Induction drugs - test 2 Flashcards

1
Q

A drug that induces a state of calm or sleep.

A

Sedative

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2
Q

A drug that induces hypnosis or sleep.

A

Hypnotic

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3
Q

A drug that reduces anxiety and that has sedation as a side effect.

A

Anxiolytic

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4
Q

A drug that reversibly depresses the activity of the CNS.

A

Sedative-Hypnotics

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5
Q

State of drug-induced unconsciousness.

A

General Anesthesia

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6
Q

What is MAC?

A

Monitored Anesthesia Care- administration of a combination of sedatives and analgesics to induce a depressed level of consciousness, allowing patients to tolerate unpleasant procedures and enabling clinicians to perform procedures effectively.

AKA Procedure Sedation/ Conscious Sedation

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7
Q

What four groups will medication be distributed to?

A

Vessel rich group (75%)
Muscle group (18%)
Fat (5%)
Vessel poor group (2%)

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8
Q

What makes up the Vessel-rich group?

A

Brain
Heart
Kidney
Liver

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9
Q

What makes up the Muscle group?

A

Skeletal muscle
Skin

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10
Q

What makes up the Vessel-poor group?

A

Bone
Tendon
Cartilage

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11
Q

What are the 5 components of General Anesthesia?

A

Hypnosis
Analgesia
Muscle Relaxation
Sympatholysis (hemodynamic stability)
Amnesia

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12
Q

What are the 4 stages of General Anesthesia?

A

Stage 1: Analgesia
Stage 2: Delirium
Stage 3: Surgical Anesthesia
Stage 4: Medullary Paralysis

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13
Q

What stage can cause death?

A

Stage 4

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14
Q

What stage consists of the lightest level of anesthesia?

A

Stage 1

(This is the stage of conscious sedation, the patient can still open their eyes on command, breathe normally, and protective reflexes maintained.)

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15
Q

Stage 1 begins with the initiation of an anesthetic agent and ends with ___________.
The patient will experience __________ and _________ depression.

A

Loss of consciousness

Sensory and mental

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16
Q

What are the 3 lower airway reflexes?

A

Coughing
Gagging
Swallowing

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17
Q

What is the upper airway reflex?

A

Sneezing

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18
Q

Stage 2 starts with the loss of consciousness to the onset of automatic rhythmicity of vital signs. This stage is characterized by excitement in what areas?

A

Undesired CV instability excitation
Dysconjugate ocular movements
Laryngospasm
Emesis.

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19
Q

What is the response to stimulation in Stage 2 like?

A

Exaggerated and violent

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20
Q

What stage will have an absence of response to surgical incision and depression in all elements of the nervous system?

A

Stage 3

Will have all 5 components of anesthesia hypnosis, analgesia, muscle relaxation, sympatholysis, and amnesia.

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21
Q

What stage is associated with cessation of spontaneous respiration and medullary cardiac reflex? What are the symptoms of this stage?

A

Stage 4 (over anesthesia)

All reflexes are absent
Flaccid Paralysis
Marked Hypotension with w/ irregular pulse.
May lead to death

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22
Q

How can you tell if a patient is out from stage 2 to stage 1 for an awake extubation?

A

Patient is about to follow commands

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23
Q

What is the benefit of using a barbiturate (thiopental) vs. diethyl ether?

A

Diethyl ether is slow, unpleasant, and more dangerous for induction of general anesthesia. Barbiturates can cover stages 1 to stage 3 in as little as 2 minutes.

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24
Q

Why are barbiturates no longer used in the U.S.?

A

Thiopental is now part of the lethal injection cocktail for capital punishment.

