity and hydrophilic exterior
169
Q

What is the composition and structure of sugammadex?

A
  • Is a modified γ-cyclodextrin with an eight-membered ring
  • Designed to encapsulate steroidal NMBDs.
  • It has extended cavity and negatively charged carboxyl groups for better binding to rocuronium.
170
Q

How does sugammadex work to counteract steroidal neuromuscular-blocking agents?

A
  • Sugammadex forms tight 1:1 complexes with steroidal NMBDs, particularly rocuronium, through van der Waals forces
  • Hydrogen bonds, and hydrophobic interactions, resulting in a high association rate and very low dissociation rate.
171
Q

Which neuromuscular-blocking agents does sugammadex bind to most effectively?

A
  • Is most effective at binding with Rocuronium
  • Followed by Vecuronium
  • Has much less affinity for Pancuronium.

Rocuronium > Vecuronium > Pancuronium

172
Q

Is sugammadex biologically active and does it bind to plasma proteins?

A
  • Sugammadex is biologically inactive
  • Does not bind to plasma proteins.
  • Its metabolism is minimal, with most of it eliminated through urine.
173
Q

How is sugammadex eliminated from the body?

A
  • About 75% is eliminated in the urine
  • 59% to 80% of the dose excreted within 24 hours after administration.
174
Q

How does renal impairment affect the clearance of sugammadex and rocuronium?

A
  • In patients with significant renal impairment, clearances of sugammadex and rocuronium decrease considerably
  • Their elimination half-lives increase.
  • Sugammadex is not recommended for patients with a creatinine clearance of <30 mL/min.
175
Q

Can dialysis effectively remove sugammadex and rocuronium from plasma?

A
  • The effectiveness of dialysis in removing sugammadex and rocuronium from plasma has not been consistently demonstrated.
176
Q

How does sugammadex affect the elimination of rocuronium?

A
  • Rocuronium is mainly eliminated by biliary excretion
  • When bound to sugammadex, this route becomes unavailable, decreasing rocuronium clearance to a value close to the glomerular filtration rate.
177
Q

What is the capability of Sugammadex in reversing neuromuscular blockade?

A
  • Sugammadex can reverse any depth of neuromuscular blockade induced by rocuronium or vecuronium to a Train-of-Four Ratio (TOFR) of ≥0.9 within 3 minutes.
178
Q

How does Sugammadex work to reverse neuromuscular blockade?

A
  • Sugammadex removes free rocuronium or vecuronium from plasma,
  • creating a concentration gradient that moves remaining molecules from the neuromuscular junction back into plasma, where they are encapsulated by Sugammadex.
179
Q

What are the recommended doses of Sugammadex for different levels of blockade?

A
  • For TOF count ≥2, use 2 mg/kg;
  • For deeper levels (only posttetanic twitches), use 4 mg/kg
  • For rapid reversal of 1.2 mg/kg rocuronium, use 16 mg/kg.
180
Q

Is Sugammadex effective in “cannot intubate, cannot ventilate” (CICV) situations?

A
  • Sugammadex should not be relied upon in CICV situations
  • It may not ensure immediate return of spontaneous ventilation, especially in obese patients.
181
Q

Against which neuromuscular-blocking drugs is sugammadex ineffective?

A
  • Succinylcholine
  • Benzylisoquinolinium NMBDs like mivacurium, atracurium, and cisatracurium, as it cannot form inclusion complexes with these drugs.
182
Q

How does sugammadex interact with oral contraceptives?

A
  • Inhibit oral contraceptives.
  • Patients are advised to use alternative contraceptive methods for 7 days after exposure to sugammadex.
183
Q

What is the incidence of anaphylactic reactions to sugammadex, and how is it diagnosed?

A
  • The incidence is about 0.04%,
  • Similar to that with rocuronium.
  • Diagnosis involves estimating plasma tryptase concentrations during the acute event and repeating it 2-6 hours and 24 hours later.
184
Q

What cardiac arrhythmias can occur post-sugammadex administration?

A
  • Bradycardia and asystole, may occur after sugammadex administration.
  • Continuous electrocardiogram monitoring and readiness with atropine and vasoactive drugs are necessary.
185
Q

What serious cardiac adverse events have been reported with sugammadex?

A
  • From 2009 to 2017, serious events like bradycardia, cardiac arrest, ventricular fibrillation, and tachycardia were reported, including 138 cases with nine deaths.
186
Q

Does sugammadex affect blood coagulation times?

A
  • May cause small increases in aPTT and PT
  • But clinically significant bleeding has not been reported.
187
Q

What are the primary purposes of monitoring neuromuscular function in clinical settings?

