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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
1. **Propofol induction dose.** 2. How is it effected in children? 3. Elderly?
1. **1.5 - 2.5** mg/kg IV 2. Higher in children 3. 25-50% decrease in elderly
26
Propfol unlike thiopental, etomidate and ketamine is not a ___________ compound
Chiral
27
Why is it not recommended to mix propofol with anything
It can cause the **colescence of oil droplets** which poses risk for **Pulmonary Embolism** - (**even 1% lidocaine**)
28
\_\_\_\_\_\_\_\_\_\_\_\_ is a low lipid formulation with \_\_\_% soy and \_\_\_\_% egg lecithin. It needs no \_\_\_\_\_\_\_\_\_\_. But there is a higher incidence of \_\_\_\_\_\_\_\_\_.
1. Ampofol 2. 5% soy 3. 0.6% egg lecithin 4. preservatives 5. pain on injection
29
\_\_\_\_\_\_\_\_\_\_ 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
1. Aquavan 2. Water soluble 3. slower onset 4. higher Vd 5. higher potency
30
What is the **context sensitive half time** after and 8 hour infusion of propofol
**40** minutes
31
True or False: Propofol alters spinal level reflexes
FALSE- no spinal cord depression
32
Why has propofol replaced thiopental?
It offers complete awakening without residual CNS effects
33
What is the antiemetic/antipruritic dose of propofol?
**10 mg IV** (can be followed by a 10 mcg/kg/min infusion)
34
What is the presumed mechanism of anticovulsant activity produced by propofol?
GABA receptor Cl- receptor activation pre and post synaptically
35
the population with the highest ED95 for propofol.
Toddlers - they require the highest dosing and increased bolusing
36
How does propofol mediate vasodilation and decreased inotrpy?
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)
37
CV effects of propofol
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)
38
Which drug has a greater decrease in BP propofol or TPL?
Propofol
39
What type of patients may have and exaggerated respone to hypotension with propofol?
1. Hypovolemic 2. Elderly 3. those with poor LV function d/t CAD 4. Rapid hydration (bolus) prior to administration is recommended
40
What happens to the **HR** with a **propofol**?
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
41
**Ventalitory** **changes** in response to **propofol** administration
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
42
Popofol and **fetal** **drug**
Propofol **crosses** the placenta, but is **rapidly removed** from the fetus - ok to use in OB anesthesia
43
**Amnestic** **dose** of propofol
**30 mcg**/kg/min
44
Potential **side effects** of propofol due to **lipid emulsion**
1. risk of **infection** 2. pain on injection 3. hyper**triglyceride**mia 4. potental for **pulmonary embolism** 5. bradycardia **(rare** 1.4/100,000**)**
45
What should unespected tachycardia durring propofol prompt?
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
How does propofol act as an **antioxidant**?
It **inhibits** **lipid** **peroxidation** (radical scavenger?)(may protect membranes)
47
**Rank the amount of myclonus** with induction drugs
Etomidate \> Propofol \> STP
48
**Propofol dosing** 1. Induction 2. GA maintenance infusion 3. Sedation infusion 4. Antiemetic/antipruretic 5. Amnestic
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
4-hydroxy-propofol
metabolite that is 1/3 as potent as propofol
50
Propofol is excreted renally, how is this effected in chronic renal failure
It does not effect clearance d/t inactive metabolites
51
Propofol has renal excretion with \_\_\_\_\_\_\_\_\_\_\_.
**\< 0.3%** unchanged
52
Etomidate **Class,** **Structure** and **pH**
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
With Etomidate physiologic activity will be ___________ in an acidotic patient
**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
Etomidate and protien binding
**Highly protein bound** to **albumin** **(****76%)**patients with decreased albumin may need a**lower****dose** due higher free drug concentration in the blood and enhanced effect.
