2. 2
History
• 1942 – Griffith & Johnson suggested
d-tubocuranine is safe to use during
surgery
• 1952 – Succinylcholine Introduced
by Thesleff & Foldes
• 1962 – Braid & Reid first used
Pancuronium
• 1980 – Vecuronium, amino steroid &
Atracurium, a benzylisoquinolinium
introduced
• 1990 – Mivacurium introduced
3. 3
Indications for NMBD’S
• Muscular relaxation before the initiation of airway management
• Therapeutic hypothermia after cardiac arrest
• Management of patients with:
• Acute respiratory distress syndrome
• Increased intraabdominal pressure
• Increased intracranial pressure
• Status asthmatics
• For patients on mechanical ventilation who require muscular
relaxation to prevent patient-ventilator asynchrony
• Muscular relaxation for a surgical procedure
• Adjunct therapy for patients undergoing electroconvulsive therapy
6. 6
Pharmacologic characteristics
• Potency of each drug is determined by constructing dose response curves,
which describe the relationship between twitch depression and dose. Because
clinically useful relaxation is attained when twitch is abolished almost
completely, the ED95, corresponding to 95% block, is more commonly used.
• The Intial Dose of NMBDs administered is based on the amount of ED95 that
can suppress twitch height by 95%. The dose required for intubation is 2–3
times the ED95 amount. Because as the dose increases, depression of the
twitch response is accelerated.
• Duration of action is the time from injection of the neuromuscular blocking
agent to return of 25% twitch height. 25% twitch height figure was chosen
because rapid reversal can normally be achieved at that level.
• Recovery index is the time interval between 25% and 75% twitch height. It
provides information about the speed of recovery once return of twitch is
manifest.
7. 7
Phases of Block in DMR
• Phase I
Peri-Junctional sodium channel cannot reopen until the end plate
repolarizes.
The end plate cannot repolarize as long as the DMR continues to
bind to the Ach receptors.
• Phase II
After a prolonged time of continuous end plate depolarization can
cause poorly understood changes in Ach receptor which result in Phase II
block.
8. 8
Phase II Block
A phase II block is a complex phenomenon that occurs slowly at junctions continuously
exposed to depolarizing agents.
The junction is depolarized by the initial application of a depolarizing relaxant, but
then the membrane potential gradually recovers toward normal, even though the
junction is still exposed to drug.
The repeated opening of channels allows a continuous efflux of potassium and influx of
sodium, and the resulting abnormal electrolyte balance distorts the function of the
junctional membrane.
Ca+2 entering the muscle through the opened channels can cause disruption of
receptors and the sub–end-plate elements themselves.
9. 9
Phase I Block - Characteristics
• Decreased Twitch Amplitude in Single Twitch
• Similar Decrease in all amplitude with TOF
• Absence of Fade with TOF ( Train Of Four )
• Absence of Post-tetanic potentiation
• Antagonism by Nondepolarizing muscle
relaxants
• Augmentation by anticholinesterase drugs
10. 10
Succinylcholine
• Succinylcholine is the only available NMBD with a rapid
onset of effect and an ultrashort duration of action.
• Is composed of two molecules of acetylcholine linked
through the acetate methyl groups.
• Is a small, flexible molecule, and like the natural ligand
acetylcholine, succinylcholine stimulates cholinergic
receptors at the neuromuscular junction and muscarinic
autonomic sites.
• ED95 of less than 0.3 mg/kg.
• Administration of 1 mg/kg of succinylcholine results in
complete suppression of response to neuromuscular
stimulation in approximately 60 seconds.
• Recovery to 90% muscle strength following administration
of 1mg/kg succinylcholine requires 9 to 13 minutes.
General Properties
PHARMACOKINETICS
AND
PHARMACODYNAMICS
11. 11
• Short duration of action of succinylcholine results
from its rapid hydrolysis by butyrylcholinesterase
(aka plasma cholinesterase/ pseudocholinesterase)
• Butyrylcholinesterase has a large enzymatic capacity
in plasma, hence only 10% of the administered drug
reaches the neuromuscular junction.
• Because little or no butyrylcholinesterase is present at
the neuromuscular junction, the neuromuscular
blockade of succinylcholine is terminated by its
diffusion away from the neuromuscular junction into
the circulation.
• Butyrylcholinesterase therefore influences the onset
and duration of action of succinylcholine by controlling
the rate at which the drug is hydrolyzed before it
reaches and after it leaves the neuromuscular junction.
