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SRNAPharmacology II > Barbiturates/non-barbiturates Agents > Flashcards

Barbiturates/non-barbiturates Agents Flashcards

1
Q

Why are barbiturates not classify as either short acting or long acting

A
  1. Residual plasma concentrations last for hours even after “ultra short-acting” drug are given for anesthesia
  2. More drug will convert a short acting to long actin
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2
Q

Ultra short Barbiturates

A

Methohexital

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3
Q

They are _________solutions so they are incompatible with _____, _____ and _______ (NOC)

A

Alkaline salts

Opioids, catecholamines, NMB agents

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4
Q

Methohexital usually ___% with a ph of ____-

A

1; 10

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5
Q

Barbiturates comes from a combination of the

A

urea and malonic acid.

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6
Q

Methohexital ________causes _____activity manifested by __________

A 
Methyl radical (methohexital), causes convulsive activity
manifesting as involuntary muscle movement
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7
Q

**Mechanism of action for Methohexital

A
  • Works on neurotransmitter GABA in the CNS/ potentiates effect (inhibitory neurotransmitter)
  • Produces sedative-hypnotic effects
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8
Q

GABA to cell work by?

A

Hyperpolarize post synaptic cell

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9
Q

Barbiturates and propofol on GABA, Mechanism of action

A

Barbiturates and propofol
⇩ dissociation of GABA from receptor
⇧duration of GABA activated opening of chloride channels

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10
Q

Barbiturates on RAS ______

• RAS promotes_________

A
  • Uniquely depress reticular activating system(RAS)
  • wakefulness(⇧ Brain activity)
  • leading to hypotension due to venodilation
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11
Q

At high doses , barbiturates does what?

A

⇩ sensitivity of postsynaptic membranes to acetylcholine inhibits Ach to bind to Ach receptors enhances muscle relaxation

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12
Q

***Fast awakening with methohexital is because

A

*****redistribution from the brain to inactive tissues

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13
Q

Elimination of methohexital is dependent on ______%metabolized

A

metabolism• <1% recovered unchanged in the urine (99% metabolized)

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14
Q

Methohexital
Effect site equillibration is _________
and Context sensitife half life is ________due to

A

Rapid effect site equilibration

prolonged ; drug sequestered in fat and skeletal muscle reenters the circulation

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15
Q

Protein binding parallels_________

• Decreased protein binding due__________ such as aspirin can =

A
  • lipid solubility
    -to displacement by drugs
  • enhanced drug effects
    ⇧ drug sensitivity in pts with uremia and cirrhosis
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16
Q

what can decrease protein binding in uremic patients ?

A

⇩ protein binding in uremic pts may be due to
competitive binding of nitrogenous waste products
(displacement by metabolites)

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17
Q

_________cause ⇩ protein binding in pts with_________

A

Hypoalbuminemia ;cirrhosis of the liver

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18
Q

Most important determinant of DISTRIBUTION

A

Lipid solubility

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19
Q

2 Other determinants of distribution other than lipid solubility

A

Ionization

Protein binding

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20
Q

For Methohexital the most important determinant of distribution is

A

Lipid solubility

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21
Q

__________is a major determinant of delivery- change in blood volume/flow may alter distribution

A

Tissue blood flow

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22
Q

***Methohexital in the brain undergo_______within _______
What is the mechanism of early awakening?

A

Methohexital undergo maximal brain uptake within
30 seconds
•Redistribution is the mechanism for early awakening after SINGLE IV dose

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23
Q

_________is the most prominent site for initial redistribution of high lipid soluble barbiturates

A

Skeletal muscle

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24
Q

During distribution • Initial ____plasma concentration________due to
• Equilibration with skeletal muscle is achieved in _______after IV dose of ________

A

⇩ ; uptake into skeletal muscles

15 minutes after IV does thiopental

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25
Q

• Need to ____dose with muscle ______perfusion (shock), _____muscle mass (elderly)

A

⇩;⇩; ⇩

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26
Q

Metabolism of Methohexital
Metabolized where?
Reserve capacity of liver is _______therefore takes ______dysfunction before you have a prolonged effect.

A

Oxybarbiturates metabolized only in hepatocytes
• Reserve capacity of liver is large -> takes extreme
hepatic dysfunction before a prolonged effect

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27
Q

Methohexital vs thiopental which has more rapid metabolism? reflecting less________
Therefore______ remains in plasma= more available for
metabolism

A

methohexital rapid ;lipid soluble

More

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28
Q

Methohexital Hepatic clearance is______than thiopental
• Early awakening after single IV dose is dependent
on _________

A

3-4 X more than thiopental

redistribution

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29
Q

For methohexital _________plays a greater role in terminating effects, than________
• Metabolism plays a role in time required for
complete____________

A

Metabolism; THIOPENTAL ;

psychomotor recovery

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30
Q

• Psychomotor functions recover faster with-______than ________

A

methohexital than thiopental

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31
Q

For Methohexital vs Thiopental: recovery time ?

A

more predictable doses than thiopental

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32
Q

What is more dependent on changes in cardiac output and hepatic blood flow ?

A

Hepatic clearance

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33
Q

Barbiturates are excreted where?

