Neuromuscular Blocking Agents/Reversal

Question 1

What are the primary functions of neuromuscular

blocking drugs?

Answer 1

To facilitate intubation and mechanical ventilation and produce
immobility during surgery.
Barash PG, Cullen BF, Stoelting RK, Cahalan MK, Stock MC,
Ortega R. Clinical Anesthesia. 7th ed. Philadelphia, PA:
Lippincott Williams and Wilkins; 2013: 523.

Question 2

During resting conditions, how does the electrical
potential on the inside of a nerve cell compare to the
outside of the cell? What happens if this potential
changes?

Answer 2

The potential on the inside of the cell is negative (around -
90mV). If the potential becomes less negative, or depolarizes,
sodium channels open that allow sodium ions to flood into the
cell. This increase in positive ions causes the inside of the
nerve cell to be more positive than the outside. This effect also
allows calcium to enter the cell.
Barash PG, Cullen BF, Stoelting RK, Cahalan MK, Stock MC,
Ortega R. Clinical Anesthesia. 7th ed. Philadelphia, PA:
Lippincott Williams and Wilkins; 2013: 525.

Question 3

Where is the primary site of action for neuromuscular

blocking agents?

Answer 3

The nicotinic cholinergic receptor on the muscle endplate
(postsynaptic).
Barash PG, Cullen BF, Stoelting RK, Cahalan MK, Stock MC,
Ortega R. Clinical Anesthesia. 7th ed. Philadelphia, PA:
Lippincott Williams and Wilkins; 2013: 523.

Question 4

All of the available neuromuscular blocking agents

bear a chemical resemblance to what chemical?

Answer 4

Acetylcholine
Katzung BG, Masters, SB, & Trevor AJ. Basic and Clinical
Pharmacology. 12th ed. New York: McGraw-Hill; 2012: 467.

Question 5

Besides their chemical similarity to acetylcholine,
what chemical structure is common to all
neuromuscular blocking agents? What is the
significance of this feature?

Answer 5

They all contain one or two quaternary nitrogens which makes
them water-soluble and prevents their entry into the central
nervous system.
Katzung BG, Masters, SB, & Trevor AJ. Basic and Clinical
Pharmacology. 12th ed. New York: McGraw-Hill; 2012: 467.

Question 6

What electrolyte abnormalities can potentiate

neuromuscular blockade?

Answer 6

Hypocalcemia will augment a nondepolarizing blockade.
Hypermagnesemia can potentiate a block by competing with
calcium at the neuromuscular junction. Hypokalemia will also
augment a nondepolarizing block.
Butterworth JF, Mackey DC, Wasnick JD. Morgan & Mikhail’s
Clinical Anesthesiology. 5th ed. New York, NY: McGraw-Hill;
2013: 214.

Question 7

How do volatile anesthetics affect the action of

neuromuscular blocking drugs?

Answer 7

Volatile anesthetics potentiate the effects of neuromuscular
blocking drugs. Desflurane produces the most significant
potentiation of nondepolarizing muscle relaxants. The degree
of potentiation in order from greatest to least is Desflurane >
Sevoflurane > Isoflurane > Nitrous/Fentanyl
Butterworth JF, Mackey DC, Wasnick JD. Morgan & Mikhail’s
Clinical Anesthesiology. 5th ed. New York, NY: McGraw-Hill;
2013: 213.

Question 8

How does hypothermia affect neuromuscular

blockade?

Answer 8

Hypothermia can augment a block by decreasing metabolism or
delaying excretion of the drug.
Butterworth JF, Mackey DC, Wasnick JD. Morgan & Mikhail’s
Clinical Anesthesiology. 5th ed. New York, NY: McGraw-Hill;
2013: 214.

Question 9

Which neuromuscular block agent undergoes no

metabolism?

Answer 9

Rocuronium undergoes no metabolism and is eliminated
unchanged by the liver and kidneys.
Butterworth JF, Mackey DC, Wasnick JD. Morgan & Mikhail’s
Clinical Anesthesiology. 5th ed. New York, NY: McGraw-Hill;
2013: 218.

Question 10

What nondepolarizing neuromuscular agents will
have a prolonged duration of action in patients with
hepatic disease?