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25
Why are we still talking about barbiturates?
This drug is still used in other countries. Critical to understand properties of barbiturates (gold standard) as comparison with other drugs.
26
What is the MOA of Barbiturates?
Potentiates GABA-A channel activity; directly mimics GABA. Acts on glutamate, adenosine, and neuronal nicotinic acetylcholine receptors
27
Barbiturates are a cerebral _____________. What will be the effect on CBF? What will be the effect on CMRO2?
Cerebral vasoconstrictor CBF decreases CMRO2 decreases by 55%
28
How do barbiturates help with seizures?
The decrease in CBF and CMRO2 will decrease the metabolic activity of the brain
29
Do barbiturates cause analgesic effects?
No Analgesia
30
What is the onset time of barbiturates? Barbiturates have a rapid redistribution at 5 minutes ________ of the total dose in the blood. How much of the total dose will be in the blood after 30 minutes?
30 seconds 50% 10%
31
What will result from a prolonged infusion time of barbiturates?
Lengthy context-sensitive half-time
32
Where is thiopental rapidly distributed to? The rate of metabolism of thiopental is equal to what?
Thiopental goes to the brain and viscera in about 1 minute. Metabolism of thiopental is equal to thiopental accumulation in the fat.
33
During emergence, the medication that was stored in the _________ and __________ will be reabsorbed in the blood and affect mentation.
fat and lean tissues
34
What is the site of the initial redistribution for barbiturates? Equilibrium at ________ minutes to plasma. When will perfusion decrease? Who has mass decrease?
Skeletal Muscles 15 minutes Perfusion decrease d/t shock The elderly will have a mass decrease
35
Why is the context-sensitive half-time for barbiturates so long?
The fat is a reservoir site for the drug, redosing/large dosing will yield cumulative effects.
36
Usually, barbiturates are dosed on ________ body weight.
lean
37
How are Barbiturates metabolized? How are they excreted? Elimination half-time consideration for pediatrics?
Hepatocytes 99% Renal Shorter half-time (higher metabolism)
38
Protein binding percentage of barbiturates? Is the barbiturate active or inactive?
Binds to albumin 70 to 85% Inactive, most of the drug will be bound to the protein. Once the drug becomes unbound and goes the VRG and crosses the BBB, that is when the drug will affect mentation.
39
When the barbiturate is non-ionized it will be ____________ soluble and _________ favors.
more lipid soluble and acidosis favors - Wants to stay in muscle and fat
40
When the barbiturate is ionized, it will be _________ soluble and _________ favors.
less lipid soluble and alkalosis favors
41
What are previous uses of barbiturates?
Premedication for Hangover Grand mal seizures (now uses benzos) Rectal administration with uncooperative/young patients Increased ICP, cerebral protection Induction
42
____ isomer is much more potent than ________ isomer, but the barbiturates are only marketed as ________ mixtures.
S- isomer R- isomer Racemic mixture
43
What are examples of oxybarbiturates?
Methohexital, Phenobarbital, Pentobarbital
44
What are examples of thiobarbiturates?
Thiopental, Thiamylal
45
What is the dose of Thiopental (sodium pentothal)?
Dose: 4mg/kg IV
46
In 30 minutes, what percentage remains in the brain for Thiopental? Because of this, what are the anesthetic considerations for this medication?
10% remains in the brain (rapid redistribution) Because of the rapid redistribution, be sure to supplement induction with other anesthetic agents so the patient can stay down during induction.
47
Where else can thiopental be redistributed? When do you decrease the dose of thiopental?
Skeletal muscles In the elderly or if the patient is in shock
48
What is the fat/blood coefficient of thiopental? The dose of thiopental is calculated on _________. The elimination half-time of thiopental is longer than __________.
11 Ideal body weight Methohexital
