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163 Cards in this Set
- Front
- Back
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what are the short acting NMB?
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sux (anectine)
mivacurium (mivacron) |
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what are the intermediate acting NMB?
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*rocuronium (zemuron)
*vecuronium (norcuron) *atracurium (tracrium) *cisatracurium (nimbex) |
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what are th long acting NMB?
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*dtubocurarine (dTC)
*pancuronium (pavulon) |
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what is the ED95 of sux?
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0.25mg/kg
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what is the ED95 of mivacurium ?
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0.09mg/kg
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what is the ED95 of roc?
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0.3mg/kg
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what is the ED95 of atracurium?
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0.25mg/kg
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what is the ED95 of cisatricurium?
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0.05mg/kg
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what is the ED95 of dTC?
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0.51mg/kg
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what is the ED95 of pavulon?
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0.07mg/kg
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what will ED95 tell you about a NMB?
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it is the dose that 95% suppression of single twitch response
*1 ED95 of ANY NMB will suppress twitches for approx 20 minutes |
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what is the intubating doese of sux?
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1-1.5mg/kg
*1.5-2 w/NDMR) |
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what is the intubating dose of mivacurium?
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0.15-0.25 mg/kg
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what is the intubating dose of roc?
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0.6-1.2 mg/kg
RSI > = 1.5 mg/kg |
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what is the intubating dose of vec?
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0.08 - 0.1 mg/kg
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what is the intubating dose of atracurium?
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0.4-0.5mg/kg
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what is the intubating dose of cisatracurium?
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0.15-0.2mg/kg
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what is the intubating dose of dTC?
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0.5-0.6mg/kg
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what is the intubating dose of pancuronium?
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0.08-0.1mg/kg
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what is the time to intubation w/sux?
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30-60sec
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what is the time to intubation w/mivacron?
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1.5-2 min
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what is the time to intubation w/roc?
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1-3 min
RSI = 1min |
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what is the time to intubation w/vec?
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2-3 min
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what is the time to intubation w/atracurium?
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2-3min
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what is the time to intubation of cisatr?
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2-3min
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what is the time to intubation of dTC?
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3-5 min
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what is the time to intubation of pancuronium?
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3-5min
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how long does it take to rec 25% of fx w/sux?
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5-10min
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how long does it take to rec 25% of fxn w/mivacron?
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16-20min
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what are the NMB that have recovery of 25% of fxn w/in 30min?
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roc, vec, atracurium
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how long does it take for 25% recovery of fxn after cisatricurium?
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40min
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what is the time frame for 25% rec of fxn w/dTC?
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60-90min
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what is the time frame for 25% rec of fxn w/pancuronium?
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80-100min
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what is the metabolism of short acting NMB?
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plasma cholinesterase
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what is the metabolism of cisatricurium?
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hoffmann elimination
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w/cisatricurium, what effects does the hoffman elimination have?
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inc pH = inc effect
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what drugs are eliminated via biliary route?
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vec & roc
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what is the metabolism of atricurium?
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ester hydrolysis and hoffman elimination
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what is the metabolism of roc?
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30% renal 70% liver
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what is the metabolism of vec?
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20% renal 80% liver
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what is the metabolism of dTC?
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70% renal 30% liver
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what is the metabolism of pancuronium?
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80% renal 20% liver
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what are the drugs who have renal elimination?
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dTC, pancuronium, doxacurium
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what drugs are eliminated through metabolism?
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sux, atracurium, cisatricurium, mivacurium
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what agents increase the block of NMB?
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*aminoglycosides
*LAs *Beta blockers *CCB *polymyxins *immunosuppressants *lidocaine *quinidine *lasix *mag *lithium *CYA *trimethephan *thermal burn injury |
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what agents decrease the block of NMB?
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*phenytoin
*hyperkalemia |
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what is the purpose of NMB paralysis?
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*intubation
*surgical exposure/manipulation *improve controlled vent |
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where are the motor nerves located in the SC
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efferents
*exit ventral cord |
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what is SAD?
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Sensory Afferents Dorsal
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what is the primary NT?
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Ach
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Describe the postsynaptic NMJ?
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*5 subunits
*Ach combines w/2 alpha nicotinic receptors |
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what ions are transferred w/an impulse @ the NMJ?
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Na & Ca into cell
K out of cell |
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what happens when ions are exchanged in the postsynaptic NMJ?
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depolarization of the motor end plate
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how many receptors must be open for a muscle AP to be generated?
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5-20%
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What terminates the action of a postsynaptic NT?
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acetylcholinesterase
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what happens when Ach is metabolized?
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motor end plate is repolarized
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what makes more Ach?
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byproduct of Ach breakdown
*choline |
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what are the pharmacokinetics of NMBD?
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quaternary ammonium groups
*highly ionized (H2O soluble) *limited lipid solubility |
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NMBD have limited lipid solubility; what are the implications of this?
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*no BBB cross; no CNS effects
*min renal tubule reabsorption *no placental transmission |
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what will affect the Vd of NMBD?