A

Renal system

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34
Q

All barbiturates filtered by renal glomeruli:
What limits filtration?
What favors reabsorption into circulation ?
What % is excreted unchanged?

A

• High degree of protein binding limits filtration
• High lipid solubility favors reabsorption of filtered
drug back into circulation
• <1% methohexital is excreted unchanged in urine

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35
Q

_________ and _________are similar for thiopental and methohexital

A

Distribution half time and Vd

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36
Q

_______ and _______differ for methohexital and Thiopental

A

• Elimination half time and clearance

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37
Q

Why is methohexital shorter elimination half time due to ?

A

• Methohexital’s shorter elimination half time due to

it’s greater hepatic clearance

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38
Q

Elimination half time of methohexital is_____

Thiopental ______

A

about 4 hours; 11 hours

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39
Q

• Principal uses of methohexital

A

Induction anesthesia
• Treatment of ⇧ ICP
• Electroconvulsive therapy
• Seizure treatment

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40
Q

Barbiturate use is declining due to 5 main reasons among many

A

Lack specificity of effect in the CNS
Lower therapeutic index than benzodiazepines
Result in tolerance more easily than benzodiazepines
Greater liability for abuse
Paradoxical reaction in elderly

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41
Q

What drug has replaced barbiturates?

A

Propofol has replaced barbiturates

• Especially when rapid awakening is desired

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42
Q

This drug has more rapid recovery of consciousness

A

Methohexital

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43
Q

What is the only barbs with actions sufficient to offer an alternative to other IV induction agents?

A

Methohexital

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44
Q

2 Disadvantages of Methohexital?

A

⇧ incidence of excitatory phenomena such as involuntary skeletal muscle movements(myoclonus) and hiccough
• High dose associated with seizures in 1/3 patients

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45
Q

The involuntary skeletal muscle movement is -_____dependent therefore premedicate with

A

• Incidence-dose dependent, can ⇩ by premedicate

with opioids & use optimum dose of (1-1.5mg/kg)

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46
Q

Potency and dose
Methohexital vs thiopental? which one more potent and why?
when dose redistribution terminates action ?

A

Methohexital is 2.5 x more potent than thiopental
⇧ potency is due to lower ionization at physiologic
pH/ Alkaline=burns on injection
- about 8.5 minutes

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47
Q

What is the dose of Methohexital dose?

A

1-1.5mg/kg

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48
Q

High dose response curve?

A

NMB agents, 80-90% of receptors to exert an effect.

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49
Q

Alkaline drugs

A

Burn on injection

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50
Q

For uncooperative patients, give methohexital

A

rectally ; 20-30mg/kg

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51
Q

Other uses of Methohexital for neurology ? USe to during

A

Useful to induce seizures
• ECT
• Temporal lobe resection of seizure producing
tissue

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52
Q

Barbs used to_____ICP, along with_____&_______. ⇩

• Barbs _____metabolic oxygen requirements

A

⇩ hyperventilation & diuresis

⇩

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53
Q

How does barb decrease ICP?

A

by decrease cerebral blood volume through drug
induced cerebral vasoconstriction and associated ⇩
in cerebral blood flow

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54
Q

Barb on EEG and head trauma patient

A
  • Isoelectric EEG=max barb effect and ⇩ CMRO2 55%

* No improved outcomes for head trauma pt

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55
Q

Barb High dose =________ = ____cerebral perfusion

pressure

A

hypotension;⇩

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56
Q

Methohexital

• Dose required to suppress EEG results in _________ & ___________ similar to isoflurane (2 MAC)

A

vasodilation & myocardial depression

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57
Q

When profound EEG depression is desired? _____ preferred over ____

A

Barbs is preferred to Isoflurane if profound EEG depression is desired

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58
Q

Methohexital Cerebral protection?
Improve brain survival in cardiac patients?
Not recommended for routine _____surgery due to _____ and _________
_______may be protective without prolonging recovery.

A

No improved brain survival in cardiac arrest
patients
• Not recommended for routine use during cardiac
surgery due to ⇧ need for inotropic support and
prolonged recovery time
• Hypothermia may be more protective without
prolonging recovery

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59
Q

Methohexital Side Effects : Cardiac

A

CV depression
Normovolemic pt- transient 10-20 mmHg ⇩ in BP
and offset by compensatory 15-20BPM ⇧ in HR
Overdose or large dose to ⇩ ICP may cause direct
myocardial depression

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60
Q

Methohexital on induction
What happens to BP?
3 reasons?

A

Induction- mild, transient ⇩ BP due to peripheral
vasodilation (mostly venous), reflecting depression of the medullary vasomotor center and ⇩ sympathetic nervous system outflow

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61
Q

Barb and hypovolemic patients?

2 classes of drugs that worsen conditions?

A

Caution , hypotension may occur
Beta blockers and centrally acting alpha 2 agonists
may accentuate this response= more profound
shock

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62
Q

For induction of anesthesia, barbs produce a dose
dependent depression of _______and ______ventilatory centers.
• Leads to 3 things?

