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Anes. Pharm I Test 1
Nondepolarizing NMB
| Question | Answer |
|---|---|
| Which non depolarizing NMBs belong to the steroidal class? | Pancuronium (Pavulon), Vecuronium (Norcuron), Pipecuronium (Arduan), Rocuronium (Zemuron), Rapacuronium (Raplon) |
| Which non depolarizing NMBs belong to the benzylisoquinoline class? | D-Tubocurarine (Curare), Atracurium (Tracrium), Cisatracurium (Nimbex), Doxacurium (Nuromax), Mivacurium (Mivacron) |
| Which non depolarizing NMB in the only short acting drug? | Mivacurium (Mivacron) |
| Which non depolarizing NMBs are intermediate acting? | Atracurium (Tracrium, Cisatracurium (Nimbex), Vecuronium (Norcuron), Rocuronium (Zemuron) |
| Which non depolarizing NMBs are long acting? | Pancuronium (Pavulon), Doxacuronium (Neuromax), Pipecuronium (Arduan) |
| What is the ED95 of Doxacurium (Nuromax)? | 0.03 mg/kg |
| What is the intubating dose of Doxacurium (Nuromax)? | 0.05 - 0.08 mg/kg |
| What is the onset and duration of Doxacurium (Nuromax)? | onset: 4 - 5 minutes duration: 60-90 minutes |
| How is Doxacurium (Nuromax) metabolized? | renal > hepatic |
| Does Doxacurium (Nuromax) have any cardiovascular effects? | No |
| What is the ED95 of Pipecuronium (Arduan)? | 0.05 mg/kg |
| What is the intubating dose of Pipecuronium (Arduan)? | 0.085 mg/kg |
| What is the onset and duration of Pipecuronium (Arduan)? | onset: 3 - 5 minutes duration: 60 - 90 minutes |
| How is Pipecuronium (Arduan) metabolized? | renal > hepatic |
| Does Pipecuronium (Arduan) have any cardiovascular effects? | No |
| Does Pipecuronium (Arduan) cause histamine release? | No |
| What is the ED 95 of Pancuronium (Pavulon)? | 0.07 mg/kg |
| What is the intubating dose of Pancuronium (Pavulon) | 0.1 mg/kg |
| What is the onset and duration of Pacuronium (Pavulon)? | onset: 3 - 5 minutes duration: 60 - 90 minutes |
| How is Pancuronium (Pavulon) metabolized? | renal > hepatic |
| How does Pancuronium (Pavulon) affect the cardiovascular system? | blocks muscarinic cardiac receptors (vagolytic). stimulates sympathetic nervous system, so 10-15% increase in HR, MAP, CO |
| Can a beta-blocker prevent the cardiovascular effects of Pancuronium (Pavulon)? | No |
| Heart rate increase withPancuronium (Pavulon) is inversely related to what? | baseline heart rate |
| Pancuronium (Pavulon) is a poor choice for patients with CAD because of its cardiac effects, but why is it the drug of choice for patients undergoing cardiac bypass? | because it counteracts the bradycardia related to heavy opioid dosage |
| Pancuronium (Pavulon) may cause dysrhthymias in a patient taking which cardiac drug? | digitalis (digoxin) |
| Why is Pancuronium (Pavulon) a good choice for babies? | babies' CO is directly related to their HR, so Pavulon helps babies maintain proper BP when under anesthesia for surgery |
| What is the ED95 of Vecuronium (Norcuron)? | 0.05 mg/kg |
| What is the intubating dose of Vecuronium (Norcuron)? | 0.1 mg/kg |
| What is the onset and duration of Vecuronium (Norcuron)? | onset: 2.3 minutes duration: 45 - 60 minutes |
| How is Vecuronium (Norcuron) metabolized? | hepatic > renal |
| Vecuronium (Norcuron) is a monoquaternary analog of which other non depolarizing NMB? | Pancuronium (Pavulon) |
| Vecuronium (Norcuron) is more _______ soluble than Pacuronium (Pavulon) | lipid |
| How does one draw up Vecuronium (Norcuron) for IV injection? | It comes in powder form, so it must be reconstituted with sterile water |
| Vecuronium (Norcuron) is mostly metabolized by the liver; however, its duration is prolonged in renal failure patients. Why? | Hepatocytes deacetylize the drug into 2 metabolites which have < 1/10th the NMB of Vecuronium. Accumulation of these metabolites in renal failure is attributed to its prolonged duration in these patients. |
| Though Vecuronium (Norcuron) rarely causes histamine release, it is important to use caution in administering this drug with other histamine releasing drugs. Why? | it can inhibit the catabolism of histamine |
| Does Vecuronium (Norcuron) have any cardiovascular effects? | No |
| Why is the duration of Vecuronium (Norcuron) prolonged in infants? | infants have immature hepatocytes, so metabolism would take much longer |
| What is the ED 95 of Mivacurium (Mivacron)? | 0.08 mg/kg |
| What in the intubating dose of Mivacurium (Mivacron)? | 0.15 - 0.2 mg/kg |
| What is the onset and duration of Mivacurium (Mivacron)? | onset: 1.5 - 3 minutes duration: 12 -20 minutes |
| How is Mivacurium (Mivacron) metabolized? | plasma cholinesterase |
| Patients with atypical plasma cholinesterase experience a longer or shorter blocked with Mivacurium (Mivacron)? | longer |
| Metabolism of Mivacurium (Mivacron) is through plasma cholinesterase. What would be the only reason for a prolonged blockade with this drug in a renal or hepatic failure patient? | If their organ (renal or hepatic) failure causes a decrease in their plasma cholinesterase activity |
| There is a histamine release with administration of Mivacurium (Mivacron) at 2x the ED95 dose. How could one avoid this histamine release? | give drug in divided doses |
| Cardiovascular effects are seen at ___ x the ED95 dose | 3x the ED95 dose |