55
**Prompt awakening** of propofol and etomidate is due to
**Etomidate** = **redistribution** **Propofol** = high drug **metabolism**
56
**Etomidate** 1. Vd 2. E1/2t 3. metabolism 4. excretion
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
Clinical uses of Etomidate
1. In the presence of an **unstable cardiovascular system**
58
What causes **myoclonic** **movemnts** and how can they be attenuated
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
Awakening after etomidate is ___________ than barbiturates and there is little to no eveidene of \_\_\_\_\_\_\_\_\_\_\_\_.
More rapid, hangover
60
Why must an **opioid** be given with Etomidate, Propofol and Barbiturates for the induction of anesthesia
They have **NO** **analgesic** **properies**, and the opioid is needed to blunt the SNS response to Laryngoscopy
61
What is a **limiting factor** in using etomidate for induction of anesthesia
It depresses aderenalcortical function
62
In what patients should use of etomidate be avoided?
1. those with history of seizures - shows excitatory activity with EEG 2. Porphyria
63
What is the **catch 22** for etomidate
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
Induction drugs and **IOP**
**ketamine** = **increased** IOP etomidate, propofol, TPL = **decreased** IOP
65
Induction drug with the most N/V
Etomidate
66
Effects of Etomidate on **ICP**
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
**Etomidate Dosing** 1. Cardiaic stable dose 2. Induction range 3. Mantenance dose 4. Sedation 5. Rectal
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
Why is there a specific cardiac stable dose of etomidate?
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
Why does etomidate have **minimal CV effect?**
1. It has minimal effect on the **SNS** and **braroreceptors**. 2. **No change** in HR,aBP, PAP, CO, SVR, PVR,
70
Etomidates effects on ventilation
1. transient decrease in TV with a compensatory increase in RR 2. Minimal change in the response of increased CO2 3. Hiccoughs (myoclonus)
71
Myoclonus with etomidate may enhance \_\_\_\_\_\_\_\_\_.
Seizure activity
72
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 \_\_\_\_\_\_\_\_\_\_\_.
1. dose-dependent 2. **cholesterol to cortisol** 3. **11 beta-hydroxylase** 4. 11-dehydroxycorticosterone 5. **17-alpha-hydroxylase** 6. Stress free anesthesia
73
The mineralcorticoid supression from etomidate lasts for _____________ after the dose is given and accounts for a decrease in _____________ and _______________ production
1. **4-8 hours** 2. decreased **mineral**coriticoid and **cortico**steroid production
74
Etomidate is metabolized in 3 ways, via \_\_\_\_\_\_\_\_\_\_\_\_, \_\_\_\_\_\_\_\_\_\_\_\_, ____________ to ______________ an incactive metabolite- 85% is excreted __________ and 13% is \_\_\_\_\_\_\_\_\_\_. 2% is excreted \_\_\_\_\_\_\_\_\_\_.
1. live, ester hydrolysis, N-deakylation 2. carboxyllic acid 3. renally 4. billiary 5. unchanged
75
**Biotransformation** of etomidate is ____________ than TPL. Therefore, etomidate has \_\_\_\_\_\_\_\_\_\_\_
5X faster, a shorter DOA
76
When studied seperatly which optical isomer of Ketamine produces MORE **analgesia,** FASTER **metabolism** and **recovery,** and LOWER incidence of **emergence reactions?**
Ketamine's **S(+) isomer** - it is **2x** more potent than the racemic mixture and **4x** more potent than the R(-) isomer!
77
**Both isomers** of ketamine exibit this cocain like effect
Inhibit uptake of **catecholamines** back into POST ganglionic sympathetic nerve endings
78
What type of receptors is Ketamine thought to interact with?
1. **NMDA** - 2. **Opioid** - mu, kappa and delta 3. Sigma receptors 4. **Monaminergic** 5. **Muscarinic** 6. Voltage gated **Na**+
79
How does ketamine act at the **NMDA** receptor?
**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
Where are **monoaminergic** receptors located?
