PHARMACOLOGY | NMB Agents Flashcards
Which subunit of the nAchR is present in receptors located at the endplate NMJ but NOT in extrajunctional receptors?
A. β
B. γ
C. δ
D. ε
D. ε
nAchRs found on skeleton muscle are 5-subunit ligand-gated ion channels, consisting of 2 α subunits and 1 each of β, ε (or γ), and δ. ε subunit is found on mature receptors, which are normally located only in the NMJ (aka at the muscle endplate).
With decreased stimulation from the neurons and muscle disuse, such as during periods of immobilization or with muscular dystrophy, stroke, or severe
burn, immature, extra-junctional receptors develop, characterized by the substitution of γ for ε subunits.
During induction of anesthesia for cesarean delivery in a 22-year-old female,
rocuronium is inadvertently substituted for succinylcholine. The neonate does not
show any sign of muscle relaxation because rocuronium is:
A. Highly protein bound
B. “Unaffected by ion trapping”
C. Lipid soluble
D. Highly ionized
D. Highly ionized
Neuromuscular-blocking drugs (NMBDs) are highly charged molecules because of the presence of a quaternary ammonium group in their structure. This makes them poorly lipid soluble so that they do not cross biologic membranes like blood–brain
barrier, renal tubular epithelium, and placenta.
Administration of these drugs thus does not produce central nervous system effects; renal tubular reabsorption is minimal, and maternal administration does not adversely affect the fetus. Issue of ion trapping can only develop if a drug gets trapped in the acidic environment of fetal blood after it has crossed the placenta.
The effect of Ach at the neuromuscular junction (NMJ) is terminated by which
of the following mechanisms?
A. Break down by acetylcholinesterase
B. Break down by pseudocholinesterase
C. Degradation by tissue esterase
D. Reuptake into the nerve terminal
A. Break down by acetylcholinesterase
After depolarization of the motor nerve and a rise in intracellular Ca+2 at the nerve
terminal, vesicles containing Ach are released into the synaptic cleft. Binding of
Ach to nAchRs on muscle cells induces muscle contraction. Ach is then rapidly
hydrolyzed by acetylcholinesterase into choline and acetic acid in the synaptic cleft
as well as at the basement membrane. Choline is subsequently reabsorbed at the
presynaptic nerve terminal.
Pseudocholinesterase is an enzyme responsible for the degradation of
succinylcholine, mivacurium, as well as ester local anesthetics. Similarly, tissue
esterases are responsible for the degradation of other pharmacologic agents, such as remifentanil and atracurium.
Neither of these enzymes plays a role in the
degradation of Ach, resulting in termination of its action at the NMJ.
What is the role of Ca++ in muscle contraction?
Ca+2 binds to and induces a conformational change in troponin which leads to formation of actin-myosin cross-bridge.
Depolarization of the skeletal muscle –> release of Ca+2 from the sarcoplasmic reticulum as well as entry of extracellular Ca+2 –> Ca+2 binds to and
induces a conformational change in troponin –> formation of actin-myosin cross-bridge –> activation of the myosin motor –> thereby producing mechanical contraction.
This NMB agent has an active metabolite almost as potent as its parent drug and accumulates in renal failure:
VECURONIUM
TRUE or FALSE
Onset is faster for the less potent NMB agent.
TRUE
Succinylcholine and rocuronium is less potent compared to Cis-atracurium and Vecuronium, hence they have FASTER ONSET.
Which of the following NMB causes precipitates when given concurrently with Thiopental?
A. Vecuronium
B. Rocuronium
C. Cis-atracurium
D. Mivacurium
A. Vecuronium
Vecuronium is a quaternary aminosteroid with only one metabolite, 3-
desacetylvecuronium. It precipitates out of solution if administered concurrently
with thiopental.
- devoid of vagolytic effects and
histamine release!
IOP increase after a single dose succinylcholine?
up to 15mmHg (ONLY lasts 5 minutes)
Normal intraocular pressure is
12 to 20 mmHg with a diurnal variation of 2 to 3 mmHg, whereas changes in position may induce increases of up to 6 mmHg.
Intraocular pressure increases up to 15 mmHg transiently (5 minutes duration) after administration of succinylcholine
Which of the following has vagolytic property thus causing tachycardia?
A. Mivacurium
B. Cis-atracurium
C. Atracurium
D. Pancuronium
D. Pancuronium
Pancuronium produces tachycardia through a vagolytic mechanism, as well as by direct sympathomimetic actions.
