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Anesthesia > IV Anesthetics > Flashcards

IV Anesthetics Flashcards

1
Q

How quickly must you use Propofol after opening?

A

6 hrs (due to emulsion amendable to bacterial growth)

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2
Q

Describe propofol metabolism

A

Rapid liver metabolism, inactive compound excreted by kidney

clearance > hepatic blood flow = extrahepatic metabolism

~30% metabolized in lungs

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3
Q

Typical wake up time after propofol bolus?

A

8-10 min (DOA 3-8 min)

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4
Q

Rapidity of wake up from propofol likely 2/2 what?

A

redistribution from highly perfused (brain) to poorly perfused (fat/muscle) tissues

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5
Q

Induction dose of propofol

A

1-2.5 mg/kg IV

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6
Q

Protein binding % of propofol

A

97%

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7
Q

MOA of propofol

A

increase chloride current via GABAa receptor

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8
Q

Major CNS effects of propofol?

A
  • hypnotic
  • decrease CBF/CMRO2/ICP/IOP

NOT AN ANALGESIC

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9
Q

CV effects of propofol (HR, SVR)

A

Large decrease in MAP via vasodilation (arteries and veins)

Decrease preload and afterload

Inhibits baroreflex = only small increase in HR

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10
Q

Respiratory effects of Propofol (RR, Vt, CO2/O2 response)

A

Induction dose = Respiratory depressant, apnea

Maintenance dose = reduce minute ventlation (decrease RR and Vt)

blunt CO2/O2 vent response

reduce upper airway responsiveness (less laryngospasm)

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11
Q

post-surgical benefit of propofol

A

anti-emetic

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12
Q

Pt with unexpected tachycardia during propofol anesthesia…what should you look for?

A

Labs- BMP

metabolic acidosis possible (propofol infusion syndrome)

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13
Q

How can you reduce injection pain with propofol?

A
  1. pre-medicate with opioid
  2. co-administer with lidocaine (50-100mg IV)
  3. Dilution
  4. use larger veins
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14
Q

What factors would decrease the required induction dose of propofol?

A

old age

pre-med with opioids/benzos

reduced CV reserve

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15
Q

What factors increase the required induction dose of propofol?

A

age (children need upwards of 2.5-3.5mg/kg IV)

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16
Q

Continuous propofol infusion rate for maintenance of anesthesia

A

100-200ug/kg/min (if combined with NO or opioids for analgesia)

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17
Q

Continuous propofol infusion rate for sedation

A

25-75 ug/kg/min

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18
Q

anti-emetic dosing of propofol

A

10-20mg IV

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19
Q

Difference between propofol and fospropofol

A

fospropofol (Lusedra) = water-solubule pro drug of propofol used for MAC

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20
Q

biproducts of fospropofol

A

propofol + phosphate + formaldehyde

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21
Q

difference between propofol and fospropofol duration

A

fospropofol = longer onset/ofset duration (due to prodrug form)

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22
Q

Major barbiturates used in IV induction

A

thiopental

methohexital

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23
Q

Major effects of barbiturates in anesthesia

A

hyponotic

sedative/general anesthetic

anticonvulsant

NOT AN ANALGESIC

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24
Q

Downfall of barbiturates (thopental/methohexital) re: solution

A

alkaline Na salt w/ pH > 10 –> precipitation with injected with acidic drugs (like neuromuscular blocking drugs)

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25
Q

Metabolism of barbiturates

exception?

A

hepatic metabolism via oxidation and N-dealkylation/desulfaration

exception = phenobarbital (renal excretion)

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26
Q

clearance of methohexital vs thiopental?

A

methohexital = more rapid than thiopental (quicker duration of action)

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27
Q

MOA of barbiturates

A

enhancement of inhibitor neurotransmiter (GABAa)

inhibition of excitatory transmission (unclear specific target)

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28
Q

Major CNS effects of barbiturate

A

Cerebral vasoconstric
Decrase CBF
Decrease ICP
Decrease CMRO2

= Flat line EEG (except methohexital = increase epileptic foci)

GREAT FOR USE IN SPACE OCCUPYING IC LESIONS

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29
Q

CV effects of barbiturates

A

Decrease BP (vasodilate, decrease sympathetic outflow)

compensatory increase in HR (blunt hypotension)

Decrease CO 2/2 decrease VR (pooling of blood in capacitance vessels)

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30
Q

Which patients will have exagerated CV response to barbiturates?

A
  • hypovolemia
  • cardiac tamponade
  • cardiomyopathy
  • CAD
  • cardiac valve disease

(** can’t compensate for decreased SVR with increased CO)

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31
Q

Respiratory effects of barbiturates

A
  • resp depressant = decreased minute vent (decreased Vt and RR)

decrease vent response to CO2/O2

LESS reduction in upper airway response (don’t use without NM blockers for DL)

32
Q

Major side effects of barbiturates

A
  1. arterial injection = pain, tissue damage from vasoconstriction
  2. sub-cut injection = pain/local tissue irritation

USE DILUTE PREPS! (2.5% thiopental, 1% methohexital)

33
Q

Induction dose of thiopental

A

3-5mg/kg IV

34
Q

Induction dose of methohexital

A

1-1.5mg/kg IV

35
Q

Benzos commonly used in anesthesia

A

diazepam, midazolam, lorazepam

36
Q

Desired effects of benzos

A

anterograde amnesia
anxiolysis

= GREAT PREMEDICATION

Also- anti-epileptic

37
Q

quickest onset benzo? why?