A

depression of the medullary and pontine ventilatory centers
⇩ response to hypercarbia
• Low respiratory rate
• Low tidal volumes

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63
Q

2 drugs with higher risk for MH

A

Succinylcholine

Volatile anesthetics

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64
Q

⇧_______when used with other CNS depressant

drugs used for preop medication

A

Apnea risk

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65
Q

Large doses needed to suppress _____and ________

A

laryngeal reflexes & cough

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66
Q

May occur during intubation?

A

Laryngospasm or bronchospasm may occur during intubation attempts- no LMA

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67
Q

Induction dose doesn’t alter_________

Induced enzyme induction =

A

-postop LFT’s
accelerated metabolism of other drugs (oral anticoagulants, phenytoin, tricyclic antidepressants) or endogenous substances (corticosteroids, bile salts and vit K)

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68
Q

• Stimulate ________in liver metabolism (____)

after 2-7 days sustained drug administration

A

⇧ in liver metabolism (enzyme inducer)

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69
Q

Barbiturates stimulate activity of ___________ which leads to _____Production of ______ and may exacerbate which condition ?

A

• Stimulate the activity of mitochondrial enzyme
• This ⇧ production of Heme, and may exacerbate
acute intermittent porphyria

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70
Q

Barbiturates, avoid in pt with _____________

A

Avoid in pt with Acute Intermittent Porphyria
• Also enhance barbs own metabolism which
contributes to tolerance

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71
Q

Barbiturates lead to a Modest _____in renal blood flow and glomerular filtration rate due to

A

⇩; ⇩ in BP and CO

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72
Q

Does barbiturate use for induction of anesthesia produce renal damage?

A

• Barbiturate use for induction of anesthesia does not

produce renal damage

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73
Q

Barbiturates and placenta?

Fetal plasma conc vs. maternal concentration

A

Barbiturates readily cross the placenta
• Fetal plasma concentrations are significantly lower
than maternal plasma concentrations

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74
Q

______occurs earlier than enzyme induction
At maximal tolerance the required effective dose
increases _______

A
  • Acute tolerance

- six-fold

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75
Q

Tolerance to the sedative effects occurs

A

sooner and is greater than the anticonvulsant and lethal effects

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76
Q 
As tolerance to the sedative effects\_\_\_\_ the
therapeutic index\_\_\_\_\_\_(narrow therapeutic index)
A

⇧; ⇩

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77
Q

With intra-arterial injection there is ?
Can cause _____ and ________
Risk ___with ___drug concentration

A

Immediate, intense vasoconstriction and excruciating pain that radiates along the distribution of the artery
Gangrene and permanent nerve damage may result
Risk ⇧ with ⇧ drug concentrations

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78
Q

Mechanism of Damage done with intra-arterial injection

A 
Precipitation of crystals in the artery leading to inflammation and arteritis, which coupled with the
micro embolization that follows causes
• Occlusion of the distal artery
• Ischemia
• Tissue necrosis
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79
Q

Intra-arterial injection

A

Treatment-immediate attempts to dilute drug,
prevention of arterial spasm, general measures to
maintain blood flow
Lidocaine, papaverine, phenoxybenzamine sympathectomy of the upper extremity produced by a brachial plexus block

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80
Q

Large role in picking out induction agents

A

Blood pressure

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81
Q

Etomidate doest not

A

increase or decrease BP or CO

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82
Q

Which induction agents will raise BP

A

Ketamine

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83
Q

Which 2 induction agents with analgesic ?

A

Precedex

Ketamine (potent analgesic properties)

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84
Q

Venous Thrombosis happens because of?

A

Deposition of barbiturate crystals in the vein
• Less risk because of ⇧ diameter of veins
• Prevented by using dilute concentrations
(1% methohexital )

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85
Q

Allergic reactions for IV barbs for induction of anesthesia most likely represent anaphylaxis but can also be anaphylactoid. What is the difference?

A

• Anaphylaxis- antigen-antibody interaction,
immune mediated and requires prior exposure
• Anaphylactoid- no previous exposure or
sensitization, not a true allergic reaction but results
in histamine release, vasodilation, wheals, and
welts

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86
Q

Treatment for allergic reaction of barbiturates

A

• Treatment- Aggressive fluid replacement & IV EPI

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87
Q

What are the NON- BARBITURATE INDUCTION AGENTS ?

A 
PDEK
Propofol (Diprivan), 
Dexmedetomidine(Precedex)
Etomidate (Amidate)
Ketamine (Ketalar)
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88
Q

What is PROPOFOL?

is it chemically different as compared to other IV sedatives?

A

Emulsion (parental fat formulation intralipid)
1% (10mg/ml)solution in an aqueous solution of 10% soybean oil, glycerol, and purified egg lecithin
FketaminChemically different from all other IV sedative/ hypnotics

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89
Q

Equivalence of propofol to thiopental?