The intubating dose of NonDepo NMB should be 2x ED95?
TRUE
Larger intubating dose SPEEDS the onset and LENGTHENS the duration
Clinical vignette:
While doing a PACU rounds, you noticed that a patient is desaturating to an O2 sat of 70-80%. Upon thorough assessment, your clinical judgement is to secure the airway using RSI technique. However, the patient underwent GA-GETA and neostigmine was used as reversal agent from his previous surgery an hour ago.
What muscle relaxant are you going to use this time and why?
ROCURONIUM 1.2mg/kg
Neostigmine, but not edrophonium, inhibits pseudocholinesterase (in addition to acetylcholinesterase) which leads to a prolonged effect of succinylcholine. Therefore, it is not recommended to administer succinylcholine in cases where surgical muscle relaxation is required
immediately after neostigmine has been administered.
Reference: Barash 9th edit | pp 1613
A patient on succinylcholine infusion has a TOF ratio of 0.3. What does this tell about the patient’s degree of paralysis?
A. Patient is in phase I block.
B. Patient is in phase II block.
C. Patient is recovering from block.
D. Cannot tell from given information.
B. Patient is in phase II block
Phase I, or accommodation, block is characterized by a uniform decrease in the
amplitude of twitches compared with baseline. There is no fade with TOF on phase I block, and adequate recovery will demonstrate return of all 4 twitches. Phase II block is characterized by fade on TOF, tetanic fade, and post-tetanus potentiation.
Which mechanism best explains the fasciculations often seen preceding a phase
I block by succinylcholine?
A. Activation of presynaptic nAchR
B. Activation of postsynaptic nAchR
C. Prolonged muscle depolarization
D. Prolonged muscle repolarization
A. Activation of presynaptic nAchR
Binding of succinylcholine to presynaptic nAchR activates those receptors, stimulating repetitive firing and Ach release from the motor nerve terminal, which are manifested as fasciculations. Succinylcholine competes with Ach for binding to the postsynaptic nAchR and is not metabolized by the acetylcholinesterase present at
the synaptic cleft, producing prolonged activation of the nAchR and muscle
depolarization.
As the depolarized muscle membrane locks voltage-gated sodium channels in the inactivated confirmation, junctional neurotransmission is blocked and flaccid paralysis ensues. This is called a phase I, or accommodation, block.
This block is terminated by unbinding and diffusion of succinylcholine away from
the NMJ back into the plasma and subsequent hydrolysis by plasma cholinesterases. Fasciculations can produce myalgia, and pretreatment with a small dose of nondepolarizing NMBs or NSAIDs has been shown to be effective for myalgia
prophylaxis.
The four most common neuromuscular blocking drugs currently used in clinical practice have an ED95 of either 0.3 or 0.05!
.
TRUE
ED95 for SUX and ROC is 0.3
ED95 for CIS and VEC is 0.05
- There is a highly significant variation between patients in response to all neuromuscular blocking drugs
Nondepolarizing neuromuscular blocking drugs bind and inhibit:
presynaptic α3β2 acetylcholine receptors
BIND - -> INHIBIT - -> MUSCLE RELAX!
Glycopyrrolate has onset and offset times similar to neostigmine.
TRUE
For these reasons, glycopyrrolate is preferred with neostigmine (dose one-fifth
that of neostigmine, 0.2-mg glycopyrrolate for every 1-mg neostigmine)
Intubating dose of ATRACURIUM:
0.5 mg/kg
twice the ED95!
For all neuromuscular blockers the usual intubating dose is 2× or 3× the ED95
TRUE
Which of the following statements provides the most accurate explanation
behind the “faster onset” of rocuronium as compared with cisatracurium?
A. Rocuronium is less potent
B. Rocuronium is more potent
C. Rocuronium is ultrashort acting
D. Rocuronium is long acting
**A. Rocuronium is less potent
The rate of onset of nondepolarizing NMBs generally depends on their potency.
Less potent agents, such as rocuronium (ED95 0.3 mg/kg), have a faster onset of
action as compared with more potent agents, such as cisatracurium (ED95 0.05 mg/kg). Rocuronium and cisatracurium are both intermediate-acting NMBs and
have a duration of action of approximately 30-50 minutes.
**LESS POTENT, FAST ONSET **
Psuedocholinesterase activity is increased in which of the following conditions?
