Ph- General Anesthesia Flashcards
(98 cards)
1
Q
What are the 5 currently used inhalation agents for general anesthesia?
A
- Nitrous oxide
- halothane
- isoflurane
- desflurane
- sevoflurane
2
Q
What are the inhalation agents used as muscle relaxants that are:
- depolarizers
- non-depolarizers?
A
- succinylcholine
2. vecuronium, rocuronium
3
Q
What is the definition of general anesthesia?
A
Drug-induced absence of the perception of all sensations.
There is still normal physiological response to stimuli, but there is no perception of them
4
Q
What are the 4 stages of the depth of anesthesia [dependent on the concentration of anesthetic agent in the brain]?
A
Stage 1:
- decreased perception, calm
Stage 2:
- excitement, delerium, irregular respiration, amnesia [Lingering in this stage is NEVER desirable]
Stage 3:
- surgical anesthesia, regular breathing or no breathing, complete absence of all perception
Stage 4:
- medullary depression/coma, no spontaneous breathing or movement, severely depressed or flat EEG [NOT desirable, but used in complex procedures requiring total circulatory arrest or interruption of cerebral blood flow]
5
Q
What determines the induction and emergence from anesthesia?
A
Induction and emergence occur as the anesthetic concentration in the brain fluctuates [achieved by clinical observation NOT measurable quantity]
- Induction - occurs rapidly as gas diffuses to tissue with highest vascularity [brain]
- emergence- occurs when redistribution to less vascular tissues reduce level of anesthetic in the brain
6
Q
What does the solubility of a gas in blood determine?
What does the blood:gas partition coefficient describe?
A
Solubility of a gas in blood determines its concentration or partial pressure.
The B:G partition coefficient describes the relative affinity of the gas for the 2 phases, thus, high B:G coefficient means that the gas has a high affinity for blood [very soluble]
7
Q
Describe the partial pressure and concentration of highly soluble gases vs low solubility gasses?
A
High solubility- move in and out of the cells easily and cross cell membranes with ease, making
- LOW partial pressure
- LOW concentration
Low solubility [low B:G gradient] means the gas will stay together as microscopic pockets that interact minimally with cells
- HIGH partial pressure
- HIGH concentration
8
Q
Anesthetic inhalation agents are effective as ______ NOT as ____________________.
The effective concentration of a gas is ________ proportional to the tension [partial pressure] and _____________________ proportional to the solubility.
A
Anesthetic agents are effective as gases NOT dissolved components in blood.
The effective concentration is DIRECTLY proportional to the tension/partial pressure and INVERSELY proportional to the solubility.
More soluble = less concentration = less partial pressure
Less soluble = more concentration = more partial pressure
9
Q
What is the relationship between Minimal Alveolar Concentration [MAC] and potency [lipophilicity]?
List the general anesthetics from most potent to least.
A
The less the MAC, the higher the potency
- Nitrous oxide [MAC 0.47]
- Halothane [MAC 0.75]
- Isoflurane [MAC 1.4]
- Sevoflurane [MAC 2]
- Desflurane [MAC 6]
10
Q
What general anesthetic is not a complete anesthetic, but has rapid onset and recovery and is used in conjunction with other agents?
A
Nitrous oxide
11
Q
What inhaled general anesthetic has the highest MAC, lowest B:G coefficient [rapid emergence] and pungency that irritate the airway?
A
Desflurane
12
Q
What inhaled general anesthetics are used primarily in pediatrics?
A
- sevoflurane [high potency/metabolism, non-pungent]
2. halothane [high potency/metabolism]
13
Q
What inhaled general anesthetic has the potential for hepatotoxicity in adults, and is used primarily in pediatrics?
A
halothane
14
Q
What 5 factors determine how quickly an inhaled anesthetic will build up to a given concentration in the alveolus?
A
- Fi [concentration of gas inspired]
- ventilation
- gas solubility
- pulmonary blood flow
- AV concentration gradient
15
Q
During induction of general anesthetic, what is the relative ratio of alveolar concentration to inspired gas concentration?
What happens to the ratio with maintenance?
Emergence?
A
Induction: because anesthetic is continually taken up by pulmonary circulation, during induction Fi will be really high. FA/Fi is less than one.
Maintainance= ratio is 1
Emergence = FA/Fi is greater than 1
16
Q
What is the effect of concentration of anesthetic in inspired air on how quickly gas builds up in the alveoli?
A
Fi [concentration] determines the max partial pressure in the alveolus.
If the anesthetic is a higher concentration, it will increase the rate of induction of anesthesia due to greater initial concentration gradient
17
Q
What is the effect of pulmonary ventilation on FA?
A
FA [alveolar partial pressure] decreases continually due to uptake, so alveolar ventilation is necessary to increase FA to compensate for continued uptake of gas into blood
18
Q
What is the effect of solubility on induction of general anesthesia?
A
The higher the B:G partition coefficient, the more soluble the anesthetic is in blood.
