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231 Cards in this Set
- Front
- Back
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What is meant by "Monoquanternary" and which NMB agent falls under this category?
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It means it has 2 Nitrogens attached to it but only ONE of them has a charge; Vecuronium
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What is meant by "Bisquanternary" and which NMB agent falls under this category?
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It means that 2 Nitrogens attached to the molecule has a charge; Pancuronium
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How is Sux metabolized?
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By plasma cholinesterase found in the blood plasma (aka butylcholinesterase or pseudocholinesterase)
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How long does Sux last and why does it last longer than ACh?
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Lasts 5-10 minutes; it's metabolized by plasmacholinesterase found in the blood; while Sux is at the NMJ (site of action) it is safe from metabolism whereas ACh gets broken down at the NMJ by ACh-esterase
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What is the duration of action of NDMR (antagonists) dependent on?
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dependent on equilibrium between plasma concentration and extracellular concentration; as plasma concentration decreases due to metabolism/degradation, etc more NMBA molecules diffuse back to the plasma (from the receptor)
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Curare and its derivatives have a Isoquinoline base structure; what does this consist of?
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2 Benzene rings with a Nitrogen on one of them
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Which class of NDMRs release Histamine? What are the 2 primary physiological results of this Histamine release?
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Isoquinolines; decreases BP and can cause bronchospasms
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Isoquinolines are well-known to release Histamine. What are the aminosteroidals well known to do, physiologically?
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Increase HR
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ALL NMBA's base structures have what added?
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amine groups
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Of the amine groups (of the NMBAs), which amine group is known to be the active binding site to the alpha subunit of the ACh receptor?
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quaternary amine group (positively charged Nitrogen)
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Medicinally, Isoquinolines are good for what?
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Clearing up rashes (fungal rashes)
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What's another name for Isoquinolines and why are they sometimes called that?
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Benzylisoquinolines, to account for the Benzene functional group that is found attached to the base isoquinoline
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What's the Duration of Action of NDMRs?
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Ultrashort=<5 minutes
Short-acting=5-20 minutes Intermediate-acting=25-55 min Long-Acting=60 minutes and > |
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All MRs are quaternary ammonium compounds; describe what "quaternary" is?
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4 carbon atoms attached to 1 Nitrogen atom
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Which molecule (Sux or NDMRs) is a small, slender molecule?
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Sux
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Which molecule (Sux or NDMRs) is a large, bulky molecule?
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NDMRs
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What causes the allergic reactions that MRs are well known for?
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the positive ammonium group
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What are "pachycurares?"
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bulky, rigid molecules ("pachy" means "thick") that cause non-depolarizing block (AKA the non-depolarizers)
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What are "Leptocurares?"
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slender molecules ("lepto" means "slim") that cause depolarizing block (AKA SUX)
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The more methyl groups that are placed on the + Nitrogen group, the (more or less) potent the NMBA?
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MORE potent
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What is the interonium distance that is optimal to fit ACh receptor alpha subunits and cause binding/block?
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20 Angstrum (or about 10 carbons)
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A shorter interonium distance than 20 Angstrum causes what kind of block?
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ganglionic block (muscarinic block)
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Longer interonium distance tend to block what?
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NMB (nicotinic block)
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Beers and Reich rules state that a rule of 4.4 Angstrum produces what action?
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Muscarinic Action
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Beers and Reich rule states that a distance of 5.9 Angstrum produces what action?
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Nicotinic
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Which NDMR has an Angstrum distance of 4.4 and therefore provides more muscarinic block than nicotinic block?
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Pancuronium (Pavulon)
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Which NMB has a Angstrum distance of 5.9 and therefore has more of a Nicotinic Block?
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Vecuronium
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Acetylcholinesterase is the enzyme that breaks down ACh; what is the enzyme that reproduces ACh?
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Choline Acetyl transferase
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What are the other 2 names for Acetylcholinesterase?
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Specific cholinesterase or True Cholinesterase
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What are the other 2 names for Plasma Cholinesterase?
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Pseudo Cholinesterase or Butyryl Cholinesterase
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Why does Sux need to be refrigerated?
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It loses it's potency at room temperature (would probably have to give a double dose)
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What's the basic chemical structure of Sux?
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2 ACh molecules bonded together
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Can Sux be broken down by ACh-Esterase?
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No
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What causes the termination of action of Sux?