A. Pregnancy
B. Liver failure
C. Obesity
D. Malignancy
C. Obesity
Pseudocholinesterase degrades succinylcholine (SCh), mivacurium, and certain local anesthetics. Intrinsic levels can be affected by certain physiologic and
pharmacologic factors, such as alcoholism or obesity, which both increase butyrylcholine (aka pseudocholinesterase) levels. Butyrylcholinesterase levels may
decrease to 75% of normal during pregnancy and to 67% of normal during
immediate postpartum period; this degree of decrease is not usually clinically
significant, but occasional prolonged apnea from SCh administration may result.
Similarly, significant decrease of synthetic liver function may also result in
prolonged apnea. In addition, plasma butyrylcholinesterase may be inhibited by
exogenous compounds, such as organophosphates (eg, insecticides, chemical warfare agents, and echothiophate, a topical glaucoma agent), anticholinesterase agents (eg, neostigmine, pyridostigmine, and edrophonium), and monoamine oxidase inhibitors (MAOIs).
Conditions with nAChR Upregulation:
SENSITIVE to succinylcholine
RESISITANT to NMBA
According to BARASH, the high-dose of ROCURONIUM is:
0.9 to 1.2 mg/kg
What is ED 95?
The average dose to ACHIEVE 95% suppression of twitch height in 50% of population.
A “defasciculating” dose of a nondepolarizing neuromuscular blocking drug:
5 - 10% of ED95
Which muscle relaxant undergoes biliary excretion?
A. Vecuronium
B. Pancuronium
C. Rocuronium
D. Succinylcholine
E. Both A and C
A. Both A and C
Nondepolarizing neuromuscular blocking drugs are:
Ionized
Hydrophilic compounds
Quaternary ammonium - exhibit limited lipid solubility
CANNOT CROSS BBB and PLACENTA
Only when the residual neuromuscular block is minimal (e.g., train-of-four count of 4 without fade or train-of-four ratio ≥0.4) is neostigmine a highly effective reversal agent.
TRUE
NEO is 0.4! dial 0.4 to get in!!!
Which of the following structures of the skeletal muscle does not change in
length as the muscle contracts?
A. A band
B. I band
C. H zone
D. Z line
A. A band
Skeletal muscle myofibril is composed of densely organized actin (thin) and myosin
(thick) filaments. Histologically, A band contains overlapping actin and myosin,
whereas I band contains actin only.
The distance between 2 Z lines is defined as a sarcomere. When muscle cell is depolarized, rising intracellular Ca+2 leads to formation of actin-myosin cross-bridges in the A band and myosin motor activation
pulls the actin filaments closer together.
Thus, the spaces occupied by I band, H
zone, and between the Z lines become shorter. The A band width remains
unchanged.
Following an intubating dose of a nondepolarizing drug, and once a clinical neuromuscular block is established, about 50% to 75% of the intubating dose is required to reestablish a deeper block.
**FALSE **
Following an intubating dose of a nondepolarizing drug, and once a clinical neuromuscular block is established, only 10% to 25% of the intubating dose is required to reestablish a deeper block (i.e., 0.05 to 0.15 mg/kg for rocuronium).
What is the predominant mechanism for SUCCINYLCHOLINE-induced tachycardia in adults?
STIMULATION of nicotinic receptors at autonomic ganglia
Does succinylcholine reduces the RISK of aspiration in patients with intact and competent esophageal sphincter?
How?
YES
Although succinylcholine may increase intragastric pressure, the lower esophageal sphincter tone is also increased, such that the intragastricesophageal pressure gradient remains the same.
Therefore, in patients with an intact and competent esophageal sphincter, there is not an increased risk of aspiration from the use of succinylcholine.
TRUE or FALSE
The speed of onset is inversely related to the potency.
TRUE
The less potent, the faster ONSET
SEQUENCE of NEUROMUSCULAR TRANSMISSION
Action potential depolarizes –> Ca++ INFLUX –> Fusions in Vesicles –> RELEASE of Ach –> Ach DIFFUSES across synaptic cleft –> binds ALPHA(not beta) subunit of NICOTINIC receptors
When Ach binds both ALPHA –> receptor ION channel OPENS:
Na+Ca++ pasok
K+ alalabas
NMB of choice for patient with ORGANOPHOSPHATE poisoning?
Sensitive to NonDepo
The metabolism of this NMB agent is INDEPENDENT of liver function thus making it ideal for patients with advanced liver pathology?
A. Cisatracurium
B. Atracurium
C. Mivacurium
D. Pancuronium
A. Cisatracurium
Cisatracurium is the cis-cis isomer of atracurium and represents 15% of
the atracurium mixture by weight but over 50% in potency.