PHARMACOKINETICS
AND
PHARMACODYNAMICS
12. 12
• Butyrylcholinesterase (BCE) is synthesized by the
liver and found in the plasma. The neuromuscular
blockade induced by succinylcholine is prolonged
when the concentration or activity of the enzyme
is decreased.
• Decreased butyrylcholinesterase enzyme activity
is NOT a major concern in clinical practice.
• Because even large decrease in activity result in
only moderate increases in the duration of action
of succinylcholine.
• In no patient, the total duration of neuromuscular
blockade exceed 23 minutes
Factors lower butyrylcholinesterase
Liver disease
Advanced age
Malnutrition
Pregnancy
Burns
Oral contraceptives
Monoamine oxidase
inhibitors
Echothiophate
Cytotoxic drugs
Neoplastic disease
Anticholinesterase drugs
Metoclopramide
Butyrylcholinesterase activity
13. 13
DIBUCAINE NUMBER
• Dibucaine (LA) inhibits normal butyrylcholinesterase to a far greater extent than
the abnormal enzyme.
• Under standardized test conditions, dibucaine inhibits the normal enzyme
approximately 80% and the abnormal enzyme approximately 20%
• Indicates the genetic makeup of an individual with respect to BCE, it does not
measure the concentration of the enzyme in the plasma substrate.
14. 14
Side effects
• Stimulates cholinergic autonomic receptors on both
sympathetic and parasympathetic ganglia (Nn type),
muscarinic (M2) receptors in the SA Node of the heart.
• This responses can be attenuated by prior use of atropine
• With large doses of succinylcholine, these effects may
become positive, causing tachycardia.
• The clinical manifestation of generalized autonomic
stimulation is the development of sinus bradycardia,
junctional rhythms, and ventricular dysrhythmias.
Cardiovascular effects
Causes Increased secretions and Bradycardia
15. 15
• Sinus bradycardia
Stimulation of muscarinic receptors in the SA node causes sinus
bradycardia. Problematic in individuals with predominantly vagal tone,
eg children, who have not received atropine. Sinus bradycardia can
occur in adults, commonly after a second dose of the drug. Bradycardia
after a second dose suggests that hydrolysis products of succinylcholine
(succinylmonocholine and choline) sensitize the heart.
• Nodal (junctional) rhythms
Greater stimulation of muscarinic receptors in the SA node, suppresses
the sinus mechanism and allowing the emergence of the atrioventricular
node as the pacemaker. The incidence is greater after a second dose.
• Ventricular dysrhythmias
Circulating catecholamine concentrations increase fourfold, and K+
concentrations increase by one third after succinylcholine
administration. Hypoxia, hypercarbia, and surgery may be additive to
the effect of causing dysrhythmias
Cardiovascular effects
16. 16
• Activation of Ach Receptor cause depolarization movement of Na+
in and K+ out of the cells.
• This increase plasma K+ levels by approx 0.5 mEq/ dL.
• This slight increase in K+ is well tolerated by most. But not
inpatients with pre-existing hyperkalemia
• Severe hyperkalemia may follow
– Metabolic acidosis
– Hypovolemia
– Major denervation injuries
– Spinal cord transection, peripheral denervation, stroke, trauma
– Extensive burns (Initial 48 hours is safe to use) – To be avoided after 2
days upto 2years after burns.
– Prolonged immobility
• Also can occur in myotonia and muscle dystrophies.
Hyperkalemia
Potassium leak
from newly
proliferated
extrajunctional
Ach receptors
17. 17
Treatment
• Immediate hyperventilation
• 1.0 to 2.0 mg of calcium chloride intravenously
• 1 mEq/kg of sodium bicarbonate
• 10 units of regular insulin in 50 mL of 50% glucose for
adults
• For children, 0.15 units/kg of regular insulin in 1.0 mL/kg
of 50% glucose.
Hyperkalemia
18. 18
• The increased IOP develops within 1 minute of injection,
peaks at 2 to 4 minutes, and subsides by 6 minutes.
• Mechanism – Not clearly defined, but it is known
to involve contraction of tonic myofibrils and/ or transient
dilatation of choroidal blood vessels.
• Sublingual administration of nifedipine may attenuate the
increase in IOP, suggesting a circulatory mechanism.
• Despite this increase in IOP, the use of sch for eye
operations is not contraindicated unless the anterior
chamber is open.
• The use of succinylcholine in patients with penetrating eye
injuries, after pre-treatment with a nondepolarizing
NMBD and with a carefully controlled rapid sequence
induction of anesthesia, can be considered.