A

1.5-2.5mg/kg IV is equivalent to 4-5mg/kg thiopental or 1.5 mg/kg methohexital

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90
Q

Dose of Propofol induction

A

1.5-2.5 mg/kg rapid IVP=unconsciousness in 30 seconds

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91
Q

Advantages of PROPOFOL

A

Rapid and complete awakening compared to other induction agents

92
Q 
Continues advantages of propofol include
? effect of CNS
?MH activation
? steroid syntheis, hepatic, histamine release
Comment contxt sensitive half time
Other effects (2)
A

Minimal residual CNS effects
• No MH activation
• Doesn’t affect steroid synthesis or ACTH response
• Does not alter hepatic or fibrinolytic function
• Does not cause histamine release
• Context sensitive half time is minimally influenced by
duration of infusion (<40 minutes for up to 8hr infusion)
• Antiemetic and antipruritic effects

93
Q

MECHANISM of ACTION of PROPOFOL
Modulate what receptors?
When activiated = ________ = ________ =____inhibition
-may also _____the rate of

A

Sedative-hypnotic effects via GABA activation
• Selective modulator of GABA receptors
• GABA receptor activated= ⇧chloride ions= hyperpolarizes cell= functional inhibition
• Propofol may also ⇩ the rate of GABA dissociation from the GABA receptor

94
Q

Methohexital volume of distribution

A

Large

95
Q 
PharmacoKINETICS of Propofol
Clearance?
Metabolism?
Excretion?
Liver and kidney patients effects?
A

Clearance (rapid)from the plasma exceeds hepatic blood flow as well as metabolism
Hepatic oxidative metabolism by cytochrome P-450 to inactive metabolites is rapid and extensive
- <0.3% excreted unchanged in the urine
-No impaired elimination in pt with cirrhosis or renal dysfunction

96
Q

What terminates the action of propofol

A

Redistribution terminates action

97
Q

What is important for removal of drug (propofol) from plasma?

A

Tissue uptake (possibly into the lungs) is important for removal of drug from plasma

98
Q

Elimination half life of Propofol?

A

0.5-1.5 hours

99
Q

Propofol Context sensitive half time is

• ________effect-site equilibration

A

<40 minutes for infusions up to 8 hours

Short

100
Q

For propofol, No evidence of impaired eliminationn

• Elderly display ⇩ rate of plasma clearance

A
  • in cirrhosis pt
    • Renal dysfunction doesn’t influence elimination
  • ⇩
101
Q

Clinical uses of Propofol MAC cases

•

A

-Induction agent of choice- especially when rapid and complete awakening is needed (MAC cases) - -Continuous IV infusion is commonly used for
conscious sedation or as part of Total Intravenous
anesthesia (TIVA)

102
Q

• ICU sedation- caution in pediatric-reports of

A

metabolic acidosis, lipemia, bradycardia, &

progressive myocardial failure

103
Q

Propofol onset of action

A

10-50 seconds

104
Q

Propofol peak effect

A

2 min

105
Q

Duration of action

A

2-5 minutes

106
Q

Advantages short

A

Short acting, Antiemetic and anxiolytic

107
Q

Some disadvantages of Propofol

A 
Dose dependent hypotension
Respiratory Depression
Apnea
NO ANALGESIA/ NO MUSCLE RELAXATION
Burns at injection site.
108
Q

Induction dose of propofol

A

Healthy adults- 1.5-2.5 mg/kg will provide blood levels of 2-6 mcg/ml & unconsciousness

109
Q

For propofol: why do KIDS require HIGHER INDUCTION DOSES?

A

Kids need higher induction dose due to higher

central distribution volume and higher clearance rate (3mg/kg)

110
Q

Who require LOWER INDUCTION DOSES and why?

A

Elderly need lower induction dose (20-25% ⇩) due
to smaller central distribution volume and ⇩
clearance

111
Q

_____effect site equillibration and _____context sensitive half time = ___________

A

Short effect-site equilibration & short context

sensitive half time= easy titration

112
Q

Conscious sedation of propofol dose?

Supplement with _________ for painful procedures

A

doses of 25-100mcg/kg/min
provide minimal amnestic effects, no analgesic
Supplement with midazolam or short acting opioid for painful procedures

113
Q

Pharmacokinetics comparison of anesthetic agents

A

not numbers but difference

114
Q

Etomidate can also cause _______another drug that can also cause that is _________

A

MYOCLONUS; METHOHEXITAL

115
Q

Maintenance of propofol

A

100-300mcg/kg/min to maintain anesthesia (combined with opiods if need analgesia)

116
Q

General anesthesia with propofol=

A

Minimal postop nausea/vomiting +Prompt awakening

Minimal residual sedative effects

117
Q

NONHYPNOTIC THERAPEUTIC USES of PROPOFOL

What is the subhypnoptic dose?

A

Antiemetic effects- post op nausea/vomiting is ⇩
when propofol is given regardless of anesthetic
type/drugs used
• Sub-hypnotic doses (10-15mg) may be given in the
post-op area-rapid onset, little side effects
• Effective treatment for chemotherapy induced N/V

118
Q

Propofol ____mg is effective in treating ________associated with _______

A

10mg is effective in treating pruritus associated with neuraxial opioids

119
Q

Anticonvulsant activity Can terminate status epilepticus- short duration
_________induce seizure activity in epileptic pts

A

• Doses of >1mg/kg IV ⇩ seizure duration 35-45% in pt
undergoing ECT
• Does NOT

120
Q

_______properties with propofol similar to vitamin ____

A

Antioxidant properties similar to vitamin E

121
Q

ORGAN EFFECTS- CNS-PROPOFOL

Effect on CMRO2? ICP? Cerebral blood flow

A

Decrease, decrease, decrease

122
Q

Neuro effects: Large doses can of propofol can cause _______and a fall in________ and _________

A

hypotension ; cerebral perfusion pressure

123
Q

• EEG changes similar thiopental_______burst
suppression
• decrease those potentials on EEG?

