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!!!!! Summer Pharm test 2 !!!!! > Non-barb induction agents > Flashcards

Non-barb induction agents Flashcards

1
Q

Define general anesthesia

A
  1. generalized reversible CNS depression
    1. No sensory perception- has sensory input
    2. Loss of conciousness
    3. immobility
    4. some supression of autonomic reflexes
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2
Q

most general anesthetics require supplimentation of an _________ for __________ to occur

A
  1. opioid
  2. analgesia
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3
Q

In absense of an opoid the body will indicate the stress response via

A
  1. Increased HR, BP
  2. SNS activation
  3. Cortisol release
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4
Q

Pre- meds/ sedation

A
  1. Anxiolytics- bezo
  2. antibiotic
  3. opioids
  4. prevent aspiration
  5. Preoxygenation
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5
Q

Induction drug

A
  1. IV or Inhalational
  2. IV = barbituate or non barbituate
  3. Inhalation = usually sevoflurane
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6
Q

Induction drugs

A

wear off in 3-5 minutes due to the distribution of the drug

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7
Q

What is the E1/2t for Propofol

A

0.5-1.5 hours

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8
Q

Propofol drug classification

A

Non-barbituate intravenous anesthetic

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9
Q

Propofol is supplied as

A
  1. 1% Egg, 10% soy and 2.5% glycerol
  2. Anapahlactoid reactions - avoid in Egg yolk and soy allergies
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10
Q

2 preservatives used in Propofol

A
  1. EDTA - preffered (diprovan)
  2. Sodium metabisulfite (Propofol)
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11
Q

Which preservative can cause bronchospasm in astmatics

A

Sodium metabasulfite

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12
Q

Preservatives in Propofol

A
  1. Propofol Inhibits phagocytosis
  2. It Supports growth of E. Coli and Pseudomona aeruginosa
  3. Preservatives likely kill off Candidia Albicans
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13
Q

Propofol Mechanism of Action

A
  1. Potentiates binding of GABA to GABAA receptor at the B1 subunit
  2. Decreases the rate of disassociation of GABA from the receptor
  3. Potentiation increases Cl- influx (hyperpolarization of the post synaptic cell membrane and functional inhabition of the post cenaptic neuron (decreased neuronal excitability)
  4. Inhabition of Glutamate ant the NMDA receptor
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14
Q

Propofols clearance ________ hepatic blood flow

A

Exceeds

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15
Q

Propofol Metabolism

A

conjugated in the liver to water souluable compounds

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16
Q

Propofol excretion

A

Renally - CRF doesn’t affect clearance

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17
Q

the drug propofol is a ___________, it is the preservative Na-metabasulfite that causes ____________ in astmatics

A
  1. Bronchodialator
  2. Bronchoconstriction
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18
Q

Even at at low doses propofol can serve as an__________ because it directly acts of ______________.

A
  1. Antiemetic
  2. Chemo receptor trigger zone
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19
Q

Propofol produces dose dependant

A

sedation and hypnosis

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20
Q

Effects of Propofol

A
  1. Sedation/hypnosis
  2. Anesthesia
  3. Amnesia
  4. Antiemetic
  5. Antiprueitic
  6. Anticonvulsant
  7. Attenuation of bronchoconstriction
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21
Q

Adverse effects of propofol

A
  1. Dose dependant respiratory depression
  2. dose dependant myocardial deprssion and vasodilatin
  3. Myoconus
  4. Lipidemia
  5. Pain on injection
  6. Infection and bronchospasm/preservatives
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22
Q

Cardiovascular effects of propofol

A
  1. Vasodilation
    1. Decreased SVR
  2. Myocardial depression
    1. Decreased SV
    2. Decreased CO
    3. Bradycardia????
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23
Q

Deaths with propofol and bradycardia

A

1.4 / 100,000

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24
Q

What if you give propofol and the patient is twitching

A

It is myoclonus

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25
Q
  1. Propofol induction dose.
  2. How is it effected in children?
  3. Elderly?
A
  1. 1.5 - 2.5 mg/kg IV
  2. Higher in children
  3. 25-50% decrease in elderly
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26
Q

Propfol unlike thiopental, etomidate and ketamine is not a ___________ compound

A

Chiral

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27
Q

Why is it not recommended to mix propofol with anything

A

It can cause the colescence of oil droplets which poses risk for Pulmonary Embolism - (even 1% lidocaine)

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28
Q

____________ is a low lipid formulation with ___% soy and ____% egg lecithin. It needs no __________. But there is a higher incidence of _________.