Answer 10

The steroidal derivatives, rocuronium, vecuronium, and
pancuronium will be prolonged in the presence of hepatic
disease.
Nagelhout JJ, Plaus KL. Nurse Anesthesia. 5th ed. St. Louis,
MO: Elsevier Saunders Company; 2014: 176.

Question 11

Which of the steroidal muscle relaxants is most

affected by renal disease?

Answer 11

All three steroidal relaxants (rocuronium, vecuronium, and
pancuronium) are affected by renal disease. Pancuronium is
about 85% dependent upon renal elimination and is the most
affected.
Nagelhout JJ, Plaus KL. Nurse Anesthesia. 5th ed. St. Louis,
MO: Elsevier Saunders Company; 2014: 177.

Question 12

What are the two major classifications of
nondepolarizing neuromuscular blockers? What
commonly used agents fall into each class?

Answer 12

Isoquinolones, which includes atracurium and cisatracurium and
steroid derivatives which includes pancuronium, rocuronium,
and vecuronium.
Katzung BG, Masters, SB, & Trevor AJ. Basic and Clinical
Pharmacology. 12th ed. New York: McGraw-Hill; 2012: 470.

Question 13

What is the intubating dose of rocuronium?

Answer 13

0.6 mg/kg to 1.2 mg/kg
Nagelhout JJ, Plaus KL. Nurse Anesthesia. 5th ed. St. Louis,
MO: Elsevier Saunders Company; 2014: 173.

Question 14

What method is used clinically to speed the onset of

rocuronium?

Answer 14

Priming, which is the administration of 10% of the intubating
dose about 1-3 minutes prior to anesthetizing the patient and
administering the remaining dose.
Nagelhout JJ, Plaus KL. Nurse Anesthesia. 5th ed. St. Louis,
MO: Elsevier Saunders Company; 2014: 173.

Question 15

How is rocuronium elimination?

Answer 15

Rocuronium is primarily eliminated in unchanged form via biliary
excretion.
Nagelhout JJ, Plaus KL. Nurse Anesthesia. 5th ed. St. Louis,
MO: Elsevier Saunders Company; 2014: 173.

Question 16

What is the duration of action of rocuronium?

Answer 16

Rocuronium is an intermediate-acting muscle relaxant. The
duration of action is dose-dependent. An intubating dose of 0.6
mg/kg to 1.2 mg/kg usually provides a duration of action
between 30 and 90 minutes.
Nagelhout JJ, Plaus KL. Nurse Anesthesia. 5th ed. St. Louis,
MO: Elsevier Saunders Company; 2014: 173.

Question 17

How does the elimination half-life of rocuronium
differ between pediatric patients, adults, and the
elderly?

Answer 17

The elimination half-life of rocuronium in children is about 38
minutes, in adults it is 56 minutes, and in the elderly it is 137
minutes.
Nagelhout JJ, Plaus KL. Nurse Anesthesia. 5th ed. St. Louis,
MO: Elsevier Saunders Company; 2014: 173.

Question 18

What cardiovascular changes may be seen with the

administration of rocuronium or vecuronium?

Answer 18

No cardiovascular changes are seen with the administration of
rocuronium or vecuronium, and no increases in histamine levels
are seen with doses up to 1.2 mg/kg of rocuronium.
Barash PG, Cullen BF, Stoelting RK, Cahalan MK, Stock MC,
Ortega R. Clinical Anesthesia. 7th ed. Philadelphia, PA:
Lippincott Williams and Wilkins; 2013: 538-539.

Question 19

How do the duration, onset, and recovery times of

vecuronium compare with that of rocuronium?

Answer 19

Rocuronium has a much faster onset than vecuronium, but the
duration and recovery times are approximately equal.
Barash PG, Cullen BF, Stoelting RK, Cahalan MK, Stock MC,
Ortega R. Clinical Anesthesia. 7th ed. Philadelphia, PA:
Lippincott Williams and Wilkins; 2013: 538.

Question 20

About what should you be cautious when using
either atracurium, vecuronium, or rocuronium in
conjunction with thiopental?

Answer 20

If administered shortly after thiopental, hese agents can react
with thiopental to produce barbituric acid, a precipitate that can
obstruct the IV.
Barash PG, Cullen BF, Stoelting RK, Cahalan MK, Stock MC,
Ortega R. Clinical Anesthesia. 7th ed. Philadelphia, PA:
Lippincott Williams and Wilkins; 2013: 539-540.