| Why does neostigmine slow the recovery of Mivacurium (Mivacron)? | it inhibits plasma cholinesterase |
| Why is Mivacurium (Mivacron) indicated for difficult airway cases but not for rapid sequence? | short duration (12 - 20 min), but not a short onset (1.5 - 3 min) |
| Why does Mivacurium (Mivacron) have an irregular pattern of onset? | It contains 3 sterioisomers, each with a different half life |
| What is the ED95 of Cisatracurium (Nimbex)? | 0.05 mg/kg |
| What in the intubating dose of Cisatracurium (Nimbex)? | 0.1 mg/kg |
| What is the onset and duration of Cisatracurium (Nimbex)? | onset: 2 - 3 minutes duration: 20 - 35 minutes |
| How is Cisatracurium (Nimbex) metabolized? | Hofmann elimination (organ independent) |
| Cisatracurium (Nimbex) is approximately __x more potent than Atracurium (Tracrium) | 3x more potent |
| Why is the production of laudanosine lessened with Cisatracurium (Nimbex) when compared with Atracurium (Tracrium)? | it is metabolized only through Hofmann elimination, with no contribution from plasma esterases |
| Why is Cisatracurium (Nimbex) a good drug for infusions? | It has no cumulative effects |
| Since Cisatracurium (Nimbex) causes minimal histamine release, it also causes minimal _________ effects | cardiovascular |
| What is the ED95 of Atracurium (Tracrium)? | 0.2 mg/kg |
| What is the intubating dose of Atracurium (Tracrium)? | 0.5 mg/kg |
| What is the onset and duration of Atracurium (Tracrium)? | onset: 2 - 3 minutes duration: 20 - 35 minutes |
| How is Atracurium (Tracrium) metabolized? | Hofmann elimination and plasma esterase (organ independent) |
| What is the name of the CNS stimulant metabolite that is formed with the breakdown of Atracurium (Tracrium)? | laudanosine |
| Although clinically significant levels of laudanosine have not been reported with Atracurium (Tracrium) use, take caution in using on _______ failure patients | renal; decreased renal function = decreased excretion of metabolite = buildup |
| Histamine release is noted with 3x the ED95 dose of Atracurium (Tracrium). What does this look like clinically? | Increased HR, decreased MAP, decreased SVR, flushing |
| What can you avoid histamine release with administration of Atracurium (Tracrium)? | slow administration and/or pretreat with H1 (benadryl) and H2 (pepcid) blockers |
| What is the ED95 of Rocuronium (Zemuron)? | 0.3 mg/kg |
| What is the intubating dose of Rocuronium (Zemuron)? | 0.6 mg/kg (dose dependent) |
| What is the onset and duration of Rocuronium (Zemuron)? | onset: 1 - 2 minutes duration: 20 - 35 minutes |
| How is Rocuronium (Zemuron) metabolized? | hepatic > renal |
| Rocuronium (Zemuron) is a derivative of ___________ but is about 6x less potent. | Vecuronium (Norcuron) |
| Why is Rocuronium (Zemuron) indicated only for rapid sequence and not for difficult airway cases? | short onset (1 - 2 min), but intermediate duration (20 - 35 min) |
| Does Rocuronium (Zemuron) cause histamine release? | no |
| _______________ reactions have been reported with Rocuronium (Zemuron) use | anaphylactoid |
| Does priming improve the onset of Rocuronium (Zemuron)? | no |
| What is the only clinical use today for the drug D-Tubocurarine (Curare) | used as a defasiculating agent |
| What is the defasiculating dose for D-Tubocurarine (Curare) | 3 mg |
| The lower the ED95, the _____ potent the drug and the _______ the onset. | more potent longer onset |
| The higher the ED95, the _______ potent the drug and the ________ the onset | less potent shorter onset |
| How is the ED95 determined? | By measuring the dose needed to produce a 95% twitch suppression of the single twitch response |
| What is the idea behind the priming principle? | a smaller dose of a non depolarizer is given prior to induction to allow some of the receptors to be occupied and minimize time required to rest of receptors to be blocked by remainder of intubating dose |
| The priming dose is usually ____ of the intubating dose or _____ of the ED95 dose | 1/10th of intubating dose 1/3rd of ED95 dose |
| Non depolarizing NMBs from different classes will _________ each other | enhance |
| If Rocuronium (Zemuron) is given for rapid intubation and Cisatracurium (Nimbex) is later given during the case for blockade, what would explain the blockade caused by Cisatracurium lasting longer than usual? | the fact that the two non depolarizing NMBs are from different classes, therefore they enhance each other's action, causing the Cisatracurium blockade to be prolonged |
| What are the agent related factors that influence the selection of the appropriate NMB for a case? | onset of action, duration of agent, side effects of agent, metabolism of agent |
| What are the patient related factors that influence the selection of the appropriate NMB for a case? | coexisting disease (renal, hepatic, cardiac, neuromuscular), current medical therapy, surgical procedure |
| What is the mechanism of action of a non depolarizing NMB agent? | they compete with ACh to bind with the alpha subunits of the postsnyaptic nicotinic receptors to prevent the ion channel from opening and therefore prevent depolarization |
| Non depolarizing NMB agents need to bind with ___ of the alpha subunits to prevent depolarization | one |
Created by:
Mary Beth
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