A
  1. Ampofol
  2. 5% soy
  3. 0.6% egg lecithin
  4. preservatives
  5. pain on injection
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29
Q

__________ is a prodrug that is produced by addint groups to the parent drug like phosphate monoesters. This will make the drug ___________. It also has a much _____________ onset and a __________ Vd and has ___________ potency

A
  1. Aquavan
  2. Water soluble
  3. slower onset
  4. higher Vd
  5. higher potency
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30
Q

What is the context sensitive half time after and 8 hour infusion of propofol

A

40 minutes

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31
Q

True or False: Propofol alters spinal level reflexes

A

FALSE- no spinal cord depression

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32
Q

Why has propofol replaced thiopental?

A

It offers complete awakening without residual CNS effects

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33
Q

What is the antiemetic/antipruritic dose of propofol?

A

10 mg IV (can be followed by a 10 mcg/kg/min infusion)

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34
Q

What is the presumed mechanism of anticovulsant activity produced by propofol?

A

GABA receptor Cl- receptor activation pre and post synaptically

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35
Q

the population with the highest ED95 for propofol.

A

Toddlers - they require the highest dosing and increased bolusing

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36
Q

How does propofol mediate vasodilation and decreased inotrpy?

A

Vasodilation is mediated via inhibition of the SNS vasoconstricor berve activity causeing subsequent vasodilation

Decreased inotropy is due to decreased intracellular Ca++ availibility (transsarcollema Ca++ influx)

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37
Q

CV effects of propofol

A
  1. Decreased BP (25-40%)
  2. dose dependent myocardial depression and vasodilation = decreased SVR, CO, and SV
  3. Heart rate is UNCHANGED (possibly due to barorecepror inhibition)
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38
Q

Which drug has a greater decrease in BP propofol or TPL?

A

Propofol

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39
Q

What type of patients may have and exaggerated respone to hypotension with propofol?

A
  1. Hypovolemic
  2. Elderly
  3. those with poor LV function d/t CAD
  4. Rapid hydration (bolus) prior to administration is recommended
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40
Q

What happens to the HR with a propofol?

A
  1. HR is relatively unchanged -
  2. there is likely baroreceptor inhabition and also Propofol likely blunts the SNS more then the PSNS resulting in a predominence oof vagal tone
  3. There is NO SA or AV nodal changes so propofol is acceptable for an ablative prcedure or WPW
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41
Q

Ventalitory changes in response to propofol administration

A
  1. Induction doses = apnea
  2. Infusion doses - decreased RR & decreased TV
  3. Decreased resposne to CO2 and hypoxia
  4. Decreased pH (acidosis)
  5. Hypoxic vasocntriction remains intact
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42
Q

Popofol and fetal drug

A

Propofol crosses the placenta, but is rapidly removed from the fetus - ok to use in OB anesthesia

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43
Q

Amnestic dose of propofol

A

30 mcg/kg/min

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44
Q

Potential side effects of propofol due to lipid emulsion

A
  1. risk of infection
  2. pain on injection
  3. hypertriglyceridemia
  4. potental for pulmonary embolism
  5. bradycardia (rare 1.4/100,000)
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45
Q

What should unespected tachycardia durring propofol prompt?

A
  1. Lab evaluation for lactic acidosis (blood gas and lactate)
  2. Early lacticacidosis reversible with discontinuation
  3. Prolonged lactic acidosis could lead to cardiogenic shock requiring ECMO
  4. Possible differential diagnosis include: hyperchloremic metabolic acidosis d/t NS infusion, Diabetic ketoacidosis or acidocis d/t release of a tournique)
46
Q

How does propofol act as an antioxidant?

A

It inhibits lipid peroxidation (radical scavenger?)(may protect membranes)

47
Q

Rank the amount of myclonus with induction drugs

A

Etomidate > Propofol > STP

48
Q

Propofol dosing

  1. Induction
  2. GA maintenance infusion
  3. Sedation infusion
  4. Antiemetic/antipruretic
  5. Amnestic
A
  1. Induction: 1.5-2.5 mg/kg
  2. GA maintenance infusion: 100-300 mcg/kg/min
  3. Sedation infusion: 25-100 mcg/kg/min
  4. Antiemetic/antipruretic: 30 mcg/kg/min
  5. Amnestic: 10 mg
49
Q

4-hydroxy-propofol

A

metabolite that is 1/3 as potent as propofol

50
Q

Propofol is excreted renally, how is this effected in chronic renal failure

A

It does not effect clearance d/t inactive metabolites

51
Q

Propofol has renal excretion with ___________.