Increased Intraocular
pressure - IOP
19. 19
• Increase in IGP is presumed to result from
fasciculations of the abdominal skeletal muscle.
• IGP > 28 cm H2O is required to overcome the competence of
GE junction. However, when the normal angle of esophagus
into the stomach is altered, as may occur with pregnancy,
abdomen distended by ascites, bowel obstruction, hiatus
hernia, the IGP required is frequently less than 15 cm H2O.
• Miller and Way found that 11 of 30 patients had essentially no
increase in IGP after succinylcholine administration, yet 5 of
the 30 had an increase in IGP of greater than 30 cm H2O.
• If fasciculations were prevented by prior administration of a
nondepolarizing NMBD, no increase in IGP was observed.
• Sch does not increase IGP appreciably in infants and children.
Increased Intragastric
pressure - IGP
20. 20
• Sch has potential to increaseICP. The mechanisms and
clinical significance of this transient increase are unknown,
but the rise in ICP does not
occur after pretreatment with nondepolarizing NMBDs.
• The incidence of muscle pain varies widely, from
0.2% to 89%.
• Waters and Mapleson postulated that pain is secondary to
damage produced in muscle by the unsynchronized
contractions of adjacent muscle fibers just before the onset of
paralysis.
• Pretreatment with a prostaglandin inhibitor (e.g., lysine
acetyl salicylate) shown to be effective in decreasing the
incidence.
• pretreatment with a nondepolarizing NMBD has ± effect.
Increased Intracranial
pressure - ICP
Myalgia
21. 21
• Increase in tone of the masseter muscle can happen in both adults
& children.
• Is an exaggerated contractile response at the neuromuscular
junction and can produce difficulty in mouth opening.
• It may be an early indicator of malignant hyperthermia, though
this finding is not consistently associated with it and cannot be
used to establish a diagnosis of malignant hyperthermia.
Masseter Spasm
• The main indication for sch is to facilitate tracheal intubation.
• In adults, a dose of 1.0 – 1.5 mg/kg yields 75 to 80% excellent
intubation conditions within 60 to 90 seconds. after
an induction sequence that includes a hypnotic (propofol or thiopental)
and a moderate opioid dose.
• The dose must be increased to 1.5 to 2.0 mg/kg if dose of
nondepolarizing blocker has been used.
Uses
22. 22
• Sch especially indicated for ― RSI (rapid sequence induction)
when a patient presents with a full stomach and the
possibility of aspiration of gastric contents.
• It has both a fast onset, to reduce the time between
induction and intubation of the airway, and a rapid recovery
• Children are more resistant to sch than adults, and doses of
1 to 2 mg/kg are required to facilitate intubation. In infants,
2 to 3 mg/kg may be required.
• Sch, at a dose of 4 mg/kg, only effective intramuscular
NMBD in children with difficult intravenous access and
provides adequate intubating conditions in about 4 minutes.
Uses
26. 26
A. Suitability for Intubation
• None of NDMR equals sch in Rapidity of action
• Onset of NDMR can be quickened by using
– Large dose
– Priming dose
• 2 to 3x ED95 is used for Intubation – Onset is faster
• ED95 – Is the dose that produce 95% twitch depression in 50% of
population.
• General Rule – More Potent , slower the speed of onset
• Priming Doses – Giving 10% to 15% of Intubating dose 5min before
induction, will occupy enough receptors and paralysis will be quick
following relaxant administration after induction.
27. 27
B. Preventing Fasciculations
• 10% to 15% of NDMR intubating dose 3-5 minutes before Sch
prevents fasciculations but may not prevent myalgias
C. Maintenance Relaxation
• Muscle paralysis need to be maintained after intubation
– To facilitate surgery
– To control ventilation
– To permit a reduced depth of anesthesia
28. 28
D. Potentiation by Inhalational Anesthetics
• Volatile agents decrease NDMR dosage by atleast 15%
• Actual degree of potentiation depends on
– Inhalational Anesthetic (Des > Sevo > Iso > Halo )
– Muscle relaxant employed ( Pancuronium > Vecuronium > Atracurium)
E. Autonomic Side Effects
• Blocking autonomic ganglion – Reduces HR variability in response to
Hypotension and other intra operative stress eg – Tubocurarine
• Blocking Vagal Muscarinic at SA node – Tachycardia eg –Pancuronium
• Newer relaxants like Atrac,Cisatrac,Vec,Rocu are devoid of autonomic
effects
29. 29
F. Histamine Release
• Histamine Release from mast cells causes
– Bronchospasm
– Skin Flushing
– Hypotension
• Pancuronium, Atracurium, Mivacurium are capable of
triggering histamine release particularly at higher doses
• Prevention
– Slow Injection Rates
– H1,H2 antihistaminic pre treatment
31. 31
A. Temperature
• Hypothermia prolongs blockade by
1.Decreasing metabolism
(eg, mivacurium, atracurium, and cisatracurium)
2.Delaying excretion
• (eg, pancuronium and vecuronium).
