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Anesthesia Orientation > IV Anesthetics, Opioids, LA, NMB > Flashcards

IV Anesthetics, Opioids, LA, NMB Flashcards

1
Q

how is propofol metabolized

A

fast! faster than hepatic blood flow so it also has extrahepatic metabolism eg plasma & lung

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2
Q
  • pharmocokinetics and dynamics of propofol

- how to adjust for age of pt

A
  • quick off b/c it is redistributing to skeletal mm and areas that are less well perfused (less hangover)
  • dec dose in elderly (smaller central compartment/slower clearance)
  • inc dose in kids (large Vd/fat + rapid clearance)
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3
Q

MOA of propofol

A

potentiateds Cl- flow thru GABA receptors

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4
Q

absolute and relative contraindications of propofol

A
  • relative: egg allergy b/c propofol has egg white in it (but no EBM to back it up)…also caution with sulfa allergy b/c of the preservatives that propofol is kept in
  • absolute: d/o of fat metabolism, caution in HLD, pancreatitis
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5
Q

CNS effects of propofol (& on EEG)

A
  • ↓ CBF, ↓ ICP, ↓ CMRO2
  • ↓ amplitude, ↑ latency, even burst suppression on EEG
  • “feel good” b/c activates nucleus accumbens
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6
Q

CV effects of propofol

A
  • ↓↓ BP 2/2 ↓ SVR (vasodilation - the most of the IV anesthetics!)
    • inhibits the baroreflex so can really tank BP
  • depresses myocardium/contractility
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7
Q

Resp effects of propofol

A
  • resp depressant (inhibits central drive)
  • inhibits aw reflex (could intubate with just propofol but would need a large dose that would drop BP a lot)
  • inc apneic threshold (ventilatory response to CO2 dec)
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8
Q

GI effects of Propofol

A
  • dec PONV (may dec serotonin in the area postrema)
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9
Q

induction dose of propofol

A

1-2.5 mg/kg

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10
Q

side effects of propofol

A
  • pain on injection
  • hypotn
  • lipid emulsion –> bacterial growth
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11
Q

side effects and toxicity of barbs? (2 main ones)

A
  • stimulates prophyrin –> AIP attacks

- chemical arteritis on accidental arterial injection

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12
Q

what problem can be encountered on injection of barbs?

A

may precipitate b/c it’s very alkaline & when it mixes with acidic NMB (roc) it can precipitate in IV –> “rock”

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13
Q

metabolism of barbiturates

A

slow hepatic oxidation –> more hangover effect

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14
Q

MOA of barbiturates

A

potentiates GABA (inc duration that Cl- channels r open), inhibits excitatory eg glutamate

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15
Q

CV effects of barbs (HR, BP)

A
  • BP: dec via dec SVR (vasodilation & venodilation)
  • HR: inc via baroreceptor unless that response is blunted (eg. BB) ** diff than propofol which blunts baroreceptor reflex
  • myocardial depression
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16
Q

Resp effects of barbs (RR, hypoxic drive, apneic threshold)

A
  • ↓ RR, ↓ TV –> apnea
  • dec hypoxic drive (O2)
  • inc apneic threshold (CO2)
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17
Q

CNS effects of barbs (and on EEG)

A
  • vasoconstrictors - ↓ CBF, ↓ ICP, ↓ CMRO2
  • can be used for focal CNS lesions
  • on EEG dose dep’t burst suppression
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18
Q

main utility of barbiturates?

A

dec ICP in neuro cases; neuroprotection from focal cerebral ischemia

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19
Q

signif about onset and offset of barbiturates?

A

onset in 30 sec
offset takes awhile b/c half life is ~ 12 hrs and it takes 3-5 half lives before the drug is out of the body so it has signif “hangover” effect

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20
Q

why do pts wake up from anesthesia?

A

redistribution!!

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21
Q

beware barbiturates in these 4 settings

A

AS, hypovolemia, AIP, sepsis

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22
Q

where in the body is an anesthetic within 1-3 min?

within 10 min?

