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neuromuscular block
| Question | Answer |
|---|---|
| acetylcholine at the end plate interact with which receptors? | nicotinic receptors (cholinergic receptors) |
| what is the mechanism of action of nondepolarizer? | competitive inhibition by binding to cholinergic receptors and deactivate them. |
| what is the mechanism of action of succynlcholine? | binds with cholinergic receptors and activates them. |
| what happens when acetylcholinesterase is inhibited by anticholinesterase? | acetylcholine builds up around receptors and compete with nondepolarizers reversing their blockade. |
| how is acetylcholine's action terminated? | hydrolysis by acetylcholinesterase at then NEuromuscular junction, not by diffusion. |
| duration of acetylcholine effect at receptors? what effect the duration? | brief less then 1 milliseconds due to rapid hydrolysis by acetylcholinesterases into choline and acetate. |
| what happens to the metabolite choline? | transported back into parasympathetic nerve endings to make more acetylcholine. |
| what is another name of plasma cholinesterase. where is it found? where is it mostly present? | another name is pseudocholinesterase. found around acetylcholine receptors and mostly also found in plasma. |
| what is butylcholinesterase? where are they found? | another cholinesterase with lower specificity to acetylcholine. mostly found in blood plasma, glia, liver, other tissues. |
| which other place can you find AchE? | Red blood cells. |
| why cant muscle relaxants cross lipid membranes? | Nondepolarizers are too large succs are too highly ionized. |
| what is the block characteristic of succs, what about nondepolarizers | succs cause phase 1 block. nondepolarizers cause phase 2 block |
| characteristic of depolarizing phase 1 block. | 1. no fade to tetanus or twitch (decrease amp) 2. withnfasciculations 3. no reversal 4. TOF ratio of 1. equal train of four 5. sustained response to single stimulus and tetanus. |
| characterstic non depolarizing block | 1. fade with tetanus and twitch 2. no fasciculations 3. post-tetanic potentiation 4. reversal with anticholinesterase |
| describe the phase 2 block and what causes it? | repeated stimulation inactivates the receptors. with non-depolarizers 1. fade with twitch and tetanus 2. sometimes reversed sometimes not 3. post-tetanic potentiation. |
| spontaneous elimination of muscle relaxant is _______ and name a few. The action is required in the presence of ____________ | hoffman elimination. atracurium - hoffman and ester hydrolysis cistarcurium - hoffman require normal body Ph and temperature. does not need renal function. |
| priming is used in order to _________, with _____dose given ___ minutes prior to full dose of ______ and ________ | to shorten the time to relaxation. 1/10th of dose 5 minutes prior vecuronium and atracurium. |
| the priming dose and intubating dose of both atracurium and vecuronium | priming atracurium - 0.08mg/kg vec - 0.01mg/kg intubating atracurium - 0.5mg/kg vecuronium - 0.1mg/kg |
| factors which potentiates neuromuscular blockade (6 points) | 1. antibiotics 2. anesthetics 3. physiologic states 4. electrolyte abnormality 5. cardiac drugs 6. anticholinesterase |
| which anesthetics potentiates neuromuscular block? | local anesthetics such as procaine volatiles such as enflurane and isoflurane more then halothane. ketamine |
| how does antibiotics potentiate neuromuscular block? | decrease release of acetylcholine |
| which 4 groups of antibiotics potentiate neuromuscular block? | 1. tetracycline 2. aminoglycosides - gentamicine, amikacin, kanamycin, tobramycin, netilmicin. 3. lincosamide - clindamycine, lincomycin 4. polymixinss - bacitracin, polymicin b |
| which antibiotics do not cause potentiation of neuromuscular block? | erythromycin, penicillin, and cephalosporins |
| which cardiac drugs cause potentiation of block? | 1. lidocaine 2. quinidine 3. calcium channel blockers - verapamil 4. lasix |
| how does electrolytes potentiates block? | 1. magnesium 2. increased Li, Na 3. decreased k, ca - alkalosis 4. lasix. |
| how does magnesium potentiate block? | potentiates both nondepolarizers and succs 1. decreases release of acetycholine 2. increased sensitivity of end plate to acetylcholine. |
| which physiologic states potentiates block? | 1. hepatic dysfunctions 2. acidosis, alkalosis 3. hypothermia |
| how much time is needed for anticholinesterase to antagonize a block? | 15-30 minutes |
| how is edrophonium compared to neostigmine and pyridositigmine? | 1. less atropine 2. shorter onset 3. less muscarinic side effect 4. volume of distribution, clearance, elimination half life, and duration are similar. |
| how much atropine does edrophonium, neostigmine, pyridostigmine require? | edrophonium - 10mcg/kg pyridostigmine and neostigmine - 15mcg/kg |