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After 5-10 minutes, it diffuses off the receptor and out of the NMJ into the plasma where it gets broken down by PLASMA Cholinesterase
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There's a Phase 1 and a Phase 2 block that occurs with Sux; what does Phase 1 consist of?
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Phase 1 Block--Sustained opening of receptor channels in depolarized post-junctional membrane which cannot respond to further ACh
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There's a Phase 1 and a Phase 2 block that occurs with Sux; what does Phase 2 consist of?
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Phase 2 Block--Desensitized repolarized post-junctional membrane remains unresponsive to ACh; occurs after large or reepeated Sux doses; unknown mechanism
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How is Sux metabolized?
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In the plasma by Plasma Cholinesterase
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Approx. how much of IV admin. Sux actually makes it to the NMJ?
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10%
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What's the mechanism behind Sux's duration of 5-10 minutes?
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Sux duration is purely a component of its protection from plasma cholinesterases once it diffuses to the extravascular NMJ
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With Sux, the use of what will help differentiate between a phase 1 and phase 2 block?
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Peripheral Nerve Stimulator
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Describe what metabolites Sux is broken down to by plasma cholinesterase.
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Succinylcholine is broken down (by plasma cholinesterase) to Succinylmonocholine and choline; Succinylmonocholine is further broken down into Succinic Acid and Choline (by plasma cholinesterase)
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Succinylmonocholine is a metabolite of Succinylcholine; what is it's potency as compared to Succinylcholine?
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1/100 of the potency of Succinylcholine although it does have some MR properties
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What's the standard INTUBATING dose of Sux?
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1-1.5 mg/kg (refrigerated)
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Sux has a ____ onset of effect and an _____ duration of action
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Rapid onset; Ultrashort Duration
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What's the ED95 dose range of Sux (not intubating dose)?
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0.51-0.63 mg/kg
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Complete suppression of response to PNS occurs with Sux in approximately _____ seconds
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60 seconds
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With Sux, recovery to 90% muscle strength requires from ____ to _____ minutes
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9 to 13 minutes (approximately 10 minutes)
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Normal recovery from Sux admin occurs in approx. 9-13 (10) minutes; what can hinder this recovery time?
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Ppl who have genotypical ABNORMAL plasma cholinesterase
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What is the main thing Sux's rapid onset (60 seconds) is good for?
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For securing an airway quickly (Rapid Sequence Intubation)
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Name the 6 quality levels of Spanish wine.
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Vino de Mesa (VdM)
Vino de la Tierra (VdlT) Vino de Calidad Producido en Región Determinada (VCPRD) Denominacion de Origen (DO) Denominacion de Origen Calificada (DOCa) Denominacion de Pago (DOP) |
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Other than Sux, what are other agents Butyrylcholinesterase metabolizes?
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Local Anesthetics, Esmolol, Mivacron, and "other drugs"
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A decreased concentration or activity of the Butyrylcholinesterase enzyme will ______ Sux's duration
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prolong
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What's the approx. incidence of ppl who have genetically decreased activity of the Butyrylcholinesterase enzyme?
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1:3000 ppl
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There are 2 types of Atypical plasmacholinesterase activity (Homozygous and Heterozygous); which one is worse with the most pronounced abnormal activity?
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Homozygous
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With Homozygous Atypical plasmacholinesterase activity, how long will Sux's duration last?
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More than an hour
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How much atypical plasmacholinesterase is present with homozygous atypical?
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More atypical (abnormal) plasmacholinesterase present then normal
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How much atypical plasmacholinesterase is present with heterogous atypical?
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some abnormal (atypical) and some normal (typical) present
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With heterozygous atypical plasmacholinesterase activity, how long will Sux's duration last?
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About an hour
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Other than a genetic mutation, what are some other things that can cause atypical butyrylcholinesterase?
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Liver disease, malnutrition, severe anemia, organophosphate poisoning
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What's the measurement test for atypical butyrylcholinesterase?
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Dibucaine test (generates a Dibucaine number)
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What is Dibucaine?
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It's a local anesthetic that uniquely inhibits plasmacholinesterase
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After a Dibucaine test, more Butyrylcholine left in the plasma (after normal plasmacholinesterase has been inhibited by Dibucaine) means there is more (typical or atypical) plasmacholinesterase? Is this a low or high degree of inhibition?