32. 32
B. Acid–Base Balance
• Respiratory acidosis potentiates the blockade of most
nondepolarizing relaxants and antagonizes its reversal.
C.Electrolyte Abnormalities
• Hypokalemia and hypocalcemia
…augment a nondepolarizing block.
• Hypermagnesemia..... potentiates a nondepolarizing
blockade by competing with ca2+ at the motor end-plate.
34. 34
F. Concurrent Disease
Neurological or muscular disease can have profound effects on an
individual’s response to muscle relaxants.
Cirrhotic liver disease and chronic renal failure – increased volume of
distribution and a lower plasma concentration for a given dose of water
soluble drugs, such as muscle relaxants
Drugs dependent on hepatic or renal excretion may demonstrate
prolonged clearance
So greater initial (loading) dose—but smaller maintenance dose might
be required in these patients.
37. 37
Atracurium
• Classification – Bisquaternary ammonium benzylisoquinoline / Intermediate acting
• Pharmacology – ED95 is 0.2 to 0.25 mg/kg Intubating Dose is 2-3× ED95
0.5mg/kg followed by 0.1mg/kg every 10 to 20 min Onset of action 3 to 5 minutes at
2 × ED95 Duration of action - 0.5 mg/kg is 30 to 40 minutes. Terminal half-life of
approximately 20 minutes. Infusion of 5-10mcg/kg/min can replace intermittent boluses
• Storage
– Must be stored at 2-8℃
– Loses 5 to 10% of potency for every month exposed to room temperature
– At room temperature, it should be used within 14days
38. 38
Atracurium
• Metabolism
No Active Metabolites
No Organ Dependent
Two metabolic pathways
A. Hofmann reaction, a nonenzymatic degradation with a rate that
increases as temperature and/or pH increases.
B. Nonspecific ester hydrolysis. The enzymes involved in this metabolic
pathway are a group of tissue esterases, which are distinct from plasma or
acetyl cholinesterases.
• Tissue esterases also involved in the degradation of esmolol and
remifentanil.
• It has been estimated that two thirds of atracurium is degraded by ester
hydrolysis and one third by Hofmann reaction.
39. 39
• Side Effects
– Histamine Release in a dose-related manner.
If large doses (≥0.5mg/kg) are administered can cause hypotension, tachycardia, and skin
flushing.
Bronchospasm may also occur.
These responses can be avoided by slow injection or by pretreatment with H1 and H2 receptor
blockade.
– The end product is laudanosine and acrylate fragments.
It has been reported as causing seizures in animals, but at doses largely exceeding the
clinical range. Laudanosine is excreted by the kidney.
– No deleterious effect of laudanosine has been demonstrated conclusively in humans.
• Special situations
– Dosage requirements are similar in various age group
– No dosage adjustment in renal or hepatic failure
– Dose increased in burn patients
Atracurium
40. 40
Cis-Atracurium
• Classification Benzylisoquinoline / Stereoisomer of Atracurium / Intermediate
acting
• Pharmacology – It is 5 Times More Potent Than Atracurium ED95 is 0.04 to
0.05 mg/kg Intubating Dose is 2-3x ED95 0.15 – 0.2 mg/kg followed by 0.02mg/kg
every 10 to 20 min Onset of action 2 to 3 minutes at 2 × ED95 Duration of action -
0.1 – 0.2 mg/kg is 40 to 50 minutes. Infusion of 1.0 – 2.0 mcg/kg/min can replace
intermittent boluses
• Storage
– Must be stored at 2-8℃
– At room temperature, it should be used within 21days
41. 41
Cis-Atracurium
• Metabolism
– No Active Metabolites
– No Organ Dependent
– Only One metabolic pathway – Hofmann reaction, a nonenzymatic
degradation with a rate that increases as temperature and/or pH
increases.
– Not by Nonspecific ester hydrolysis.