A

1-3: brain

10 : skel mm/lean tissue

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23
Q

which benzo works fastest and why

A

midazolam - most lipid soluble (gets into brain and spinal cord fast from the blood); action terminates from rapid redistribution

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24
Q

metab of benzos

A

all hepatic (oxdn which dec w/age, cirrhosis or other chronic liver dz) then renally excreted

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25
Q

mech of benzos

A

enhance GABA (inc freq of Cl- channel openings)–> hyperpolarization

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26
Q

CNS effects of benzos

A
  • CNS: ↓ CMRO2, ↓ CBF, nc/↓ ICP
  • prevent/control grand mal seizures
  • amnesia, sedative, antianxiety effects
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27
Q

CV effects of benzos (on HR & BP)

A
  • ↑ HR

- ↓ BP, ↓ CO, ↓ PVR slightly (midazolam > diazepam)

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28
Q

Resp effects of benzos

A
  • minimal if given alone

- dec response to CO2

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29
Q

antagonism of benzos and dose

A

Flumazenil 8-15 ug/kg

- competitively binds GABA…(seff: anxiety, w/d, ↑ ICP, seizure, **n/v)… resedation may occur

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30
Q

which pt populations should i be careful with benzos

A

eldery

ppl who are altered already

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31
Q

unique feature of ketamine that sets it apart from other hypnotics

A
  • ANALGESIA, “dissociative” amnesia (thalamus not synced w/limbic system), hypnosis
  • low protein binding
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32
Q

metabolism of ketamine

A

P450 hepatic

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33
Q

MOA of ketamine

A
  • inhibits excitatory NMDA receptor but also works on a bunch of other receptors in the body “dirty drug” aka can really mess you up
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34
Q

what other drug is good to give before induction with ketamine?

A

glycopyrralate b/c ketamine inc salivation. nb…glyco is used vs atropine b/c glyco doesn’t cross the BBB

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35
Q

why is ketamine’s use limited?

A

dissociative drug - dissoc b/w thalamus to limbic system. distorted visual/tactile sensations (but less in kids), experience delirium (give Versed)

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36
Q

CNS effects of ketamine (& on EEG)

A
  • **vasodilator… ↑ ICP, ↑ CBF
  • ? falsely high BIS
  • ↑ amplitude but dec latency on EEG
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37
Q

CV effects of ketamine (BP, HR)

A
  • ↑ SNS therefore small ↑ HR, BP, CO but beware use in critically ill pt with already decreased SNS stores. (ok in hypovolemic shock)
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38
Q

resp effects of ketamine (3)

A
  • no resp depression
  • bronchodilator (ok for - reactive aw dz)
  • ↑ salivation may promote laryngospasm
39
Q

induction dose of ketamine

A

1-2 mg/kg IV

4-6 up to 10 per Schell mg/kg IM

40
Q

what situations is ketamine especially useful?

which are contraindications?

A

ggod: uncooperative pts,
ppl with reactive airways

  • contra: pulm HTN ↑ PAP, inc IOP (b/c causes nystagmus)
41
Q

what situation is etomidate especially useful for & why?

A

ppl with bad hearts b/c it is an IV hypnotic with minimal hemodynamic effects

42
Q

metab of etomidate

A

ester hydrolysis (plasma & hepatic)

43
Q

which drug should be utilized for pts with multiple allergies?

A

Etomidate

44
Q

what effect can be observed during etomidate induction

A

myoclonus & pain @ IV on induction

45
Q

MOA of etomidate

A
  • potentiates GABA

- fast onset (bound to albumin, lipid soluble)

46
Q

CNS effects of etomidate (& on EEG)

A
  • vasoconstrictor… ↓ CBF, ↓ ICP, ↓ CMRO2
  • ↑ amplitude but still ↓ latency on EEG (like Ketamine)
  • contraindicated in seizure pts (can induce epileptiform activity on EEG)
47
Q

CV effects of etomidate (on HR and BP)

A
  • ***minimal - dec SVR but no effect on BP
  • good drug for heart cases
  • dec CBF & myocardial O2 demand
48
Q

Resp effects of etomidate

A
  • min resp depression (dec TV but inc RR)
49
Q

what unique side effects does etomidate have (3)