49
What is the partition coefficient?
Describes the distribution of a given agent at equilibrium between two substances at the same temperature, pressure, and volume. (50% of thiopental is available in arterial blood and 50% is available in the vessel poor group, rich group, and muscle, since they are at equilibrium that will be the partition coefficient)
50
What is the blood-gas coefficient?
Describes the distribution of an anesthetic between blood and gas at the same partial pressure.
51
What does a higher blood-gas coefficient correlate with?
Higher solubility of anesthetic in the blood and thus slowing the rate of induction. The blood can be considered a pharmacologically inactive reservoir.
52
Methohexital has a lower lipid solubility than which drug?
Pentothal
53
At a normal pH, what percentage of methohexital is non-ionized? What is the metabolism and recovery of methohexital?
76% (methohexital) 61% (pentohal) Fast metabolism and rapid recovery (induction only, not continuous infusion).
54
What are the excitatory phenomena with methohexital?
Myoclonus and Hiccups
55
What is the IV dose of methohexital?
1.5 mg/kg IV
56
What is the rectal dose of methohexital?
20-30 mg/kg (rectal)
57
With continuous methohexital infusion, there can be post-op ____ activity in 1 out of 3 patients.
Seizure
58
Methohexital can induce seizures in patients undergoing what procedure?
temporal lobe resection (lower seizure threshold, easier for seizures to occur)
59
Methohexital will decrease seizure durations by what percentage in ECT patients?
35 to 45% Don’t give methohexital if the patient has a history of seizures, but if they are in an active seizure, go ahead and use methohexital.
60
What are the CV effects of barbiturates (5mg/kg of thiopental)?
SBP: Transient 10-20 mmHg decrease, HR: 15 to 20 bpm increase
61
For patients that are hypovolemic, have CHF, and are on beta blockers, what response will barbiturates lack?
baroreceptor Just don’t give barbiturates to anyone with these conditions.
62
Barbiturates will cause what release?
Histamine Usually asymptomatic, thiopental can lead to an anaphylactoid response with previous exposure.
63
What are the side effects of ventilation with barbiturates?
Dose-dependent. The increasing dose will depress ventilatory centers (medullary and pontine).
64
How do barbiturates affect sensitivity to CO2?
Decrease sensitivity to CO2. This means we need a higher level of ETCO2 in order to trigger the medullary and pontine center for spontaneous respiration. May need an ETCO2 of 50 or 55 to trigger a breath
65
How do you return to spontaneous ventilation with barbiturates?
Slow frequency or decrease tidal volume.
66
What is the side effect of barbiturates through intra-arterial injection?
Immediate intense vasoconstriction and pain. Obscure distal arterial pulses. Blanching, followed by cyanosis. Gangrene and permanent nerve damage. Treatment: Vasodilators - lidocaine and papaverine to sustain adequate blood flow (heat pads)
67
Scoliosis surgery with barbiturates will require what monitoring?
Somatosensory Evoked Potentials (SSEP) Commonly used to detect changes in nerve conduction and prevent impending nerve injury.
68
2 to 7 days of barbiturate infusion will _________ metabolism of anticoagulation, phenytoin, TCAs, digoxin, corticosteroids, bile salts, and vit K. May persist for 30 days. Barbituates will cause a modest transient decrease in ________ and _________.
accelerate metabolism more frequent dosing will be required Renal blood flow and glomerular filtration rate
69
Propofol is a what type of agonist?
Gamma Aminobutyric Acid (GABA) agonist
70
What is the dose of propofol for induction?
Induction: 1.5 to 2.5mg/kg IV
71
What is the dose of propofol for conscious sedation?
Conscious sedation: 25 to 100 µg/kg/min
72
What is the dose of propofol for maintenance?
Maintenance: 100 to 300 µg/kg/min
73
Rapid injection of propofol will produce unconsciousness within how many seconds?