| dose of neostigmine | 1.5-3 mg |
| what effect does neostigmine produce in a higher dose? which dose? | greater then 5 mg. will potentiate block |
| in renal failure, neostigmine will____ | last longer then pancuronium. |
| the average clinical adult dose of ____ of cistaracurium will last ______ | 0.2mg/kg will last 1 hour. |
| when can there be a marked prolongation of neostigmine excretion? | end stage renal failure or chronic renal failure |
| about how much percentage of neostigmine is eliminated by the kidneys? dosing of neostigmine in end stage renal failure and severe renal dysfunction? | about 80 % cleared by kidneys. in severe renal dysfunction (creatinine clearance of 10-50 ml/min) dose is decreased by 50 %. and in end stage renal (creatinine clearance of less then 10ml/min) dose decreased to 75%. |
| what are the 3 causes of resistance to nondepolarizers? | 1. increased serum K and potassium 2. burns 3. paralyzed extremity |
| extubation criterial after reversal is used | 1. normal vitals, circulatory, alert and awake 2. head lift sustained, strong grip greater then 5 seconds 3. MIF more negative then - 20. ViTAL CAPACITY GREATER THEN 15cc/kg. 4. blood gas with 40% fio2 - pao2 > 80, paco2 < 50, normal ph |
| pancuronium elimination, ionization, metabolism | 1. 80% unchanged in urine 2. highly ionized 3. hepatic metabolism. |
| what is an important advantage of vecuronium? | minimal cardiac side effects |
| vecuronium metabolism, excretion, elimination and what prolongs elimination? | hepatic metabolism and biliary excretion (50-60%). prolonged in liver failure with a dose of 0.2mg/kg but not at 0.1mg/kg. prolonged in renal failure |
| what prolongs elimination half life of atracurium? | abnormal ph and temperature. (not dependent upon renal or liver function, as it is eliminated by hoffman and ester hydrolysis spontaneous degredation in plasma). |
| cisatracurium in comparison to atracurium. | 1. only by hoffman not ester hydrolysis too 2. about threefold as potent 3. no dose related changes in plasma histamine release 3. duration and rate of recovery are similar. |
| reversal of cisatrcurium can be accomplished in ____ | 10 minutes |
| how is cisatracurium advantageous? | 1. has no metabolite 2. cardiac stability similar to vecuronium (heart rate and MAP). 3. noncumulative 4. inexpensive. |
| rocuronium dosing for 1. intubation 2. maintenance 3. infusion. 4. onset and duration | 1. intubation - 0.06-1 mg/kg iv 2. maintenance n- 0.1mg/kg iv 3. infusion - 5mcg/kg/min 4. onset - 60-90 seconds, duration 30 minutes. |
| rocuronium is a _______ and can be used as a _____ | rapid acting vecuronium derivative. can be used as a substitute to succynlcholine with rapid sequence induction. |
| in which setting can rocuronium be used? | substitute to succs in setting of rapid sequence for patients with open eye and full stomach or hyperkalemic and full stomach. |
| rocuronium elimination, excretion. | elimination primarily biliary but 30% by renal excretion |
| precautions for roc? | duration is increased in renal and hepatic failure. |
| rocuronium does not cause _______ | histamine release and is cardiac stable |
| how does botulism toxin (botox) cause potentiation of block? | calcium dependent release of acetylcholine producing a state of denervation (paralysis). |
| when reversal is not achieved after administration of anticholinesterase. what should you do? | stay on mechanical ventilator because the risk of second dose of anticholinesterase will potentiate further blockade. |
| how is succs terminated? | there is little or no pseudocholinesterase at the NM junction, so most of the drug diffuses away from the motor end plate. |
| action of pseudocholinesterase | very rapid hydrolysis of succs before it reaches the NM junction. |
| what indicates the quality but not the quantity of pseudocholinesterase? | dibucaine number. |
| what happens when pseudocholinesterase is absent? decreased? | succs is broken down by nonezymatic hydrolysis - will take 1-5 hours. if liver disease, pseudocholinesterase decreases will take 15-20 minutes for succ to wear off. |
| pseudocholinesterase is made in the ______ | liver |
| dibucaine value and incidence | normal pseudocholinesterase - 80% heterozygous - 60% 1:480 homozygous atypical 20% 1: 3200 |
| 4 complications of succs? | 1. hyperkalemia (burns, neurolical disorders, trauma). 2. increased eye pressure - afferent discharge of muscle spindles 3. muscle pain 4. increased intragastric pressure - but barrier pressure is also increased. |
| how is the 'fade' assesed? | dividing the fouth amplitude with the first response. the Train of four ratio decreases with more blockade. |
| how is the stimulus applied in the TOF? | four stimulus over 2 seconds. each stimulus 0.5 seconds with 2 hz. |
