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Mo and Mik > m and m 9 - IV anes > Flashcards

m and m 9 - IV anes Flashcards

1
Q

Barbiturates mechanism of action is ________, and their main location of action is _______

A

Increase duration of opening of GABA receptors

Reticular activating system

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2
Q

Thiopental and Thiamylal both have higher lipid solubility, greater potency and more rapid onset of action than other barbiturates. Whym structurally?

A

Substitution of oxygen with sulfur on C-2 increases lipid solubility, both thiopental and thiamylal have sulfurs at this position

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3
Q

While thiopental and thiamylal have higher lipid solubility, greater potency and more rapid onset, what is a disadvantage of these drugs? (3)

A
  • Very alkaline (pH over 10)
  • Unstable (2 week shelf life)
  • Painful on injection, assoc with venous thrombosis
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4
Q

What is the major reason for termination of effect of barbiturates, redistribution, metabolism or elimination?

A

Redistribution - mainly to muscle will decrease concentration of central barbiturates to about 10% of peak doses by 20-30 mins

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5
Q

What are some factors that can alter pharmacokinetics of barbiturates?

A
  • Low albumin (highly protein bound)
  • Hypovolemia (decrease Vd)
  • Acidosis
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6
Q

Under what situations is the duration of action / half life of barbiturates become context sensitive?

A

With prolonged administration (i.e. drips or redosing) the peripheral compartments become saturated, making duration of action dependent on elimination

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7
Q

Where is the principal site of metabolism of barbiturates? are the metabolites active or inactive?

A

Liver, water soluble inactive metabolites

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8
Q

Why is recovery from methohexital faster than from other barbiturates?

A

Methohexital has greater hepatic extraction and is therefore cleared more rapidly by the liver

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9
Q

What are the effects of barbiturates on cardiovascular system?

A

Can be unpredictable based on underlying volume status, autonomic tone. Generally, Will cause decreased BP (primary) and reflex tachycardia. Will maintain CO due to tachycardia and reflex increase in contractility

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10
Q

What are conditions that make patients prone to wide swings in CV function after barbiturates?

A
  • Hypovolemia
  • Poorly controlled hypertension
    Under these conditions, may be unable to maintain CO and would have wide swings in BP/HR. Can prevent with adequate preop hydration
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11
Q

Effect of barbiturates on respiratory function?

A

Will depress medullary ventilatory center, decreasing response to hypoxia and hypercapnia

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12
Q

True or false, barbiturates will blunt response to airway Instrumentation, decreasing propensity for bronchospams/laryngospasm.

A

False, in suceptible patients (asthmatics), barbiturates alone won’t block airway reflexes, therefore can have bronchospasm. Can also have laryngospasm in lightly anesthetized patients

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13
Q

What is the effect of barbiturates on cerebral blood flow, cerebral perfusion pressure, intracranial pressure, etc?

A

Will constrict cerebral vasculature, causing decrease in cerebral blood flow, cerebral blood volume and intracranial pressure. However, cerebral perfusion pressure increases because arterial blood pressure drops LESS than intracranial pressure

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14
Q

Although barbiturates decrease cerebral blood flow, why is this usually inconsequential?

A

It induces an even greater drop in cerebral O2 consumption

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15
Q

What are EEG changes seen with barbiturates?

A

Baseline low voltage fast activity (small doses) to high voltage slow activity with burst suppresion to electrical silence with maximal doses

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16
Q

True or false, barbiturates are also analgesic.

A

False, in some causes may lower pain threshold

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17
Q

True or false, barbiturates can cause muscle relaxation

A

False, can actually cause Involuntary skeletal muscle contraction e.g. methohexital

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18
Q

What is a disease state where barbiturates should absolutely be avoided?

A

Acute intermittent porphyria (can promote aminolevulinic acid synthetase, which increases formation of porphyrin)

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19
Q

What class of barbiturates are more likely to cause histamine release? Significance?