30 seconds
74
Propofol is a constitution of 1% solution, how many mg/mL is that? What would 2% be?
1% (10mg/mL) 2% (20mg/mL)
75
What are the components of propofol?
Propofol is 10% soybean oil, 2.25% glycerol, 1.2% purified egg phosphatide (lecithin).
76
What are the disadvantages of propofol?
Supports bacteria growth, causes increased plasma triglyceride concentrations (prolonged use), pain on injection (give lidocaine IV before).
77
What are the commercial preparations for propofol?
Ampofol (low lipid emulsions with no preservatives, higher incidence of pain on injection), Aquavan (prodrug that eliminates pain on injection, byproduct will produce pain, larger Vd, higher potency) Nonlipid with Cyclodextrins (clinical trials).
78
Propofol is a relative modulator of what receptors?
GABA-A
79
Where is GABA the principal inhibitory NT? GABA-A receptor activation will increase transmembrane conductance of _________.
Brain Chloride (hyperpolarization of the postsynaptic cell membrane and functional inhibition of the post-synaptic neuron, no transmission of impulse)
80
Immobility of propofol is not caused by drug-induced ____.
Spinal cord depression
81
What clears propofol more than hepatic blood flow? Tissue uptake of propofol is greater when it is being metabolized by _________.
Lungs Cytochrome P450
82
What metabolizes propofol?
Hepatic enzyme cytochrome P450 ## Footnote It metabolizes to water soluble sulfate and glucuronic acid metabolites, excreted by the kidneys.
83
What is the elimination half-time of propofol?
0.5 to 1.5 hours
84
What is the context-sensitive half-time of propofol?
40 minutes (8-hour infusion) ## Footnote Note that it is shorter than thiopental, because propofol is not as lipid-soluble as barbiturates.
85
What are the pharmacokinetic properties of propofol?
Elimination Half Time: 0.5-1.5 hrs, Vd: 3.5-4.5 L/kg, Clearance: 30-60 mL/kg/min, SBP trend: Decreased, HR trend: Decreased.
86
What are the pharmacokinetic properties of Etomidate?
Elimination Half Time: 2-5 hrs, Vd: 2.2-4.5 L/kg, Clearance: 10-20 mL/kg/min, SBP trend: No change to decrease, HR trend: No change.
87
What is the elimination half time of Ketamine?
2-3 hrs
88
What is the volume of distribution (Vd) of Ketamine?
2.5-3.5 L/kg
89
What is the clearance rate of Ketamine?
16-18 mL/kg/min
90
What is the SBP trend associated with Ketamine?
Increase
91
What is the HR trend associated with Ketamine?
Increase
92
What are the awakening times of Propofol in patients with cirrhosis of the liver?
Similar awakening time with alcoholic and normal patients.
93
Does renal dysfunction affect Propofol clearance?
No influence on propofol clearance.
94
What are the concerns about Propofol with pregnancy?
Propofol will cross the placenta but is rapidly cleared in the neonatal circulation.
95
What are the clinical uses of Propofol?
Induction DOC Continuous IV infusion (by itself or with other anesthetics, TIVA)
96
What percentage solution of Propofol is used in ICU to reduce lipid emulsion?
2% (20 mg/mL)
97
What is the Propofol induction dose for children?
3.0 to 3.5 mg/kg IV Higher dose due to larger central distribution volume and clearance rate.
98
What is the Propofol dose consideration for the elderly?
Lower induction dose by 25% to 50% 1 mg/kg or even less than that.
99
What are the plasma levels of Propofol during unconscious induction and awakening?
Unconscious on induction: 2 to 6 μg/mL Awakening: 1.0 to 1.5 μg/mL
100
What are the effects of intravenous sedation of Propofol?
Minimal analgesic and amnestic effects. Prompt recovery without residual sedation. Low incidence of postop PONV. Anti-convulsant properties. Midazolam or Opioid used as adjuncts.
101
What is Propofol the agent of choice for?
Brief GI endoscopy procedures.
102
How does Propofol's anti-emetic effect compare to Zofran?
Propofol is more effective than Zofran. ## Footnote Propofol depresses the subcortical pathways and has a direct depressant effect on the vomiting center.
103
