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Neuro 2 > IV Anesthesia > Flashcards

IV Anesthesia Flashcards

1
Q

What is special about induction agents?

A

they have a short onset of action

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2
Q

List the induction agents used in IV anesthetics.

A

Thiopental
Propofol
Etomidate

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3
Q

List the additional agents (with longer onset of actions) used in IV anesthetics.

A
  • Ketamine
  • Diazepam, Lorazepam, Midazolam
  • Morphine, Meperidine, Fentanyl, Remifentanil
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4
Q

What are the 4 components of achieving balanced anesthesia?

A
  • Relieve Anxiety
  • Relax Muscles
  • Induce unconsciousness
  • Prevent secretions
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5
Q

How does balanced anesthesia contrast with “neurolept” analgesia?

A

Use of neurolept analgesia produces pain relief and provides a state of indifference (patient is responsive to command but is not compromised by situational anxiety)

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6
Q

What agents are used for neurolept analgesia?

A

Droperidol

Fentanyl

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7
Q

What does droperidol do to the patient?

A

state of indifference, anti-emetic, anti-convulsant

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8
Q

What does fentanyl do for the patient?

A

analgesia

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9
Q

What do you add to droperidol and fentanyl to get neurolept ANESTHESIA?

A

N2O

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10
Q

What other combination can you use for neurolept analgesia in preparation for surgery (dry secretions + provide analgesia)?

A
  • Atropine

- Opiate (morphine or meperidine)

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11
Q

What problem does the high level of lipid solubility pose for lipophillic (IV) anesthetics?

A

difficult to formulate them for injection

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12
Q

What are two “tricks” for making lipophillic anesthetics more soluble for injection?

A
  • Adjust pH
  • Use surfactant like propylene glycol or glycerol
  • Use 2nd generation pro-drugs that yield same pharmacologically active product only once they are inside the body
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13
Q

What problems may adding surfactant to a lipophillic anesthetic pose?

A

can sometimes give rise to a direct toxicity to the lining of the vein into which it is being administered; this can sometimes be avoided by diluting the drug and giving it more slowly

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14
Q

What is the main MOA for IV anesthetics?

A

reinforcing the inhibitory action of GABA and glycine

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15
Q

Which two IV anesthetics also have aneffect on the NMDA receptor for glutamate?

A

Ketamine (major inhibition)

Propofol (minor inhibition)

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16
Q

List the IV anesthetics that are major inhibitors of GABA.

A

Barbiturates
Propofol
Etomidate

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17
Q

List the IV anesthetics that are major inhibitors of glycine.

A

Propofol

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18
Q

MOA of barbiturates.

A

prolong the binding of GABA to the receptor (increases the strength of the inhibitory effects of endogenous GABA, so increase efficacy)

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19
Q

MOA of benzodiazepines.

A

Produce only an allosteric change in receptor activity, that is to say, they shift the dose response curve for GABA binding to the left, the increase potency but not efficacy.

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20
Q

True or false: barbiturates and benzodiazepines both have a “ceiling effect”

A

FALSE: With increasing dose barbiturates produce greater and greater CNS depression, ultimately leading to coma and death.

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21
Q

True or false: it is just as easy to overdose on barbiturates as it is on benzodiazepines.

A

FALSE: benzodiazepines are much safer and difficult to overdose with unless combined with drugs or alcohol (CNS depressants).

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22
Q

What is the benzodiazepine antagonist that can rapidly reverse acute toxicities if they occur?

A

flumazenil

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23
Q

What neurotransmitter is used in the consciousness pathway that activates the thalamus?

A

Ach

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24
Q

What part of the brain is activated by Histamine, Serotonin, and GABA in the consciousness pathway?

A

cortex

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25
Q

How do inhaled anesthetics compare to IV induction agents in terms of onset?

A

When compared with the onset of anesthesia with an inhaled anesthetic, the effects of an IV induction agent are almost instantaneous.

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26
Q

Where do IV anesthetics distribute to in the body?

A

Out of plasma into high flow organs then re-distributes to other organs (eventually adipose tissue if dosage is high enough)

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27
Q

What is happening when a patient awakens after IV anesthetia?

A

Awakening of the patient is due only to drug re-distribution, the timescale is far too short for metabolism or excretion to have had a meaningful impact upon drug load in the body.

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28
Q

What is the rate-limiting step in final elimination of the drug following surgery?

A

release of drug from adipose tissue

29
Q

What two IV anesthetics have half lives that increase dramatically with the duration of drug administration (due to accumulation and release from fat, metabolism and elimination)?

A

Diazepam

Thiopental

30
Q

What is the barbiturate used in IV anesthesia?

A

Thiopental

31
Q

MOA: Reinforce the inhibitory effects produced by endogenous GABA binding to its receptor system.

A

Etomidate

32
Q

MOA: Reinforce the inhibitory effects produced by endogenous GABA binding to its receptor system (can function like GABA at high concentrations). Also can block the binding of glutamate to its receptor

A

Propofol

33
Q

TOXICITY:

  • Depress cerebral blood flow, cerebral O2 consumption and ICP.
  • Slight increase in HR, inhibition of cardiac output.
  • Inhibit respiratory rate and minute volume.
  • Porphyria*
A

Thiopental

34
Q

What affect does thiopental have on CYPs?

A

induction

35
Q

TOXICITY:

  • Depress cerebral blood flow, cerebral O2 consumption and ICP.
  • Slight increase in HR, inhibition of cardiac output.
  • Inhibit respiratory rate and minute volume.
  • Anti-emetic*
A

Propofol

36
Q

What is propofol infusion syndrome?