Question 21

What is the intubating dose of vecuronium?

Answer 21

0.1 mg/kg
Nagelhout JJ, Plaus KL. Nurse Anesthesia. 5th ed. St. Louis,
MO: Elsevier Saunders Company; 2014: 175.

Question 22

How is vecuronium eliminated?

Answer 22

Vecuronium ungergoes hepatic and renal elimination. The
majority of is eliminated in the bile.
Nagelhout JJ, Plaus KL. Nurse Anesthesia. 5th ed. St. Louis,
MO: Elsevier Saunders Company; 2014: 173.

Question 23

What may be responsible for the prolonged duration
of action of vecuronium when used in intensive care
unit patients?

Answer 23

One of vecuronium’s metabolites, 3-OH vecuronium, accounts
for about 60% of the activity of vecuronium and is excreted by
the kidneys. The reduced clearance of this metabolite in the
presence of altered renal status can result in a prolongation in
the action of vecuronium.
Barash PG, Cullen BF, Stoelting RK, Cahalan MK, Stock MC,
Ortega R. Clinical Anesthesia. 7th ed. Philadelphia, PA:
Lippincott Williams and Wilkins; 2013: 539.

Question 24

What is the intubating dose of pancuronium?

Answer 24

0.07 mg/kg
Longnecker DE, Newman MF, Brown DL, Zapol WM.
Anesthesiology. 2nd ed. New York: McGraw-Hill; 2012: 503.

Question 25

What difficulty does the use of pancuronium present

in noncardiac surgery?

Answer 25

It is associated with a higher incidence of postoperative muscle
weakness and is more difficult to reverse than intermediateacting
agents.
Barash PG, Cullen BF, Stoelting RK, Cahalan MK, Stock MC,
Ortega R. Clinical Anesthesia. 7th ed. Philadelphia, PA:
Lippincott Williams and Wilkins; 2013: 537.

Question 26

What cardiac effect of pancuronium has increased

its usefulness in the cardiac surgery setting?

Answer 26

Pancuronium can cause an increase in heart rate, blood
pressure, and cardiac output via a vagolytic effect at the
postganglionic nerve terminal, an increase in catecholamine
release, and an antimuscarinic effect. This offsets the
bradycardia associated with large doses of fentanyl used in
cardiac surgery.
Barash PG, Cullen BF, Stoelting RK, Cahalan MK, Stock MC,
Ortega R. Clinical Anesthesia. 7th ed. Philadelphia, PA:
Lippincott Williams and Wilkins; 2013: 537.

Question 27

What is the intubating dose of atracurium?

Answer 27

0.5 mg/kg
Nagelhout JJ, Plaus KL. Nurse Anesthesia. 5th ed. St. Louis,
MO: Elsevier Saunders Company; 2014: 175.

Question 28

What are the most common side effects of

atracurium administration?

Answer 28

Atracurium can cause significant histamine release which can
result in hypotension, tachycardia, flushing, and bronchospasm.
Barash PG, Cullen BF, Stoelting RK, Cahalan MK, Stock MC,
Ortega R. Clinical Anesthesia. 7th ed. Philadelphia, PA:
Lippincott Williams and Wilkins; 2013: 535.

Question 29

What are the metabolic byproducts of the
metabolism of atracurium and what side effects can
result from them?

Answer 29

Laudanosine and acrylate are metabolic byproducts of the
degradation of atracurium. Laudanosine has been reported to
cause seizures in animals but only in doses larger than clinically
relevant.
Barash PG, Cullen BF, Stoelting RK, Cahalan MK, Stock MC,
Ortega R. Clinical Anesthesia. 7th ed. Philadelphia, PA:
Lippincott Williams and Wilkins; 2013: 535.

Question 30

What is the structural difference between atracurium
and cisatracurium? What are the clinical effects of
this difference?

Answer 30

Cisatracurium is a potent isomer of atracurium that, unlike
atracurium, is devoid of any histamine release. Cisatracurium
has a higher potency and requires less of the drug to be
administered to reach the same clinical endpoint. As a result,
less laudanosine and acrylate byproducts are produced and the
toxic effects of these agents is essentially nonexistent.
Barash PG, Cullen BF, Stoelting RK, Cahalan MK, Stock MC,
Ortega R. Clinical Anesthesia. 7th ed. Philadelphia, PA:
Lippincott Williams and Wilkins; 2013: 536.