– Laudanosine production is there but 5 Times lesser than Atracurium
• Side Effects
– No histamine release
– No autonomic effects
42. 42
Pancuronium
• Classification – Steroid ring on which two modified Ach are positioned / Long
acting
• Pharmacology – ED95 is 0.06 to 0.07 mg/kg Intubating Dose is 0.08-0.12
mg/kg (2× ED95) followed by 0.02mg/kg every 30 – 40 min for maintenance
Onset of action 3 to 5 minutes at 2 × ED95 Duration of action - 0.1 mg/kg is >
50 minutes.
• Storage
Stored at 2-8 but can use
℃ upto 6months at room temprature
43. 43
Pancuronium
• Metabolism
– It undergoes deacetylation to produce 3 metabolites in Liver (20%)
– Most potent of these 3 metabolites is 3-OH , accumulates in renal failure;
it has 2/3rd the potency and duration of action similar to Pancuronium.
– Primarily Renal 80% excretion – Unchanged ; 15% excretion – Bsssile
• Side effects
–Cardiovascular
• Hypertension and Tachycardia
Vagal blockade
Sympathetic stimulation,
Catecholamine release and Decreased
catecholamine reuptake
• Hence Bolus doses should be given with caution in patients whom increasing
HR would be determinantal
Eg – CAD, Stenotic VHD, HOCM
44. 44
Pancuronium
• Side effects
–Arrythmias
• Ventricular arrythmias
due to increased catecholamine release and AV conduction
• Comibnation of TCA / Pancuronium / Halothane is ARRYTHMOGENIC.
–Allergic Reactions
• Hypersensitive to bromides may exhibit allergic reactions with
Pancuronium
–Renal Failure
• Excreion is slowed down and blockade is prolonged
–Liver Failure
• Large initial dose due to increased Vd and reduced maintenance dose
because of decreased clearance.
45. 45
Vecuronium
• Classification – aminosteroid / Intermediate acting / demethylation of
Pancuronium – Reduces side effects without altering the potency.
• Pharmacology –
ED95 is 0.04 to 0.05 mg/kg
Intubating Dose is 0.1-0.2 mg/kg (2-3 × ED95)
followed by 0.01mg/kg every 15-20 min for
maintenance Onset of action 3 to 5 minutes at 2 × ED95
Duration of action - 0.1 mg/kg is 40 minutes.
Terminal half-life of approximately 20
minutes. Infusion Dose 1-2 mcg/kg/min
46. 46
Vecuronium
• Metabolism
– Vecuronium undergoes deacetylation to produce 3-OH metabolites in Liver (40%)
– Most potent of these metabolites, 3-OH Vec, accumulates in renal failure; it has
≈80% the potency of vecuronium and may be responsible for delayed recovery in
ICU patients
• Excretion
– Metabolites Primarily biliary excretion 60% and secondarily renal 40%
• Side effects
1. Cardiovascular – No significant effects
2. Liver Failure – Liver dependent metabolism & biliary excretion
but prolongation is usually not seen.
47. 47
Rocuronium
• Classification – Monoquatenary Steroid / Intermediate acting
• Pharmacology
More
Rapid Onset – Addition of Cyclic substituents other than piperidine at the
2 and 16 positions of vecuronium or pancuronium.
6 to 10 times less potent – methyl group in vec / pancuronium is
replaced by an allyl group in rocuronium.
Stable in solution – Acetyl ester in A ring replaced by Hydroxy group
• ED95 is 0.25 – 0.52 mg/kg
• Intubating Dose is 0.6 – 1.2 mg/kg (2-3 × ED95)
followed by 0.1mg/kg every 20 - 30 min for maintenance
48. 48
Rocuronium
• Pharmacology
• Onset of action
– 2 to 3 minutes at 0.6 mg/kg
– 60 to 90 seconds at 1.2 mg/kg – Nearly approaches the onset of
Succinylcholine. Used as alternative to Sch in RSI.
• Duration of action
– 0.6 mg/kr is 30 – 40 minutes.
– 0.12 mg/kg is 60 – 80 minutes.
• Metabolism & Excretion
– No metabolism and No active Metabolites
– Excretion Primarily biliary >70% and secondarily renal 10-25%
49. 49
Rocuronium
• Side effects
– Prolonged duration in liver failure, pregnancy, elderly
– Not significantly affected in renal disease
– Cardiovascular – Mild Vagolytic in high doses
– Mild Histamine release
• Clinical Consideration
– Rocuronium at doses of 0.9 to 1.2mg/kg has ONSET that approaches
succinylcholine 60 to 90 seconds
– This makes Rocuronium a suitable alternative for RSI situations with the
problem of MUCH LONGER duration of action
– SUGGAMADEX - modified gamma-cyclodextrin, dose of 8 mg/kg, given 3 min
after 0.6 mg/kg of rocuronium, TOF ratio to 0.9 was observed within 2 min.