It is also metabolized by Hofmann elimination but, unlike atracurium, it does not release histamine. Metabolism is independent of liver function.
Nondepolarizing neuromuscular blocking drugs bind to one or both alpha subunits of the nicotinic acetylcholine receptor WITHOUT causing any activation of these ion receptor channels
TRUE
TRUE or FALSE
Succinylcholine should be avoided in GBS due to the danger of hyperkalemia, a risk that can persist after recovery from GBS.
TRUE
If NMB is needed for surgical exposure, then a short-acting NMB should be used.
Depending on the phase of the disease, patients may be resistant or sensitive
to these drugs, so objective nerve function monitoring is important
Where is pseudocholinesterase produced?
A. Liver
B. Lung
C. Kidney
D. Plasma
A. Liver
Pseudocholinesterase is produced in the liver and circulates in the plasma.
The SHORT duration of succinylcholine is due to:
A. Lipid Metabolism
B. Rapid Hydrolysis
C. ED50
D. ED95
B. Rapid Hydrolysis
TRUE or FALSE
In patients with type II diabetes the duration of ROCURONIUM is prolonged and residual paralysis risk is increased.
TRUE
Hoffman elimination is faster when the pH is higher and the temperature is lower?
FALSE
**High pH, High Temperature = FASTER ELIMINATION via Hoffman elimination **
During a Hofmann elimination reaction, quaternary ammonium groups are converted to tertiary amines by cleavage of a carbon nitrogen bond.
The Hofmann reaction is both pH- and temperature-dependent, with higher pH and temperature favoring elimination.
Compared with the phase I block elicited by succinylcholine, the phase II block has which of the following characteristics?
A. Same twitch strength with repetitive stimulation
B. Posttetanic potentiation
C. Similarity with depolarizing block
D. Posttetanic depression
B. Posttetanic potentiation
Usually, administration of intubating doses of succinylcholine produces a short, depolarizing neuromuscular blockade referred to as the phase I block. The force of
muscle contractions is reduced; however, the twitch strength does not change in
response to repetitive stimulation (eg, TOF or tetany).
Administration of large doses of succinylcholine (>3-5 mg/kg), prolonged
exposure (>30 min), or the presence of abnormal/atypical plasma cholinesterases can lead to a phase II block, which resembles the level of paralysis generated by nondepolarizing NMBs. Fade of twitch strength is observed after repetitive
stimulation and potentiation, or stronger twitches, is produced after a period of
tetany.
ROUTE of SUX can be thru EXCEPT:
A. intravenously
B. Intraosseous
C. Intralingual
D Intramuscular
E. Endotracheal
E. Endotracheal
Succinylcholine is usually administered intravenously, but intraosseous, intralingual, and intramuscular routes have been reported when intravenous access is unavailable.
Succinylcholine depolarizes both postsynaptic and extrajunctional receptors
TRUE
SUX –> POST & EXTRAJUNCTIONAL –> MUSLCE RELAX!
TRUE of succinylcholine:
A. Induces maximum blockade within 1 minute and lasts for approximately 45 minutes to 1 hour
B. Despite paralysis at the adductor pollicis muscle, the diaphragm may start to contract, and spontaneous breathing may resume as fast as 2 minutes after 1 mg/kg
C. About 75% of the original intravenous dose reaches the neuromuscular junction
D. If pretreatment is used, it is recommended to INCREASE the dose of succinylcholine (up to 2 mg/kg).
D. If pretreatment is used, it is recommended to INCREASE the dose of succinylcholine (up to 2 mg/kg).
Statement A is wrong because succinylcholine blockade lasts for up to 15 minutes.
Spontaneous breathing may resume as fast as 5 minutes after the dose of 1mg/kg
About 10% of the original intravenous dose reaches the NMJ
The lowest train-of-four count for depth of block is called “shallow,”
TOF count: ____
TOF ratio: ____
TOF count - 4
TOF ratio - < 0.4
Succinylcholine Contraindications:
Burn more than 24 hrs
AKI with Uremia
Conditions with Upregulated receptors
MH-susceptible
In the absence of any tactile or visual recognition of fade with train-of-four subjective assessment, the train-of-four ratio can be as low as 0.3 to 0.4.