A

⇩⇩
somatosensory evoked potentials (SSEP) and
motor evoked potentials (MEP)

124
Q 
Propofol vs thiopental? CV effect
Systemic BP?
CO and SVR?
BP effects exaggerated in \_\_\_\_\_\_\_, \_\_\_\_\_\_\_and pt with \_\_\_\_\_\_\_\_\_\_ due to \_\_\_\_\_\_\_\_\_
Required prior to propofol?
A

⇩ in systemic BP( ⇩ preload) greater than
equivalent thiopental dose
• ⇩ BP often accompanied by changes in cardiac output and SVR
• BP effects exaggerated in hypovolemic, elderly, & pt
with compromised LV function due to CAD
• Adequate hydration recommended prior to administering
propofol

125
Q

Propofol induces _______of smooth muscle and is due to ______________

A

• Relaxation of smooth muscle is due to inhibition of

sympathetic vasoconstrictor nerve activity

126
Q

Stimulaiton of ______and _______ does what to BP effects of propofol?

A

Stimulation of laryngoscopy and intubation reverses

BP effects of propofol

127
Q

_________ and __________have been seen in
healthy patients despite prophylactic anticholinergics
• Risk- is ____________
•

A

Profound bradycardia and asystole

1.4 in 100,000

128
Q

_________and _________in children in ICU with prolonged use

A

Severe, refractory and fatal bradycardia

129
Q

What can occur in the pediatric population with propofol?

A

⇧ in incidence of oculo-cardiac reflex in pediatric strabismus surgery despite prior prophylaxis with anticholinergics

130
Q

Propofol and pulmonary system?

What can counteract this effect?

A

Dose dependent depression of ventilation
Apnea occurring in 25-35% of pts after induction
• Effect enhanced with preoperative opioids
• Painful stimuli may counteract this effect

131
Q

Propofol on Vt and RR
Effect on asthma?
effect on ventilatory response to CO2 and arterial hypoxemia?

A

• Maintenance doses of propofol ⇩ Vt and RR
• Causes bronchodilation and ⇩ incidence of
intraoperative wheezing in asthma pt
• ⇩Ventilatory response to CO2 & arterial hypoxemia

132
Q

Propofol on Liver? Kidneys?

May cause ____Urine why?

A

Liver; No adverse effect on the liver
Kidneys :No adverse effect on the kidneys
May cause GREEN URINE due to the presence of phenols in the urine

133
Q

Effects of Propofol on intraoccular pressure?

A

Associated with SIGNIFICANT ⇩ in IOP which may lead to false readings

134
Q

Caution with Propofol ?

Prolonged________repored with ________

A

Allergic reaction to phenol nucleus & diisopropyl side chain
- May lead to anaphylaxis
- May lead to bronchoconstriction
- Prolonged myoclonus has been reported in pt with
meningismus

135
Q

Propofol and bacterial contamination?

A

• Potential for bacterial contamination. Propofol strongly supports the growth of E-coli and pseudomonas aeruginosa

136
Q

Propofol general aseptic techniques?

A

Use aseptic technique
•** Discard unused portion in 6 hours
•*** Change infusion line q 12 hours
• HIGH abuse potential- high risk of death

137
Q

Propofol infusion syndrome
Symptoms
Dose associated with PIS

A
  • s/s Lactic acidosis, bradycardia unresponsive to treatment, fat infiltrated liver,rhabdomyolysis
  • Pediatric and adults
  • High dose infusions (>75mcg/kg/min) for longer than 24 hours
  • Reversible if discontinued
138
Q

Propofol airway?

A

Airway Protection
Inhaled and IV anesthetics alter pharyngeal function with associated risk of impaired upper airway protection and pulmonary aspiration

139
Q

Propofol pain at injection site

A

Occurs <10% of pts if large vein is used
• Precede injection with lidocaine
• Precede with potent short acting opioid
• Incidence of thrombosis or phlebitis is <1%
• Arterial inject= severe pain but no vascular
compromise

140
Q

Etomidate, Amidate

A

Carboxylated imidazole-containing compound
chemically unrelated to other anesthesia induction
agents

141
Q

Disadvantage of etomidate

A

Decrease ability to produce cortisol

142
Q

Aqueous solution is unstable at __________ pH and

is formulated in a________% solution with 35%__________________ (pH6.9)

A

Aqueous solution is unstable at physiologic pH and is formulated in a 0.2% solution with 35% propylene glycol (pH6.9)

143
Q

ETOMIDATE and Injection site

A

Contributes to high incidence of pain at injection site and occasional venous irritation

144
Q

Which isomer is active with EtomIDATE , ? potency?