A
  • depresses endocrine system… inhibits 11-B-hydroxylase which inhibits cortisol and aldosterone synthesis
  • worst PONV “vomidate”
  • myoclonus
50
Q

induction dose of etomidate

A

0.2-0.3 mg/kg IV

51
Q

mech of dexmedetomidine

A
  • a2 agonist on presynaptic terminal inhibits NE release –> sedation, dec MAC
52
Q

main utility of dexmedetomidine

A

in ICU when want sedating pt but want them to be able to wake up and interact

53
Q

MOA of opioids

A

bind opioid receptor (mu) to activate G protein –> ↓ excitatory NT (Ach, substance P)

54
Q

where do opioids exihibit their MOA?

A

analgesia via binding receptors in the sensory neurons of peripheral nervous system, neuraxial: dorsal horn (inhibits passage of pain info), medulla (potentiates inhibitory pathways which modulate pain signals, & cortex (dec perception of pain & emotional response to it)

55
Q

most potent opioids

A
  • most potent = Sufentanil > Remi > Fentanyl > hydromorphone > morphine
56
Q

most lipid soluble opioids

A

fentanyl, sufentanil > alfentanil… remembr bolus front-end and back-end graph

57
Q

how are opioids metabolized?

what specific metabolites are active?

A

metab by liver (morphine –> M6G which is active; meperidine–>normeperidine –> seizures)

58
Q

what is unique about codeine and tramadol?

A

they are prodrugs changed into active froms (morphine and another version of tramadol)

59
Q

effect of opioids on circulation (HR and BP)

A
  • ↓ HR via vagus nerve – esp fentanyl (so dec CO)…exception meperidine ↑ HR
  • BP: ↓ from ↓ sympathetic tone (↓ venous and arterial P) but can have cardiac stability when used as single agent
60
Q

seff of methadone & meperidine

A

prolong QT interval

61
Q

unique about morphine re: seff

A

causes histamine release

62
Q

respiratory effects of opioids re: RR, apneic threshold, hypoxic drive

A
  • dec RR, dec MV via Mu receptor
  • ↑ apneic threshold (↑ PaCO2)
  • ↓ hypoxic drive
  • histamine induced bronchospasm (more with morphine)
  • chest wall rigidity (more with Fentanyl, rapid/hi doses… Tx: NMB)
63
Q

opioid effects on CNS

A
  • CNS: ↓ CMRO2, ↓ CBF, ↓ ICP; no effect on EEG
  • sedative effects
  • dec MAC
64
Q

effect of opioids on eyes and GI

A
  • miosis (stim edinger-westphal nucleus)
  • GI: constipation from inc mm tone, sphincter of Oddi contraction (used to visualize on ERCP); chemoreceptor zone –> n/v
65
Q

indications for opioids

A
  • post-op shivering tx Meperidine 10-25 mg

- sedation, analgesia, anti-tussive

66
Q

what is the opioid receptor antagonist

A

Naloxone (seff tachy, ventricular irritability, HTN, pulm edema…brief action 30-45 min)

67
Q

describe Propofol infusion syndrome

A
  • in peds/younger pt
  • high infusion rate (>150-100 ug/kg/min) x hrs-days metabolic acidosis, bradyarrhythmia, cardiac arrest nonresponsive to tx, death.
  • Mech? mitochondrial toxicity/lipid overload
68
Q

contraindications to etomidate

A
  • pt w/seizure hx

- pt w/AIP as can induce attack

69
Q

how does myasthenia gravis change response to non-depolarizing NMB? how about depolarizing agents like SCh?

A
  • MG have fewer ACh receptors on mm therefore….
  • MG sensitive to NDMB
  • MG resistant to Sux
70
Q

how does myasthenic syndrome (Lambert-Eaton syndrome) change response to non-depolarizing NMB? how about depolarizing agents like SCh?

A
  • LES has less ACh released at myoneural jxn but # of receptors is normal
  • LES sensitive to both as already have underlying weakness present
71
Q

Which benzo changes from water soluble to lipid soluble upon venous injection?