Question 31

What are the two metabolic pathways for atracurium

and cisatracurium?

Answer 31

The first means of metabolism of atracurium and cisatracurium
is via Hofmann elimination, which is a nonenzymatic
degradation of the drug. The second is via degradation by the
same tissue esterases that degrade remifentanil and esmolol.
About 1/3 of atracurium undergoes Hofmann elimination and
the remainder undergoes degradation by tissues esterases.
Barash PG, Cullen BF, Stoelting RK, Cahalan MK, Stock MC,
Ortega R. Clinical Anesthesia. 7th ed. Philadelphia, PA:
Lippincott Williams and Wilkins; 2013: 535.

Question 32

What is the intubating dose of cisatracurium?

Answer 32

0.1 mg/kg
Nagelhout JJ, Plaus KL. Nurse Anesthesia. 5th ed. St. Louis,
MO: Elsevier Saunders Company; 2014: 175.

Question 33

What are the muscle relaxants of choice for the

patient with renal disease?

Answer 33

Atracurium and cisatracurium are the preferred muscle
relaxants in patients with renal disease. The onset and duration
are not affected by renal impairment.
Nagelhout JJ, Plaus KL. Nurse Anesthesia. 5th ed. St. Louis,
MO: Elsevier Saunders Company; 2014: 177.

Question 34

How does succinylcholine affect serum potassium

levels?

Answer 34

Succinylcholine increases the serum potassium level by about
0.5 mEq/L in most patients. A defasciculating dose of a
nondepolarizing muscle relaxant does not have any effect on
the increase in potassium, but large doses of nondepolarizing
muscle relaxants will abolish it. The increase in potassium is
much more dramatic and can be life-threatening in patients with
denervation injuries in which there is an upregulation in
extrajunctional receptors. This includes patients with spinal
cord transection, stroke, extensive burns, trauma, muscular
dystrophies, and prolonged immobility due to disease.
Barash PG, Cullen BF, Stoelting RK, Cahalan MK, Stock MC,
Ortega R. Clinical Anesthesia. 7th ed. Philadelphia, PA:
Lippincott Williams and Wilkins; 2013: 533.

Question 35

How do nondepolarizing neuromuscular blocking

agents affect a depolarizing phase I block?

Answer 35

Typically, small doses of nondepolarizing muscle relaxants will
antagonize a phase I block produced by succinylcholine
because by occupying some of the acetylcholine receptors, they
inhibit depolarization.
Butterworth JF, Mackey DC, Wasnick JD. Morgan & Mikhail’s
Clinical Anesthesiology. 5th ed. New York, NY: McGraw-Hill;
2013: 208.

Question 36

What is fasciculation and with what drug does it

occur?

Answer 36

Fasciculation is disorganized muscle activity that occurs after
the administration of succinylcholine but before muscle
paralysis occurs.
Barash PG, Cullen BF, Stoelting RK, Cahalan MK, Stock MC,
Ortega R. Clinical Anesthesia. 7th ed. Philadelphia, PA:
Lippincott Williams and Wilkins; 2013: 531.

Question 37

What are the contraindications to the use of

succinylcholine?

Answer 37

Hyperkalemia, severe muscle trauma, severe burns,
denervation injuries, renal failure with hyperkalemia, malignant
hyperthermia, Duchenne muscular dystrophy, Guillain-Barre
syndrome, and severe sepsis. It is recommended for use in
children under the age of 8 only in emergency situations.
Nagelhout JJ, Plaus KL. Nurse Anesthesia. 5th ed. St. Louis,
MO: Elsevier Saunders Company; 2014: 168-169.

Question 38

What is the drug of choice to produce neuromuscular

blockade when succinylcholine is contraindicated?

Answer 38

Rocuronium
Longnecker DE, Newman MF, Brown DL, Zapol WM.
Anesthesiology. 2nd ed. New York: McGraw-Hill; 2012: 504.

Question 39

What is the primary metabolite of succinylcholine

and what are the effects of this metabolite?