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Atypical; low inhibition (there's little to no typical or "normal" plasmacholinesterase to inhibit)
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With the Dibucaine test, what does a large amount of inhibition mean?
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It means there is a large amount of "normal" or typical cholinesterase that is available in the blood to be inhibited by Dibucaine
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What does normal plasmacholinesterase metabolize Butyrylcholine into?
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Succinylcholine and Choline
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Is atypical plasmacholinesterase inhibited by Dibucaine?
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NO
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After a Dibucaine test is performed, more butyrylcholine in plasma = more (typical or atypical) butyrylcholinesterase?
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ATYPICAL
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After a Dibucaine test is performed, more atypical butyrylcholinesterase = (more or less) inhibition
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LESS inhibition
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According to the Dibucaine test, what Dibucaine number (%) is equivalent to a LOW inhibition, meaning a greater amount of atypical butyrylcholinesterase is present?
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20-30%
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Which Dibucaine Number correlates with Homozygous Atypical (the worst kind)?
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20-30
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Which Dibucaine number correlates with Heterozygous Atypical (some normal and some abnormal plasmacholinesterase)?
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50-60
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Which Dibucaine number correlates with Homozygous TYPICAL (normal plasmacholinesterase)?
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70-80
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What does the Dibucaine number indicate?
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the percentage of enzyme inhibited
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What are the factors that lower plasmacholinesterase activity?
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Liver disease, advanced age, malnutrition, severe anemia, pregnancy, burns, oral contraceptives, monoamine oxidase inhibitors (MAOIs), echothiophate, cytotoxic drugs, neoplastic disease, anticholinesterase drugs, tetrahydroaminacrine, hexafluorenium, metoclopramide, Bambuterol, Esmolol
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What is VERY important to do after you admin Sux but before you admin a NDMR?
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Twitch the patient to make sure the Sux has metabolized
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Is low plasmacholinesterase activity a significant problem in clinical practice? Why or why not?
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NO; even large decreases in plasmacholinesterase enzyme create only a moderate increase in DOA; In no patient did the total duration of NM blockade exceed 23 minutes; just have to protect their airway and wait it out
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What are the VAST side effects of Succinylcholine?
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allergic reactions, CV effects, Fasciculations, muscle pains (myalgia), hyperkalemia, myoglobinuria, sustained muscle contraction with myotonias, increased intraocular, intragastric and intracranial pressures, malignant hyperthermia risk (trigger), plasma cholinesterase deficiencies are unmasked
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What are the allergic reactions from Sux caused by?
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related to positive ammonium group (unique to ALL NMBAs) and Sux releases Histamine
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What physiological effects occur from Sux's Histamine release?
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decreased BP, hives, wheezing, bronchospasms
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Why is it bad to get children Sux (based on CV effects)?
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Sux causes bradycardia and brady-arrythmias (children's BP depends on HR so want HR up, not down)
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Why is bradycardia, brady-arrythmias, asystole a problem with Sux admin?
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Sux stimulates ALL Cholinergic autonomic receptors (all nicotinic and muscarinic receptors); has a significant affinity for muscarinic receptors which is responsible for the bradycardia
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What cardiac result can occur with otherwise healthy children after Sux admin?
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Cardiac Arrest
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When cardiac arrest does occur after Sux admin, what other 3 things often accompany it?
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Hyperkalemia, rhabdomyolysis, and acidosis
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Which population of children are at a higher risk of cardiac arrest after Sux. Admin and why?
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Children with Duchenne's Muscular Dystrophy (due to the up-regulation of ACh receptors); they get rapid hyperkalemia which causes cardiac arrest
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Is Sux contraindicated in children (age 8 and younger)?
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YES
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When's the only time Sux should be administered to a child age 8 or younger?
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In an emergency situation
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What is the NDMR that could replace Sux for admin. to children (it also has an onset of NM blockade of 60 secs)?
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Rocuronium
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Although Sux and Roc have similar NM blockade onset times (60 seconds), what is a disadvantage of Roc that doesn't occur with Sux?
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Roc doesn't "go away" for 45-55 minutes, unlike Sux that "goes away" in 5-10 minutes
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If you must use Sux in a child, what might you also need to administer to them to keep them from getting bradycardic?
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Atropine
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What specific mechanism causes bradycardia after Sux admin?
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Stimulation of cardiac muscarinic receptors in the sinus node
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What often causes sinus bradycardia in adults after Sux admin?