What is propofol's MOA for it's anti-emetic effect?
Propofol depresses the subcortical pathways and has a direct depressant effect on the vomiting center
104
What is the sub-hypnotic dose of Propofol? How many mLs is it?
10 to 15 mg IV followed by 10 μg/kg/min 1 to 1.5 mL of 1% propofol
105
What is the dose of Propofol for anti-pruritic effects? How much will you give if you have 1% propofol?
10 mg IV 1% propofol is 10mg/mL so 1 mL.
106
What is the dose of Propofol as an anticonvulsant agent?
1 mg/kg IV
107
What are other benefits of Propofol?
Propofol as a bronchodilator Analgesia at low doses Potent antioxidant Does not trigger MH
108
What does Propofol decrease? Autoregulation is related to ____ and PaCO2 is ____.
CMRO2, CBF, and ICP Autoregulation related to CBF and PaCO2 is maintained.
109
What effect do large doses of Propofol have on cerebral perfusion pressure?
Decrease CPP - need to support MAP
110
What are the EEG changes from Propofol similar to?
Thiopental
111
What are SSEPs? What is propofol's effect on SSEPs?
Somatosensory evoked potentials (SSEPs) are brain and spinal cord responses elicited by sensory stimuli. Most of the clinically used SSEPs are elicited by electrical stimulation to the peripheral nerve, although more natural stimuli such as pain or touch sensation can yield SSEPs. Propofol has no SSEP suppression, unless volatiles or nitrous is added.
112
Does Propofol produce seizures?
It does cause excitatory movements on induction/emergence, but does not produce seizures.
113
How does the SBP of Propofol compare to Thiopental?
The decrease in SBP in propofol is higher than in thiopental due to inhibition of the SNS, vascular smooth muscle relaxation, and decrease SVR…also decreases the level of intracellular calcium.
114
What are the CV side effects of Propofol in patients with hypovolemia, elderly, or LV compromised?
Exaggerated (might consider etomidate instead)
115
What is the effect on HR with Propofol?
Bradycardia due to decreased SNS response, may depress baroreceptor reflexes. Profound bradycardia and asystole happens even in healthy adults.
116
What are the pulmonary side effects of Propofol?
Dose-dependent ventilation depression will cause Apnea. Synergistic effect with opioids. Intact hypoxic pulmonary vasoconstriction response. Painful surgical stimulation counteracts the ventilatory depressant effects.
117
What is the effect of Propofol on liver transaminase enzymes or creatine concentration?
Normal
118
What injury can prolonged infusion of Propofol cause?
Hepatocellular
119
What syndrome causes green urine from phenols without alteration in renal function? What is the cloudy urine caused by?
Propofol Infusion Syndrome Uric acid crystallization (no alternation to renal function)
120
What causes PRIS and what are its effects? Signs/sx? Reversible?
High dose infusion, greater than 75 μg/kg/min for 24 hours. Cause severe, refractory, and fatal bradycardia in children. Symptoms: Lactic acidosis, bradycardia, rhabdomyolysis, green urine. Reversible in the early stages.
121
What is the treatment for someone with PRIS in cardiogenic shock?
Extracorporeal membrane oxygenation (ECMO)
122
What are the side effects of Propofol on other organs?
Decrease Intraocular pressure. Inhibits platelet aggregation. Allergic Reactions. Prolonged myoclonus. Abuse and Misuse.
123
Even though Methohexital (Brevital) has a higher non-ionized component (76%) at normal pH than pentothal (61%). Why does Methohexital have a lower lipid solubility than pentothal?
Oxybarbitruates (Methohexital) have oxygen at the second position. Replacement of the oxygen with sulfur atom results in the corresponding thiobarbiturates (Pentothal) which are much more lipid soluble and have greater potency. Basically, percent ionization can not be the sole factor to determine solubility. In this example, chemical structure determines lipid solubility.
124
When giving a highly lipid-soluble drug, why would a lower dose be administered to someone with a high fat-to-bodyweight ratio (obese and geriatrics)?