A

Midazolam

72
Q

Which opioid depresses cardiac contractility the most?

A

Meperidine

73
Q

Which drugs augment NDMB?

A
  • inhaled gases
  • aminoglycoside antibiotics (gentamycin, streptomycin, neomycin, tobramycin) + (Clindamycin, lincomycin) *Erythromycin is a macrolide and does not affect NDMB
  • Mg
  • IV local anesthetics
  • Lasix
  • Dantrolene
  • CCB
  • Lithium
74
Q

Which drugs/states antagonize NDMB?

A

Calcium!!!! Also hyperPTH & hypercalcemia can be resistant to NDMB

75
Q

Which anticholinesterase agents work the fastest of

edrophonium, pyridostigmine, neostigmine

A

Edro > neo > pyrido

- need to use atropine w/edro (atropine x BBB :( )

76
Q

What is the effect of acute hyperkalemia on NDMB and depolarizing agents?

A
  • NDMB: resistant

- Sux: sensitive b/c hyperkalemia hyperpolarizes cell membrane

77
Q

what % of receptors can still be blocked when 5 sec head lift is sustained?

A

50%

78
Q

effect of dexmedetomidine on HR and BP

A
  • dec HR

- dec BP

79
Q

effect of dexmedetomidine on RR?

A

minimal does not depress respiratory fxn

80
Q

MOA of local anesthetics

A
  • -inhibit VG-Sodium channels (at nodes of Ranvier) selectively when the nerves are actively firing so ↓ rate of depolarization… works at type A fibers (delta…pain, temp) and type c fibers (dorsal root…pain)
81
Q

which nerve fibers are more sensitive to LA blockade?

A
  • smaller, myelinated fibers are more sensitive to blockade (first things to go is sympathetics > pain > temp then touch)
  • mantle fibers also more sensitive (outer surface of the nerve)
82
Q

describe chemical properties of LA

A

all are weak bases

  • B from crosses membrane
  • BH+ is active @ sodium channels
83
Q

how does pKa influence LA action?

A
  • pKa closer to physiologic pH will have faster onset since molecule will have relatively more B form which can cross lipid membrane
  • bicarb can be added to LA injection to speed onset of action
  • onset of action proportional to pKa
84
Q

how will inc protein binding of LA influence its action?

A

duration of action is prolonged w/inc protein binding

85
Q

how are LA metabolized?

A
  • ester: plasma esterases pseudochoinesterase) in blood…fast
  • amide: liver p450…slow
86
Q

at which injection sites do LA’s absorb the fastest?

A

IV > tracheal > intercostal

87
Q

Seff of LA

A

*CNS develop before
CVS
- CNS excitatory: circumoral numbness 1st, blurred vision, then nervous/restless/agitated/twitching —> CNS depression, tonic-clonic seizures….
- then CV inhibitory: collapse and prolonged coding

88
Q

Tx of seizures in LAST vs LAST in general

A
  • benzos, hyperventilate (dec CO2 vasoconstricts cerebral vessels, dec CBF
  • lipid emulsion
89
Q

What is transient neurologic syndrome (TNS)? How to treat it

A
  • 12-24 hrs post spinal anesthesia
  • severe pain radiating down both legs but **NO sensory or motor deficits!
  • moreso w/Lido
  • Rx: NSAIDs
90
Q

Cardiac effects of LA (contractility, vasculature…which LA is most cardiotoxic?

A
  • inhibits Na channels so depresses contractility
  • all are vasodilators except cocaine
  • bupiv most cardiotoxic
91
Q

MOA of cocaine?

A

inhibits NE reuptake –> adrenergic stim (HTN, ventricular ectomy, MI)…Tx NTG then maybe BB

92
Q

which allergy can be observed with LA?

A

ester> amide b/c ester –> PABA (sunscreen)

93
Q

which LA can cause methemoglobinemia and what is the rx for it?

A
  • prilocaine (EMLA) + benzocaine
  • oxidize the Fe in heme to 3+ state in which it can’t bind O2
  • pulse ox falsely low twd 85%
  • Tx: methylene blue 1 mg/kg

Anesthesia Orientation (5 decks)

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