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84 Cards in this Set
- Front
- Back
Droperidol: mechanism of action
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Binds to postsynaptic GABA receptors in Chemoreceptor Trigger Zone
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Droperidol: indication(s)
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Prophylaxis of post-operative nausea and vomiting, adjunct to general anesthesia
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Droperidol: Important side effects
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May bind to and block dopiminergic receptors and postsynapti alpha adrenergic receptors> therefore causes hypotension and tachycardia; sedation and generalized loopiness, PROLONGED QT/ Torsades
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Droperidol: who would you not administer this drug to? Special considerations?
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Anyone with prolonged QT (Can cause fatal arrhythmia); must get 12 lead EKG before and 2-3 hours after administration
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Sufentanil: mechanism of action
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Mu opiod receptor agonist
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Sufentanil: more or less potent than Fentanyl? How many times?
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10x more potent than Fentanyl; 500-700 times more potent than Morphine
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Sufentanil: relative duration of action:
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doesn't hang around post op as long as fentanyl (leading to resp. depression after extubation)...but provides post op pain relief longer than remifentanil
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Sufentanil: what do you do if your patient develops chest wall rigidity?
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Give NMB
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Sufentanil: high doses can cause:
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Vagus mediated bradycardia, chest wall rigidity
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Sufentanil: what effect does this have on cerebral blood flow?
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Decreased CBF, decreased CRMO2
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Sufentanil: when do you give?
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can give up front to intubate and run as infusion throughout case
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Sevoflurane: Mechanism of action and MAC
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GABA? 2%
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Sevoflurane: Effect on heart rate
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No effect on HR
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Sevoflurane: good for induction because:
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Quick onset of action, no irritating smell
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Sevoflurane: to whom would you not give this agent?
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Renal Failure Patients (d/t concerns of nephrotoxicity with Compound A)
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Zofran: indication
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Anti-emetic
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Zofran: side effects
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Headache, malaise, dizziness; can cause prolonged QT (but not nearly as significant as Droperidol)
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Zofran: mechanism of action
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Works on 5HT3 Serotonin receptors
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Rocuronium: Use and mechanism of action
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Non-depolarizing neuromuscular blocker; Competes with acetylcholine at Nicotinic receptors
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Rocuronium: onset and duration
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Onset: within two minutes; intermediate duration
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Rocuronium: metabolism and excretion
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Metabolized by liver and excreted by kidneys
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Rocuronium: side effects
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None (possible allergic reaction)
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Rocuronium: effect with isoflurane
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Takes longer for spontaneous recovery when combined with isoflurane
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Phenylephrine: use
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Hypotension (especially useful with spinal anesthesia)
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Phenylephrine: receptor site
What does this mean? |
alpha-1 receptors;
Increases blood pressure by constricting vasculature, increases SVR, and coronary artery perfusion; no effect on cardiodynamics (although reflex bradycardia may result) |
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Phenylephrine: metabolism
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MAO and sulfotransferase enzymes in liver; excreted in urine
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Phenylephrine: side effects
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Increased pulmonary vascular resistance (pulmonary hypertension), reflex bradycardia, extravasation if given peripherally
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Morphine: mechanism of action
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Binds to mu and kappa opioid receptors
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Morphine: effects
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Analgesia, sedation, and respiratory depression
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Morphine: onset and duration of action
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Slower to come on and off than other opioids d/t lipid solubility
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Morphine: metabolism and excretion
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Active metabolite ( M6G) as well as inactive metabolite (M3G) are excreted from kidneys
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Morphine: to which patient populations should you avoid giving this drug?
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Renal failure (excretion of active metabolites); also causes histamine release which can cause hypotension and/or bronchospasm
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Desflurane: MAC
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6%
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Desflurane: Blood gas coefficient/speed of onset
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0.42 (most rapid onset)
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Desfurane: use in induction
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Not used for inhalation induction in pediatrics d/t risk of bronchospasm (bad smell, airway irritant)
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Desflurane: effect on HR
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No effect at dose < 1 MAC, Tachycardia at > 1 MAC
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Desflurane: what is so great about it?
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Cardiac stable, does not decrease CO
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Isoflurane: MAC
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1% (most potent inhalation agent)
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Isoflurane: effect on HR
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Increases by 20%
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Isoflurane: What is good about it?
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stability, predictability, lack of toxicity, low solubility
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Isoflurane: can it be used for induction?
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No, can be an airway irritant and is pungent.
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Isoflurane: MAC
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1.15%
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Isoflurane: effect on BP
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Decreases SVR and may cause hypotension
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Ephedrine: Drug class/ mechanism of action
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Noncatecholamine; causes release of catecholamines (norepi) from vesicles in terminal end of postganglionic neurons
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Ephedrine: receptors
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Non-selective Alpha and Beta agonist, so causes increased HR, contractility, BP, SVR (although not as much as Epi, although lasts longer- about 10 min duration)
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Ephedrine: tachyphylaxis (what does this mean)?
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Quick tolerance; after use, vesicles are depleted of NE and second dose does not get same effect, may require increased dose
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Ephedrine: effect on fetus
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Acidosis; used to be indicated for antepartum use because it allows blood flow to placenta, but now NE is used d/t fetal acidosis
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Ephedrine: who would you not give this drug to?
