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Apex Review > Intravenous anesthetics 2 > Flashcards

Intravenous anesthetics 2 Flashcards

1
Q

Ketamine: (select 3)
a. causes emergence delirium
b. agonizes the N-methyl-D-aspartate receptor
c. relieves somatic pain
d. increases the risk of depression
e. increases the cerebral metabolic rate of oxygen consumption
f. promotes bronchoconstriction

A

a. causes emergence delirium
c. relieves somatic pain
e. increases the cerebral metabolic rate of oxygen consumption

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2
Q

What is the primary mechanism of action of ketamine?

A

NMDA antagonist (creates a dissociated state)

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3
Q

What is the secondary mechanism of action of ketamine?

A

many secondary receptor targets including opioid, MAO, serotonin, NE, muscarinic, and Na+ channels

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4
Q

What is the onset of IV ketamine?

A

30-60 seconds

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5
Q

What is the onset of IM ketamine?

A

2-4 minutes

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6
Q

What is the onset of PO ketamine?

A

variable

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7
Q

What is the duration of action of ketamine?

A

10-20 minutes (may require 60-90 minutes to return to full orientation

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8
Q

What is the clearance of ketamine?

A

liver

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9
Q

What is the active metabolite of ketamine?

A

norketamine

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10
Q

What is the IV, IM, and PO induction doses of ketamine?

A

IV: 1-2 mg/kg
IM: 4-8 mg/kg
PO: 10 mg/kg

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11
Q

What is the opioid sparing dose of ketamine?

A

0.1-0.5 mg/kg or 1-3 mcg/kg/min.

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12
Q

What are the respiratory effects of ketamine?

A

maintains respiratory drive, increased oral secretions, bronchial dilation

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13
Q

What are the CV effects of ketamine?

A

Increased SNS tone, SVR, HR, and Cardiac output
increased pulmonary vascular resistance

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14
Q

What are the CNS effects of ketamine?

A

increased ICP, IOP, nystagmus, and analgesia
also causes emergence delirium & lowers the seizure threshold

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15
Q

Subhypnotic doses of ketamine may be used to

A

treat severe depression

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16
Q

Ketamine should be avoided with

A

acute intermittent porphyria

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17
Q

What is the pKa of ketamine?

A

7.5

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18
Q

Ketamine works by

A

dissociating the thalamus (sensory) from the limbic system (awareness)

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19
Q

Chronic ketamine use _______ the enzymes that metabolize it

A

induces

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20
Q

Ketamine is excreted via the

A

renal system

21
Q

Because ketamine increases the SNS tone it is useful in ______ but harmful in

A

useful if the patient is hemodynamically unstable but harmful if severe CAD

22
Q

Ketamine is a ________ myocardial depressant. The CV effects require an

A

direct; intact SNS

23
Q

The myocardial depressant effects of ketamine will be unmasked in patients with

A

depleted catecholamine stores (sepsis) or sympathectomy

24
Q

How does ketamine affect the CO2 response curve?

A

it does not significantly shift it

25
Q

Emergence delirium presents as

A

nightmares and hallucinations

26
Q

_______ are the most effective way to prevent emergence delirium

A

benzodiazepines

27
Q

Risk factors for emergence delirium include

A

age >15 years, female gender, ketamine dose >2 mg/kg and hx of personality disorder

28
Q

What kind of pain is ketamine good for?

A

somatic> visceral pain

29
Q

The analgesic properties of ketamine make it good for

A

burn patients (frequent dressing changes) and those with pre-existing chronic pain syndromes

30
Q

Chronic ketamine can cause

A

ulcerative cystitis

31
Q

The S enantiomer (esketamine) is marketed as a nasal spray that’s indicated for

A

treatment-resistant depression in adults as well as depressive symptoms in adults with major depressive disorder with acute suicidal ideation or behavior

32
Q

Describe ketamines protein binding.

A

smallest amount of plasma protein binding as compared to the other induction agents at 12%

33
Q

Central nervous system effects of etomidate include (select 2):
a. cerebral vasodilation
b. myoclonus
c. analgesia
d. decreased intracranial pressure

A

b. myoclonus
d. decreased intracranial pressure

34
Q

The mechanism of action of etomidate is

A

GABA-A agonist

35
Q

The onset of action of etomidate is

A

30-60 seconds

36
Q

The duration of action of etomidate is

A

5-15 minutes

37
Q

The clearance of etomidate is

A

liver + plasma esterases

38
Q

The active metabolite of etomidate is

A

none

39
Q

The induction dose of etomidate is:

A

0.2-0.4 mg/kg IV

40
Q

The respiratory effects of etomidate include

A

mild respiratory depression

41
Q

The CV effects of etomidate include

A

minimal- cardiac stability
SVR is decreased which accounts for a small reduction in BP

42
Q

The CNS effects of etomidate include

A

decreased ICP
decreased CMRO2
decreased CBF
no analgesia

43
Q

Rapid awakening with etomidate is due to

A

redistribution (NOT metabolism)

44
Q

Etomidate does not block the SNS response to

A

laryngoscopy; should consider an opioid or esmolol

45
Q

Which anesthetic agent increases mortality in the patient with Addisonian crisis?
a. etomidate
b. propofol
c. dexmedetomidine
d. midazolam

A

a. etomidate

46
Q

A single dose of etomidate suppresses adrenocortical function for

A

5-8 hours (some books say up to 24 hours)

47
Q

Etomidate is a known inhibitor of

A

11-beta-hydroxylase
17-alpha-hydroxylase

48
Q

Key side effects of etomidate include:

A

myoclonus (this is not a seizure)
etomidate does not cause seizures if the patient does not have a hx. of seizures
suppression of adrenocortical function for up to 24 hours
nausea & vomiting (greater than any other induction agent)
acute intermittent porphyria

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