There will be less blood volume to kilogram ratio. It is important to administer certain drugs by ideal body weight. Just think less lean muscle = lower drug dose
125
Etomidate is the only (chemical structure) __________-containing compound. What does that mean?
carboxylated imidazole This means that etomidate is water-soluble at an acidic pH and lipid-soluble at physiological pH (7.4)
126
What carrier agent does etomidate use that causes pain at the injection site?
propylene glycol (35%) Make sure to use lidocaine before to numb the internal structures of the vein (excluding cardiac patients).
127
Etomidate has a high incidence of _________.
myoclonus - the most significant adverse side effect of etomidate
128
What is the unique absorption characteristic of etomidate?
Etomidate is the only induction drug with direct systemic absorption in the oral mucosa that bypasses hepatic metabolism. (the percentage of the active drug does not decrease if given PO due to bypassing hepatic metabolism)
129
What is the mechanism of action of Etomidate?
Selective modulator of GABA-Alpha receptors.
130
What percent of etomidate is bound to albumin?
76% Remember: drugs bound to albumin are inactive. The free-floating drugs are the ones that are active.
131
How does the volume of distribution (Vd) of etomidate affect clearance?
Etomidate has a large Vd, resulting in a clearance that is 5 times faster than thiopental. You'll get prompt awakening with etomidate (the large Vd of etomidate counteracts the 76% binding capacity to albumin)
132
How is Etomidate metabolized?
Hydrolysis by hepatic microsomal enzymes and plasma esterases.
133
What is the elimination half-time for Etomidate? Percent of etomidate eliminated in the urine and bile?
2-5 hours 85% eliminated in the urine, 10-13% eliminated in the bile.
134
What is the dose and onset time for etomidate?
Range: 0.2 to 0.4 mg/kg IV. Onset: 1 minute.
135
For clinical use, etomidate is a great alternative to _______ or _____ for IV induction of anesthesia.
Propofol or Barbiturates Etomidate also has no hangover or cumulative drug effects, unlike pentothal and thiopental.
136
Etomidate is best suited for what type of patients for induction?
Unstable Cardiovascular patients, especially the ones with little or no cardiac reserves.
137
What are the analgesic effects of etomidate?
There are no analgesic effects. Opioids are used with etomidate during direct laryngoscopy and tracheal intubation.
138
What can be given to attenuate the myoclonic effects of etomidate prior to administration?
Opioids (*Fentanyl 1 to 2 mcg/kg) or BZD.
139
What is the incidence rate of myoclonus with etomidate?
50-80% ## Footnote Caution use in patients with seizure history.
140
Etomidate causes myoclonus due to alteration in the balance of inhibitory and excitatory influences on the ________ tract.
Thalamocortical Tract.
141
Fentanyl concentration: 50 mcg/mL. Patient’s weight is 100 kg. Administer 1 mcg/kg to attenuate myoclonus, how many ml will you administer?
2 mL.
142
How does etomidate affect adrenocortical response?
Etomidate will cause adrenocortical suppression. (Dose-dependent inhibition of the conversion of cholesterol to cortisol, decrease stress response)
143
What will be the result of adrenocortical suppression from etomidate? How long will enzyme inhibition last after the initial dose?
Severe hypotension, Longer Mechanical Ventilation. 4-8 hours
144
When might we need to keep our cortical response intact and consider an alternative besides etomidate?
When dealing with septic or hemorrhagic patients.
145
What does the graph indicate about etomidate?
Etomidate is associated with a decrease in the plasma concentration of cortisol.
146
CNS side effects of etomidate include a decrease in ______ and ________.
Decrease in Cerebral Blood Flow (CBF) and Cerebral Metabolic Rate of O2 (CMRO2) CBF and CMRO2 decrease by 35% to 45%.
147