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Second dose of the drug given approx. 5 minutes after the first
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What causes Nodal (junctional) Rhythms after Sux admin?
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Suppression of the sinus mechanism (emergence of the AV node as the pacemaker)
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What increases the incidence of junctional rhythm after Sux admin?
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Incidence increases after a second dose of succinylcholine
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What intervention prevents junctional rhythm occurrences with Sux admin? Why?
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Previous admin of dTc (Curare); a small "defasciculating" dose of a NDMR prevents junctional rhythms because they block ACh receptors, taking them "offline," not allowing them to get depolarized
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How does Sux contribute to ventricular dysrhythmias?
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lowers the threshold of the ventricle to catecholamine-induced dysrhythmias
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What are some things that may contribute to ventricular dysrhythmias by promoting increased catecholamine release?
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Endotracheal intubation, hypoxia, hypercapnia and surgery
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Other than Sux, what are some other drugs that lower the threshold of the ventricle to catecholamine-induced dysrhythmias?
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Digitalis, tricyclic antidepressants, monoamine oxidase inhibitors (MAOIs), exogenous catecholamines and Halothane
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What population has a higher incidence of Sux-induced fasciculations?
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younger adults and muscular build
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What intervention can lessen or eliminate Sux-induced fasciculations? How?
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prior administration of NDMR (ex. Curare); not as many ACh receptors get depolarized (they are taken "offline"), so the fasciculations are decreased or eliminated
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What are the Sux-induced Myalgias (muscle pains) often related to?
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Fasciculations
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What's the incidence of muscle pain (myalgias)? What population has the higher incidence?
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0.2-89%; higher incidence in younger and muscular patients (like with the fasciculations), also women and ambulatory patients
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What may be administered prior to Sux to help decrease incidence of Sux-induced myalgias (muscle pain)?
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pre-treatment with NDMR may decrease incidence
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What is the primary mechanism of hyperkalemia after Sux admin?
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Massive sustained depolarization causes potassium to be released by cells (into the blood)
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with Sux admin, how much does potassium typically increase?
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average serum increase= 0.5-1 meq/dl
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What will the EKG show with hyperkalemia?
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tall, spiked T waves, ventricular ectopy
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Sux-induced Hyperkalemia requires immediate treatment; how would you treat? Why?
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Hyperventilation (induces respiratory alkalosis) and Na Bicarbonate admin (1 mEq/kg); alkalizing the blood forces potassium back into the cell, correcting the hyperkalemic state; you can also admin calcium chloride (1-2 g) and/or glucose (25-50g) plus soluble insulin (10-20 U)
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What patient populations are most at risk for Sux-induced Hyperkalemia?
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Burns, Trauma, Nerve damage, NM disease, (all of the above due to up-regulation of ACH receptors), Intra-abdominal infections for more than a week, severe acidosis with hypovolemia, renal failure and renal neuropathy
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How long do trauma patients risk getting Sux-induced hyperkalemia after their initial insult (due to up regulation of receptors)?
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60 days after massive trauma or until adequately healed
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Increased number of ACh receptors develop in response to burns (major up regulation); a lot of these "new" receptors have the epsilon subunit(adult type receptors) replaced with what?
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gamma subunit (immature fetal type receptors)
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Should you avoid using Succinylcholine 24 hours post burn? Why or why not?
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YES; massive up-regulation occurs after 24 hours; massive depolarization would occur and massive hyperkalemia would result due to the large numbers of potassium released into the blood from the cell
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Because hyperkalemia has occurred as many as 463 days post burn, how long should you avoid Sux admin?
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Sux should be avoided for at least 1-2 years after the skin has healed
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In burn patients, Is hyperkalemia associated with the EXTENT of the burn?
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NO
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In burn patients, can you admin Sux BEFORE 24 hours post burn?
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Yes, to secure the airway
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Hemiplegia and paraplegia are associated with hyperkalemia for the first ___ months after injury (due to up-regulation of receptors)
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6 months
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Unlike burns where hyperkalemia is not associated with the extent of the burn, in NM diseases, hyperkalemia DOES correlate with the extent of muscle involvement; what does this mean?
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the more muscle disease, the more up-regulation of ACh receptors and the larger the extent of hyperkalemia
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In burn patients, when does the upregulation of receptors typically subside?
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When skin has regrown and infection has resolved
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Is Sux-induced hyperkalemia in NM disease patients attenuated by prior admin of NDMR?
