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84 Cards in this Set

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Droperidol: mechanism of action
Binds to postsynaptic GABA receptors in Chemoreceptor Trigger Zone
Droperidol: indication(s)
Prophylaxis of post-operative nausea and vomiting, adjunct to general anesthesia
Droperidol: Important side effects
May bind to and block dopiminergic receptors and postsynapti alpha adrenergic receptors> therefore causes hypotension and tachycardia; sedation and generalized loopiness, PROLONGED QT/ Torsades
Droperidol: who would you not administer this drug to? Special considerations?
Anyone with prolonged QT (Can cause fatal arrhythmia); must get 12 lead EKG before and 2-3 hours after administration
Sufentanil: mechanism of action
Mu opiod receptor agonist
Sufentanil: more or less potent than Fentanyl? How many times?
10x more potent than Fentanyl; 500-700 times more potent than Morphine
Sufentanil: relative duration of action:
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
Sufentanil: what do you do if your patient develops chest wall rigidity?
Give NMB
Sufentanil: high doses can cause:
Vagus mediated bradycardia, chest wall rigidity
Sufentanil: what effect does this have on cerebral blood flow?
Decreased CBF, decreased CRMO2
Sufentanil: when do you give?
can give up front to intubate and run as infusion throughout case
Sevoflurane: Mechanism of action and MAC
GABA? 2%
Sevoflurane: Effect on heart rate
No effect on HR
Sevoflurane: good for induction because:
Quick onset of action, no irritating smell
Sevoflurane: to whom would you not give this agent?
Renal Failure Patients (d/t concerns of nephrotoxicity with Compound A)
Zofran: indication
Anti-emetic
Zofran: side effects
Headache, malaise, dizziness; can cause prolonged QT (but not nearly as significant as Droperidol)
Zofran: mechanism of action
Works on 5HT3 Serotonin receptors
Rocuronium: Use and mechanism of action
Non-depolarizing neuromuscular blocker; Competes with acetylcholine at Nicotinic receptors
Rocuronium: onset and duration
Onset: within two minutes; intermediate duration
Rocuronium: metabolism and excretion
Metabolized by liver and excreted by kidneys
Rocuronium: side effects
None (possible allergic reaction)
Rocuronium: effect with isoflurane
Takes longer for spontaneous recovery when combined with isoflurane
Phenylephrine: use
Hypotension (especially useful with spinal anesthesia)
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)
Phenylephrine: metabolism
MAO and sulfotransferase enzymes in liver; excreted in urine
Phenylephrine: side effects
Increased pulmonary vascular resistance (pulmonary hypertension), reflex bradycardia, extravasation if given peripherally
Morphine: mechanism of action
Binds to mu and kappa opioid receptors
Morphine: effects
Analgesia, sedation, and respiratory depression
Morphine: onset and duration of action
Slower to come on and off than other opioids d/t lipid solubility
Morphine: metabolism and excretion
Active metabolite ( M6G) as well as inactive metabolite (M3G) are excreted from kidneys
Morphine: to which patient populations should you avoid giving this drug?
Renal failure (excretion of active metabolites); also causes histamine release which can cause hypotension and/or bronchospasm
Desflurane: MAC
6%
Desflurane: Blood gas coefficient/speed of onset
0.42 (most rapid onset)
Desfurane: use in induction
Not used for inhalation induction in pediatrics d/t risk of bronchospasm (bad smell, airway irritant)
Desflurane: effect on HR
No effect at dose < 1 MAC, Tachycardia at > 1 MAC
Desflurane: what is so great about it?
Cardiac stable, does not decrease CO
Isoflurane: MAC
1% (most potent inhalation agent)
Isoflurane: effect on HR
Increases by 20%
Isoflurane: What is good about it?
stability, predictability, lack of toxicity, low solubility
Isoflurane: can it be used for induction?
No, can be an airway irritant and is pungent.
Isoflurane: MAC
1.15%
Isoflurane: effect on BP
Decreases SVR and may cause hypotension
Ephedrine: Drug class/ mechanism of action
Noncatecholamine; causes release of catecholamines (norepi) from vesicles in terminal end of postganglionic neurons
Ephedrine: receptors
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)
Ephedrine: tachyphylaxis (what does this mean)?
