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Barry Anesthesia
Barry Anesthesia NMB meds
| Question | Answer |
|---|---|
| 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
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