NMBD - part II
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Created by:
Maryjononnemacher on July 15, 2012
Description:
lecture two, starting at slide 28
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52 terms
Terms | Definitions |
|---|---|
 Which class of antibiotics affect NDMB? How does this happen? | aminoglycosides potentiate NDMB - decreased release of ACh or stabilize postjunctional receptor - greater effect on steroidal agents stuff that ends in MYCIN |
| Which antibiotic was given in a large dose and produced neuromuscular blockade WITHOUT actually giving the patient a muscle relaxant? What is the dose cutoff for this drug | Clindamycin - avoid giving in doses >40mg/kg ***never push clindamycin |
| How do local anesthetics affect neuromuscular blocking agents | - can potentiate depolarizing and NDMB - interfere w/ prejunctional release of ACh - desensitize postjunctional membrane to ACh - directly depression skeletal muscle fibers |
| Which subclass of local anesthetics can interfere with succinylcholine? Why/how? | Ester locals - compete for plasma cholinesterase. - possibly prolong effect of succs and mivacron |
| How can lasix alter neuromuscular blockade? | - small dose can enhance blockade --> inhibition of cAMP production (cAMP and calcium needed for ACh release) - large dose can antagonize blockade --> increased production of cAMP - increased ACh release which antagonizes NDMB |
| True or false: mannitol can prolong neuromuscular blockade | FALSE - osmotic diuresis does NOT affect neuromuscular blockade |
| How do lithium and magnesium affect neuromuscular blockade? | - decrease release of ACh - stabilization of postjunctional membrane |
| Chronic anticonvulsant therapy (increases/decreases) dose requirements for neuromuscular blocking agents | INCREASES |
| Conditions that can alter responses to nondepolarizing blockade (6 conditions) | 1) hypothermia 2) changes in serum potassium levels 3) burn injury 4) paresis or hemiplegia 5) allergic reaction 6) steroid use |
| Hypothermia (shortens/prolongs) neuromuscular blockade. Why? | Prolongs - decreased liver metabolism, renal excretion. Decreased degradation by Hofmann elimination bc it is influenced by temperature and pH of blood |
| Acute hypokalemia causes an (decreased/increased) resting transmembrane potential | INCREASED - harder to generate action potential |
| Succs response to hypo and hyper kalemia | Hypokalemia - increased resistance Hyperkalemia - increased sensitivity (remember succs has potential to release 0.5-1mEq potassium, leading to arrhythmias) |
| Nondepolarizing drugs response to hypo and hyper kalemia | hypokalemia - increased sensitivity Hyperkalemia - increased resistance |
| Hyperkalemia causes an (decreased/increased) resting transmembrane potential | DECREASED - easier to generate action potential |
| Burn injuries cause an (increased/decreased) resistance to non-depolarizing drugs | INCREASED RESISTANCE - begins 10 days post-burn, peaks at 40 days if >30% body burned |
| What changes about the cholinergic receptor after a burn injury? | substitution of epsilon unit for gamma subunit |
| Trauma/Burns can increase the production of what protein? | alpha-1 glycoprotein |
| Factors that INCREASE non-depolarizing neuromuscular blockade (15+ factors) ***TEST*** | - Antibiotics: "mycins" - Local anesthetics - Volatile agents - Hypokalemia - Hypermagnesemia - Respiratory acidosis - Antiarrythmic agents - Diuretics - Ca channel blockers - Renal disease (pancuronium) - Hepatic disease (Rocuronium, vecuronium) - Myasthenia Gravis - Age > 60 - Lithium - Hypothermia |
| Factors that Decrease Nondepolarizing Neuromuscular Blockade | - Anticonvulsants - Burn injury > 30% BSA |
| Histamine release from mast cells induced by: (3 factors) | 1) antigen/antibody reaction: true anaphylaxis 2) activation of ompletement system (IgG or IgM) - IgG has anaphylactoid rxn 3) direct action on mast cells |
| Two types of mast cells and where they are found | Mucosal - bronchial system and GI tract Serosal - vascular endothelium, skin, and connective tissue |
| Why are women at higher risk for an allergic reaction to muscle relaxants? | Higher incidence d/t sensitization from cosmetics, foods and soaps. |
| What population should pavulon be avoided in? Why? | Elderly d/t decreased clearance (decreased renal function, decreased hepatic function) also vagolytic effects (increased HR, CO, MAP) --> elderly may not be able to tolerate |