A

• Only D-isomer is active and 5 times as potent

145
Q

Etomidate MECHANISM OF ACTION

What does etomidate not do?

A
  • Binds GABA and enhances the affinity of the inhibitory neurotransmitter (GABA) for these receptors
  • Etomidate does not modulate other ligand gated ion channels at clinically relevant concentrations
146
Q

Pharmacokinetics of Etomidate?
Vd?
pka_____, ___% ionized at physiologic ph

A

• Large Vd, suggesting considerable tissue uptake
• Distribution into body water is favored by moderate
lipid solubility and existence as a weak base
• pKa 4.2, 99% unionized at physiologic pH

147
Q

Etomidate Penetrates brain _____reaches peak levels__________
______%protein bound to albumin

A

rapidly, within 1 minute

76%

148
Q

Prompt awakening with ETOMIDATE is the result of

A

redistribution to inactive tissues

149
Q 
****Metabolism of Etomidate
MEtabolized by ?
What is responsible for hydrolysis? 
Clearance compared to thiopental? =
Elimination half time is \_\_\_\_hours
A

Rapidly metabolized by hydrolysis of the ethyl ester
side chain to water-soluble, inactive compound
• Hepatic microsomal enzymes and plasma esterases are responsible for hydrolysis
• Clearance is about 5 times that of
thiopental=shorter elimination half time of 2-5
hours

150
Q

KETOFOL

A

Combined ketamine and propofol to prevent hypotension cause by ketamine.

151
Q

Precedex is a

A

Centrally acting alpha 2 antagonists

152
Q

Induction dose of Etomidate

A

• Induction dose- 0.2-0.4 mg/kg IV

153
Q

Excellent amnestic

A

ETOMIDATE

154
Q

• Can result in loss of airway reflexes

A

ETOMIDATE

155
Q

Etomidate Onset of unconsciousness occurs in______________circulation

A

one arm-to-brain circulation

156
Q

Involuntary myoclonic movements are common with ________can be attenuated by ________
awakening compared to barbiturates?

A

***Attenuated by opioids
Awakening- more rapid than barbs, with little/no
hangover or cumulative drug effects

157
Q

PRINCIPAL LIMITING FACTOR of ETOMIDATE

A

Principle limiting factor is transient depression of

adrenocortical function

158
Q

ETOMIDATE on PONV

A

• May ⇧ PONV

159
Q

No need to know half life of_____know that it is

A

propofl ; short

160
Q

ETOMIDATE on CBF, CMRO2, ICP?

Maintain what? ideal for?

A

• ⇩ cerebral blood flow and CMRO2
• ⇩ ICP
• Maintains cerebral perfusion pressure
Ideal for head injury pt

161
Q

Caution of etomidate in those neuro patients ? because it is used to __________in patient undergoing _________

A

Caution in pt with history of seizures, and focal
epilepsy
Used to facilitate localization of seizure foci in pt undergoing cortical resection of epileptogenic
tissue

162
Q

For ETOMIDATE, what is the dose for CV stability ?

A

CV stability is characteristic with 0.3mg/kg IV

induction dose

163
Q

**ETOMIDATE on HR, stroke volume or cardiac

output? BP?

A

BEST FOR PATIENTS with HR and OTHER HEART DISEAS
Minimal changes• Minimal effects on myocardial activity with induction doses in pt with little/no cardiac reserve
• Mean BP may ⇩ 15% due to fall in SVR

164
Q

Propofol, worried about recall may give

A

VERSED

165
Q

Who can have sudden hypotension with ETOMIDATE?

A

• Acutely hypovolemic pt could have sudden

hypotension

166
Q

What dose of ETOMIDATE can cause decrease in BP and CO?

A

• Dose of 0.45mg/kg may cause a significant ⇩ in BP

and CO

167
Q

ETOMIDATE effect on Resp system? compared to barb?
TV, RR
how long does the effect last?

A

Ventilatory depressant effects are less than with
barbs but apnea may occur after rapid IV injection
• Causes a ⇩ in tidal volume that is offset by ⇧in RR
• Effects on breathing are transient, lasting 3-5
minutes

168
Q

ETOMIDATE on renal ?

A

Does not ⇩ renal blood flow

169
Q

ETOMIDATE at injection site?

What is recommended?

A
  • Pain on injection
  • Pain with IV inject is frequent (80%)
  • Administration of lidocaine or opioid prior to injection recommended (Stabilize myocardium, Not to require Increase O2)
170
Q

MYOCLONUS

A

Excitatory effects that manifest as spontaneous movements, dystonia and tremors

171
Q

• MOA of myoclonus

What % of patients affected?

A

Inhibition of subcortical structures that normally suppress extrapyramidal motor activity
• Occur in >50% of pts

172
Q

How can you decrease the incidence of myoclonus?

A

• Can ⇩ myoclonus incidence with 1-2mcg/kg fentanyl or a benzodiazepine prior to etomidate injection

173
Q

Not good for LMA

A

Etomidate

174
Q

Etomidate and ENDOCRINE ?

How long does that effect lasts?