TRUE
Succinylcholine-induced HYPERKALEMIA happens in these following condition:
ACUTE renal failure with Uremia
Sepsis
Encephalitis
Severe trauma
Chronic denervation states (SPINAL CORD INJURY, PROLONGED BED REST, BURN of > 24 hours)
Open globe (anterior chamber)
A patient was maintained on a succinylcholine infusion for 8 hours during
surgery and does not regain spontaneous ventilation 30 minutes after the infusion was discontinued. TOF yields 1 twitch. Which of the following is the best course of action?
A. Give neostigmine.
B. Send pseudocholinesterase activity test.
C. Give naloxone.
D. Wait for spontaneous recovery.
D. Wait for spontaneous recovery
WHY?
This patient likely has a phase II block as a result of a prolonged succinylcholine
infusion. The recommended course of action at this time would be to continue
sedation and mechanical ventilation until spontaneous recovery of muscle strength
has occurred.
Although theoretically anticholinesterase drugs can antagonize phase II block by
increasing the amount of Ach available in the synaptic cleft, the response is difficult
to predict because those drugs will also prevent the degradation of succinylcholine
and are therefore best avoided in this situation. Atypical pseudocholinesterase or
pseudocholinesterase deficiency may be suspected if the patient developed a phase
II block and prolonged paralysis after a single dose of succinylcholine.
Naloxone is a reasonable choice if patient has full motor recovery (no fade on TOF) and still fails to initiate spontaneous ventilation, pointing to other causes of apnea, such as opioid overdose.
Bradycardia observed after a single dose of Succinylcholine to children is attributed to what mechanism?
MUSCARINIC stimulation at the sinus node
Which of the following Non-depolarizing NMB has the highest VAGOLYTIC effect:
A. Mivacurium
B. Vecuronium
C. Atracurium
D. Pancuronium
D. Pancuronium
Vagolytic effects from highest to lowest:
PAN > ROC > VECU
NMB of choice for patient with GBS?
Sensitive to Succinylcholine
SUCCINYLCHOLINE and DIBUCAINE number:
DIBUCAINE NUMBER - % of NORMAL pseudocholinesterase INHIBITED by dibucaine(NOT ABNORMAL pseudo)
Dibucaine - amide local anesthetic; inhibits normal plasma pseudocholinesterase by about 80% or greater.
Normal - 80%
homozygous atypical - 20%
heterozygous atypical - 40 to 60%
HOMO –> Paralysis extend up to 4-8 hrs
HETERO –> Paralysis extend 50% up to 100%
Succinylcholine short duration is due to:
A. Rapid hydrolysis
B. Volume of distribution
C. Liver extraction ratio
D. Diffusion to ECF
A. Rapid Hydrolysis
Ca+2 binding to which component of the NMJ induces muscle contraction?
A. Actin
B. Thin filaments
C. Troponin
D. Nicotinic acetylcholine receptor
C. Troponin
Binding of Ach to nAchRs causes a conformational change that lets Na+ into the cell while K+ out of the cell, depolarizing skeletal muscle. Depolarization leads to
release of Ca+2 from the sarcoplasmic reticulum as well as entry of extracellular
Ca+2.
Ca+2 binds to and induces a conformational change in troponin, allowing formation of actin-myosin cross-bridge and activation of the myosin motor, thereby producing mechanical contraction.
Ca+2 DOES NOT directly bind to actin, also known as thin filaments.
Calcium kay TROPONIN
Which of the following muscle relaxant is metabolized by pseudocholinesterase?
A. Cis-atracurium
B. Vecuronium
C. Pancuronium
D. Mivacurium
D. Mivacurium
Which statement regarding the phase II block that can be associated with succinylcholine administration is TRUE?
A. Phase II block occurs only after prolonged exposure to succinylcholine.
B. Receptor desensitization is a mechanism responsible for phase II block.
C. Inhalation anesthetics delay the onset of phase II block.
D. Phase II block results in train-of-four (TOF) fade but not tetanic fade.
B. Receptor desensitization is a mechanism responsible for phase II block.
Phase II block occurs after repeated boluses or prolonged infusion of succinylcholine. It can also occur after a single bolus of succinylcholine in patients with pseudocholinesterase deficiency.
Phase II block is characterized by fade of the
TOF twitch response, tetanic fade, and posttetanic potentiation. Several mechanisms have been proposed to explain the phase II block, including succinylcholine binding and inhibition of the presynaptic nAchR, postsynaptic receptor desensitization (locking of the receptor in an inactivated state unresponsive to further agonist binding), and membrane potential repolarization by activation of Na/K ATPase.
Inhaled anesthetics accelerate, not delay, the onset of a phase II block.
