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NUNA 680 - Pharm > Pentothal, Brevital, Etomidate, & Dexmedetomidine > Flashcards

Pentothal, Brevital, Etomidate, & Dexmedetomidine Flashcards

1
Q

Define “intravenous anesthetic agent.”

A

Typically, a drug injected IV to induce unconsciousness at the beginning of general anesthesia, but allows rapid recovery after the end of its effect.

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2
Q

By which MOAs does an intravenous anesthetic agent typically work?

A

It changes level of consciousness by depressing the reticular activating system either by enhancing inhibition properties of GABA or inhibiting the NMDA excitatory synapses.

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3
Q

Which IV anesthetic agent is the “gold standard” to which all other agents are compared?

A

Thiopental (Sodium Pentothal)

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4
Q

What is the primary mechanism for terminating the central effect of IV induction agents?

A

Their redistribution from the central, highly-perfused compartment to the larger and less-well perfused “peripheral” compartments (skeletal muscles)

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5
Q

What is the alpha phase of pharmacokinetics?

A

Redistribution - plasma concentration declines so drug moves out of vessel-rich central group and to peripheral group

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6
Q

What is the beta phase of pharmacokinetics?

A

Elimination - metabolism and excretion

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7
Q

Describe the “ideal” IV anesthetic.

A

Water soluble/chemically stable/IV fluid compatible
Rapid onset w/o myoclonus or unpredictable CV or CNS SE
Anticonvulsant/antiemetic/analgesic/amnestic
Rapid onset (lipid soluble) and predictable recovery
No impairment of renal/hepatic function, steroid synthesis, or teratogenicity
No pain on injection
Low potential for histamine release/anaphylaxis
Rapidly metabolize to inactive substances/minimal accumulation
“Dialable”/rapidly responsive to titration
Cerebroprotective - dec metabolism in proportion to dec CBF, no inc in ICP
No hangover/HA

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8
Q

What drug class is thiopental?

A

Barbiturate - Thiobarbiturate (sulfur)

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9
Q

Describe the 2.5% preparation of thiopental

A

2.5% sodium salt (25 mg/ml) is water-soluble but highly alkaline pH 10.5 therefore bacteriostatic

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10
Q

How long will thiopental stay stable after reconstituted from a powder?

A

6 days at room temperature, 2 weeks in the refrigerator

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11
Q

What can occur when thiopental is mixed with opioids, catecholamines, NMB, and LR, which are more acidic? If injected intraarterially?

A

Precipitation!!

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12
Q

Is thiopental (2.5%) painful upon injection?

A

Minimally; irritating if extravascular but NOT necrotic

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13
Q

What is the MOA of thiopental?

A

Increases duration of GABA on its receptor (Cl- channels open longer –> hyperpolarization) AND mimics GABA on its receptor (directly causing Cl- channels to open)

Also activates glutamate, adenosine, and nACh receptors (SNS causes hemodynamic depression & desensitizes nACh receptors to depolarizing effects of ACh (large doses)

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14
Q

How do the hemodynamic effects of thiopental compare to propofol?

A

They are minimal in magnitude

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15
Q

What are the cardiovascular effects of thiopental?

A

Transient decrease in BP (arterial AND venous); increase in HR (carotid sinus baroreceptor - can be absent with beta blockade or hypovolemia); peripheral vasodilation (venous pooling, decreased venous return/CO) usually offset by sympathetic activation; HISTAMINE RELEASE.

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16
Q

Can you decrease CV effects of thiopental through SLOW administration?

A

No

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17
Q

How do myocardial depressant effects of thiopental compare with volatile agents?

A

Less; no direct myocardial depressant effect.

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18
Q

What are the respiratory effects of thiopental?

A

Decreases sensitivity of medullary ventilatory center to CO2 stimulation; respiration returns with small TV and slow RR; AW reflexes intact

Apnea potentiated with opioids, benzos, and other depressant drugs

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19
Q

Why might thiopental require concurrent administration of propofol for a general anesthetic?

A

Because airway reflexes remain intact, allowing the possibility of a laryngospasm

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20
Q

What are the CNS effects of thiopental?

A

Decreased ICP by cerebral vasoconstriction; decrease CMRO2 by 55%

Hypotension with large doses can decrease CPP below adequate

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21
Q

How much does thiopental decrease CMRO2?

A

55%

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22
Q

By what mechanism and under what conditions does thiopental provide cerebral protection?

A

Mechanism: reduction of CMRO2 is greater than decrease in CBF (demand less than supply)

Conditions: Successful in incomplete cerebral ischemia (CBP, hypotension, circ. arrest); NO protection for global ischemia (cardiac arrest)

Doses adequate to provide cerebral protection cause vasodilation/myocardial depression; hypothermia does same thing without these SE.

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23
Q

Does thiopental cause liver and kidney damage?

A

No; slight decrease in flow d/t reduction in BP, but no damage

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24
Q

What blood condition contraindicates use of methohexital and thiopental?

A

Porphyria; stimulates/increases production of heme

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25
Q

Does thiopental cross the placenta? If so, is it safe for the fetus?

