1
RNFA
RNFA MASTER EXAM TEST
QUESTIONS AND ANSWERS UPDATED
(2024/2025) (VERIFIED ANSWERS)
DEPOLARIZING BLOCKERS - ANS ✓Succinylcholine is the only depolarizing
neuromuscular blocker used clinically in the USA. succinylcholine remains
popular because it is the only ultrarapid onset/ultrashort duration
neuromuscular blocker available.
• Succinylcholine binds to the nicotinic receptor and acts like acetylcholine
to cause depolarization of the end plate. This in turn spreads and
depolarizes adjacent membranes, causing transient fasciculations,
especially in chest and abdomen, though general anesthesia and prior
administration of a small dose of a nondepolarizing muscle relaxant tends
to attenuate them. Succinylcholine is not metabolized effectively at the
synapse, therefore the membrane remains depolarized and unresponsive
to additional impulses. A flaccid paralysis results. This is called Phase I
block, or depolarization block. Phase I block is augmented, not reversed, by
acetylcholinesterase inhibitors.
• The onset of neuromuscular blockade is very rapid, usually within 1
minute. Because of its rapid hydrolysis by plasma butyrylcholinesterase
(pseudocholinesterase), duration of neuromuscular block is 5-10 minutes.
• With a single large dose, repeated doses, or prolonged continued infusion
of succinylcholine (30-60 minutes) the membrane repolarizes; despite this
repolarization, the membrane can't be depolarized again because it is
desensitized.
The channels behave as if they are in a prolonged closed state. This is called
phase II block or desensitization block. Phase II block may be reversed by
acetylcholinesterase inhibitors.
RNFA MASTER
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RNFA
PHARMACOKINETICS OF NEUROMUSCULAR BLOCKERS - ANS ✓• All
neuromuscular blocking agents contain one or two quaternary ammonium
groups, which makes them highly polar and very poorly soluble in lipid.
• Neuromuscular blockers are inactive if given by mouth. They are always
given IV or IM. They penetrate membranes very poorly and do not enter
cells or cross the blood-brain barrier.
NON-DEPOLARIZING BLOCKERS - ANS ✓Highly ionized. They don't cross
membranes well and have limited volume of distribution of 80-140 mL/Kg -not
much larger than blood volume.
They have durations of action that range from 20 to 90 minutes, which can
be extended by supplemental dosing.
Non-depolarizing blockers can be classified into: long-, intermediate-, and
short-acting.
SHORT-ACTING
Mivacurium
INTERMEDIATE-ACTING
Atracurium
Rocuronium
Cisatracurium
Vecuronium
LONG-ACTING
Tubocurarine
Pancuronium
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METABOLISM - ANS ✓The duration of neuromuscular blockade produced by
nondepolarizing relaxants is strongly correlated with the elimination half-life.
Drugs that are excreted by the kidney typically have longer half-lives,
leading to longer durations of action.
Drugs eliminated by the liver tend to have shorter half-lives and durations
of action.
Atracurium is inactivated by hydrolysis by non-specific plasma esterases
and by a spontaneous reaction (Hoffman elimination). Duration of
neuromuscular block produced by atracurium is not altered by the absence
of renal function.
One of atracurium metabolites is laudanosine. Laudanosine may cause
transient hypotension and, in higher doses, seizures.
Cisatracurium, a stereoisomer of atracurium, undergoes Hoffman
elimination to form laudanosine. Because cisatracurium is more potent
than atracurium and lower doses are required, laudanosine concentrations
following cisatracurium administration are lower. Cisatracurium also
causes less histamine release. Therefore, cisatracurium has largely
replaced atracurium in clinical practice.
Mivacurium has short duration of action. Hydrolysis by
butyrylcholinesterase is the primary mechanism for inactivation of
mivacurium. Not dependent on liver or kidney.
Rocuronium has the most rapid onset among nondepolarizing blockers.
Can be used as alternative to succinylcholine for rapid sequence intubation.
DEPOLARIZING BLOCKERS - ANS ✓The extremely short duration of action of
succinylcholine (5-10 minutes) is due to its
rapid hydrolysis by plasma (and hepatic) butyrylcholinesterase.
Neuromuscular blockade by succinylcholine (and mivacurium) may be
prolonged in patients with an abnormal variant of butyrylcholinesterase.
Prolonged paralysis from succinylcholine caused by abnormal
RNFA MASTER
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butyrylcholinesterase should be treated with continued mechanical
ventilation until muscle function returns to normal.
Because of the rarity of these variants, butyrylcholinesterase testing is not
routine clinical procedure.
ADVERSE EFFECTS - ANS ✓...
NON-DEPOLARIZING BLOCKERS - ANS ✓• Some benzylisoquinolines may
produce hypotension due to histamine release and ganglionic blockade.
• Some ammonio steroids may produce tachycardia due to blockade of
muscarinic receptors, which may lead to arrhythmias. These drugs should
be used cautiously in patients with cardiovascular disease.
HISTAMINE RELEASE - ANS ✓Tubocurarine, and to a lesser extent, mivacurium
and atracurium can produce
hypotension as a result of histamine release. Tubocurarine is seldom used
clinically at this time.
Clinical signs of histamine release are erythema at the face and upper chest,
a transient decrease in blood pressure, and an increase in heart rate.
More severe reactions of histamine release include bronchospasm and
circulatory collapse.
Antihistamines can counteract responses that follow histamine release,
particularly if given before the neuromuscular blocker.
GANGLION BLOCKADE - ANS ✓Tubocurarine may cause some blockade of
nicotinic receptors of the autonomic ganglia
and the adrenal medulla; this results in a fall in blood pressure and
tachycardia.