A

< 0.3% unchanged

52
Q

Etomidate Class, Structure and pH

A
  1. Non-barbiturate induction agent
  2. Carboxylated Imidazole compound - pH of 6.9 and water soluable
  3. At physiologic pH it becomes LIPID soluble (base: pH = 8.2, pK = 4.2 and 99% non-ionized at physiologic pH)
53
Q

With Etomidate physiologic activity will be ___________ in an acidotic patient

A

Less, but not much. it is a basic solutionwith a pH of 8.2, however the pKa is 4.2 and it is 99% ionized at physiologic pH

54
Q

Etomidate and protien binding

A

Highly protein bound to albumin (76%)patients with decreased albumin may need alowerdose due higher free drug concentration in the blood and enhanced effect.

55
Q

Prompt awakening of propofol and etomidate is due to

A

Etomidate = redistribution

Propofol = high drug metabolism

56
Q

Etomidate

  1. Vd
  2. E1/2t
  3. metabolism
  4. excretion
A
  1. Vd = 2.5-4.5 L/kg
  2. E1/2t = 2-5 hours
  3. metabolism = hydrolysis of elthyl ester side chain to carboxylic acid
  4. excretion = 85% renal with <3% unchanged in the urine, 10-15% bile
57
Q

Clinical uses of Etomidate

A
  1. In the presence of an unstable cardiovascular system
58
Q

What causes myoclonic movemnts and how can they be attenuated

A
  1. Myoclonus = alteration in balance between exciatory and inhibitory influences on the thalamocotical tract
  2. Disinhibiting of the extrapyamidal system- class
  3. Myoclonus can be attenuated by prior administration of an opioid
59
Q

Awakening after etomidate is ___________ than barbiturates and there is little to no eveidene of ____________.

A

More rapid, hangover

60
Q

Why must an opioid be given with Etomidate, Propofol and Barbiturates for the induction of anesthesia

A

They have NO analgesic properies, and the opioid is needed to blunt the SNS response to Laryngoscopy

61
Q

What is a limiting factor in using etomidate for induction of anesthesia

A

It depresses aderenalcortical function

62
Q

In what patients should use of etomidate be avoided?

A
  1. those with history of seizures - shows excitatory activity with EEG
  2. Porphyria
63
Q

What is the catch 22 for etomidate

A

It may increase epileptic foci, it also may help facilitate localization of seizure activity. In contrast Etomidate has been used to terminate status epilepticus. Use as a last resort in seizure activity

64
Q

Induction drugs and IOP

A

ketamine = increased IOP

etomidate, propofol, TPL = decreased IOP

65
Q

Induction drug with the most N/V

A

Etomidate

66
Q

Effects of Etomidate on ICP

A
  1. Etomidate produces a direct vasoconstirction which results in decreased CBF, CMRO2, and ICP.
  2. CPP is unlikely to change because of the minimal changes in BP with Etomidate
67
Q

Etomidate Dosing

  1. Cardiaic stable dose
  2. Induction range
  3. Mantenance dose
  4. Sedation
  5. Rectal
A
  1. Cardiaic stable: 0.3 mg/kg
  2. Induction range: 0.2 - 0.6 mg/kg
  3. Mantenance: 10 mcg/kg/min w/ N20 and Opioid
  4. Sedation: 5-8 mcg/kg/min
  5. Rectal: 6.5 mg/kg Pediatrics
68
Q

Why is there a specific cardiac stable dose of etomidate?

A
  1. Cardiac stable dosing is 0.3 mg/kg
  2. When the dose is greater than 0.45 there is significant decreases in SVR, BP and CO
69
Q

Why does etomidate have minimal CV effect?

A
  1. It has minimal effect on the SNS and braroreceptors.
  2. No change in HR,aBP, PAP, CO, SVR, PVR,
70
Q

Etomidates effects on ventilation

A
  1. transient decrease in TV with a compensatory increase in RR
  2. Minimal change in the response of increased CO2
  3. Hiccoughs (myoclonus)
71
Q

Myoclonus with etomidate may enhance _________.

A

Seizure activity

72
Q

Etomidate causes ___________ adrenocortical supression via inhibition of the coversion of _________ to __________. The main enzyme inhibited _______________ is evidenced by the accumualtion of ______________. Another enzyme that may be inhibitied is _________. This one is minor inhibition. This inhibition may provide an advantage of having ___________.

