IV Anesthetics Flashcards

1
Q

What is th MOA of ketamine?

A

NMDA receptor antagonist
Inhibits post synaptic receptors in the spinal cord
Dissociates the thalamus (sensory impulses) from the limbic system (awareness)

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2
Q

When are peak plasma levels of ketamine achieved when injected IM?

A

10-15 minutes

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3
Q

How lipid soluble is ketamine?

A

More so than thiopental and less protein bound so very fast brain uptake

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4
Q

What is distribution half life of ketamine?

A

10-15 minutes

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5
Q

How is ketamine biotransformed?

A

In the liver

It has a high elimination half-life

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6
Q

How are the end products of ketamine excreted?

A

Renally

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7
Q

What are the CV effects of ketamine?

A

Increase Bp, CO, HR, PAP, myocardial work

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8
Q

How does it cause the CV effects it causes?

A

By inhibiting the reputable of norepinephrine

By stimulating the central sympathetic nervous system

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9
Q

What does ketamine do to the heart at high doses?

A

It is a direct myocardial depressant by inhibition calcium

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10
Q

How is ventilatory drive affected with ketamine?

A

Minimal unless administered with opioids

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11
Q

What are the respiratory effects of ketamine?

A

Potent bronchodilator

Increased secretions

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12
Q

What are the cerebral effects of ketamine?

A

It increases CBF, CMRO2, and ICP except with BZDs

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13
Q

What does diazepam do to ketamine?

A

Prolongs it’s half-life

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14
Q

What does diazepam and midazolam due to ketamine’s cardiovascular effects?

A

it attenuated the cardio stimulators effects

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15
Q

What anesthetics does ketamine act synergistically?

A

Volatile anesthetics

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16
Q

What anesthetics is ketamine additive with?

A

Propofol, BZDs, GABA agents

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17
Q

What happens when using alpha and beta antagonists with ketamine?

A

The myocardial depressant effects are unmasked

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18
Q

What is the MOA of etomidate?

A

Depresses the RAS and mimics GABA

Disinhibition of the extra pyramidal tract

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19
Q

What are the side effects of etomidate?

A

Adrenal insufficiency
Myoclonus
PONV

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20
Q

What is unique about the structure of etomidate?

A

It has an imidazole ring like midazolam that gives it water solubility in acidic solutions?

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21
Q

What does etomidate have to be injected with?

A

Propylene glycol because it is water soluble in acidic solutions

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22
Q

What is the consequence of injecting with propylene glycol?

A

It burns

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23
Q

How is etomidate rapid onset?

A

Highly lipid soluble at physiologic ph

Large nonionized fraction

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24
Q

How is etomidate biotransformed?