Like most of our barbiturates (thiopental), etomidate is a potent direct cerebral _________. What does this do to ICP?
Vasoconstrictor Decrease ICP
148
Compare EEG changes between Thiopental and Etomidate.
Etomidate will have more frequent excitatory spikes because it lowers the seizure threshold.
149
What are the CV effects of Etomidate?
Most CV stable induction agent with minimal changes in HR, SV, CO, and contractility. Mild decrease in MAP d/t decrease in SVR. No intra-arterial damage and no histamine release. Etomidate can cause sudden hypotension with hypovolemia
150
What are the respiratory side effects of etomidate?
Less ventilation depressant than barbiturates, d/t rapid clearance. Rapid injection will lead to apnea. Decrease Vt is offset by a compensatory increase in RR (transient, will last 3-5 mins)
151
What is the formula for minute ventilation?
Tidal Volume x Respiratory Rate.
152
Etomidate _________the CO2 drive through the stimulation process.
preserves.
153
Ketamine is a derivative of _______. Why is the drug used for induction?
Phencyclidine (PCP) Angel Dust. Ketamine is used for its amnestic and intense analgesic properties.
154
Describe the dissociative anesthesia of Ketamine.
The patient will resemble being in a cataleptic state (dazed) in which eyes are open with a slow nystagmic gaze. Signs and sx: uncommunicative but wakefulness is present; hypertonus and purposeful skeletal muscle movements
155
What advantages does ketamine have over propofol and etomidate?
No pain on injection (lipid emulsion not required) Profound analgesia at subanesthetic doses.
156
What are the disadvantages of ketamine?
Frequent emergence delirium, Abuse potential.
157
What is the preservative of ketamine? What is the significance of this?
Benzethonium Chloride This preservative inhibits nicotinic acetylcholine receptors, which will cause SNS.
158
Describe S(+) Ketamine.
- Left-handed optical isomer. - More Intense Analgesia: 2x greater than racemic ketamine, 4x greater than R(-) ketamine. - Faster metabolism and recovery - Less salivation - Lower incidence of emergence
159
What does racemic Ketamine inhibit?
Racemic Ketamine inhibits the uptake of catecholamines back into postganglionic sympathetic nerve endings.
160
What patients should you use ketamine with caution?
A-fib, coronary artery disease, SVT, Hx of v-fib, Hx of MI
161
Patients that receive racemic ketamine will have less ________ and ________.
Less fatigue and less cognitive impairment.
162
What is the mechanism of action of ketamine?
Binds noncompetitively to N-methyl-D-aspartate (NMDA) receptor- This inhibits the activation of NMDA receptors by glutamate and decrease the presynaptic release of glutamate It also binds to opioid receptors and weak bind to sigma receptors It also has weak actions at GABA-a receptors
163
What is the onset time of action for ketamine?
Peak plasma concentration at 1 minute (IV) and 5 minutes for IM (pediatric patients).
164
What is the duration of action for ketamine?
10-20 minutes.
165
What is the lipid solubility of ketamine?
High (5x to 10x than Thiopental) - goes to the brain, does not bind with albumin, distributed to the tissues
166
What is the volume of distribution (Vd) of ketamine?
Large Vd (3L/kg), elimination half-time 2-3 hours.
167
What is the hepatic clearance rate of ketamine?
1L/min.
168
How is ketamine metabolized? What is its metabolite, active or nonactive? How is ketamine excreted?
The hepatic enzyme, cytochrome P450. Metabolite: Norketamine, active, one-third potency, prolonged analgesia. Excreted through the kidneys.
169
With ketamine, there is increased tolerance and potential for abuse/dependence with _____ patients.
burn.
170
What is the induction dose of ketamine IV and IM?
IV induction dose: 0.5 - 1.5 mg/kg; IM induction dose: 4 - 8 mg/kg.
171
What is the maintenance dose of ketamine IV and IM?
IV maintenance dose: 0.2 - 0.5 mg/kg; IM maintenance dose: 4 - 8 mg/kg.
172
What is the analgesic dose of ketamine IV?