A

ADRENAL CORTICOL SUPPESSION
Produces a dose dependent inhibition of the conversion of cholesterol to cortisol
Effects last 4-8 hours

175
Q

Use Etomidate in those endocrine patients? 2 types of patients

A

Use with caution or avoid in pt that may require an
intact **cortisol response(Sepsis or hemorrhage patients)
May result in “stress free” surgery

176
Q

Incidence of allergic reaction with ETOMIDATE

A

Very low

ETOMIDATE KEEPS EVERYTHING EVEN

177
Q

What is Ketamine?

A

Phencyclidine derivative that produces a “dissociative anesthesia”
KETAMINE INCREASES EVERYTHING

178
Q

Good with asthma 2

A

Propofol
Ketamine (Bronchodilator) and Respiratory depression
Ketamine cause amnesia

179
Q

What is dissociative anesthesia?

A

• Dissociative anesthesia resembles cataleptic state
• Eyes open, slow nystagmic gaze
• Appears awake, non communicative
• Varying amounts of hypertonus and purposeful skeletal
muscle movement

180
Q

Ketamine causes

A

Amnesia

And INTENSE ANALGESIA with SUB anesthetics

181
Q

Ketamine concentrations

A

Supplied in 10, 50, 100mg/ml(IM injection )

182
Q

Ketamine concentration for IM injection

A

100mg/ml

183
Q

Ketamine structures resembles

A

Phencyclidine

184
Q

S isomer of Ketamine associated with

A

intense analgesia more than S

185
Q

MOA of Ketamine

A

Interacted with N-Methyl-D aspartate (NDMA) receptors, and may affect opioid receptors, monoaminergic receptors, muscarinic receptors, voltage sensitive NA channels and calcium channels

186
Q

NDMA is a member of

A

glutamate recepotr, ligand gates ion channle. EXCITATORY neurotransmitter with glycine as an obligatory coagonist

187
Q

Ketamine

A

inhibits activation of the NMDA receptor by
glutamate, ⇩presynaptic release of glutamate and
potentiates GABA

188
Q

Ketamine and opioid receptor activiety

A

Mu, delta, kappa receptors•

189
Q

Some studies have suggested that ketamine may be

an

A

antagonist at mu receptors and an agonist at

kappa receptors

190
Q

Ketamine is Partially antagonized by

This suggests ketamine is an

A

anticholinesterase drugs

antagonist at the muscarinic receptor

191
Q

Ketamine produces anticholinergic symptoms

A

(emergence delirium, bronchodilation, sympathomimetic action)

192
Q

Ketamine Pharmacokinetics
Resembles?
Onset, duration of action, lipid solubility, pka

A

Resembles thiopental
• Rapid onset of action, short duration of action, high lipid solubility
pK 7.5 at physiologic pH
High lipid solubility (5-10x thiopental)= rapid
transfer across BBB

193
Q

Protein binding of Ketamine?

A

Peak plasma concentration after 1 minute IV, 5

minutes IM Not highly protein bound

194
Q

Ketamine redistribution
Hepatic clearance Vd
Hepatic Extraction?

A 
Redistributed
• High hepatic clearance- 1 liter/minute
• Large Vd- 3 liters/kg
• High hepatic extraction ratio suggests alterations in
hepatic blood flow may effect clearance
195
Q

Ketamine metabolism
Active metabolites yes or no?
what slows metabolism of Ketamine?

A

Metabolized-liver microsomal enzymes(CYP-450)
• Norketamine-active metabolite 1/5-1/3 as potent
and may contribute to prolonged effects
• Diazepam slows the metabolism
• Chronic use = enzyme induction and may explain
tolerance of analgesic effects
• Tolerance can occur with >2 short interval
exposures

196
Q

Ketamine unique induction agents why?
recommended to administer_________why?
Which agent is preferred?
What may increase emergency

A

Recommend to administer antisialagogue
preoperatively to prevent coughing and
laryngospasm due to ketamine induced salivary
secretions
GLYCOPYRROLATE may be preferred(doesn’t cross
BBB) atropine, scopolamine may ⇧emergence
delirium

197
Q

Always want to give

A

Versed before Ketamine

198
Q

Ketamine and analgesia dose

A

• Dose of 0.2-0.5mg/kg can produce intense

analgesia

199
Q

Induction dose of KETAMINE
which dose is higher?
CAREFUL

A

1-2mg/kg IV or 4-8mg/kg IM
• Consciousness lost 30-60 seconds after IV, 2-4
minutes after IM
KNOW IM vs IV dose

200
Q

with Ketamin return of consciouness_____

fulll orientation______

A

Return of consciousness usually in 10-20 minutes
• Return of full orientation, additional 60-90 minutes
• Emergence times are ⇧ after repeated dose or
continuous infusion
• Useful for burn dressing changes
• Useful in hypovolemic pt due to CV stimulating
effects

201
Q

Ketamine induction
May be a __________if endogenous____________
Induction of anethesia with ___________ and _________followed by ________is proposed For _______ patient