Answer 39

Succinylcholine is rapidly metabolized into succinylmonocholine
and then to succinic acid. Succinylmonocholine is believed to
stimulate cholinergic receptors in the sinoatrial node, resulting
in bradycardia.
Butterworth JF, Mackey DC, Wasnick JD. Morgan & Mikhail’s
Clinical Anesthesiology. 5th ed. New York, NY: McGraw-Hill;
2013: 209

Question 40

Why does succinylcholine have such a short
duration of action compared to the nondepolarizing
agents?

Answer 40

Succinylcholine is rapidly hydrolyzed by pseudocholinesterase
in the plasma and to a lesser extent, butyrylcholinesterase in
the liver.
Katzung BG, Masters, SB, & Trevor AJ. Basic and Clinical
Pharmacology. 12th ed. New York: McGraw-Hill; 2012: 468.

Question 41

What is the intubating dose of succinylcholine and
how long does it typically last until full neuromuscular
recovery?

Answer 41

The intubating dose is 1-1.5 mg/kg. It takes 12-15 minutes on
average before full neuromuscular recovery occurs.
Nagelhout JJ, Plaus KL. Nurse Anesthesia. 5th ed. St. Louis,
MO: Elsevier Saunders Company; 2014: 165.

Question 42

How does the intubating dose of succinylcholine in

children compare with that of adults?

Answer 42

Children require a higher dose of succinylcholine than adults,
typically requiring 1-2 mg/kg. Infants require an even higher
dose of 2-3 mg/kg to facilitate intubation. Defasciculating doses
of nondepolarizing neuromuscular blockers are rarely given
because fasciculations are uncommon in children.
Barash PG, Cullen BF, Stoelting RK, Cahalan MK, Stock MC,
Ortega R. Clinical Anesthesia. 7th ed. Philadelphia, PA:
Lippincott Williams and Wilkins; 2013: 533.

Question 43

In what way does the administration of
succinylcholine affect the masseter muscle and
adductor pollicis differently in some individuals?
Why?

Answer 43

Succinylcholine can cause rigidity for several minutes in the
masseter muscle and to a smaller degree, the adductor pollicis.
The reason for this is not completely understood, but it is
believed that it is mediated by acetylcholine receptors as large
doses of nondepolarizing muscle relaxants block this response.
Barash PG, Cullen BF, Stoelting RK, Cahalan MK, Stock MC,
Ortega R. Clinical Anesthesia. 7th ed. Philadelphia, PA:
Lippincott Williams and Wilkins; 2013: 531.

Question 44

How does succinylcholine affect intracranial

pressure?

Answer 44

Succinylcholine may increase intracranial pressure, but this
effect is blocked by the administration of a defasciculating dose
of a nondepolarizing muscle relaxant.
Barash PG, Cullen BF, Stoelting RK, Cahalan MK, Stock MC,
Ortega R. Clinical Anesthesia. 7th ed. Philadelphia, PA:
Lippincott Williams and Wilkins; 2013: 532.

Question 45

How does succinylcholine affect intragastric

pressure?

Answer 45

Succinylcholine increases intragastric pressure, but this effect is
prevented by administration of a defasciculating dose of a
nondepolarizing muscle relaxant.
Barash PG, Cullen BF, Stoelting RK, Cahalan MK, Stock MC,
Ortega R. Clinical Anesthesia. 7th ed. Philadelphia, PA:
Lippincott Williams and Wilkins; 2013: 532.

Question 46

How does succinylcholine affect intraocular

pressure?

Answer 46

The administration of succinylcholine can raise intraocular
pressure by 5 to 15 mmHg. The administration of a
defasciculant has little to no affect on this increase. Although
there is no documented cases where the administration of
succinylcholine has led to blindness or the extrusion of ocular
contents, the use of succinylcholine in open-eye injuries is
widely avoided.
Barash PG, Cullen BF, Stoelting RK, Cahalan MK, Stock MC,
Ortega R. Clinical Anesthesia. 7th ed. Philadelphia, PA:
Lippincott Williams and Wilkins; 2013: 506.

Question 47

What is succinylcholine-induced myalgia, and how

can it be prevented?