A

Thiobarbiturates (sulfure containing) can cause histamine release, significant for asthmatic or atopic patients

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20
Q

True or false, CNS depressants potentiate the effects of barbiturates.

A

True - alcohol, opioids and antihistamines are examples

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21
Q

Benzos vs barbiturates, how does function at GABA receptor differ?

A

Barbs increase duration of opening, benzos increase frequency of opening

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22
Q

What property (structural) of midazolam improves its water solubility (vs other benzos)?

A

Imidazole ring

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23
Q

Benzos, (midaz, loraz and diazepam) are available PO, IM and IV. What is the exception that isn’t FDA approved for PO use?

A

Midaz is not approved for PO use, despite the use in this route in pediatrics

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24
Q

Which of the commom benzos isn’t as well tolerated IM (Pain) with unpredictable absorption?

A

Diazepam

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25
Q

Which of the common Benzos has the slowest onset? Why?

A

Lorazepam, because it is the least lipid soluble

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26
Q

What pharmacokinetic property accounts for awakening after benzo administration?

A

Redistribution

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27
Q

True or false, benzos are highly protein bound?

A

True, up to 90-98%

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28
Q

What is the major organ associated with benzo biotransformation? Excretion?

A

Metabolism is liver, excretion is urine

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29
Q

Which benzo has an active phase 1 metabolite? Which can a second peak in plasma concentrations 6-12 hours post administration and why?

A

Diazepam and diazepam. Second peak is from enterohepatic circulation

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30
Q

Renal failure will cause prolonged sedation in patient who receive which benzo?

A

Midazolam, due to accumulation of alpha-hydroxymidazolam

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31
Q

Benzos do not depress cardiac function except when _____

A

Coadministered with opioids

32
Q

What is the effect of benzos on respiration?

A

Will cause respiratory depression, ESPECIALLY if administered IV

33
Q

What is the effect of benzos on cerebral oxygen consumption, cerebral blood flow and intracranial pressures?

A

Decreases all these parameters, but not to the extent of barbiturates

34
Q

True or false, benzos cause muscle relaxation mediated at the neuromuscular junction?

A

False, the muscle relaxation is mediated at the spinal cord level

35
Q

True or false, induction with benzos is as fast as seen with thiopental and propofol

A

False, it is significantly slower, with a slower recovery

36
Q

What are three drugs that are known to interact with benzos?

A

Cimetidine - decreases metabolism of diazepam (decreases activity of CYP-450)
Erythromycin - blocks metabolism of midazolam, increasing it duration of action
Heparin - increases free drug concentrations by displacing diazepam from free drug binding sites

37
Q

What is the mechanism by which ketamine works, beyond NMDA antagonism?

A

Dissociative anesthetic, dissociates thalamus from limbic system

38
Q

What drug of abuse is ketamine structurally similar to? How do potencies compare?

A

Phencyclidine, Ketamine is 10% as potent

39
Q

What are specific clinical situations where ketamine is useful?

A

Trauma, hypovolemia - produces sympathetic stimulation

40
Q

What is the induction agent that can be used IM for children and uncooperative adults?

A

Ketamine

41
Q

What is a way to decrease the hallucinogenic effects of ketamine?

A

Co-admin with a benzo (e.g. Midazolam) or propofol

42
Q

Awakening from ketamine is from [redistribution / metabolism]?

A

Redistribution

43
Q

Ketamine has multiple metabolites that are chemically active. Which is chemically active? Where is it mainly metabolized?

A

Active metabolite is norketamine, metabolized in the liver

44
Q

Major route of ketamine metabolite excretion is the ____

A

Kidney

45
Q

Ketamine [increases/decreases] HR, CO and BP. These effects are mediated by [central/peripheral] effects, main mechanism?

A

Increases, unique among IV anesthetics
Central effects
Inhibit re-uptake of NE after release from nerve terminals

46
Q

A group of patients to avoid ketamine bolus (i.e. induction dose) in? A group that it might benefit?

A

Avoid in patients with CAD - Increase myocardial work

Beneficial in patients with shock

47
Q

Under what conditions does ketamine cause apnea?