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NO
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How does Sux produce Myoglobinuria?
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Sux causes sustained depolarization which breaks down muscles into relatively large proteins; these proteins are usually cleared by healthy kidneys
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Is Sux-induced Myoglobinuria a concern with renal insufficiency or disease?
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YES; avoid in these patients unless absolutely necessary
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Sux produces myotonias. What are myotonias?
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Sustained, continual muscle contractions continued after Sux effects wear off
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Myotonia patients may be at a higher risk for what potentially fatal complication?
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Malignant Hyperthermia
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What is the onset and duration of Sux-induced increased intraocular pressure?
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occurs 1 minute after injections, peaks at 2 to 4 minutes and subsides by 6 minutes
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What are some ways you can eliminate Sux-induced IOP?
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sublingual admin of Nifedipine, admin 3 mg Curare (dTc), 1 mg Pancuronium or 3-5 mg Rocuronium (all above are small, defasciculating doses); make sure they are well anesthetized (straining and coughing will increase IOP)
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Sux is NOT contraindicated for INDUCTION with increased IOP unless what is occurring?
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Unless the anterior chamber is open (open globe injury) and vitreous humor is leaking out; in this case, don't use Sux at ALL
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With increased IOP it's ok to use Sux for induction; What would be better to use for intubation and maintenance if possible?
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A NDMR if possible
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If Sux is the only thing available and the patient has increased IOP with an open globe injury, but needs their airway secured, do you use Sux?
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YES; have to look at risk/benefit; it's "better to save a life than to save an eye"
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How does Sux increase intragastric pressure?
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Due to fasciculations of abdominal skeletal muscle
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What is the biggest complication that can occur due to Sux-induced increased intragastric pressure?
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Regurge and aspiration possible at this time
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In a patient with already increased intragastric pressure, what pressure should you not mask ventilate over?
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15-20 cm H2O
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What are some conditions that produce an increase in intragastric pressure?
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pregnancy, abdomen distended by ascites, bowel obstruction or hiatal hernia
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What type of intubation technique is necessary with increased intragastric pressure? Why?
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Rapid Sequence Intubation; don't want to increase intragastric pressure
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How can you attenuate Sux-induced Increases in ICP?
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pretreatment with NDMR (small, defasciculating dose)
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How does pretreatment with a NDMR attenuate the Sux-induced increases in ICP?
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It decreases Sux-induced fasciculations and the Valsalva effect (the Valsalva effect decreases venous drainage which impeded blood flow out of the brain, increasing ICP)
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Does a Masseter Muscle spasm (of the jaw) indicate definite Malignant Hyperthermia?
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NO; while it is a frequent response to MH (and can be an early indicator), it is not consistently associated with MH (esp when it's the only isolated sign)
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Sux is known to be a trigger for Malignant Hyperthermia; what other class of drugs is known to be a trigger?
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Volatile Inhaled Anesthetics
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What conditions produce the most exaggerated hyperkalemic response after Succinylcholine admin (due to major up-regulation of receptors)?
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CVA hemiplegia or paraplegia, Muscular Dystrophies, Guillain-Barre Syndrome
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What is the major potentially fatal condition that can occur due to Sux-induced Hyperkalemia?
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Cardiac Arrest
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What do "defasciculating doses" of NDMR before Sux-admin attenuate?
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Attenuates increases in intragastric and intracranial pressures; also minimizes the incidence of fasciculations
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When should you admin "defasciculating dose" of NDMR in relation to Sux admin?
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2 minutes before Sux
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When a patient is resistance to Succinycholine (for whatever reason), what Sux dose changes should be made?
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Dose should be increased by 50%
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After Sux has been administered for induction, what should be admin for maintenance?
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NDMR
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When switching from an induction agent (Sux) to a maintenace agent (NDMR), what should take place before starting the NDMR?
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Always check NM function (twitch or TOF) before administering NDMR to identify Pseudocholinesterase deficiencies
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Why should Sux admin be avoided after reversal of NDMRs with CIs?
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Sux will last up to 60 minutes when given soon after the administration of Neostigmine (5 mg)
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Which drug is the original isoquinoline MR of which all the others are derivatives of?
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Curare
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Describe the chemical structure of Isoquinoline NMBAs
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Isoquinoline back bone with ester bridge
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What major physiological effect is seen MOST OFTEN with Histamine release?