| Pavulon's onset, duration, dosing (initial, maintenance), vial concentration | Onset: 3-5 min Duration: 60-90 minutes Initial dose: 0.08-0.1mg/kg Maintenance: 0.01mg/kg Vial concentration: 1mg/ml OR 2mg/ml |
| Pavulon's structure | Bisquaternary aminosteroid compound |
| Vecuronium's brand name and structure | Norcuron monoquarternary structure 2-desmethyl analog of pavulon --> increased lipid solubility |
| Cardiovascular effects of vecuronium | None - no histamine release, no vagolytic effects |
| Metabolism/Clearance of vecuronium | - primary biliary excretion - Hepatic metabolism and elimination - 40% excreted in bile - 30% excreted unchanged in urine - elimination half-time prolonged in renal failure |
| Active metabolite of vecuronium | 3-OH metabolite - can accumulate and prolong block |
| Vecuronium's onset, duration, dosing (initial, maintenance, infusion), vial concentration | Onset: 3-5 min Duration: 20-35 min Initial dose: 0.08-0.1mg/kg Maintenance: 0.01-0.15mg/kg Infusion: 1mcg/kg/min Vial concentration: powder mixed to 1mg/ml |
| Rocuronium's onset, duration, dosing (initial, maintenance, infusion), vial concentration | Onset: 1-2 min Duration: 20-35 min Initial dose: 0.6mg/kg (0.45mg/kg onset 4 min) RSI = 1.2mg/kg (onset < 90 sec) Maintenance: 0.1-0.2mg/kg for TOF 3/4 Infusion: 0.01-0.02mg/kg/min Vial concentration: 10mg/ml |
| Rocuronium's brand name and structure | Zemuron monoquarternary aminosteroid - resembles vec except hydroxyl group added |
| Rocuronium CV effect | minimal - however reports of anaphylaxis in literature |
| Metabolism/Clearance of rocuronium | - primarily eliminated by biliary excretion - increased Vd w/ hepatic disease - duration slightly prolonged in elderly d/t decreased clearance - small amt excreted in urine (10-30%) - DOA may be prolonged in renal failure |
| Atracurium's brand name and structure | tracrium bisquaternary benzyl isoquinolium structure |
| Metabolism/Clearance of atracurium | Hofmann Elimination - 1/3 of degradation - non-enzymatic degradation at body temp and pH Hydrolysis of nonspecific plasma esterases - 2/3 of degraded atracurium - UNRELATED to plasma cholinesterase |
| Atracurium metabolite and side effects | Laudanosine - seizures at high doses. not active at NMJ |
| Cardiovascular effects of atracurium | may cause histamine release at high doses administered rapidly, slight increase in HR if histamine released |
| Atracurium's onset, duration, dosing (initial, maintenance, infusion), vial concentration | Onset: 3-5 min Duration: 20-35 min Initial dose: 0.4-0.5mg/kg (2yrs and older) Maintenance: 0.1mg/kg (20-45 min after initial dose) Infusion: 9-10 mcg/kg/min Vial concentration: 10mg/ml |
| Cisatracurium's brand name and structure | Nimbex Benzylisoquinolinium nondepolarizing agent 1R'-cis configuration of atracurium - 1 of 10 stereoisomers |
| Metabolism/Clearance of cisatracurium | Hofmann elimination - 77% of metabolism minor role of plasma esterase in clearance - independent of hepatic/renal function - pharmacokinetic profile minimally influenced by aging |
| Cisatracurium metabolites and side effects | Laudanosine - seizures at high doses Monoquaternary acrylate |
| Cisatracurium's onset, duration, dosing (initial, maintenance, infusion), vial concentration | Onset: 3-5 min Duration: 20-35 min Initial dose: 0.15-0.2mg/kg (adults) 0.1mg/kg (children) Maintenance: 0.03mg/kg Infusion: 1-2 mcg/kg/min Vial concentration: 2mg/ml OR 10mg/ml |
| 6 characteristics of "the ideal relaxant" | 1) Nondepolarizing 2) rapid onset 3) dose-dependent duration 4) no side-effects 5) elimination independent of organ function 6) no active or toxic metabolites |
| Succinylcholine's brand name and structure | anectine, quelicin, suxamethonium diacetylcholine - two ACh molecules |
| Metabolism/Clearance of succinylcholine | Metabolism by plasma cholinesterase aka pseudocholinesterase, to succinylmonocholine and choline Renal excretion: 10% |
| Dosages for succinylcholine (adult, peds, IM) | A: 1-1.5 mg/kg P: 1.5-2 mg/kg IV 3-5 mg/kg IM |
| Onset and duration of succinylcholine | Onset: 20-50 seconds Duration: 3-5 minutes |
| Vial concentration of succinylcholine | 20mg/ml |
| Pavulon's route of excretion | Renal excretion - avoid in renal failure pts and elderly |
| Cardiovascular effects of succinylcholine | Bradycardia d/t direct stimulation of muscarinic receptors of the SA node. |
| Succinylcholine's effect on autonomic ganglia | Modest stimulation |
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