A

If given as a bolus, especially with opioids on board

48
Q

Generally, what is the effect of ketamine on the respiratory system?

A

It is a bronchodilator

49
Q

What is the effect of ketamine on salivation? How is this mitigated?

A

Increases salivation, may need to pretreat with glycopyrrolate

50
Q

What is the effect of ketamine on cerebral O2 consumption, blood flow and intracranial pressure?

A

It increases all these parameters

51
Q

What is the effect of ketamine on the MSK system?

A

Can cause myoclonic activity, which may not be detected on EEG

52
Q

What drugs can be used to attenuate the cardiostimulatory effects of ketamine?

A

Diazepam, midazolam

53
Q

What happens if ketamine is co-administered with adrenergic antagonists?

A

This will unmask the cardio-depressive effects of ketamine, which are usually overwhelmed by its sympathetic stimulation

54
Q

What is the major MSK effect associated with etomidate? What is the mechanism? How can this be attenuated?

A

30-60 % incidence of myoclonus
Mechanism is disinhibition of CNS areas that control extrapyramidal motor activity
Attenuate with opioids

55
Q

What is the mechanism for awakening from etomidate (metabolism, redistribution, etc)?

A

Redistribution

56
Q

Where is etomidate metabolized

A

Metabolized in the liver by hepatic microsomal enzymes and plasma esterases

57
Q

Effects of etomidate on CV system?

A

Minimal

58
Q

True Or false, etomidate by itself is enough anesthetic for direct laryngoscopy?

A

False, will end up with increased HR and BP from this stimulation

59
Q

Effect of etomidate on Respiratory system?

A

Minimal, even induction doses of etomidate don’t result in apnea

60
Q

What is the effect of etomidate on SSEP?

A

It increases the amplitude of somatosensory evoked potentials

61
Q

Etomidate is associated with [increased/decreased] PONV?

A

Assoc with increased PONV

62
Q

What is the effect of etomidate on the endocrine system?

A

Inhibits enzymes assoc with cortisol and aldosterone synthesis. Long term use assoc with increased mortality in septic patients

63
Q

True or false, egg allergy is a contraindication for propofol use?

A

False. Although propofol has egg lecithin, it is from the egg yolk, while most egg allergies are to egg white (albumin).

64
Q

What way is propofol associated with sepsis?

A

The formulation can cause growth of microorganisms. Needs to be used within 6 hours of opening the container

65
Q

How should propofol dosing be altered in the elderly? Why?

A

Decrease dose in the elderly, because of decreased Vd (less muscle mass)

66
Q

What is propofol infusion syndrome?

A

Long Term use in critically Ill children or young NSG patients causes lipemia, metabolic acidosis and death

67
Q

Effect of propofol on CV system?

A

Decrease BP, SVR, preload and cardiac contractility

68
Q

Effects of propofol on the baroreflex?

A

Blunts this reflex, leading to more hypotension

69
Q

In what group of patients is the CV depressant effects of propofol most marked? (3)

A
  • Extremes of age
  • Beta blockers use
  • Impaired ventricular function
70
Q

Effects of propofol on respiratory system?

A

blocks response to hypoxia and hypercarbia

71
Q

True or false - propofol can cause release of histamine, causing wheezing in asthmatic patients

A

True, however, incidence of wheezing is less with propofol compared to etomidate and barbiturates

72
Q

Effect of propofol in cerebral blood flow and intracranial pressure?

A

Decreases both

73
Q

Significance of propofol use on cerebral perfusion pressure?

A

Can cause significant decrease in CPP, because it also decreases arterial pressure, therefore may need to support arterial pressure to maintain adequate CPP

74
Q

Effect of propofol on PONV?

A

Decreases PONV

75
Q

True or false, propofol is contraindicated in epileptic patients?

A

False, propofol has actually been used to treat seizures

76
Q

Midazolam [increases/decreases] amount of propofol needed for anesthetic purposes

A

Decreases

Mo and Mik (9 decks)

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