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Decrease in BP
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What is the ester bridge of the isoquinolines broken down by?
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Plasma Esterases
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What is the purpose of the isoquinoline ester bridge?
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Spreads N+ (positive ammonium) groups out to place them in their optimal distance from one another (approx. 20 Angstrum linear distance)
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What is the more technical chemical name for the isoquinoline series of MRs?
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Benzylisoquinolinium series
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What part of the isoquinoline molecule is where enzymatic breakdown occurs?
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At the ester linkages
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What's the intubation dose of Curare (AKA d-Tubocurarine or dTc)?
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0.5-0.6 mg/kg
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With Curare, what's the onset to maximum block?
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5.7 minutes (5-6 minutes)
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What's the DOA of Curare?
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81 minutes (LONG-acting)
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Does Curare release Histamine?
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YES
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Curare is a ganglionic blocker; what physiological effects does that cause?
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Decreased Pulse and BP
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What's the other name for Atracurium?
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Tracrium
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What's the intubation dose of Atracurium?
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0.5-0.6 mg/kg
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With Atracurium, what's the onset to maximum block?
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3.2 minutes (about half of Curare)
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What's the DOA of Atracurium?
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46 minutes (INTERMEDIATE-acting)
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Is Atracurium metabolized by the Liver or Kidney?
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NO
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How is Atracurium (Tracrium) metabolized?
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Hofmann elimination (Just falls apart) and Ester hydrolysis
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Does Atracurium release Histamine?
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YES, but in larger doses (less Histamine release than Curare)
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What's one major benefit of using Atracurium over Curare?
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Onset of action is faster and DOA is shorter
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What's the other name for Cis-atracurium?
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Nimbex
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Which isoquinoline is the most popular isoquinoline MR used in practice today?
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Cis-atracurium (Nimbex)
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What's the intubation dose of Nimbex?
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0.15-0.2 mg/kg
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With Cis-Atracurium, what's the onset to maximum block?
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1.9-7.7 minutes
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Is Nimbex metabolized by the Liver or Kidney?
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NO
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What's the DOA of Cis-atracurium (Nimbex)?
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46-91 minutes (although usually 45-55 minures); Intermediate/Short Acting
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Is Cis-atracurium a good drug for renal patients? Why or why not?
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YES; not metabolized by renal
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How is Cis-atracurium (Nimbex) metabolized?
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Hofmann elimination (just falls apart) and Ester hydrolysis
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Does Cis-atracurium release Histamine?
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NO
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The degradation curve of Cis-atracurium drops off very quickly; what does this mean?
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allows for quick, sudden return of function in approx. 50 minutes; they will go from minimal to no twitches to 4 twitches all of a sudden (not much in-between)
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What's the other name for Doxacurium?
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Nuromax
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What's the intubation dose of Doxacurium (Nuromax)?
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0.05-0.08 mg.kg
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With Doxacurium (Nuromax), what's the onset to maximum block?
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4.4-7.6 minutes
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What's the DOA of Doxacurium (Nuromax)?
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77-123 minutes (LONG-acting)
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Which isoquinoline MR is known to have minimal CV side effects?
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Doxacurium (Nuromax)
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How is Doxacurium metabolized?
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excreted 70% unchanged in the urine, as well as in the bile
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Does Daxacurium have any active metabolites?
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NO
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What's the intubation dose of Mivacurium?
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0.2-0.25 mg/kg
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With Mivacron, what's the onset to maximum block?
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2.1-3.3 minutes
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What's the DOA of Mivacurium?
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14.5-21 minutes (Intermediate/Short acting)
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Which isoquinoline MR is closest to Sux in DOA and recovery?
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Mivacurium
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How is Mivacurium metabolized?
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By plasma cholinesterase
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Can Mivacurium be reversed by anticholinesterases?
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YES
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What's the ED95 (under N2O) of Curare?
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0.5 mg/kg
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What's the ED95 (under N2O) of Doxacurium?
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0.025 mg/kg
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What's the ED95 (under N2O) of Atracurium?
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0.23 mg/kg
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What's the ED95 (under N2O) of Cis-atracurium?
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0.05
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What's the ED95 (under N2O) of Mivacurium?
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0.08 mg/kg
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What's the dosage for relaxation of Curare when used with Nitrous? Volatiles?
