Drugs For Anesthesia At A Glance Exa

Front 1

Droperidol: mechanism of action

Back 1

Binds to postsynaptic GABA receptors in Chemoreceptor Trigger Zone

Front 2

Droperidol: indication(s)

Back 2

Prophylaxis of post-operative nausea and vomiting, adjunct to general anesthesia

Front 3

Droperidol: Important side effects

Back 3

May bind to and block dopiminergic receptors and postsynapti alpha adrenergic receptors> therefore causes hypotension and tachycardia; sedation and generalized loopiness, PROLONGED QT/ Torsades

Front 4

Droperidol: who would you not administer this drug to? Special considerations?

Back 4

Anyone with prolonged QT (Can cause fatal arrhythmia); must get 12 lead EKG before and 2-3 hours after administration

Front 5

Sufentanil: mechanism of action

Back 5

Mu opiod receptor agonist

Front 6

Sufentanil: more or less potent than Fentanyl? How many times?

Back 6

10x more potent than Fentanyl; 500-700 times more potent than Morphine

Front 7

Sufentanil: relative duration of action:

Back 7

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

Front 8

Sufentanil: what do you do if your patient develops chest wall rigidity?

Back 8

Give NMB

Front 9

Sufentanil: high doses can cause:

Back 9

Vagus mediated bradycardia, chest wall rigidity

Front 10

Sufentanil: what effect does this have on cerebral blood flow?

Back 10

Decreased CBF, decreased CRMO2

Front 11

Sufentanil: when do you give?

Back 11

can give up front to intubate and run as infusion throughout case

Front 12

Sevoflurane: Mechanism of action and MAC

Back 12

GABA? 2%

Front 13

Sevoflurane: Effect on heart rate

Back 13

No effect on HR

Front 14

Sevoflurane: good for induction because:

Back 14

Quick onset of action, no irritating smell

Front 15

Sevoflurane: to whom would you not give this agent?

Back 15

Renal Failure Patients (d/t concerns of nephrotoxicity with Compound A)

Front 16

Zofran: indication

Back 16

Anti-emetic

Front 17

Zofran: side effects

Back 17

Headache, malaise, dizziness; can cause prolonged QT (but not nearly as significant as Droperidol)

Front 18

Zofran: mechanism of action

Back 18

Works on 5HT3 Serotonin receptors

Front 19

Rocuronium: Use and mechanism of action

Back 19

Non-depolarizing neuromuscular blocker; Competes with acetylcholine at Nicotinic receptors

Front 20

Rocuronium: onset and duration

Back 20

Onset: within two minutes; intermediate duration

Front 21

Rocuronium: metabolism and excretion

Back 21

Metabolized by liver and excreted by kidneys

Front 22

Rocuronium: side effects

Back 22

None (possible allergic reaction)

Front 23

Rocuronium: effect with isoflurane

Back 23

Takes longer for spontaneous recovery when combined with isoflurane

Front 24

Phenylephrine: use

Back 24

Hypotension (especially useful with spinal anesthesia)

Front 25

Phenylephrine: receptor site

What does this mean?

Back 25

alpha-1 receptors;

Increases blood pressure by constricting vasculature, increases SVR, and coronary artery perfusion; no effect on cardiodynamics (although reflex bradycardia may result)

Front 26

Phenylephrine: metabolism

Back 26

MAO and sulfotransferase enzymes in liver; excreted in urine

Front 27

Phenylephrine: side effects

Back 27

Increased pulmonary vascular resistance (pulmonary hypertension), reflex bradycardia, extravasation if given peripherally

Front 28

Morphine: mechanism of action

Back 28

Binds to mu and kappa opioid receptors

Front 29

Morphine: effects

Back 29

Analgesia, sedation, and respiratory depression

Front 30

Morphine: onset and duration of action

Back 30

Slower to come on and off than other opioids d/t lipid solubility

Front 31

Morphine: metabolism and excretion

Back 31

Active metabolite ( M6G) as well as inactive metabolite (M3G) are excreted from kidneys

Front 32

Morphine: to which patient populations should you avoid giving this drug?

Back 32

Renal failure (excretion of active metabolites); also causes histamine release which can cause hypotension and/or bronchospasm

Front 33

Desflurane: MAC

Back 33

6%

Front 34

Desflurane: Blood gas coefficient/speed of onset

Back 34

0.42 (most rapid onset)

Front 35

Desfurane: use in induction

Back 35

Not used for inhalation induction in pediatrics d/t risk of bronchospasm (bad smell, airway irritant)

Front 36

Desflurane: effect on HR

Back 36

No effect at dose < 1 MAC, Tachycardia at > 1 MAC

Front 37

Desflurane: what is so great about it?

Back 37

Cardiac stable, does not decrease CO

Front 38

Isoflurane: MAC

Back 38

1% (most potent inhalation agent)

Front 39

Isoflurane: effect on HR

Back 39

Increases by 20%

Front 40

Isoflurane: What is good about it?

Back 40

stability, predictability, lack of toxicity, low solubility

Front 41

Isoflurane: can it be used for induction?

Back 41

No, can be an airway irritant and is pungent.