TRUE or FALSE
Pretreatment with a small dose of a nondepolarizing neuromuscular blocking drug has not been shown to prevent this hyperkalemic response
TRUE
Pretreatment is NOT applicable to upregulated or downregulated receptors.
The most important level of block is “recovered,” where the train-of-four count is 4 and the train-of-four ratio is ≥0.9.
TRUE
Which of the following is the correct sequence of signals, leading to skeletal
muscle contraction?
A. Release of Ach → ligand-gated Na+ channels → motor nerve depolarization → voltage-gated Ca++ channels → muscle depolarization
B. Motor nerve depolarization → voltage-gated Ca++ channels → release of Ach → ligand-gated Na+ channels → muscle depolarization
C. Motor nerve depolarization → ligand-gated Na+ channels → release of Ach → voltage-gated Ca++ channels → muscle depolarization
D. Ligand-gated Na+ channels → voltage-gated Ca++ channels → release of Ach → motor nerve depolarization → muscle depolarization
B. Motor nerve depolarization → voltage-gated Ca++ channels → release of Ach → ligand-gated Na+ channels → muscle depolarization
Regarding Succinylcholine: Approximately 10%, of the original intravenous dose reaches the neuromuscular junction.
TRUE
Pseudocholinesterase has a great capacity to hydrolyze succinylcholine and only a small fraction, approximately 10%, of the original intravenous dose reaches the neuromuscular junction.
All of the following are side effects of anticholinesterase drugs, EXCEPT:
A. Excessive salivation
B. Increased bowel motility
C. Bradycardia
D. Bronchodilation
D. Bronchodilation
Administration of anticholinesterase agent leads to accumulation of acetylcholine, manifesting increased cholinergic actions in the body. Vagal stimulation causes bradycardia and, if not antagonized by concomitant administration of a cholinergic agent, may lead to cardiac standstill.
Anti-sialagogue actions of these
agents are also helpful in reducing the excessive salivation induced by parasympathetic overactivity of acetylcholine generated by inhibition of
cholinesterase. Disruption of gastrointestinal anastomosis is another consideration, secondary to increased peristalsis of the bowel. Cholinergic activity may also lead to bronchospasm and not bronchodilation.
TRUE or FALSE
In obese patients who need RSI, the dose of succinylcholine should be calculated based on actual body weight rather than ideal body weight
TRUE
Depo - ACTUAL body weight
NonDepo - IDEAL body weight
In normal patients, the increase of K after succinylcholine dose is limited to approximately
0.5 mEq/L
This NMB agent has metabolite “laudanosine” that can cause neuroexcitation and seizures:
ATRACURIUM
TOF of > 2
SUGAMADEX 2mg/kg will reverse the paralysis in 2 minutes up to 4 minutes!
In children, the onset and the duration of rocuronium are reduced, and the dose requirement is slightly higher?
TRUE
This NMB agent undergoes no clinically significant metabolism and is cleared primarily by the liver via BILE EXCRETION:
ROCURONIUM
incidence of anaphylaxis with the use of SUCCINYLCHOLINE:
1:10,000
VERY COMMON!
High yield tip: AGENTS implicated in ALLERGIC REACTION during GENERAL ANESTHESIA
Muscle relaxant is the most common culprit of allergic reaction intraoperatively.
Conditions with nAChR Downrgulation are:
A. sensitive to non-depolarizing agent
B. sensitive to depolarizing agent
A. sensitive to non-depolarizing agent
RESISTANT to succinylcholine
SENSITIVE to NMBA
This is the only muscle relaxant that, at equipotent doses, causes greater neuromuscular block at the vocal cords than at the adductor pollicis:
A. succinylcholine
B. rocuronium
C. vecorunium
D. pancorunium
A. succinylcholine
Succinylcholine is the only muscle relaxant that, at equipotent doses, causes greater neuromuscular
block at the vocal cords than at the adductor
pollicis.
Miller | 9th ed
After intubating a 20 y.old ASA I patient, you noticed that the value of your TOF count is 0 and PTC(post-tetanic count) >1. Qualitatively, this is considered as:
A. Deep blockade
B. Complete blockade
C. Moderate blockade
D. Shallow blockade
A. Deep blockade
PTC 0 Complete blockade
PTC >1 Deep blockade
Moderate depth of blockade corresponds to a TOF count of 1-3. What is the estimated receptor occupancy when moderate blockade is achieved?
A. 50 - 60%
B. 70 - 90%
C. 40 - 60%
B. 70 - 90%
