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Barry Anesthesia

Barry Anesthesia NMB meds

Nueromuscular blocking drugs are also called muscle relaxers, paralytics
What is the neuromuscular junction Location where a motor nerve ending activates muscle to contract
Neuromuscular junction consists of prejuntional nerve terminal, a synaptic cleft, and highly folded post junctional membrane
What triggers an action potential An electrical stimulus that changes a resting membrane potential (~-70) to a higher value called the threshold potential (~-55).
What is an action potential a short lasting event in which a cell’s membrane potential rapidly rises (less neg.) and then falls (more neg.)
What ion generates the action potential in the nerve terminal voltage- gated Ca++ ion channels open causes an influx of Ca++into the cytoplasm
Ca++ ions inside the nerve do what trigger the release of Ach from their storage vesicles
Nicotinic Cholinergic receptors (nAchR) are composed of what subunits 2 alpha, 1 beta, 1 gamma, and 1 delta
What is the only nAchR that binds Ach alpha; when both alphas are occupied there is a conformational change in the subunits opening a channel for Na+ and Ca ++ to flow in and K+ to flow out
Acetylcholinesterase (true cholinesterase) does what hydrolyzes Ach into acetic acid and choline
Where is Acetylcholinesterase found in the folds of the motor end plate
What are the 2 classes of NMBs depolarizers and non-depolarizers
Describe depolarizers they resemble Ach and mimic its action (causes muscle contraction(fasiculations), followed by relaxation)
ACh agonists are what type of NMB ? depolarizing
Ach Competative antagonists are what type of NMB non-depolarizing
How are depolarizers metabolized They diffuse off the receptors and get Metabolized by psuedocholinesterase (plasma cholinesterase) .
What is the ONLY depolarizing NMB succinylcholine (Anectine)
What are the side effects of Succinylcholine stimulates nicotinic and muscarinic (bradycardia) Ach receptors, Myalgia(can prevent with DTc or other non-depol, Hyperkalemia, Malignant Hyperthermia,myoglobinuria, increased ICP, IOP, IGP, Trismus
What do you do if you suspect MH Stop use of all potentiating agents, call for help, cool, bicarb 1-2Meq/kg, Dantrolene, No Ca blockers
Earliest Diagnostic signs of MH increased EtCo2 (also increased HR, hypoxia d/t increased oxygen demand
Caffeine halothane test is for what determine if someone has MH
How do you administer dantrolene (20mg/50cc sterile water) 2.5mg/kg IV Q5min, Max dose 10mg/kg. Followed by 1mg/kg q 6hrs
What is the onset, duration and dose of Anectine onset: 30-60 sec, duration-3-10min, dose: 1-2 mg/kg IV, or 4-5mg/kg IM in children
What is Phase I block (when relating to succ) When the depolarized postjunctional membrane cannot respond to Ach (because receptors are full)
What is Phase II block (when relating to succ) Occurs when large or repeated dose given (3-5mg IV), post junct. Membrane has repolarized but cannot response to Ach because of conformational changes in the receptor (result of prolonged depolarization)
What causes a problem with succ metabolism decreased pseudocholinesterase levels
What is myasthenia gravis autoimmune disorder that attacks and damages Ach receptors
What causes decrease pseudocholinesterase Atypical pseudocholinesterase, severe liver disease, anticholinesterase administration (insecticides, drugs for myasthenia gravis, some chemo drugs)
What anticholinesterases (cholinesterase inhibitors) do Indirectly Increase Ach by decreasing acetylcholinesterase (used to reverse non-dep.)