RNFA MASTER
RNFA
RNFA MASTER EXAM TEST
QUESTIONS AND ANSWERS UPDATED
(2024/2025) (VERIFIED ANSWERS)
DEPOLARIZING BLOCKERS - ANS ✓Succinylcholine is the only depolarizing
neuromuscular blocker used clinically in the USA. succinylcholine remains
popular because it is the only ultrarapid onset/ultrashort duration
neuromuscular blocker available.
• Succinylcholine binds to the nicotinic receptor and acts like acetylcholine
to cause depolarization of the end plate. This in turn spreads and
depolarizes adjacent membranes, causing transient fasciculations,
especially in chest and abdomen, though general anesthesia and prior
administration of a small dose of a nondepolarizing muscle relaxant tends
to attenuate them. Succinylcholine is not metabolized effectively at the
synapse, therefore the membrane remains depolarized and unresponsive
to additional impulses. A flaccid paralysis results. This is called Phase I
block, or depolarization block. Phase I block is augmented, not reversed, by
acetylcholinesterase inhibitors.
• The onset of neuromuscular blockade is very rapid, usually within 1
minute. Because of its rapid hydrolysis by plasma butyrylcholinesterase
(pseudocholinesterase), duration of neuromuscular block is 5-10 minutes.
• With a single large dose, repeated doses, or prolonged continued infusion
of succinylcholine (30-60 minutes) the membrane repolarizes; despite this
repolarization, the membrane can't be depolarized again because it is
desensitized.
The channels behave as if they are in a prolonged closed state. This is called
phase II block or desensitization block. Phase II block may be reversed by
acetylcholinesterase inhibitors.
RNFA MASTER
, 2
RNFA
PHARMACOKINETICS OF NEUROMUSCULAR BLOCKERS - ANS ✓• All
neuromuscular blocking agents contain one or two quaternary ammonium
groups, which makes them highly polar and very poorly soluble in lipid.
• Neuromuscular blockers are inactive if given by mouth. They are always
given IV or IM. They penetrate membranes very poorly and do not enter
cells or cross the blood-brain barrier.
NON-DEPOLARIZING BLOCKERS - ANS ✓Highly ionized. They don't cross
membranes well and have limited volume of distribution of 80-140 mL/Kg -not
much larger than blood volume.
They have durations of action that range from 20 to 90 minutes, which can
be extended by supplemental dosing.
Non-depolarizing blockers can be classified into: long-, intermediate-, and
short-acting.
SHORT-ACTING
Mivacurium
INTERMEDIATE-ACTING
Atracurium
Rocuronium
Cisatracurium
Vecuronium
LONG-ACTING
Tubocurarine
Pancuronium
RNFA MASTER
, 3
RNFA
METABOLISM - ANS ✓The duration of neuromuscular blockade produced by
nondepolarizing relaxants is strongly correlated with the elimination half-life.
Drugs that are excreted by the kidney typically have longer half-lives,
leading to longer durations of action.
Drugs eliminated by the liver tend to have shorter half-lives and durations
of action.
Atracurium is inactivated by hydrolysis by non-specific plasma esterases
and by a spontaneous reaction (Hoffman elimination). Duration of
neuromuscular block produced by atracurium is not altered by the absence
of renal function.
One of atracurium metabolites is laudanosine. Laudanosine may cause
transient hypotension and, in higher doses, seizures.
Cisatracurium, a stereoisomer of atracurium, undergoes Hoffman
elimination to form laudanosine. Because cisatracurium is more potent
than atracurium and lower doses are required, laudanosine concentrations
following cisatracurium administration are lower. Cisatracurium also
causes less histamine release. Therefore, cisatracurium has largely
replaced atracurium in clinical practice.
Mivacurium has short duration of action. Hydrolysis by
butyrylcholinesterase is the primary mechanism for inactivation of
mivacurium. Not dependent on liver or kidney.
Rocuronium has the most rapid onset among nondepolarizing blockers.
Can be used as alternative to succinylcholine for rapid sequence intubation.
DEPOLARIZING BLOCKERS - ANS ✓The extremely short duration of action of
succinylcholine (5-10 minutes) is due to its
rapid hydrolysis by plasma (and hepatic) butyrylcholinesterase.
Neuromuscular blockade by succinylcholine (and mivacurium) may be
prolonged in patients with an abnormal variant of butyrylcholinesterase.
Prolonged paralysis from succinylcholine caused by abnormal
RNFA MASTER
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butyrylcholinesterase should be treated with continued mechanical
ventilation until muscle function returns to normal.
Because of the rarity of these variants, butyrylcholinesterase testing is not
routine clinical procedure.
ADVERSE EFFECTS - ANS ✓...
NON-DEPOLARIZING BLOCKERS - ANS ✓• Some benzylisoquinolines may
produce hypotension due to histamine release and ganglionic blockade.
• Some ammonio steroids may produce tachycardia due to blockade of
muscarinic receptors, which may lead to arrhythmias. These drugs should
be used cautiously in patients with cardiovascular disease.
HISTAMINE RELEASE - ANS ✓Tubocurarine, and to a lesser extent, mivacurium
and atracurium can produce
hypotension as a result of histamine release. Tubocurarine is seldom used
clinically at this time.
Clinical signs of histamine release are erythema at the face and upper chest,
a transient decrease in blood pressure, and an increase in heart rate.
More severe reactions of histamine release include bronchospasm and
circulatory collapse.
Antihistamines can counteract responses that follow histamine release,
particularly if given before the neuromuscular blocker.
GANGLION BLOCKADE - ANS ✓Tubocurarine may cause some blockade of
nicotinic receptors of the autonomic ganglia
and the adrenal medulla; this results in a fall in blood pressure and
tachycardia.
RNFA MASTER