They are **ainti-nociceptive** receptors that are in the descending inhibatory pathways
81
How do NMDA receptors work
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
NMDA receptors are thought to be both\_\_\_\_\_\_\_\_\_.
**Ligand** gated and **voltage** dependent.
83
The **pharmakokinetics** of Ketamine resembles TPL in that ....
**Ketamine** also has a **rapid** **onset**, **short** **DOA** and **high** **lipid** **solubility**
84
**pKa** of Ketamine
**7.5** at physiological pH
85
Ketamine 1. Hepatic Clearance 2. Vd 3. Elimination half time 4. Compartment model
1. Hepatic Clearance: **1 L/minute** 2. Vd : **3 L/kg** 3. Elimination half time: **2-3 hours** 4. Compartment model = **2**
86
Ketamine metabolism and excretion
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
Can ketamine be subject to **tolerence**
**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
Type of anesthesia produced by Ketamine - what does it entail?
"Disassociative Anesthesia" EEG distinction between the talamocortical and limbic systems
89
What **additional** **preoperative** **drug** is recommended to be added to an induction with **ketamine**
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
Ketamine is given and then plasma concentrations are measuserd and they have a high norketamine concentration. What does this tell me
Ketamine has a high first pass effect when it is administered orally
91
what is norketamine hydroxylated to?
hydroxynorketamine
92
Total body clearance of ketamine
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
**Ketamine Dosing** 1. Induction: 2. Infusion: 3. IM: 4. Sedation/analgesia/spinal:
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
Where are the NMDA receptors in the **spinal cord**? why is this relevent with **spinal anaesthesia**?
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
Induction drug withought pain or irritation
Ketamine
96
Often times these two drugs are combined for TIVA (Total IV anesthesia)
**Propofol and ketamine** - there have been reports of this producing more **stable** **hemodynamics** than that of fentanyl and poropofol
97
Ketamine and pharyngeal and laryngeal reflexes
they are maintained or only slightly depressed
98
What can be expected for the return of conciousness with fentanyl?
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
What would be a good **induction** **drug** for the acutely **hypovolemic**? Why?
**Ketamine- it has CV stimulating effects** (still has depressant effects and is reliant on the patinets endogenous catecholamines and sympathetic activity)
100
Ketamine and **ICP** effects
1. **Direct** cerebral vasodialator - (Ca++ inhibition?) 2. Can **increase** **CBF** up to **60%** 3. **Increased** **ICP** 4. **Increased** **CMRO2** 5.
101
Ketmaine effecs on the eye
1. Increased IOP 2. Nystagmus 3. Pupillary dilation
102
Onset, peak effect and termination of effect: 1. Propofol 2. Etomidate 3. Ketamine 4. TPL
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
What causes the disassociative state for Ketamine?
1. **Depressed** neuronal function in the **cerebral** **cortex** and **thalamus** 2. **stimulation** of the **hoppocampus** (limbic system)
104
Which drug class has more prominent amnesia? Benzos or ketamine?
**Benzos**! Ketamine doesn't depress sensations of sight and hearing
105
Awakening is the most rapid and complete with this drug
Propofol
106
Principal **hemodynamic** effects of ketamine
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
Unexpected decreased in blood pressure and cardiac ouput after giving ketmaine may reflect 1.\_\_\_\_\_\_\_\_\_\_\_ 2.\_\_\_\_\_\_\_\_\_\_\_ 3. \_\_\_\_\_\_\_\_\_\_\_.
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
Where is the sympathomimmetic NMDA effect mediated?
LIkely due to NMDA receptor activity in the **nucleus tractus solitarious**
109
Which enantiomer has some Mu activivity and is likely responsible for the effect of spinal analgesia of ketamine
S enateomer- the only wone with the affinity fo rhte NMDA receptors
110
Ketamine Respiratory effects
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
Contraindictaions to ketamine
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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