A

Yes; maternal doses up to 4 mg/kg are safe for fetus

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26
Q

Dr. Cahoon knew of a resident who died in the call room from an overdose of which drug?

A

Thiopental; can cause tolerance and physical dependence

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27
Q

Thiopental can cause _________ and __________ reactions. (negative)

A

anaphylactoid; anaphylaxis

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28
Q

What is thiopental’s redistribution 1/2 life?

A

2-4 minutes

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29
Q

What is thiopental’s elimination 1/2 life?

A

10-12 hours (long beta phase!)

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30
Q

Thiopental (is/is not) highly lipid soluble and (non/ionized) at physiologic pH.

A

is lipid soluble; nonionized

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31
Q

Thiopental is __% protein bound.

A

85; protein binding effects the diffusion rate of the drug - the more bound, the slower the diffusion

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32
Q

What is the dose of thiopental?

A

3-5 mg/kg (less for elderly and early pregnancy)

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33
Q

What is the onset of thiopental?

A

30 seconds

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34
Q

What is the duration of thiopental?

A

5-10 minutes

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35
Q

How many redistribution 1/2 lives are required for termination of effect?

A

3-4

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36
Q

Summarize the properties of thiopental as an IV anesthetic.

A

“Gold standard,” minimal CV effects, good cerebral protection, minimal pain on injection, hangover, moderate emetic, precipitation

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37
Q

What is the drug class of methohexital?

A

Barbiturate - oxybarbiturate (less lipid soluble than thiopental)

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38
Q

What is the advantage of 1% methohexital over 2% methohexital?

A

Decreased risk of venous thrombosis

39
Q

How long is refrigerated methohexital stable after reconstitution?

A

6 weeks

40
Q

What is the MOA of methohexital?

A

Increases duration of GABA on its receptor (Cl- channels open longer –> hyperpolarization) AND mimics GABA on its receptor (directly causing Cl- channels to open)

Also activates glutamate, adenosine, and nACh receptors (SNS causes hemodynamic depression & desensitizes nACh receptors to depolarizing effects of ACh (large doses)

41
Q

What limits the central effects of methohexital and thiopental?

A

Redistribution to the peripheral compartment

42
Q

Methohexital is metabolized _-_x faster than thiopental due to ______ ______ __________ which causes _________ VOD and keeps ____ methohexital in the plasma.

A

3; 4; decreased lipid solubility; smaller; more

43
Q

Since methohexital is metabolized faster than thiopental, this results in…

A

Less hangover and more rapid awakening after repeated doses

44
Q

What is the elimination 1/2 time for methohexital?

A

~4 hours (much shorter than thiopental ~12 hours)

45
Q

What is the advantage of methohexital over pentothal?

A

More rapid recovery

46
Q

What is the disadvantage of methohexital compared to pentothal?

A

More excitatory activity - myoclonus, hiccoughs; infusions associated with postop seizures!!!

47
Q

How can you prevent the excitatory nervous activity associated with methohexital?

A

Small doses (up to 1.0-1.5 mg/kg?), pretreat with opioids

48
Q

Methohexital is ___x more potent than thiopental due to _______ nonionized at blood pH.

A

2.5; higher percentage

49
Q

How do CV effects of methohexital differ from pentothal?

A

Similar but perhaps less hypotension due to better preserved HR; NO HISTAMINE RELEASE

50
Q

How do CNS effects of methohexital compare to pentothal?

A

Slightly less cerebral protection; increased excitatory activity

51
Q

Methohexital and thiopental can exacerbate acute intermittent _______.

A

porphyria

52
Q

Induction dose of methohexital

A

1-2 mg/kg (less in elderly)

53
Q

Sedation dose of methohexital

A

0.2-0.4 mg/kg

54
Q

Onset of methohexital

A

30 seconds

55
Q

Duration of methohexital

A

5-10 minutes

56
Q

Distribution 1/2 time of methohexital

A

5.6 minutes

57
Q

Elimination 1/2 time of methohexital

A

2-5 hours (much faster than thiopental!)

58
Q

Summarize how methohexital compares to thiopental

A

More rapid recovery, more excitatory activity (hiccoughs), moderate emetic (same as pentothal)

59
Q

Chemical structure of etomidate?

A

Carboxylated imidazole [ring]-containing compound; water soluble at acidic pH and lipid soluble at physiologic pH

60
Q

Etomidate is sometimes dissolved in _______ ________ at what pH? Causes what? Concentration? Alternative preparation?

A

propylene glycol; 6.9; pain on injection; 0.2%; fat emulsion (minimal pain on injection)

61
Q

What is the MOA of etomidate?

A

Mimics inhibitory effects of GABA by increasing receptor affinity to GABA, depressing RAS

62
Q

How do neuromotor effects compare with etomidate vs. thiopental?

A

Etomidate has excitatory activity causing myoclonus in 30-60% of patients (50-80% without benzos, opioids, or SMALL etomidate dose); MOA - disinhibition of subcortical structures that usually suppress extrapyramidal motor activity

63
Q

What is the cardiovascular SE profile like for etomidate?