A
  1. dose-dependent
  2. cholesterol to cortisol
  3. 11 beta-hydroxylase
  4. 11-dehydroxycorticosterone
  5. 17-alpha-hydroxylase
  6. Stress free anesthesia
73
Q

The mineralcorticoid supression from etomidate lasts for _____________ after the dose is given and accounts for a decrease in _____________ and _______________ production

A
  1. 4-8 hours
  2. decreased mineralcoriticoid and corticosteroid production
74
Q

Etomidate is metabolized in 3 ways, via ____________, ____________, ____________ to ______________ an incactive metabolite- 85% is excreted __________ and 13% is __________. 2% is excreted __________.

A
  1. live, ester hydrolysis, N-deakylation
  2. carboxyllic acid
  3. renally
  4. billiary
  5. unchanged
75
Q

Biotransformation of etomidate is ____________ than TPL. Therefore, etomidate has ___________

A

5X faster, a shorter DOA

76
Q

When studied seperatly which optical isomer of Ketamine produces MORE analgesia, FASTER metabolism and recovery, and LOWER incidence of emergence reactions?

A

Ketamine’s S(+) isomer - it is 2x more potent than the racemic mixture and 4x more potent than the R(-) isomer!

77
Q

Both isomers of ketamine exibit this cocain like effect

A

Inhibit uptake of catecholamines back into POST ganglionic sympathetic nerve endings

78
Q

What type of receptors is Ketamine thought to interact with?

A
  1. NMDA -
  2. Opioid - mu, kappa and delta
  3. Sigma receptors
  4. Monaminergic
  5. Muscarinic
  6. Voltage gated Na+
79
Q

How does ketamine act at the NMDA receptor?

A

Inhibits the activation of the receptor by glutamate by either by inhibiting pre-synaptic release of glutamate or directly blocking glutamate from activating the channel

80
Q

Where are monoaminergic receptors located?

A

They are ainti-nociceptive receptors that are in the descending inhibatory pathways

81
Q

How do NMDA receptors work

A
  1. They are excititory ionotropic receptors that facilitate long term potentiation
  2. Activation of NMDA results in opening of nonslecticve cation channels
  3. Na+ and Ca++ flow into the cell and K+ leaves
  4. Ca++ influx is thought to be critical for synaptic pasticity and formation of new memories
82
Q

NMDA receptors are thought to be both_________.

A

Ligand gated and voltage dependent.

83
Q

The pharmakokinetics of Ketamine resembles TPL in that ….

A

Ketamine also has a rapid onset, short DOA and high lipid solubility

84
Q

pKa of Ketamine

A

7.5 at physiological pH

85
Q

Ketamine

  1. Hepatic Clearance
  2. Vd
  3. Elimination half time
  4. Compartment model
A
  1. Hepatic Clearance: 1 L/minute
  2. Vd : 3 L/kg
  3. Elimination half time: 2-3 hours
  4. Compartment model = 2
86
Q

Ketamine metabolism and excretion

A
  1. Hepatic microsomal enzymes demethylation to NORKETAMINE = active metabolite; 1/5 as potent
  2. Norketamine eventually hydroxylated then conjucagted to H2O soluable inactive glucuronide metabolites excreted by the kidneys
  3. < 4% unchanged in urine and < 5% fecal excretion
87
Q

Can ketamine be subject to tolerence

A

Yes! it may stimulate the very microsomal enzyme that is responsible for its metabolism. Burn patients may develop tolerance as well as those with ketamine dependence

88
Q

Type of anesthesia produced by Ketamine - what does it entail?

A

“Disassociative Anesthesia” EEG distinction between the talamocortical and limbic systems

89
Q

What additional preoperative drug is recommended to be added to an induction with ketamine

A

An anti-saligogue like glycopyrolate - becasue it does not cross the BBB like atropine and scopolamine and has less llikelyhood to exacerbate/increase emergence delerium

90
Q

Ketamine is given and then plasma concentrations are measuserd and they have a high norketamine concentration. What does this tell me

A

Ketamine has a high first pass effect when it is administered orally

91
Q

what is norketamine hydroxylated to?