0.2 - 0.5 mg/kg IV.
173
What is the post-op sedation and analgesia dose of ketamine (pediatric surgery)?
1 - 2 mg/kg/hr.
174
What is the neuraxial analgesia dose of ketamine for epidural and spinal?
Epidural: 30 mg mixed in a drip; Spinal: 5 - 50 mg/mL saline.
175
Ketamine can induce ________. Therefore, the maintenance of pharyngeal and laryngeal reflexes (coughing/laryngospasm) is crucial. What can be given to mitigate this?
salivary secretions Glycopyrrolate (0.2 mg)
176
What is the time for loss of consciousness (LOC) for ketamine?
LOC: 30-60 seconds (IV); 2-5 minutes (IM).
177
What is the time to return to consciousness (ROC) for ketamine? Full consciousness?
ROC: 10 - 20 minutes. Full: 60-90 minutes
178
How long does amnesia persist after ROC with ketamine?
Persistence of amnesia after ROC: 60 - 90 minutes.
179
What are the clinical uses of ketamine?
Great for acutely hypovolemic patients, asthmatic patients, pediatric induction, burn dressing changes, reversal of opioid tolerance, improvement of psych disorders, and restless leg syndrome.
180
What are the components of the coronary artery disease cocktail?
Diazepam 0.5mg/kg IV, Ketamine 0.5mg/kg IV, Continuous Ketamine infusion 15-30 mcg/kg/min IV.
181
What patients do you want to avoid giving ketamine to?
Pulmonary: Systemic/Pulmonary HTN; Neuro: Increase ICP. (increase SNS effect from ketamine)
182
What are the CNS side effects of ketamine?
Potent cerebral vasodilator. Can increase CBF by 60%.
183
There will be no further increase of ICP with what IV dose of ketamine?
0.5 to 2 mg/kg IV.
184
Does ketamine’s excitatory activity in EEG alter seizure threshold?
No, but there is still a risk for myoclonus.
185
Ketamine will increase amplitude with Somatosensory Evoked Potential (SSEP). This can be reduced with what?
Nitrous.
186
What do the CV effects of ketamine resemble?
SNS stimulation. Increase in SBP, PAP, HR, CO and MRO2 Increase plasma epi and NE levels
187
How can the CV effects of ketamine be mitigated?
Premedicate with BZD or inhaled anesthetics or nitrous.
188
Ketamine can result in unexpected drops in SBP and CO due to _______.
Depleted catecholamines stores. Ephedrine will not help b/c it is an indirect vasoconstrictor. Give a direct vasoconstrictor (phenylephrine) instead.
189
What are the respiratory effects of ketamine?
- No significant depression on ventilation. - Ventilatory response to CO2 is maintained. - PaCO2 is unlikely to increase more than 3mm Hg. - Upper airway skeletal muscle tone and reflexes are maintained and intact. - Increase salivary secretions. Increase bronchodilator activity. - No histamine release.
190
5 to 30% of patients on ketamine will have ________. Signs/Sx:
Psychedelic Effects (Emergence Delirium) S/Sx: Visual, auditory, proprioceptive, and confusional illusion, delirium, vivid dreams up to 24 hours.
191
How does ketamine cause emergence delirium?
Depression of the inferior colliculus and medial geniculate nucleus (responsible for separating reality and fantasy).
192
How do you mitigate emergence delirium?
Giving BZD 5 minutes prior to ketamine administration
193
What are two drugs to give prior to ketamine?
Glycopyrrolate and Versed.
194
Other side effects of ketamine include inhibition of _______.
Platelet aggregation, can induce bleeding Inhibits cytosolic free calcium concentration which can enhance NMBD. Inhibits plasma cholinesterase which will prolong apnea from Succinylcholine.
195
What are the drug interactions with ketamine?
Volatile anesthetics: Hypotension; NDNMB: Enhanced; Succinylcholine: Prolonged.
196
What are the risks and benefits of ketamine in OSA?
Risk: Psych effects, SNS activation, hypersalivation; Benefits: Upper airway preservation and ventilatory function, bronchodilator effect.
197
What is Ketafol?
Ketamine and Propofol. Best practice is to separate your meds, don’t mix.
198
What is the immediate use rule for single-dose medication?
Meds that are sterilely compounded must be used in one hour.