A

Hepatic enzymes and plasma esterases

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25
How is etomidate excreted?
In the urine
26
What are the CV effects of etomidate?
Mild reduction in peripheral vascular resistance
27
What are the cerebral effects of etomidate?
Decreases CMR, CBF, ICP
28
What are the endocrine effects of etomidate?
Inhibition of the synthesis of cortisol and aldosterone
29
What does fentanyl do to etomidate?
It increases the plasma level and prolongs the elimination half-life of etomidate
30
What drugs decrease the myoclonus caused by etomidate?
Opioids
31
What is the MOA of Propofol?
It facilitates the inhibitory signals of GABA and increases the binding affinity for GABAa receptor.
32
Why must Propofol bottles be used in 6 hours?
Because the formulation can grow bacteria
33
How quickly do people wake up from Propofol and why?
2-8 minutes due to short initial distribution half-life
34
What is a determining factor in the amount of Propofol to use in a TIVA?
Age
35
How is Propofol biotransformed?
In the liver and other sites | Excreted in Urine
36
What is Propofol infusion syndrome?
Metabolic acidosis Lipemia Death Green urine
37
What are the CV effects of Propofol?
Decreased BP Impaired barorerceptor response Increase coronary sinus lactate
38
What are the factors associated with Propofol induced hypotension?
Age Large doses Rapid injection
39
What are the respiratory effects of Propofol?
Apnea Histamine release (but less bronchospasm than etomidate or barbs) Inhibits hypoxia vent drive
40
What are the cerebral effects of Propofol?
Decrease CBF and ICP | Also, decreases CPP due to its effect on BP
41
What does Propofol do to intraocular pressure?
Decreases it
42
What is the loading dose of dexmedetomidine
0.5-1mcg/kg over 10 minutes | 70 kg person = 35-70 mcg
43
What is the infusion rate of dexmedetomidine
0.4-1.2 mcg/kg/HR
44
What is the terminal half life of dex?
2 hours
45
What are the side effects of dex?
Hypotension Bradycardia Heart block
46
What properties does dex have?
Hypnotic Analgesic Opioid sparing Minimal respiratory depression
47
What is the mechanism of action of dexmedetomidine?
Alpha 2 agonist | Imidazoline agonist
48
How does dexmedetomidine differ from clonidine?
It is 8 times more specific at the alpha 2 receptors
49
How much time until onset of action of dexmedetomidine?
15 minutes (due to redistribution)
50
How long does it take for peak concentration to be achieved?
1 hour
51
What is the elimination half-life of dexmedetomidine at 0.2-0.7 mcg/kg/hr?
2-2.5 hours
52
What are the routes of administration of dexmedetomidine?
IV, oral, transdermal, IM
53
How is dexmedetomidine metabolized?
P450 enzymes via glucuronide conjugation and biorransformation Metabolites are excreted in urine
54
What is the major site by which dexmedetomidine causes analgesia?
Th spinal cord
55
What other sites produce the analgesic effect of dexmedetomidine?
Decreased conduction through A and C fibers Release of encephalin Alpha 2
56
What happens first with Propofol?
Hypnosis | Cardiovascular effects are delayed
57
How is ketamine metabolized?
P450
58
What kind of pain is ketamine effective for?
Nociceptive | Neuropathic
59
When is ketamine contraindicated?
``` ischemic heart disease Chronic heart failure Intracranial mass and spontaneous ventilation Open eye injury Vascular aneurysms Psychiatric disease ```
60
What does etomidate do to CPP?
Maintains it because it does not affect MAP
61
What drugs are painful on injection?
Etomidate Rocuronium Propofol
62
What does 11-betahydroxylase do?
It converts deoxycorticosterone to corticosterone and 11-deoxycorticosterone cortisol to cortisol Therefore blocking this enzyme inhibits cortisol and aldosterone production
63
How is dexmedetomidine metabolized?
Extensively in the liver
64
What is preserved with dexmedetomidine
Hypercapnic ventilatory response so causes limited respiratory at high doses
65
Why doesn't liver disease affect Propofol metabolism?
Due to the high extraction ratio of Propofol (all of Propofol that reaches the liver will be metabolized, regardless of enzyme induction
66
Which drugs depend on liver blood flow?
``` Propofol Ketamine Lidocaine Metoprolol Diltiazem Propanolol Fentanyl ```
67
What is unique about Propofol metabolism?
Some of it is extra hepatic because the extraction ratio is more than the cardiac output that the liver sees
68
How should Propofol be dosed for induction?
Based on lean body weight
69
How should Propofol be dosed on infusion?
TBW
70
What are the risk factors for Propofol infusion syndrome?
Kid 4-5mg/kg/hr or 65-80 mg/kg/min greater than 24 hours Concurrent catecholamines or corticosteroid administration Concurrent neurological or inflammatory disease Concurrent lipid metabolism disorders
71
What is the pathophysiology of Propofol. Infusion syndrome?
Impaired fatty acid metabolism and utilization leading to anaerobic metabolism Causes cardiac and skeletal muscle damage, renal failure, rhabdo, pancreatitis
72
What is fospropofol?
A prodrug that must be first metabolized to Propofol
73
What is the onset of action of fospropofol?
4-10 minutes
74
What is the principal pathway of metabolism of Propofol?
Glucoronidation
75
What happens to the rate of induction in a left to right cardiac shunt?
It would decrease because there is recirculating of blood in the pulmonary system
76
What happens to rate of induction in a right to left cardiac shunt?
It would increase because more blood is bypassing the pulmonary circulation and going straight to the brain
77
What are the risk factors for ketamine emergence delirium?
``` Older age Female Neurotic Outgoing Larger bolus dose Has dreams at home ```