A

hydroxynorketamine

92
Q

Total body clearance of ketamine

A

Total body clearence is equal to liver blood flow; decreased HBF could make a differene in metabolism, but it is not likely to have clinical significance

93
Q

Ketamine Dosing

  1. Induction:
  2. Infusion:
  3. IM:
  4. Sedation/analgesia/spinal:
A
  1. Induction: 0.5-2 mg/kg
  2. Infusion: 1-2 mg/kg/hr
  3. IM: 4-6 mg/kg (peak = 5 min)
  4. Sedation/analgesia/spinal: 0.2-0.5 mg/kg
94
Q

Where are the NMDA receptors in the spinal cord? why is this relevent with spinal anaesthesia?

A

NMDA receptors in the dorsal horn of the spinal cord; they are designed developmentally to react to pain associated with touch an injusred limb or body part. Ketamine is blocking this reaction: also the S enantomer has the affinity for the NMDA receptor

95
Q

Induction drug withought pain or irritation

A

Ketamine

96
Q

Often times these two drugs are combined for TIVA (Total IV anesthesia)

A

Propofol and ketamine - there have been reports of this producing more stable hemodynamics than that of fentanyl and poropofol

97
Q

Ketamine and pharyngeal and laryngeal reflexes

A

they are maintained or only slightly depressed

98
Q

What can be expected for the return of conciousness with fentanyl?

A
  1. Return of conciousness in about 15 minutes, but return to full orientation ususally takes about 60-90 minutes (amnesia usually is in this 60-90 min as well - but DO NOT ASSUME amnesia- these patients have intact vision and hearing)
99
Q

What would be a good induction drug for the acutely hypovolemic? Why?

A

Ketamine- it has CV stimulating effects (still has depressant effects and is reliant on the patinets endogenous catecholamines and sympathetic activity)

100
Q

Ketamine and ICP effects

A
  1. Direct cerebral vasodialator - (Ca++ inhibition?)
  2. Can increase CBF up to 60%
  3. Increased ICP
  4. Increased CMRO2
    5.
101
Q

Ketmaine effecs on the eye

A
  1. Increased IOP
  2. Nystagmus
  3. Pupillary dilation
102
Q

Onset, peak effect and termination of effect:

  1. Propofol
  2. Etomidate
  3. Ketamine
  4. TPL
A
  1. Propofol: (O = 20-30 sec) (P = ? min) (D = 5-10 min)
  2. Etomidate: (O = 1 min) (P = 1 min) (D = 3-10 min)
  3. Ketamine: (O = 30 sec) (P = 1 minute) (D = 15 min)
  4. TPL: (O = ? min) (P = ? min) (D = 5-8 min)
103
Q

What causes the disassociative state for Ketamine?

A
  1. Depressed neuronal function in the cerebral cortex and thalamus
  2. stimulation of the hoppocampus (limbic system)
104
Q

Which drug class has more prominent amnesia? Benzos or ketamine?

A

Benzos! Ketamine doesn’t depress sensations of sight and hearing

105
Q

Awakening is the most rapid and complete with this drug

A

Propofol

106
Q

Principal hemodynamic effects of ketamine

A
  1. Resembles SNS stimulation (Sympatheticomimmetic NMDA Effect)
  2. will see INCREASED BP, HR, CO
  3. Inhibits reuptake of NE stores = increased myocardial work and increased O2 Consumption
  4. However, Ketamine is a DIRECT myocardial depressant
107
Q

Unexpected decreased in blood pressure and cardiac ouput after giving ketmaine may reflect 1.___________ 2.___________ 3. ___________.

A
  1. Depletion of endogenous catecholamine stores.
  2. Or exhaustion of SNS compensatory mechanisms which will lead to an unmasking of ketamines direct myocardial depressant effetct
  3. Often seen in critically ill patients
108
Q

Where is the sympathomimmetic NMDA effect mediated?

A

LIkely due to NMDA receptor activity in the nucleus tractus solitarious

109
Q

Which enantiomer has some Mu activivity and is likely responsible for the effect of spinal analgesia of ketamine

A

S enateomer- the only wone with the affinity fo rhte NMDA receptors

110
Q

Ketamine Respiratory effects

A
  1. Minimal, no change in CO2 response curve
  2. Brochocilation (d/t increased circulating catecholamines) - good for asthmatics
  3. Increased PVR = Do not use with PHTN
  4. Increased salivation - consider glycopyrolate
111
Q

Contraindictaions to ketamine

A
  1. Eye: Increased IOP, Open eye injury
  2. CAD as the sole anesthetic- may be safe in combination with opioids or propofol
  3. HTN, Angina
  4. Vascular aneurisms
  5. Uncontrolled or systemic or Pulmonary HTN
  6. Psychiatric diseases like PTSD

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