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Anyone on MAOI antidepressants (can cause excessive hypertension and possible intracranial bleeding); anyone you are concerned about tachycardia
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Ketamine: mechanism of action and effect
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NMDA receptor antagonist, causes dissociative anesthesia/amnesia
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Ketamine: onset, metabolism, exretion
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Rapid onset, metabolized by liver, excreted by kidneys
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Ketamine: effect on cardiovascular dynamics
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increases SNS activity and increases HR, BP, CO, cardiac workload, and myocardial O2 demand
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Ketamine: who would you not use this drug for?
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Seizure disorder, elevated ICP (increases cerebral blood flow) anyone you don't want to elevate HR or BP (CAD)
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Ketamine: who is this drug especially good for?
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Potent bronchodilator- great for asthmatics or in bronchospasm, also good for hypovolemic patients (trauma)
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Dexmedetomidine (Precedex): mechanism of action and use
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decreases sns activity - selective alpha 2 adrenergic agonist; used for sedation in ventilated and non-ventilated patients (especially good for awake crani)
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Dexmedetomidine (Precedex): side effects
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Bradycardia, hypotension (if given too rapidly/ high dose),
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Precedex: what is great about it?
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Sedates with no respiratory depressant effect
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Fentanyl: class and mechanism of action
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Opoid analgesic, highly lipid soluble and rapidly crosses the blood brain barrier
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Fentanyl: metabolism and excretion
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Hepatic metabolism and renal excretion
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Fentanyl: who is it good for?
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Just about everyone! Used as the primary anesthetic for patients undergoing CV surgery or patients with poor cardiac function because it does not release histamine and direct depressant effects on the myocardium are minimal. Only mildly decreases blood pressure.
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Fentanyl: potential side effect?
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High dose/ rapid administration can cause muscle rigidity (chest wall rigidity). Treat with NMB
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Midazolam: uses and mechanism of action
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Premedication, sedation, induction. Provides antegrade amnesia; (reduces CBF, CRMO2, ICP), anticonvulsant
Promotes the binding of GABA |
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Midazolam: Reversal
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Flumazenil, but note shorter half-life of flumazenil (re-sedation may occur, or re-dosing may be necessary)
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Midazolam: Who would you not want to give this drug to?
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Liver failure, pregnancy
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Midazolam: side effects
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Mild decrease in SVR, hypotension, respiratory depression; can hang around a long time
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Propofol: Mechanism of action
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Largely unknown, binds to and blocks GABA receptors causing sedation/hypnosis
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Propofol: why do we love it?
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It is especially desirable because of its rapid and complete awakening
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propofol: side effects
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Decrease in arterial blood pressure due to a drop in systemic vascular resistance, cardiac contractility, and preload. (Large doses, rapid injection, and old age may contribute to this); respiratory depression, histamine release,
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Propofol: should be used within
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6 hours or discarded
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propofol causes pain _____
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At injection site, may be mixed with lidocaine
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Propofol: effect on cerebral dynamics
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Decreases CBF, Decreases CMRO2, decreases ICP
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Glycopyrolate: mechanism of action and receptor sites
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Anticholinergic, muscarinic antagonist that works on the PNS post-ganglionic junction of cardiac and skeletal smooth muscle and the presynaptic nerve terminals in the coronary vessels, myocardium and peripheral vasculature
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Glycopyrrulate works by:
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Competitively binding with muscarnic acetylcholine receptors to block the negative effects caused by these receptors
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Robinul is used to reverse:
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Neostigmine
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Robinul should not be given to:
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Myasthenia Gravis, patients with glaucoma, pregnant women (does not cross placenta, so does not block muscarinic effects in fetus),
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Succinylcholine is a _____
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Depolarizing neuromuscular blocker
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Depolarization with succinylcholine is observed by
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Fasiculations
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Succinylcholine works by:
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combines with the cholinergic receptors of the motor end plate to produce depolarization, causes receptors to remain blocked so that acetylcholine cannot bind
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Succinylcholine is metabolized by
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Plasma cholinesterase
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Succs has the _____ duration of action of all neuromuscular blocking agents
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shortest
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Who would you not want to administer succinylcholine to? Why?
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Anyone who is likely to have upregulated receptors at the neuromuscular junction (long term bedridden patients, burns after the first couple days, children under 5 (d/t risk of undiagnosed neuromuscular disease)- can cause hyperkalemia
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Lidocaine: mechanism of action
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inhibition of Na-ion channels--blocks transmission of action potential therefore blocks subsequent sensory nerve transmission
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Lidocaine: pharmacokinetics
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Rapid onset. Hepatic metabolism. crosses blood-brain barrier and placental barriers
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Lidocaine: toxicity is evidenced by
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Main side effects with increased plasma concentration are neuro (facial tingling, vertigo, tinnitus, slurred speech). CV-(bradycardia, hypotension) and local (pain, ecchymosis, hematoma, infection, profound hypotension, myocardial depression, resp depression, neurotoxicity, CNS depression
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Cisatracurium: method of metabolism
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Hofman's elimination (organ independent); excellent for use in renal failure
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