INSOLUBLE portions contribute to partial pressure, so the more soluble the anesthetic is, the longer the induction of anesthesia
19
Q
What is the effect of pulmonary blood flow on induction of general anesthetic?
A
High blood flow slows the buildup of anesthetic in the alveolus.
Low blood flow accelerates the rise of FA [due to dilution effects]
20
Q
What is the effect of the AV concentration gradient on induction of general anesthesia?
A
Upon induction, A-V gradient is at its highest.
- if there is no diffusion of anesthetic agent into peripheral tissue, venous partial pressure would become equal to arterial and there would be no further uptake of gas
- if anesthetic is taken up by peripheral tissue, a substantial A-V gradient is established–> allowing continued uptake of gas [as long as FA/Fi <1]
21
Q
What is the major route for elimination of inhaled anesthetics?
What 3 factors will increase the rate of elimination?
A
Diffusion is the major route for elimination. Rate is increased by: 1. low blood solubility 2. low V/Q mismatch 3. increased ventilation
22
Q
What is the order of metabolism for inhaled general anesthetics?
A
Halothane > Sevoflurane> isoflurane> Desflurane> Nitrous oxide
23
Q
What is the MAC of Nitrous Oxide?
What does this say about the potency?
What is the B:G partition for nitrous oxide?
What does this say about the onset of action and recovery?
A
MAC = 100% meaning that it is very low potency.
[100% inspired NO will fail to achieve surgical anesthesia]
B:G partition is low which means it will have rapid onset of action
24
Q
What are the 2 primary uses of Nitrous Oxide?
What are the major contraindications?
A
- supplement other anesthetics to lower their MACs
- minor surgeries [dental] when combined with opioids
Contraindications: NO can diffuse into air-filled cavities 3x more rapidly than nitrogen can diffuse out of the cavity so: 1. pneumothorax 2. intestinal obstuction 3. air embolus 4. intracranial air 5. tympanic membrane grafting 6. TRAUMA PATIENTS [potential for undiagnosed trapped air]
25
What is the potency and induction/emergence of halothane?
What is it used for?
What is the major contraindication?
Potency: VERY [low MAC]
Induction/Emergence: slow due to high B:G
Used for:
Pediatric anesthesia due to pleasant odor
Contraindication:
Causes autoimmune hepatotoxicity [helothane hepatitis] in adults due to high degree of hepatic metabolism
26
What is the primary inhalation anesthetic used in adults in the USA due to its cheap nature?
Isoflurane
27
In what 3 groups of people should you avoid desflurane? Why?
1. children - due to its rapid emergence, kids experience delerium
2. Asthmatics
3. Heavy smokers
[causes airway irritation more than other agents because it is not metabolized, but rather nearly completely eliminated through the lungs]
28
What inhalation anesthetic has the lowest B:G partition coefficient?
What does this say about the solubility?
What does it allow for us to control?
Desflurane has the lowest B:G which means it has a low solubility.
It allows for RAPID control of depth of anesthesia
29
What is sevoflurane used for?
| What is the major contraindication?
It is popular in pediatrics for inhalation induction and is often combined with NO for induction because it is :
1. higher solubility than desfluorane [need NO for induction]
2. more potent than desfluorane but w/o airway irritation
Contraindications:
Renal dysfunction due to theoretical toxic by-products
30
What inhalation anesthetics:
1. decrease mean arterial pressure
2. increase HR
3. have minimal cardiovascular effects?
1. HISD
2. ISD
3. nitrous oxide
31
What inhalation anesthetics cause:
1. decrease in minute ventilation
2. depress respiratory response to hypercapnia and hypoxia
1. HISD [everything but NO]
| 2. all of them
32
How is the goal of inhalation anesthesia and IV anesthesia different for respiratory depression?
Inhalation - you want respiratory depression/apnea so you can assume comtrol of respiration by mechanical ventilation
IV- you want to maintain spontaneous respiration in patients
33
What is meant by "luxury perfusion"?
What is the drawback?
What anesthetic gases have this effect?
It means there is:
1. decreased cerebral metabolic activity [CMR]
2. increased cerebral blood flow [CBF]
The drawback to the effect on CNS is that increased CBF raises ICP [problem if it is already elevated or if you are doing a neurosurgical procedure
ALL inhaled anesthetics have this effect
34
What is the effect of all inhaled anesthetics on the kidney?
| How are the effects minimized?
They cause a dose-dependent decrease in GFR and urine output [due to decreased cardiac output and BP]
Effects are minimized by adequate hydration. In addition, they rapidly reverse upon cessation of the drug
35
What is the effect of all inhaled agents on the liver?
1. All decrease hepatic blood flow
| 2. halothane has specific hepatotoxicity
36
What is malignant hyperthermia due to?
What inhalation anesthetics have the potential to cause malignant hyperthermia?
How will these patients present?
What will their labs show?
What causes susceptibility to this condition?
If you know your patient is susceptible, what can you do?