A

May be a myocardial depressant, especially if endogenous catecholamine stores are depleted and sympathetic nervous system responses are impaired
• Induction of anesthesia with diazepam 0.5mg/kg, &
ketamine 0.5mg/kg IV followed by 15-30 mcg/kg/min is proposed anesthesia for CAD pt
• Sub anesthetic doses + propofol for TIVA = more
stable hemodynamics then propofol + fentanyl,
without emergence reactions that may occur with
high dose ketamine

202
Q

Ketamine may cause

A

Nystagmus not ideal for eye surgery

203
Q

Only drugs of Induction causing induction delirum

A

Ketamine

204
Q

Ketamine side effects include

A

Unique in its ability to stimulate the CV system
• Unique in its ability to cause emergence delirium
• May ⇧ ICP placing pts with intracranial pathology at
risk

205
Q

CV effects of Ketamine

A

Produces CV effects that resemble sympathetic nervous system stimulation
• ⇧ systemic and pulmonary arterial pressure, cardiac
work and myocardial oxygen requirements
• ⇧ in systolic BP 20-40mmHg

206
Q

Ketamine Direct stimulation of CNS leads to ______

May enhance the _________of Epi (make myocardial more sensitive)

A

Direct stimulation of CNS leads to sympathetic nervous system outflow
• Evidence =ability of inhaled anesthetics, ganglionic
blockade, cervical epidural anesthesia and spinal
cord transection to prevent ketamine induced
increases in systemic BP and HR
• May enhance the dysrhymogenic ability of
epinephrine

207
Q

Hallmark with KETAMINE

A

No SIGNIFICANT RESPIRATORY DEPRESSION effect.

208
Q

Ketamine + VA may =

A

hypotension
• VA depresses the sympathetic nervous system outflow,
unmasks the direct myocardial depressant effects of
ketamine

209
Q

**Ketamine and Diazepam and midazolam-

A

also effective in preventing the cardiac stimulating effects of ketamine

210
Q

Verapamil attenuates

A

the BP elevating effects, drug induced ⇧in HR is enhanced

211
Q

Ketamine and NDNMB
Succinylcholine
Pancuronium
Seizure

A

Enhances action of nondepolarizing neuromuscular- blocking agents due to interference with calcium ion binding or its transport
• Decreases sensitivity of post junctional membranes
to neuromuscular blockers
• Duration of apnea after succinylcholine is ⇧ due to
inhibition of plasma cholinesterase
• Pancuronium enhances the cardiac stimulating
effects of ketamine
• Seizures have been reported in asthmatic pts
receiving aminophylline after ketamine

212
Q

Ketamine Emergencen delirium

% of patients

A

Dreams and hallucinations can occur up to 24
hours after administration
5-30%

213
Q

WHat are the factors that increase the incidence of Emergence delirium?

A
  • Factors that ⇧incidence
  • Age > 15yrs
  • Female
  • Doses >2mg/kg
  • History of personality disorder or frequent dreaming
214
Q

No significant long term personality differences with which drugs?

A

present in adults receiving ketamine

215
Q

Emergence delirium is less frequent when

A

ketamine is repeated

216
Q

PREVENTION OF EMERGENCE DELIRIUM with KETAMINE

A

Benzodiazepine- most effective
• Midazolam > diazepam
Give benzo 5 min prior to induction
Inclusion of thiopental or inhalational agents may⇩
incidence
Atropine or droperidol may ⇧ incidence of
emergence delirium with ketamine
Pt easily aroused but appear calm and comfortable

217
Q

DEXMEDETOMIDINE, PRECEDEX

A

• Highly selective, specific and potent full alpha 2
adrenergic agonist(1600 times the affinity for the
receptor)
• Indicated as an adjunct for anesthesia and ICU sedation
Produces hypnotic, sedative and analgesic effects
Produces pharmacologic effects similar to
clonidine-clonidine is partial alpha 2 agonist
Initial dose 1mcg/kg IV, load over 10 minutes
then 5-10mcg/kg/hour= TIVA without ventilatory
depression
0.2-1.5mcg/kg/hr -postop sedation

218
Q

No significnat resp depression associated with

A

Precedex

219
Q

Pharmacokinetics of Precedex

A 
2-3 hours compared to clonidine 6-10 hours
• Large Vd
• Highly protein bound (>90%)
• Undergoes extensive hepatic metabolism
• Renal excretion
220
Q

Precedex side effects

A

Most serious reactions
• Hypotension, severe bradycardia, sinus arrest, arrhythmias atrial fibrillation

Common reactions
hypotension, TRANSIENT HTN, NAUSEA< BRADYCARDIA
Nausea, bradycardia, fever, vomiting, hypoxia
Tachycardia, anemia, DRY MOUTH thirst

221
Q

Depresses transmission in the sympathetic nervous

system ganglia -

A

hypotension due to venodilation

222
Q

Comparative thiopental to methohexital Rapid distribution time

A

Metho 5.6

Thio 5.6

223
Q

minimal effect on hemodynamics

A

Etomidate

224
Q

Comparative thiopental to methohexital elimination half time

A
  1. 9 hours metho

11. 6 thio

225
Q

Comparative thiopental to methohexital: clearance

A

Metho 10.9

Thio 3.4

SRNAPharmacology II (32 decks)

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