| how are twitches delivered? | every 1 - 10 seconds (1 hz = 1 cycle/second). |
| increasing level of block is associated with decreased evoked response to electrical stimuli. these stimuli are | 200 microseconds in duration, square wave, and of equal current intensity. |
| what is an indicator of adequate reversal but not necesarily complete? | sustained tetanus of 5 seconds in 50 or 100 hz. |
| the order of muscle recovery from blockade | adductor policis comes after diaphragm, abdominis, orbicularis oculi, laryngeal muscles. |
| what is post-tetanic potentiation? what is the cause? | tetanic stimulation during a partial non depolarizing blockade may increase the evoked response to subsequent twitch. falsifying degree of recovery. due to transient increase release of ach |
| repeated stimulation inactivates the receptor | phase 2 block. |
| list of things that may reduce choliensterase activity | BLOMP burns liver disease organophosphates echothiophiate malnutrition pregnancy. |
| when can neostigmine last longer then pancuronium? | renal failures |
| what causes resistance to non-depolarizers | burns paralysis increase serum calcium and potassium. |
| pancuronium elimination, metabolism, solubility, effect of mac | 80% eliminated in urine, renal failure slows the elimination of pancuronium much more then d-tc. highly ionized, hepatic metabolism, decreases mac by 25% |
| intubating and maintenance dose of mivacurium | 0.15mg/kg, 0.1mg/kg. |
| significance of mivacurium | first rapid acting nondepolarizer. onset intubation 2.5 minutes maintenance dosing give extra 15 minutes of duration. |
| mivacurium in children | faster onset and shorter duration intubating dose is higher 0.2mg/kg. |
| duration of action of mivacurium | 2-3 times as long as succs one third as long as the intermediate acting nondepolarizers. onset with intubating dose is 2.5 minutes maintenance duration about 15 minutes. |
| when is mivacurium duration prolonged? | renal-liver failure |
| most frequent adverse event of mivacurium | transient flushing. |
| drug-NM block interaction - same as card which talks about potentiation. | 1. volatile, drugs which inhibits pseudocholinesterase (echothiophiate, trimethaphan, anticholinesterase, pancuronium) 2`. increase mg, li, Na, potentiate 3. decreased K, ca, potentiate 4. procaine, botulism, antibiotics (aminoglyc, tetracycline, lin.. |
| why does edrophonium duration less then neostigmine and pyridostigmine? | edrophonium binds to acetylcholinesterase electrostaticallyn(to negative charge of enzyme) and only reversible inhibition while neo and pyri... binds covalently to ACHesterase forming carbamylated complex which is then hydrolyzed back to ACHesterase. |
| onset of edrophonium and neostigmine | edrophonium = less then 5 minutes neostigmine = 7-8 minutes. |
| side effects of anticholinesterase and which of these have the least side effect. | muscarinic effects - SA and AV node slowing (bradycardia), GI peristalsis, secretions, bronchoconstriction. edrophonium has least muscarinic effects. |
| why does the duration of action of edrophonium is similar to ________ because of __________ | similar to neostigmine because their total body clearance is similar. |
| which anticholinesterase inhibits plasma cholinesterase? and what does it affect? | neostigmine. succs will last longer after a neostigmine reversal. |
| the pharmacodynamics of neostigmine and edrophonium is similar despite theri differences in mechanism of action. this means that ------- | reparalysis due to longer action of relaxants compared to reversal agents are not seen with clinically use doses even in liver and renal failure. |
| burn patients and interaction with blockers. | increased sensitivity to succs causes hyperakalemia with succs resistance to neostigmine |
| succs should not be given to burn patients due to | 1. hyperkalemia between 10-60 days after burn and longer in presence of infection is dose related, varies with extent of the burn |
| why are burn patients resistant to nondepolarizer blocker? | increased number of junctional receptors. |
| list the factors that lowers pseudocholinesterase thereby prolonging succs duration | liver disease, Methoclopramide, hexaflourenium, echothiophate, phenelzine, ACHEinhibitors, pregnancy, cancer, cytotoxic, drugs, first six months of life. |
| the nerve stimulator negative electrode should be __________ for maximal response. | distal |
| the power source battery of nerve stimulator should be capable of delivering | 60-70 mA, but no more then 80mA. |
| the ideal stimulus of a nerve stimulator should be | monophasic with a rectangular waverform and length of pulse does not exceed 0.2-0.3 miliseconds. |
| in a nerve stimulator what is a determinant of stimulation? | constant current |
Created by:
michelledaryanani