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*protein binding
*hypovolemia *dehydration |
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what are the effects of VAA on NMBD?
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dec plasma concentration of NMBD needed to produce blockade
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what is the depolarizing NMBD?
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sux
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what is sux composed of?
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2 Ach molecules linked together
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where does sux bind?
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nicotinic receptors
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does sux have single or multiple contractions?
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single
(contracts muscle) |
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how long is the DOA of sux?
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the channel stays open until sux diffuses back into circulation and is metabolized by plasma cholinesterase
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what are the other names for plasma cholinesterase?
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*pseudocholinesterase
*butyrocholinesterase |
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how long is the blockade of sux?
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directly r/t diffusion away from NMJ
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what can lead to increased block of sux?
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*lvr dz
*pregnancy *malignancy *malnutrition *hypothyroidism |
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where is plasma cholinesterase produced?
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liver
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what does plasma cholinesterase metabolize?
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*sux
*mivacurium *ester LA |
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what are the relative Contraindications of sux?
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*peds d/t rhabdo, hyperkalemia, masseter spasm
*MH |
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what is a phase I blockade w/sux?
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all muscles are contracted at once (or depolarizing NMB)
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what is the phase II block of sux?
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*large/repeated doses
*repolarized postjunctional membranes are unresponsive to Ach |
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what does and at what doese does sux resemble?
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*nondepolarizing
*dose > 3-5mg/kg |
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what is the normal sux metabolism?
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80
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what is heterozygous atypical plasma cholinesterase?
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*1:480 pts
*40-60 metabolism |
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what is the length of time/dose of sux will last in heterozygous atypical plasma cholinesterase?
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30 min
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what is the metabolism of homozygous atypical plasma cholinesterase?
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20
*1:3200 pts *1mg/kg may last 3 hrs |
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your pt is having an IOL. He is given sux 1mg/kg. The case is completed in less than 1 hr, but your pt does not respond to nerve stimulation. What are the implications?
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pt could have a homozygous atypical plasma cholinesterase problem.
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what is upregulation SE w/sux?
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an increased # of extrajunctional receptors along a muscle (mor Ach receptors)
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hyperkalemia is a problem w/some pts. What pt populations is sux contraindicated in?
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*burn
*TBI *para/hemiplegia |
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why would you avoid sux in pts w/increased potassium levels?
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*inc of 0.5meq/l in normal pts
*5-10meq/l in upregulated pts (burn, TBI, etc) |
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what are the SE of sux?
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*myalgia
*bradycardia *AV block/sinus arrest *inc IOP *MH *inc ICP *inc intragastric pressure |
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what are the nondepolarizing NMB?
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*mivacurium
*atracurium *cisatricurium *vecuronium *roc *dTC *metocurrarine *pancuronium *gallamine *pipercuronium *doxacurium |
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what is a nondepolarizing NMB?
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competitive block to Ach subunits
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where do nondepolarizers bind?
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nicotinic receptors
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how many receptors must be blocked to produce evidence of blockade
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70%
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what is the ED95 of pancuronium?
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0.07mg/kg
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what is the intubating dose of pancuronium?
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0.08-0.1mg/kg
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what is the time to intubation w/pancuronium?
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3-5min
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what is the duration to 25% recovery of pancuronium?
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25-30 min
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how is pancuronium eliminated?
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80% renal 20% biliary
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what is the ED95 of vec?
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0.06mg/kg
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what is the intubating dose of vec?
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0.08-0.1mg/kg
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what is the time to intubation of vec?
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2-3 min
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what is the time to 25% recovery w/vec?
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25-30min
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how is vec eliminated?
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20% renal and 80% biliary
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what is a priming dose of NMB?
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1/3 of intubating dose given ~ 3 min before intubation; occupies receptors and dec time to intubation by 50%
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which NMB produce histamine?
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*sux
*mivacurium *atracurium *dTC *metrocurarine |
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what NMB produce autonomic ganglionic block?
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*dTC
*metocurarine |
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why does sux cause bradycardia?
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*stimulates the muscarinic receptors of the SA node
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what NMB cause tachycardia?
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*atracurium
*dTC *metocurarine *pancuronium *gallamine |
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what NMB cause hypotentsion?
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*sux
*dTC *metocurarine |
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what NMB cause hypertension?
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*pancuronium
*gallamine |
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what is MH?
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an inherited myopathy w/a hypermetabolic state after exposure to a triggering agent.
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what is the test for definitive dx of MH?
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caffeine & halothane contracture test
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what are the triggering agents of MH?
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sux
VAA |
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what is the cause of MH?
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defect in sarcoplasmic reticulum --> dec Ca uptake
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how much does ECF Ca increase in MH?
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500%; leads to sustained muscle contraction, glycolysis, and heat production
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how many kids/adults are affected by MH?
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1:15,000 kids
1:50,000 adults |
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what is the first sign of MH?
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inc ETCO2
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what are other s/s of MH?
