m and m 9 - IV anes Flashcards

(76 cards)

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
Which of the common Benzos has the slowest onset? Why?
Lorazepam, because it is the least lipid soluble
26
What pharmacokinetic property accounts for awakening after benzo administration?
Redistribution
27
True or false, benzos are highly protein bound?
True, up to 90-98%
28
What is the major organ associated with benzo biotransformation? Excretion?
Metabolism is liver, excretion is urine
29
Which benzo has an active phase 1 metabolite? Which can a second peak in plasma concentrations 6-12 hours post administration and why?
Diazepam and diazepam. Second peak is from enterohepatic circulation
30
Renal failure will cause prolonged sedation in patient who receive which benzo?
Midazolam, due to accumulation of alpha-hydroxymidazolam
31
Benzos do not depress cardiac function except when _____
Coadministered with opioids
32
What is the effect of benzos on respiration?
Will cause respiratory depression, ESPECIALLY if administered IV
33
What is the effect of benzos on cerebral oxygen consumption, cerebral blood flow and intracranial pressures?
Decreases all these parameters, but not to the extent of barbiturates
34
True or false, benzos cause muscle relaxation mediated at the neuromuscular junction?
False, the muscle relaxation is mediated at the spinal cord level
35
True or false, induction with benzos is as fast as seen with thiopental and propofol
False, it is significantly slower, with a slower recovery
36
What are three drugs that are known to interact with benzos?
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
What is the mechanism by which ketamine works, beyond NMDA antagonism?
Dissociative anesthetic, dissociates thalamus from limbic system
38
What drug of abuse is ketamine structurally similar to? How do potencies compare?
Phencyclidine, Ketamine is 10% as potent
39
What are specific clinical situations where ketamine is useful?
Trauma, hypovolemia - produces sympathetic stimulation
40
What is the induction agent that can be used IM for children and uncooperative adults?
Ketamine
41
What is a way to decrease the hallucinogenic effects of ketamine?
Co-admin with a benzo (e.g. Midazolam) or propofol
42
Awakening from ketamine is from [redistribution / metabolism]?
Redistribution
43
Ketamine has multiple metabolites that are chemically active. Which is chemically active? Where is it mainly metabolized?
Active metabolite is norketamine, metabolized in the liver
44
Major route of ketamine metabolite excretion is the ____
Kidney
45
Ketamine [increases/decreases] HR, CO and BP. These effects are mediated by [central/peripheral] effects, main mechanism?
Increases, unique among IV anesthetics Central effects Inhibit re-uptake of NE after release from nerve terminals
46
A group of patients to avoid ketamine bolus (i.e. induction dose) in? A group that it might benefit?
Avoid in patients with CAD - Increase myocardial work | Beneficial in patients with shock
47
Under what conditions does ketamine cause apnea?
If given as a bolus, especially with opioids on board
48
Generally, what is the effect of ketamine on the respiratory system?
It is a bronchodilator
49
What is the effect of ketamine on salivation? How is this mitigated?
Increases salivation, may need to pretreat with glycopyrrolate
50
What is the effect of ketamine on cerebral O2 consumption, blood flow and intracranial pressure?
It increases all these parameters
51
What is the effect of ketamine on the MSK system?
Can cause myoclonic activity, which may not be detected on EEG
52
What drugs can be used to attenuate the cardiostimulatory effects of ketamine?
Diazepam, midazolam
53
What happens if ketamine is co-administered with adrenergic antagonists?
This will unmask the cardio-depressive effects of ketamine, which are usually overwhelmed by its sympathetic stimulation
54
What is the major MSK effect associated with etomidate? What is the mechanism? How can this be attenuated?
30-60 % incidence of myoclonus Mechanism is disinhibition of CNS areas that control extrapyramidal motor activity Attenuate with opioids
55
What is the mechanism for awakening from etomidate (metabolism, redistribution, etc)?
Redistribution
56
Where is etomidate metabolized
Metabolized in the liver by hepatic microsomal enzymes and plasma esterases
57
Effects of etomidate on CV system?
Minimal
58
True Or false, etomidate by itself is enough anesthetic for direct laryngoscopy?
False, will end up with increased HR and BP from this stimulation
59
Effect of etomidate on Respiratory system?
Minimal, even induction doses of etomidate don't result in apnea
60
What is the effect of etomidate on SSEP?
It increases the amplitude of somatosensory evoked potentials
61
Etomidate is associated with [increased/decreased] PONV?
Assoc with increased PONV
62
What is the effect of etomidate on the endocrine system?
Inhibits enzymes assoc with cortisol and aldosterone synthesis. Long term use assoc with increased mortality in septic patients
63
True or false, egg allergy is a contraindication for propofol use?
False. Although propofol has egg lecithin, it is from the egg yolk, while most egg allergies are to egg white (albumin).
64
What way is propofol associated with sepsis?
The formulation can cause growth of microorganisms. Needs to be used within 6 hours of opening the container
65
How should propofol dosing be altered in the elderly? Why?
Decrease dose in the elderly, because of decreased Vd (less muscle mass)
66
What is propofol infusion syndrome?
Long Term use in critically Ill children or young NSG patients causes lipemia, metabolic acidosis and death
67
Effect of propofol on CV system?
Decrease BP, SVR, preload and cardiac contractility
68
Effects of propofol on the baroreflex?
Blunts this reflex, leading to more hypotension
69
In what group of patients is the CV depressant effects of propofol most marked? (3)
- Extremes of age - Beta blockers use - Impaired ventricular function
70
Effects of propofol on respiratory system?
blocks response to hypoxia and hypercarbia
71
True or false - propofol can cause release of histamine, causing wheezing in asthmatic patients
True, however, incidence of wheezing is less with propofol compared to etomidate and barbiturates
72
Effect of propofol in cerebral blood flow and intracranial pressure?
Decreases both
73
Significance of propofol use on cerebral perfusion pressure?
Can cause significant decrease in CPP, because it also decreases arterial pressure, therefore may need to support arterial pressure to maintain adequate CPP
74
Effect of propofol on PONV?
Decreases PONV
75
True or false, propofol is contraindicated in epileptic patients?
False, propofol has actually been used to treat seizures
76
Midazolam [increases/decreases] amount of propofol needed for anesthetic purposes
Decreases