A

fatal cardiovascular and organ-systems failure of unknown etiology with protracted use

37
Q

TOXICITY:

  • Depress cerebral blood flow, cerebral O2 consumption and ICP.
  • NO side effects with heart*
  • Inhibit respiratory rate and minute volume.
  • Inhibition of Steroidogenesis→ fatalities in elderly
A

Etomidate

38
Q

Which IV anesthetic is NOT used in the ICU?

A

Etomidate

39
Q

MOA: physical occulsion of the glutamate channel

A

Ketamine

40
Q

What are the major ways in which ketamine’s toxicity differs from the other IV anesthetics?

A
  • INCREASE in cerebral blood flow, NO EFFECT on cerebral O2 consumption, and INCREASE in ICP
  • INCREASE HR, CO and MAP
  • NO effect on respiratory system
  • Analgesic
  • Bronchodilatory
  • Hallucinations
41
Q

What does it mean when you call ketamine a “dissociative anesthetic”?

A

Analgesic that preserves pharyngeal and laryngeal reflexes (patients can be unconscious with eyes open)

42
Q

How do you treat ketamine hallucinations?

A

benzodiazepine

43
Q

Why aren’t benzodiazepines used to produce unconsciousness?

A

they have a long onset of effect

44
Q

What do benzodiazepines do to a patient?

A
  • Anticonvulsant
  • Antiemetic
  • NO ANALGESIA
45
Q

What are the 3 most commonly used benzodizapeines in IV anesthesia?

A

Diazpeam
Lorazepam
Midazolam

46
Q

Metabolism of midazolam.

A

Rapidly inactivated (halflife is 2-4 hours)

47
Q

Metabolism of diazepam.

A

3 active metabolites (halflife is 20-40 hours)

48
Q

Metabolism of lorazepam.

A

conugated for elimination

49
Q

What happens when venodilation (decreased venous return) or reduced CO occur with administration of a benzodiazepine?

A

immediate compensation by increasing HR and myocardial contractility. Also, blood is shunted from the spleen and intestines into the portal system to increase venous return

50
Q

When would the net effect of benzodiazepines be a depressant?

A

When compensatory reactions to venodilation and reduced CO cannot occur due to things like cardio-active drug preventing increases in HR or contractility or hemorrhage preventing blood mobilization from the periphery

51
Q

List some advantages of opioid therapy.

A
  • Absence of direct effects on the heart
  • Maintenance of regional blood flow autoregulation
  • Decreased airway reflexes (facilitates intubation)
  • Pain relieved but patient arousable
  • Non-organotoxic (no malignant hyperthermia)
52
Q

List some disadvantages of opioid therapy.

A
  • Incomplete amnesia
  • Histamine-related reactions
  • Increased blood requirements
  • Prolonged respiratory depression in ICU
  • CV instability (bradycardia, hypo- or hypertension; addition of N2O results in CV depression)
53
Q

Which opioid is favored for a 20 minute procedure?

A

fentanyl (short duration of action, onset in seconds, no N/V)

54
Q

Which opioid is favored for long lasting analgesia?

A

Morphine (poor BBB penetration but longer duration of action)

55
Q

List the CV effects of opiates.

A

Dependent on speed of injection and presence of other CV agents.

  • Hypotension (secondary to histamine release)
  • Hypertension (reflex with light analgesia)
  • R-A-A effect
  • Intense pressor effect with naloxone
56
Q

List the respiratory effects of opiates.

A

dose dependent respiratory depression due to unresponsiveness to CO2 in carotid bodies (reversible with naloxone or nalmefene)

57
Q

List the other toxicities of IV opiates.

A
  • Muscle rigidity (wooden chest)
  • Increased ICP
  • N/V, constipation, miosis
58
Q

What is the overdose triad for opiates?

A

Pinpoint pupils
Decreased respiration
Coma

59
Q

How does remifentanil differ from other opioid agents?

A

Remifentanil is an ultra-short acting drug that must be given by IV infusion. AND you must give analgesic coverage prior to terminating remifentanil infusion

60
Q

True or false: effects of remifentanil are cumulative.

A

FALSE

61
Q

What causes malignant hyperthermia?

A

Succinylcholine and volatile anesthetics leads to intracellular calcium release from the SR

62
Q

Who gets malignant hyperthermia?

A

most commonly in young men as a result of genetic predisposition

63
Q

What genetic predisposition exists for malignant hyperthermia?

A

Several genetic loci are implicated, most especially that of the ryanodine receptor (RYR1)

64
Q

What is the presentation of a patient with malignant hyperthermia?

A

heat generation, increase (X 2-3) in end tidal CO2, total body rigidity, unexpected tachycardia and tachypnea, respiratory and metabolic acidosis
OR
unexpected cardiac arrest

65
Q

How do you treat malignant hyperthermia?

A
  • Stop giving trigger agent
  • Cool patient
  • Acid-base support (hyperventilate with O2)
  • Dantrolene
66
Q

MOA of dantrolene.

A

permits the calcium to be repackaged back into the sarcoplasmic reticulum

67
Q

DDI of dantrolene

A

CCBs (which interfere with calcium entry at the cell surface)

68
Q

Prognosis for malignant hyperthermia.

A

in young males with undiagnosed cardiomyopathy (50% mortality)

Neuro 2 (11 decks)

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