What is the primary clinical use of cholinesterase inhibitors (anticholinesterase) reversal of non-depolarizers
Pseudocholinesterase is also called plasma cholinesterase or false cholinesterase
What is atypical pseudocholinesterase genetic production of atypical pseudocholinesterases, which are unable to hydrolyze the ester bonds in succinylcholine
What is the dibucaine test exposure of blood to dibucane. Dibucaine inhibits normal plasma cholinesterase (not atypical) by about 80%. The amt of inhibited cholinesterase is measured: 80% = all normal cholinesterase was found; 40-60% then heterozygous atypical psuedocholinesterase
Non-depolarizes act by competitive antagonism. Do not mimic Ach
2 classifications of non-depolarizing Steroid derivatives (vagolytic-tachy) & Benzylisoquinolones (release histamine-vasodilation, hypotension, tachy)
Name 5 non-depolarizing agents that are steroid derivatives Pancuronium(Pavulon), Pipercuronium Rocuronium, Vecuronium
Name 3 non-depolarizing benzylisoquinolines atracurium, Cisatracuronium(Nimbex), mivacurium, d-tubocurarine
Long acting NMB Pancuronium, Pipecuronium, d-tubocurarine, doxcurium,
Intermediate acting NMB Vecuronium, Rocuronium, Atracurium, Cisatracurium
Short acting NMB Mivacurium (pulled from market)
Pancuronium (Pavulon) side effects vagolytic tachycardia, may stimulate SNS, excreted primarily renal (prolonged blockade in pts with renal failure)
Pancuronium Bromide (Pavulon) dose, onset, duration long acting non-dep., dose: intub= 0.08-.12mg/kg, maint 0.01mg/kg, onset 3-5min, duration 60-90min
Pipecuronium Bromide (Arduan) dose dose inb: 0.06-0.1mg/kg
Doxacurium dose, onset intub dose: 0.05mg/kg; onset:4-6min
What is Sugammadex rocuronium reversal agent, not yet on the market
What is Dtc used for and the dose used to prevent fasciculations; 3mg IV 3-5min prior to succinyl
Vecuronium dosages, onset, duration, type of excretion (Norcuron), intub dose: 0.08-.12mg/kg IV, maint dose: .01mg/kg, infusion: 1-2 mcg/kg/min, onset 3-5min, duration: 40-60min. primarily biliary excretion
Rocuronium dosages, onset, duration, type of excretion (Zemuron) intub dose: .6mg/kg IV , for RSI 1.2mg/kg IV , rapid onset 30-90sec, duration: 40-60min, little metabolism excreted unchanged in the bile
Rocuronium neg side effect low side effect profile
Atracurium dose, metabolism (Tracurium) intub dose: 0.5 mg/kg over 30-60sec (to decrease histamine release), maint: 0.1mg/kg, infusion : 5-10mcg/kg/min, Hoffman elimination:spont on enzymatic degradation at normal ph and temp; Laudanosine toxicity
What is Laudanosine toxicity cause by a Hoffman elimination of atracurium and cisatracurium(less), associated with CNS excitation
Atracurium neg. side effect histamine release, avoid in severe asthma
Because of its Hoffman elimination atracurium or cisatracurium may be a good choice for this type of pt renal
Cisatracurium dose,onset, metabolism intub: .1-.15mg/kg, infusion: 1-2mcg/kg/min, slower onset that atracurium, Hoffman elimination
The indirect increase in Ach Anticholinesterases/cholinesterase inhibitors causes an increase in Ach effects on all cholinergic receptors (brady, bronchoconstriction, N/V)
How do we decrease the neg. effects of anticholinesterases administration of and anticholinergic (block ach muscarinic receptors), atropine or glycopyrolate
List 5 common anticholinesterases neostigmine, pyridostigmine, edrophonium , physostigmine
What is the dose of neostigmine and the antichol used with it 0.04-0.07mg/kg IV of neostig, with 0.2mg of glycopyrolate per mg of neostig
What are the two commonly used anticholinergics atropine and glycopyrolate
Physostigmine is the only anticholinesterase that crosses the BBB, d/t increased lipid solubility; used to tx central anticholinergic toxicity/syndrome, Not used to reverse non-dep
Too much anticholinesterase can cause a blockade (weakness) due to excessive amt of Ach
Anticholinesterase does what to succinylcholine prolong
Cholinergic syndrome caused by too much anticholinesterase or organophosphates
Cholinergic syndrome s/s and tx miosis, salivation, bronchoconstriction, brady, abd cramping, weakness; confusion, seizures coma; tx with atropine (can cross BBB)- 35-70mcg/kg, pralidoxime 15mg/kg IV q 20 min (reactivates acetylcholinesterase), benzos for seizures
Anticholinergic syndrome/toxicity caused by too much atropine/scopolamine (blocked muscarinic Ach receptors)
Anticholinergic syndrome/toxicity s/s and tx restlessness, hallucinations, mania, agitation; midriasis, dry mouth, tachy, dry flushed skin, hypotension, rash on face/chest; tx with physostigmine 15-60mcg/kg IV
Created by: dupy6