50. 50
• The compound is a cyclodxtrine, made up of 8 sugar molecules forming a
ring with centre to accommodate the rocuronium molecule.
Sugammadex binds with Rocuronium in 1:1 ratio. Hence 3.6 mg( or mg/kg)
of Sugammadex binds with 1 mg( or mgkg) of Rocuronium. Binding is tight
but is not irreversible.
Terminal half loife is 2hours. Both Sugammadex and Sugammadex
Rocuronium complex excreted unchanged via kidney.
On return of 2nd
twitch in Train of Four, 2-4mg/kg of Sugammadex will
return the Train of Four Ratio 0.9 in 2 minutes approx.
In failed intubation, if Rocuronium dose of 0.6 mg/kg is used, 8mg/kg of
Sugammadex will help reversing the action in 3 minutes. If 1.2mg/kg
Rocuronium is used, them 16mg/kg of Sugammadex to be used.
Sugammadex
52. 52
Gantacurium
• Classification
– New class of NDMR called Chlorofumarates
– It is lyophilized powder as it is not stable in aqueous solution
• Pharmacology
– ED95 is 0.19mg/kg
– Intubation dose 2-3x ED95
– Onset is RAPID < 90 seconds
– Ultra Short Duration of action <10 min
• Metabolism
– Metabolised by 2 pathways
–Adduction with Cysteine – fast and ester hydrolysis – slow
53. 53
Gantacurium
• Recovery can be accelerated by Edrophonium and Cysteine.
• Histamine release observed following use of higher doses
AV002 (CW002)
• Investigational stage NDMR
• Is a Benzylisoquinolinium fumarate ester based compound
• Intermediate duration of action
• Metabolism & elimination is similar to gantacurium.
66. 66
Question 3
•The MOST important parameter
that determines the speed of onset
for NMB drugs is:
• Potency
• Lipophilicity
• Ionization
• Plasma clearance
• Receptor affinity
67. 67
Question 3
• Potency is the primary determinant of, and
inversely proportional to, the speed of onset for
NMB drugs. While the other factors may play a
small role in the speed of onset for NMB drugs,
potency is by far the most critical. A very low-
potency drug, such as rocuronium or
succinylcholine, will require relatively larger
total doses (i.e., number of molecules) to achieve
the desired effect than a high-potency drug such
as vecuronium.
68. 68
Question 4
• A patient taking which of the following drugs would most
commonly be associated with resistance to (nondepolarizing)
NMB drugs:
• Phenytoin
• Quinidine
• Cyclophosphamide
• Aminoglycosides
• Magnesium
69. 69
Question 4
• The duration of action of nondepolarizing neuromuscular
blocking agents can be shortened by the administration of some
medications, including
Calcium
Anticonvulsant: (phenytoin, carbamazepine, primidone,
sodium valproate)
Steroids.
Cholinesterase inhibitors
Calcium increases ACh release while maintaining action potential
at the neuromuscular junction
Magnesium reduces muscle contraction in proportion to its
concentration in the blood and accelerates the effects of NMBDs.
70. 70
Question 5
•When administering sugammadex through
a peripheral IV, it is important to note that
the drug has a physical incompatibility
with all of the following drugs except:
• Dexamethasone
• Verapamil
• Ranitidine
• Odansetron
71. 71
Question 6
• Use of succinylcholine to facilitate endotracheal intubation
would be acceptable (“safe”) in which one of the following
situations:
• 27 y. o. female with myasthenia gravis
• 80 y.o. female patient 2 days after 40% body surface area burn
• 18 y. o. male one week after spinal cord transection injury
• 12 y.o. with Duchene’s muscular dystrophy
• 22 y. o. with evolving respiratory failure secondary to Guillian-
Barre’
72. 72
Question 6
• Patients with myasthenia gravis results in down regulation of
the ACh receptor number at the NMJ and have a less
predictable neuromuscular blocking response and duration of
action to succinylcholine.
All of the other choices actually result in UP regulation of the
number of ACh receptors, and thus make those patients
vulnerable to a (potentially lethal) hyperkalemic response to the
injection of succinylcholine.
73. 73
Question 7
In obese patients, succinylcholine
dosage should be calculated based on
A) Ideal body weight.
B) Actual body weight.
C) The pediatric dosing.
D) Weight falling between ideal and actual.