Front 42

Isoflurane: MAC

Back 42

1.15%

Front 43

Isoflurane: effect on BP

Back 43

Decreases SVR and may cause hypotension

Front 44

Ephedrine: Drug class/ mechanism of action

Back 44

Noncatecholamine; causes release of catecholamines (norepi) from vesicles in terminal end of postganglionic neurons

Front 45

Ephedrine: receptors

Back 45

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)

Front 46

Ephedrine: tachyphylaxis (what does this mean)?

Back 46

Quick tolerance; after use, vesicles are depleted of NE and second dose does not get same effect, may require increased dose

Front 47

Ephedrine: effect on fetus

Back 47

Acidosis; used to be indicated for antepartum use because it allows blood flow to placenta, but now NE is used d/t fetal acidosis

Front 48

Ephedrine: who would you not give this drug to?

Back 48

Anyone on MAOI antidepressants (can cause excessive hypertension and possible intracranial bleeding); anyone you are concerned about tachycardia

Front 49

Ketamine: mechanism of action and effect

Back 49

NMDA receptor antagonist, causes dissociative anesthesia/amnesia

Front 50

Ketamine: onset, metabolism, exretion

Back 50

Rapid onset, metabolized by liver, excreted by kidneys

Front 51

Ketamine: effect on cardiovascular dynamics

Back 51

increases SNS activity and increases HR, BP, CO, cardiac workload, and myocardial O2 demand

Front 52

Ketamine: who would you not use this drug for?

Back 52

Seizure disorder, elevated ICP (increases cerebral blood flow) anyone you don't want to elevate HR or BP (CAD)

Front 53

Ketamine: who is this drug especially good for?

Back 53

Potent bronchodilator- great for asthmatics or in bronchospasm, also good for hypovolemic patients (trauma)

Front 54

Dexmedetomidine (Precedex): mechanism of action and use

Back 54

decreases sns activity - selective alpha 2 adrenergic agonist; used for sedation in ventilated and non-ventilated patients (especially good for awake crani)

Front 55

Dexmedetomidine (Precedex): side effects

Back 55

Bradycardia, hypotension (if given too rapidly/ high dose),

Front 56

Precedex: what is great about it?

Back 56

Sedates with no respiratory depressant effect

Front 57

Fentanyl: class and mechanism of action

Back 57

Opoid analgesic, highly lipid soluble and rapidly crosses the blood brain barrier

Front 58

Fentanyl: metabolism and excretion

Back 58

Hepatic metabolism and renal excretion

Front 59

Fentanyl: who is it good for?

Back 59

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.

Front 60

Fentanyl: potential side effect?

Back 60

High dose/ rapid administration can cause muscle rigidity (chest wall rigidity). Treat with NMB

Front 61

Midazolam: uses and mechanism of action

Back 61

Premedication, sedation, induction. Provides antegrade amnesia; (reduces CBF, CRMO2, ICP), anticonvulsant

Promotes the binding of GABA

Front 62

Midazolam: Reversal

Back 62

Flumazenil, but note shorter half-life of flumazenil (re-sedation may occur, or re-dosing may be necessary)

Front 63

Midazolam: Who would you not want to give this drug to?

Back 63

Liver failure, pregnancy

Front 64

Midazolam: side effects

Back 64

Mild decrease in SVR, hypotension, respiratory depression; can hang around a long time

Front 65

Propofol: Mechanism of action

Back 65

Largely unknown, binds to and blocks GABA receptors causing sedation/hypnosis

Front 66

Propofol: why do we love it?

Back 66

It is especially desirable because of its rapid and complete awakening

Front 67

propofol: side effects

Back 67

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,

Front 68

Propofol: should be used within

Back 68

6 hours or discarded

Front 69

propofol causes pain _____

Back 69

At injection site, may be mixed with lidocaine

Front 70

Propofol: effect on cerebral dynamics

Back 70

Decreases CBF, Decreases CMRO2, decreases ICP

Front 71

Glycopyrolate: mechanism of action and receptor sites

Back 71

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

Front 72

Glycopyrrulate works by:

Back 72

Competitively binding with muscarnic acetylcholine receptors to block the negative effects caused by these receptors

Front 73

Robinul is used to reverse:

Back 73

Neostigmine

Front 74

Robinul should not be given to:

Back 74

Myasthenia Gravis, patients with glaucoma, pregnant women (does not cross placenta, so does not block muscarinic effects in fetus),

Front 75

Succinylcholine is a _____

Back 75

Depolarizing neuromuscular blocker

Front 76

Depolarization with succinylcholine is observed by

Back 76

Fasiculations

Front 77

Succinylcholine works by:

Back 77

combines with the cholinergic receptors of the motor end plate to produce depolarization, causes receptors to remain blocked so that acetylcholine cannot bind

Front 78

Succinylcholine is metabolized by

Back 78

Plasma cholinesterase

Front 79

Succs has the _____ duration of action of all neuromuscular blocking agents

Back 79

shortest

Front 80

Who would you not want to administer succinylcholine to? Why?

Back 80

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

Front 81

Lidocaine: mechanism of action

Back 81

inhibition of Na-ion channels--blocks transmission of action potential therefore blocks subsequent sensory nerve transmission

Front 82

Lidocaine: pharmacokinetics

Back 82

Rapid onset. Hepatic metabolism. crosses blood-brain barrier and placental barriers

Front 83

Lidocaine: toxicity is evidenced by

Back 83

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

Front 84

Cisatracurium: method of metabolism

Back 84

Hofman's elimination (organ independent); excellent for use in renal failure