A

Most minimal SEs of all IV anesthetic agents! Slight decrease in MAP, SVR, least inotropic depression, no decrease in renal BF, NO HISTAMINE

64
Q

What are the respiratory effects of etomidate?

A

Less than barbiturates

Decrease TV, increase RR (opposite of opioids); airway reflexes maintained, can maintain spontaneous ventilation.

Increased depression with rapid injection or combo with volatile or opioids.

65
Q

What are the CNS side effects of etomidate?

A

Only decrease CMRO2 35-45% (thiopental 55%); CPP well maintained; excitatory (avoid in seizure patients - some myoclonus does have EEG seizure activity with etomidate).

Prevent myoclonus with opioid premedication.

66
Q

What is the major disadvantage of etomidate?

A

Causes adrenocortical suppression! :(

67
Q

What is the MOA of etomidate adrenocortical suppression?

A

Inhibits conversion of cholesterol to cortisol (11-beta-hydroyxlation reaction)

68
Q

How long does it take cortisol and aldosterone levels to decrease after etomidate injection?

A

30 minutes

69
Q

How long does adrenocortical suppression last with etomidate?

A

4-8 hours (up to 48 hours???)

70
Q

What patients need to have an appropriate stress response that could theoretically be prevented by etomidate?

A

Septic and bleeding patients

71
Q

What pharmacokinetic characteristics cause etomidate’s fast onset?

A

High lipid solubility, large nonionized percentage

72
Q

What limits etomidate’s duration of action?

A

Redistribution (like barbiturates)

73
Q

How does etomidate’s rate of clearance compare to thiopental? What causes this difference?

A

It is 5 times faster than thiopental. Metabolism is by hepatic microsomal enzymes and plasma esterases.

74
Q

What is the dose of etomidate?

A

0.3 mg/kg

75
Q

What is the onset of etomidate?

A

14-45 seconds (similar to barbiturates ~30 sec)

76
Q

What is the duration of etomidate?

A

3-12 minutes

77
Q

What is the distribution 1/2 time of etomidate?

A

2-4 minutes (same as thiopental)

78
Q

Elimination 1/2 time of etomidate?

A

2-5 hours (like methohexitol)

79
Q

Summarize the characteristics of etomidate as an IV anesthetic.

A

Pain on injection, emetic, adrenocortical suppression, GOOD CV support, excitatory CNS activity (myoclonus, seizures)

80
Q

What is the drug class of dexmedetomidine?

A

Alpha2-adrenergic agonist

81
Q

How does dexmedetomidine compare to its cousin clonidine?

A

8x more selective for alpha2 receptors

82
Q

What is the MOA of dexmedetomidine?

A

In spinal cord and pontine locus ceruleus:

Hyperpolarization with efflux of K+
Reduce NE release due to prevention of Ca+ release in presynaptic area
Decrease cAMP concentration by inhibiting adenylyl cyclase

83
Q

What may happen with a dexmedetomidine loading dose due to its effect on both alpha2Beta and alpha2Alpha receptors?

A

Hypertension

84
Q

What other CV effects may occur with an infusion of dexmedetomidine?

A

Decrease HR (be careful with heart block!), BP (hypotension more common with infusion vs bolus and in those with high sympathetic tone such as diabetic, elderly, hypovolemic)

85
Q

Describe the sedation provided by dexmedetomidine.

A

Sedation similar to physiologic sleep, easily rousable; NOT approved for GA.

Little depression of ventilation, can use to wean patient off vent.

Less delirium than benzos, less grogginess.

Amnesia not reliable.

86
Q

What effect does dexmedetomidine have on MAC?

A

Greater than 905 reduction with halothane; 35-48% with isoflurane

87
Q

What factor makes dexmedetomidine an appealing sedative for use in MRI?

A

Does not cause apnea which is good because you can’t be in the room with the patient in MRI.

However, requires longer recovery than propofol and requires a higher dose for MRI (2 mcg/kg/hr vs normal 1)

88
Q

What medication is appropriate for an awake fiberoptic intubation during which you need the patient cooperative and sedated but not apneic?

A

dexmedetomidine

89
Q

What is dexmedetomidine’s effect on secretions?

A

Antisialagogue

90
Q

What is the redistribution 1/2 life of dexmedetomidine?

A

6-8 minutes

91
Q

What is the loading dose of dexmedetomidine? Infusion dose?

A

0.5-1 mcg/kg over 10 minutes; 0.2-1.4 mcg/kg/hr

92
Q

What property of dexmedetomidine allows it to serve as an adjunct to spinal and supraspinal anesthesia or in multimodal analgesia?

A

The analgesic effect

93
Q

What is the effect of dexmedetomidine on thermoregulation?

A

Reduces shivering through alpha2 effects; inhibits central thermoregulatory control and vasoconstriction, making patient more susceptible to hypothermia

94
Q

What effect does dexmedetomidine have on PONV? Emergence delirium?

A

Decreases; prophylactic

NUNA 680 - Pharm (8 decks)

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