A
  • The purposes are to administer appropriate doses of NMBDs
  • To ensure adequate recovery from their residual effects
  • Guaranteeing patient safety.
188
Q

What are the complications associated with residual postoperative paralysis?

A
  1. Upper airway obstruction
  2. Aspiration
  3. Hypoxemia.
189
Q

Why are clinical bedside criteria considered inadequate for assessing neuromuscular recovery?

A
  • Bedside criteria like a 5-second head lift are insensitive indicators of neuromuscular recovery, as they don’t accurately reflect residual neuromuscular blockade
190
Q

What is the difference between subjective and objective neuromuscular monitoring?

A
  • Subjective monitoring relies on qualitative evaluation of muscular responses
  • Objective (quantitative) monitoring involves real-time measurement of the TOFR.
191
Q

Why is quantitative monitoring essential in neuromuscular function assessment?

A
  • Accurately measures TOFR in real time
  • Crucial for assessing neuromuscular recovery
  • Prevents residual blockade.
192
Q

What are the limitations of subjective evaluation using a Peripheral Nerve Stimulator (PNS) for neuromuscular blockade?

A
  • Is unreliable for determining recovery from neuromuscular blockade and may miss residual weakness.
  • It struggles to assure readiness for tracheal extubation (TOFR ≥0.90)
  • Often fails to detect fade at TOFR approaching 0.40.
193
Q

How is subjective neuromuscular monitoring performed?

A
  • It involves using a PNS to stimulate a nerve observing the number
  • Strength of muscle twitches (TOFC) by tactile or visual means.
194
Q

What are the different objective techniques for neuromuscular blockade monitoring?

A
  • Electromyography (EMG)
  • Mechanomyography (MMG- is Gold standard)
  • Acceleromyography
  • Kinemyography

Each with distinct methods and limitations.

195
Q

What is Electromyography (EMG) and how is it used in neuromuscular monitoring?

A
  • EMG measures muscle action potentials in response to nerve stimulation
  • Is subject to electrical interference
  • Does not analyze muscle movement.
196
Q

Why is Mechanomyography (MMG) considered the gold standard in neuromuscular blockade monitoring?

A
  • MMG measures force from muscle contraction in response to electrical stimuli
  • Is considered the gold standard, but its clinical use is limited due to preparation requirements.
197
Q

How are Acceleromyography and Kinemyography used in neuromuscular monitoring?

A
  • Acceleromyography: measures muscle acceleration and requires free thumb movement, limiting its use.
  • Kinemyography: uses a mechanosensor strip but may not correlate well with MMG.
198
Q

How do responses to nerve stimulation differ between depolarizing and nondepolarizing NMBD blockades?

A
  • Depolarizing block (succinylcholine) shows no fade or posttetanic potentiation
  • Nondepolarizing blockades exhibit fade and can cause posttetanic potentiation.
199
Q

How do different muscle groups respond to NMBDs?

A
  • Central muscles like the diaphragm are more susceptible to NMBDs and recover faster compared to peripheral muscles like the adductor pollicis.
200
Q

Which muscle group should be monitored for assessing neuromuscular blockade recovery?

A
  • The adductor pollicis muscle, in response to ulnar nerve stimulation, is recommended for monitoring to exclude residual weakness.
201
Q

How do laryngeal and diaphragmatic muscles respond to NMBDs?

A
  • These muscles are more resistant to NMBDs
  • Develop blockade faster
  • Recover quicker than peripheral muscles like the adductor pollicis
202
Q

Is monitoring facial muscles reliable for assessing neuromuscular blockade?

A
  • Monitoring facial muscles, like the corrugator supercilii or orbicularis oculi, is less reliable than monitoring the adductor pollicis muscle.
203
Q

What is the difference in residual paralysis incidence when monitoring facial muscles vs. hand muscles?

A
  • Monitoring eyebrow responses showed a 52% incidence of residual paralysis
  • compared to 22% with hand muscle monitoring.
204
Q

Name the Monoquaternary compounds:

A
  1. Tubocurarine
  2. Vecuronium
  3. Rocuronium
205
Q

Majority of Nondepolarizing NMBD are considered:

A
  • Bisquaternary Ammonium Compounds.
206
Q

The parasympathetic nervous systems uses Acetylcholine as:

A
  • Preganglionic and Postganglionic neurotransmitter.
207
Q

Chronic anticonvulsant therapy can lead to resistance to nondepolarizing NMBDs except:

A
  • Mivacurium
  • Atracurium

UPR-RCM SRNA PHARM I (7 decks)

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