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*tachycardia
*HTN *dysrhythmia *hyperthermia *cyanosis *met acidosis by ABG *hyper - kalemia, calcemia, phosphatemia *myoglobinuria |
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what is the Cr kinase level in MH?
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>1000 iu
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what is a sign a child has MH?
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Massiter muscle rigidity
*controversial as to whether to proceed w/case |
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what is the tx fo MH?
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*CALL for Help
*turn off all VAA/anesth agents *100% O2/hyperventilate *Dantrolene 2.5mg/kg Q5min *lasix, mannitol |
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what is the cardiac drug that is used in MH?
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procainamide
*mag is also used 2-5mg/kg |
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what labs should be followed for 48hrs after MH?
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creatine kinase
*urn myoglobin *coags |
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what reverses nondepolarizers?
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anticholinesterases
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what is the MOA of anticholinesterases?
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inc Ach @ NMJ by dec activity of acetylcholinesterase
*dec hydrolysis of Ach |
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what do anticholinesterases do?
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inc speed of recovery from NMB
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when are anticholinesterases given?
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when spontaneous recovery has begun
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where do anticholinesterases work?
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both nicotinic and muscarininc receptors
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what is the goal of NMB reversal?
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maximize nicotinic transmission
*minimize muscarinic transmission |
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what are the SE of Ach @ muscarinic receptors?
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*CV: dec HR/dysrhythmia
*pulm: bronchospasm/inc secretions *GI: inc peristalsis/gland secretions GU: inc bladder tone Eye: pupillary constriction |
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what is the SLUDGE response?
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s: salivation
l: lacrimation u: urination d: defication g: gastro e: eye r/t muscarinic SE of anticholinesterases |
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what is the most commonly used combo of anticholinesterases and anticholinergics?
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neostigimine & glycopyrolate
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what is the dose of neostigmine & robinol?
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0.05-0.07mg/kg + 0.2mg
(for every 1mg of neostigmine add 0.2mg of glycopyrolate) |
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when do we use nerve stimulators?
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*induction
*maintenance *emeregence of anesthesia |
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how is the frequency of nerve stimulation stated?
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hertz (Hz)
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what is 10Hz?
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10 stimuli/second
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in a single twitch, what happens when 80% of the receptors are blocked?
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decrease in the height of the twitch
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what are the problems w/a single twitch?
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*you need control twitch before NMB given
*you have to remember height of control twitch |
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what is the TOF?
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4 twitches given @ 0.5sec over 2 seconds
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what happens w/TOF and nondepolarizers?
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there is fade of the twitch
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what happens w/TOF and depolarizers?
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all four twitches are the same height
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to test a depolarizer, how are nerves stimulated?
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TOF/Tetanus/TOF
*repeated @ 1,2,3, & 4 min |
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in a depolarizer (sux) what does the TOF look like?
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the intensity, not the character of the response, is changed
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what are the advantages of the TOF?
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*more sensitive than single twitch
*no control necessary *differentiate b/w depolarizer & nondepolarizer *detects Phase II block of sux |
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what is double burst stimulation?
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3 0.2 ms stims separated by 750ms
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what is the primary use of double burst?
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detect residual NMB
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compare DBS & TOF?
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fade is more rapidly detected in double burst
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what is post tetanic stimulation?
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50 or 100Hz single stim for 5 sec
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how does post tetanic stim show in deplarizers?
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depressed amplitude
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how does post tetanic stim show in nondepolarizers?
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fade
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what Hz will NMJ show max effort?
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50Hz
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how often should post tetanic stim be repeated?
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Q2min
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what does post tetanic facilitation show?
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how adequately reversed the pt is
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the TOF post tetanic will indicate what?
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the strength of the twitches is inversely proportional to the depth of the block
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what is Wedensky inhibition?
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poorly sustained tetanic response in interval 2 of checking nerve stim
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what happens in interval 2 of post tetanic stim?
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initial response of 1 TOF rapidly diminishes and may disappear completely, tetanus is poorly sustained, inc TOF stim post-tetanic
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what happens in interval 3 of post tetanic stim?
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Wedensky inhibition is harder to detect visually, but post-tetanic facilitation is clearly visible
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what happens in interval 4 of post tetanic stim?
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Wedensky inhibition is almost impossible to detect visually, but post-tetanic stim can be detected
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what is the std for NMB reversal?
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whenever a nondepolarizer has been used in the past 4hrs, reversal should be administered
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what needs to be illicited for a reversal agent to be given?
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1 strong twitch of the TOF
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what are cyclodextrines?
|
*starch molecule w/high stereoselectivity for target drug (in this case Roc)
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what is the brand name for the cyclodextrine?
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Sugamadex (made by same company as Roc)
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what does sugamadex do?
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encapsulates the NDMR reversing the effects of the paralysis rapidly & independently of degree of block
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how doe we measure the speed of block ?
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small skeletal muscles block before abdominal
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the orbicularis oculi will indicate block where?
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larynx
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the adductor pollicis will indicate block where?
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diaphragm
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induction = ?
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eye
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emergence = ?
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thumbs up
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