Answer 47

Myalgia can occur 24-48 hours after the administration of
succinylcholine in a large percentage of patients. It primarily
affects young, ambulatory patients (particularly females).
Although the degree of fasciculations seen do not have a
correlation with the degree of myalgia, administering a
defasciculating dose of a nondepolarizing muscle relaxant prior
to the succinylcholine has been shown to prevent myalgia.
Barash PG, Cullen BF, Stoelting RK, Cahalan MK, Stock MC,
Ortega R. Clinical Anesthesia. 7th ed. Philadelphia, PA:
Lippincott Williams and Wilkins; 2013: 532.

Question 48

What explains why pediatric patients may have a

higher dose requirement for succinylcholine?

Answer 48

The quaternary ammonium structure of succinylcholine is
responsible for the high water solubility of the drug and its
volume of distribution is therefore confined to the extracellular
space. Since pediatric patients have a relatively larger
extracellular space than adults, their volume of distribution for
water soluble drugs is larger. Thus, they require a larger dose
on a milligram per kilogram basis.
Butterworth JF, Mackey DC, Wasnick JD. Morgan & Mikhail’s
Clinical Anesthesiology. 5th ed. New York, NY: McGraw-Hill;
2013: 208-209.

Question 49

What is the difference between a phase I block and

a phase II block with succinylcholine?

Answer 49

A phase I block is a depolarizing block that is antagonized, not
reversed by cholinesterase inhibitors. Succinylcholine is the
only drug available in the US that can produce a phase I block.
A phase II block is also known as a desensitizing block. This
can occur with prolonged exposure to succinylcholine (from
large or repeated doses) in which the initial end plate
depolarization decreases and the membrane repolarizes again.
A phase II block becomes clinically indistinguishable from the
block produced by nondepolarizing muscle relaxants and can,
in some cases, be reversed by cholinesterase inhibitors.
Katzung BG, Masters, SB, & Trevor AJ. Basic and Clinical
Pharmacology. 12th ed. New York: McGraw-Hill; 2012: 469-471.

Question 50

What are some non-genetic causes of a decrease in

plasma cholinesterase activity?

Answer 50

Pregnancy, liver disease, uremia, burns, malnutrition, oral
contraceptives, and plasmapheresis will all decrease plasma
cholinesterase and possibly result in a prolonged duration of
action of succinylcholine.
Barash PG, Cullen BF, Stoelting RK, Cahalan MK, Stock MC,
Ortega R. Clinical Anesthesia. 7th ed. Philadelphia, PA:
Lippincott Williams and Wilkins; 2013: 532.

Question 51

What is the significance of a dibucaine number?

Answer 51

Dibucaine is used to diagnose the different genetic forms of
plasma cholinesterase deficiency. A patient with a dibucaine
number of 70-80 is normal and the duration of action of
succinylcholine will be normal. A patient with a dibucaine
number of 50-60 is considered to have heterozygous atypical
plasma cholinesterase and the duration of action of
succinylcholine will be prolonged by 8-20 minutes. A patient
with a dibucaine number of 20-30 is considered to have
homozygous atypical plasma cholinesterase and the duration of
succinylcholine will be markedly prolonged.
Yao FF. Anesthesiology: Problem-Oriented Patient
Management. 7th ed. Philadelphia: Lippincott, Williams, and
Wilkins; 2012: 1188.

Question 52

What are the two types of genetically-induced

plasma cholinesterase deficiency?

Answer 52

About 1 in 2000 individuals have a homozygous plasma
cholinesterase deficiency, which results in an inability to
metabolized succinylcholine and may suffer prolonged paralysis
of 2-6 hours or more after the administration of a normal dose of
succinylcholine. The heterozygous form occurs in about 1 in 30
patients and results in a slight increase in the duration of
succinylcholine.
Barash PG, Cullen BF, Stoelting RK, Cahalan MK, Stock MC,
Ortega R. Clinical Anesthesia. 7th ed. Philadelphia, PA:
Lippincott Williams and Wilkins; 2013: 532.

Question 53

Are the cholinesterase inhibitors edrophonium,
neostigmine, and pyridostigmine lipid-soluble? Why
or why not?

Answer 53

Edrophonium, neostigmine, and pyridostigmine are quaternary
ammoniums that are not lipid-soluble.
Nagelhout JJ, Plaus KL. Nurse Anesthesia. 5th ed. St. Louis,
MO: Elsevier Saunders Company; 2014: 179.