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0.3 mg/kg; 0.15 mg/kg
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What's the dosage for relaxation of Doxacurium when used with Nitrous? Volatiles?
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0.02 mg/kg; 0.02 mg/kg
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What's the dosage for relaxation of Atracurium when used with Nitrous? Volatiles?
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0.3 mg/kg; 0.15 mg/kg
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What's the dosage for relaxation of Cis-atracurium when used with Nitrous? Volatiles?
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0.05 mg/kg; 0.04 mg/kg
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What's the dosage for relaxation of Mivacurium when used with Nitrous? Volatiles?
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0.1 mg/kg; 0.08 mg/kg
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How much of an initial dose of NDMR would you give as a bolus during maintenance?
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About a 4th of initial dose for intermediate and short-acting NDMR and about a 10th for long-acting NDMR
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What physiological effect do aminosteroidals typically have on HR?
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Tend to increase HR
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How are aminosteroidal MR typically metabolized (generally speaking)?
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Primarily Liver metabolism with some degree of renal excretion
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Pancuronium is considered to be more potent than Roc and Vec. Why?
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It has a methyl group attached to the Nitrogen group; the more methyl groups, the more potent
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What's the intubation dose of Pancuronium (Pavulon)?
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0.08-0.12 mg/kg
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With Pancuronium, what's the onset to maximum block?
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4 minutes
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What's the DOA of Pancuronium?
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100 minutes (LONG-acting)
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What's the CV side effect of Pancuronium?
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Vagolytic---causes tachycardia (by blocking Muscarinic ACh receptors as well as Nicotinic receptors)
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Does Pancuronium release Histamine?
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NO
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Which aminosteroidal MR has Butyrylcholinesterase-inhibiting properties (although not significant clinically)?
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Pancuronium (Pavulon)
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What's the intubation dose of Vecuronium (Norcuron)?
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0.1-0.2 mg/kg
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With Vecuronium (Norcuron), what's the onset to maximum block?
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2.4 minutes
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What's the DOA of Vecuronium?
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44 minutes (Intermediate)
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Which aminosteroidal MR is the most CV stable MR there is? Why?
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Vecuronium; it does not increase HR as other Aminosteroidals do, which is especially desirable in an ischemic patient (using Vec)
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What form does Vecuronium come in? Why is this good?
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Lyophilized powder; good for transport
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What's the other name for Pipecuronium?
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Arduan
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What's the intubation dose for Pipecuronium?
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0.08-1 mg/kg
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With Pipecuronium, what's the onset to maximum block?
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3.6 minutes
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What's the DOA of Pipecuronium?
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94 minutes (LONG-acting)
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What's the other name for Rocuronium?
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Zemuron
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What's the intubation dose of Rocuronium?
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0.6-1.2 mg/kg
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With Rocuronium, what's the onset to max block?
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1.5-2 minutes
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What's the DOA of Rocuronium?
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30-50 minutes (Intermediate)
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Which Aminosteroidal MR has the greatest amount of vagalytic activity (Increased HR)?
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Pancuronium
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With ANY MR, if you increase the dose (ex. double) you will also increase (double) the _____ ______
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onset time (make it twice as fast); for example, if you double the dosage of Roc, you'll increase the onset time from approx. 2 minutes to 1 minute
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What's the ED95 dose of Pancuronium (under N2O)?
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0.07 mg/kg
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What's the dosage for relaxation of Pancuronium when given with N2O? Volatiles?
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0.05 mg/kg; 0.03 mg/kg
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What's the ED95 dose of Vecuronium (under N2O)?
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0.05 mg/kg
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What's the dosage for relaxation of Vecuronium when given with N2O? Volatiles?
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0.05 mg/kg; 0.03 mg/kg
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What's the ED95 dose of Rocuronium (under N2O)?
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0.3 mg/kg
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What's the dosage for relaxation of Rocuronium when given with N2O? Volatiles?
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0.3 mg/kg; 0.15 mg/kg
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If you want a faster onset of a MR, what must you do?
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Increase the dose (it's a NUMBERS game)
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High potency drugs will have a (high or low) ED95?
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LOW
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While LOW potency MRs cause a more rapid onset, what do they do to the DOA? Why?
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Shortens the DOA due to weaker binding
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The more POTENT the MR the ______ the duration
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Longer (doesn't want to let go of receptor once it's there)
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What's the "priming" dose of a MR?
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10% of the ED95
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