Quick tolerance; after use, vesicles are depleted of NE and second dose does not get same effect, may require increased dose
Ephedrine: effect on fetus
Acidosis; used to be indicated for antepartum use because it allows blood flow to placenta, but now NE is used d/t fetal acidosis
Ephedrine: who would you not give this drug to?
Anyone on MAOI antidepressants (can cause excessive hypertension and possible intracranial bleeding); anyone you are concerned about tachycardia
Ketamine: mechanism of action and effect
NMDA receptor antagonist, causes dissociative anesthesia/amnesia
Ketamine: onset, metabolism, exretion
Rapid onset, metabolized by liver, excreted by kidneys
Ketamine: effect on cardiovascular dynamics
increases SNS activity and increases HR, BP, CO, cardiac workload, and myocardial O2 demand
Ketamine: who would you not use this drug for?
Seizure disorder, elevated ICP (increases cerebral blood flow) anyone you don't want to elevate HR or BP (CAD)
Ketamine: who is this drug especially good for?
Potent bronchodilator- great for asthmatics or in bronchospasm, also good for hypovolemic patients (trauma)
Dexmedetomidine (Precedex): mechanism of action and use
decreases sns activity - selective alpha 2 adrenergic agonist; used for sedation in ventilated and non-ventilated patients (especially good for awake crani)
Dexmedetomidine (Precedex): side effects
Bradycardia, hypotension (if given too rapidly/ high dose),
Precedex: what is great about it?
Sedates with no respiratory depressant effect
Fentanyl: class and mechanism of action
Opoid analgesic, highly lipid soluble and rapidly crosses the blood brain barrier
Fentanyl: metabolism and excretion
Hepatic metabolism and renal excretion
Fentanyl: who is it good for?
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.
Fentanyl: potential side effect?
High dose/ rapid administration can cause muscle rigidity (chest wall rigidity). Treat with NMB
Midazolam: uses and mechanism of action
Premedication, sedation, induction. Provides antegrade amnesia; (reduces CBF, CRMO2, ICP), anticonvulsant

Promotes the binding of GABA
Midazolam: Reversal
Flumazenil, but note shorter half-life of flumazenil (re-sedation may occur, or re-dosing may be necessary)
Midazolam: Who would you not want to give this drug to?
Liver failure, pregnancy
Midazolam: side effects
Mild decrease in SVR, hypotension, respiratory depression; can hang around a long time
Propofol: Mechanism of action
Largely unknown, binds to and blocks GABA receptors causing sedation/hypnosis
Propofol: why do we love it?
It is especially desirable because of its rapid and complete awakening
propofol: side effects
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,
Propofol: should be used within
6 hours or discarded
propofol causes pain _____
At injection site, may be mixed with lidocaine
Propofol: effect on cerebral dynamics
Decreases CBF, Decreases CMRO2, decreases ICP
Glycopyrolate: mechanism of action and receptor sites
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
Glycopyrrulate works by:
Competitively binding with muscarnic acetylcholine receptors to block the negative effects caused by these receptors
Robinul is used to reverse:
Neostigmine
Robinul should not be given to:
Myasthenia Gravis, patients with glaucoma, pregnant women (does not cross placenta, so does not block muscarinic effects in fetus),
Succinylcholine is a _____
Depolarizing neuromuscular blocker
Depolarization with succinylcholine is observed by
Fasiculations
Succinylcholine works by:
combines with the cholinergic receptors of the motor end plate to produce depolarization, causes receptors to remain blocked so that acetylcholine cannot bind
Succinylcholine is metabolized by
Plasma cholinesterase
Succs has the _____ duration of action of all neuromuscular blocking agents
shortest
Who would you not want to administer succinylcholine to? Why?
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
Lidocaine: mechanism of action
inhibition of Na-ion channels--blocks transmission of action potential therefore blocks subsequent sensory nerve transmission
Lidocaine: pharmacokinetics
Rapid onset. Hepatic metabolism. crosses blood-brain barrier and placental barriers
Lidocaine: toxicity is evidenced by
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
Cisatracurium: method of metabolism
Hofman's elimination (organ independent); excellent for use in renal failure