Question 54

What anticholinesterase drug is able to cross the

blood-brain barrier?

Answer 54

Physostigmine crosses the blood-brain barrier and, for this
reason, is not used as a reversal agent for neuromuscular
blockade.
Barash PG, Cullen BF, Stoelting RK, Cahalan MK, Stock MC,
Ortega R. Clinical Anesthesia. 7th ed. Philadelphia, PA:
Lippincott Williams and Wilkins; 2013: 1275.

Question 55

What is the maximum recommended dose of

neostigmine?

Answer 55

The maximum dose is 0.08 mg/kg up to a total of 5 mg in adults.
Butterworth JF, Mackey DC, Wasnick JD. Morgan & Mikhail’s
Clinical Anesthesiology. 5th ed. New York, NY: McGraw-Hill;
2013: 228.

Question 56

What is the dose of pyridostigmine for the reversal of

neuromuscular blockade?

Answer 56

Pyridostigmine is about 1/5 as potent as neostigmine. The
dose for reversal of neuromuscular blockade is 0.4 mg/kg up to
a total dose of 20 mg in adults.
Butterworth JF, Mackey DC, Wasnick JD. Morgan & Mikhail’s
Clinical Anesthesiology. 5th ed. New York, NY: McGraw-Hill;
2013: 229.

Question 57

What is the longest-acting cholinesterase inhibitor?

Why?

Answer 57

Pyridostigmine is the longest-acting of the cholinesterase
inhibitors because the pyridostigmine-enzyme complex
hydrolyzes slowly.
Nagelhout JJ, Plaus KL. Nurse Anesthesia. 5th ed. St. Louis,
MO: Elsevier Saunders Company; 2014: 180.

Question 58

What is the onset and duration of edrophonium?

Answer 58

Edrophonium is the fastest-acting cholinesterase with an onset
of 30-60 seconds after IV administration and a duration of about
5-10 minutes.
Nagelhout JJ, Plaus KL. Nurse Anesthesia. 5th ed. St. Louis,
MO: Elsevier Saunders Company; 2014: 179

Question 59

What symptoms can cholinesterase inhibitors

produce?

Answer 59

Cholinesterase inhibitors produce increased salivary secretion,
miosis, bronchoconstriction, decreased heart rate and
conduction velocity, increased intestinal motility, contraction of
the detrusor muscle, and increased insulin secretion.
Butterworth JF, Mackey DC, Wasnick JD. Morgan & Mikhail’s
Clinical Anesthesiology. 5th ed. New York, NY: McGraw-Hill;
2013: 227.

Question 60

What dose of glycopyrrolate is typically administered
to counteract the muscarinic side effects of
neostigmine? What are the advantages of
glycopyrrolate over atropine for this purpose?

Answer 60

Glycopyrrolate 0.2 mg per 1 mg of neostigmine is administered
to counteract the muscarinic effects of neostigmine.
Glycopyrrolate has an onset of action that closely matches
neostigmine and results in less tachycardia than atropine.
Butterworth JF, Mackey DC, Wasnick JD. Morgan & Mikhail’s
Clinical Anesthesiology. 5th ed. New York, NY: McGraw-Hill;
2013: 236.

Question 61

What are the doses of glycopyrrolate and atropine
that should be administered to reverse the
muscarinic side effects of pyridostigmine? Which is
preferred?

Answer 61

Glycopyrrolate 0.05 mg per 1 mg of pyridostigmine will
antagonize the muscarinic side effects. The dose of atropine
for the same purpose is 0.1 mg per 1 mg of pyridostigmine.
Glycopyrrolate is preferred because the onset of action more
closely matches that of pyridostigmine and it results in less
tachycardia.
Butterworth JF, Mackey DC, Wasnick JD. Morgan & Mikhail’s
Clinical Anesthesiology. 5th ed. New York, NY: McGraw-Hill;
2013: 229

Question 62

If atropine is used to antagonize the muscarinic side

effects of neostigmine, what dose should be used?

Answer 62

0.4 mg of atropine should be administered per mg of
neostigmine.
Butterworth JF, Mackey DC, Wasnick JD. Morgan & Mikhail’s
Clinical Anesthesiology. 5th ed. New York, NY: McGraw-Hill;
2013: 235.