A

midazolam (versed)

most lipid soluble (rapid distribution to brain, then redistribution to inactive tissue sites)

38
Q

MOA of benzos

A

activate GABAa, increase Cl current, hyperpolarize neuron, reduce excitability

most in cerebral cortex, post-synaptic nerve endings

minimal effects outside CNS

39
Q

most potent benzo

A

Midazolam = higher affinity for benzo receptor (x2 diazepam)

40
Q

CNS effects of benzos

A

decrease CBF and CMRO2 (less than barbs and propofol though)

ceiling effect

not neuroprotective like barbs

41
Q

CV effects of benzos

A

minimal decrease in BP (Midazolam>diazepam)

worse in volume depleted patients

42
Q

Resp effects of benzos

A

minimal vent depression…increased with opioids

43
Q

Clinical uses of benzos

A
  1. preop medication
  2. IV sedation
  3. IV induction of anesthesia
  4. suppress seizure activity
44
Q

Versed dosing for premedication (IV)

A

1-2mg IV

45
Q

PO premedication dosing of Versed in peds

A

0.5mg/kg PO 30 min before induction

46
Q

Induction dose Versed

A

0.1-0.3mg/kg IV

facilitate with small dose opioid (fentanyl 50-100ug IV) 1-3 min pre benzo dosing

47
Q

Major desired effect of Ketamine

A

ANALGESIA

dissociative anesthesia

48
Q

Ketamine onset, ofset

A

rapid, high lipid solubility

rapid, redistribution to inactive tissue

49
Q

protein binding of ketamine

A

low 12% (unique)

50
Q

Major MOA of ketamine

A

inhibition of NMDA receptor

51
Q

Side effects of katamine

A
  • open eyes, dilated, nystagmus

- lacrimation/salvation increased (premedicate with anticholinergic)

52
Q

How can you diminish emergence reactions with ketamine?

A

benzos

less reactions in kids

53
Q

CNS effects of ketamine

A

Vasodilate cerebral vessesls = increase CBF
Increase CMRO2

DO NOT USE IN PATIENTS IWTH INCREASED ICP/INTRACRANIAL PATH

54
Q

CV effects of Ketamine

blunt them how?

A

significant/transient increase in BP, HR, CO 2/2 sympathetic outflow increase

blunt w/ opioids, benzos, inhaled anesthetics

55
Q

Why may ketamine be a poor choice in critically ill patient?

A

Direct myocardial depressant

critically ill = decreased ability to increase sympathetic output = blunt increase bp/hr/co = cardiogenic shock issues

56
Q

Respiratory effects of ketamine

A

No significant resp depression

large bolus doses can cause transient hypovent/short apnea

bronchodilation = good for asthma

laryngospasm possible = increased salivation (DON’T ASSUME AIRWAY IS PROTECTED)

57
Q

Induction dose Ketamine

A

1-2mg/kg IV

4-6mg/kg IM

58
Q

Maintenance dose Ketamine

A

Alone - 30-90ug/kg/min IV

With 50-70% NO - 15-45ug/kg/min IV

59
Q

Analgesic dose ketamine

A

0.2-0.8mg/kg IV

60
Q

Etomidate effects

A

hyponotic

NO ANALGESIA

61
Q

Typical concentration of etomidate

A

2mg/ml solution

62
Q

Major metabolism site of etomidate

A

serum esterase, excreated into urine/bile

63
Q

Relative duration of etomidate

A

Dose dependent, linear

100sec unconsciousness per 0.1mg/kg given

64
Q

MOA of etomidate

A

GABA like effects, potentiate GABAa receptor effects

65
Q

CNS effects of etomidate

A

potent cerebral vasoconstrictor

decrease CBF and ICP

NOT NEUROPROTECTIVE

66
Q

CV effects of etomidate

A

CV stability after bolus injection

BP decrease modest/absent

hypovolemia = some decrease in SVR

Minimal change in HR or cardiac contractility

67
Q

resp effects of etomidate

A

resp depressant (less than barbiturates)

apnea (after bolus doses ) possible

increased resp effects w/ opioids/inhaled anesthetics

68
Q

worrisome side effect of etomidate

A

adrenocortical suppression (dose dependent inhibition of AaB-hydroxylase)

lasts 4-8 hrs after induction dose

69
Q

Induction dose of Etomidate

A

0.2-0.3mg/kg IV

70
Q

What is dexmedetomidine?

A

highly selective alpha-2 blocker

71
Q

Context sensitive half time of dexmedetomidine?

A

Significant increase w/ dose
10 min after 4 min inffusion

250min after 8hr infusion

72
Q

MOA of dexmedetomidine?

A

hyponosis from stim of alpha-2 in locus ceruleus

analgesia from SC level

73
Q

CNS effectts of dexmedetomidine?

A

decrease CBF

no signifcant change in ICP or CMRO2

74
Q

CV effects of dexmedetomidine

A
  • moderate decrease in HR and SVR

Bolus dose = transient increase in SVR, decrease HR (peripheral activation of alpha-2)

75
Q

respiratory changes of dexmedetomidine

A
  • small decrease in Vt

- no change in RR

76
Q

Major uses of dexmedetomidine?

A
  1. short term sedation for intubated/ventilated patients (ICU)
  2. adjunct to general anesthesia
  3. sedation for awake fiberoptic intubation
  4. in conjunction with regional anesthesia
77
Q

Dexmedetomidine dosing

A

0.5-1ug/kg IV (initial over 10-15 min) + infusion 0.2-0.7 ug/kg/hr

Anesthesia (9 decks)

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