Malignant hyperthermia is caused by hypermetabolic muscles [due to mutated ryanadine receptors]. It is Autosomal dominant
All can cause malignant hypertension except NO.
The patients will be hypercapnic, hypertensive, and tachycardia.
Labs will show lactic acidosis and hyperkalemia, increased tone, hyperthermia.
Susceptibility: auto dom. mutation in ryanadine receptor
If a patient has a potential family history, give them:
1. NO and IV anesthesia
2. any non-depolarizing muscle relaxant [not succinylcholine]
37
In addition to the inhalation anesthetics [minus NO], what other agent has the potential to cause malignant hyperthermia?
succinylcholine [a depolarizing muscle relaxant]
- in susceptible patients, you should use a non-depolarizing muscle relaxant
38
What are the 5 steps of treatment if a person is presenting with malignant hyperthermia?
1. cease the anesthetic agent
2. rapid/aggressive cooling attempts
3. IV hydration
4. IV dantrolene
5. Ca channel antagonist
39
What is the Meyer-Overton Principle?
Inhaled anesthetics decrease neuronal activity by partitioning into cell membrane lipid bilayers disrupting the membrane dynamics and distorting the ion channels, thus altering or abating the production of action potentials. *Indirect/nonspecific
[supported by the fact that more lipophilic = more potent w/ lower MAC]
40
What facts oppose Meyer-Overton principle and rather support that inhaled anesthetics work by direct interactions with neuronal membrane proteins to alter ion channel activity?
1. steep dose-response curve [although indirect action could produce a secondary messenger that binds and disrupts ion channels]
41
What is the proposed effect of anesthetics of NMDA channels and GABA receptors?
NMDA glutamate receptors are the major excitatory neurotransmitters of the CNS. Volatile anesthetics inhibit certain Ca channels [including them]
GABAa receptors are the major inhibitors of the CNS and are Cl channels. Volatile anesthetics bind and open the channels to increase inhibition of neurons
42
Neuromuscular blocking agents produce _________ NOT ______________.
paralysis NOT anesthesia
43
What are the 2 major uses of neuromuscular blocking agents?
1. paralyze muscle so you can intubate with an endotracheal tube
2. achieve surgical relaxation
44
What is the structure of succinylcholine?
What is the mechanism of action?
What are the 3 major uses?
It is 2 Ach joined together.
MOA: Ach receptor agonist, but not metabolized by AchE so results in longer depolarization. Metabolized by pseudocholinesterase in the liver
Primary uses:
1. emergent intubation
2. rapid induction on a full stomach [prevent aspiration]
3. very short surgical procedures
45
What are the 4 major side effects of succinylcholine?
1. bradycardia
- stimulates muscarininc receptors in SA node
- children are esp. susceptible so do IV atropine prior
2. hyperkalemia
- induces depolarization throughout the body which raises serum K
- life threatening of K is already high [burn victims]
- myopathies, denervation injury, immobilization have a greater K increase
- cardiac arrest is refractory to resuscitation
3. malignant hyperthermia
- avoid in peds
4. drug interactions
46
What are the general characteristics of the 2 non-depolarizing muscle relaxants?
How do they work?
Vecurium and rocurium are competitive antagonists for the Ach receptor
They differ from succinylcholine because they do NOT change the conformation of the channel and thus there is NO membrane depolarization
47
What 4 things potentiate the blockade of a non-depolarizing muscle relaxant [vecuronium, recuronium[?
1. hypothermia
2. acidosis
3. electrolyte abnormalities
4. concurrent disease
48
How do vecuronium and recuronium differ?
Vecuronium has onset in 3-4 minutes and rocuronium in 1 minute.
They both act for 30-60 min and have biliary excretion
49
What are the 2 nondepolarizer reversal drugs?
1. cholinesterase inhibitor
- inactivates breakdown of Ach raising the concentration compared to vecuronium or recuronium
* *be careful bc it will potentiate depolarization blockade
2. anticholinergics
50
What are the IV induction agents?
Why are they preferable to gas?
What is the one situation where you would use gas>IV for induction?
Propofol [and/or maintenance/sedation + amnestic]
Etomidate
Thiopental [barbituate]
Preferable to gas because they minimize/abolish stage 2 anesthesia [excitement/irreg respirations and heart rate]
The one situation where gas is used is in children lacking IV access.
51
Maintenance of anesthesia is typically achieved with gas, but what 3 IV agents are potent enough to be the sole anesthetic in shorter, less stimulating surgeries?
Propofol [also amnestic]
Dexmedetomidine [ also analgesic]
Ketamine [also sedative, amnestic and analgesic]
52
What are benzodiazepines used for in IV anesthesia?
Midazolam is less potent and too slow acting for induction, but it is used to provide sedation in the perioperative period
53
A typical general anesthetic for major surgical procedures includes what 6 components?
1. amnestic/sedative
2. analgesic
3. induction agent
4. muscle relaxant
5. maintenance anesthetic
6. relaxant reversal
54
What are the 2 primary uses of midalozam?
| What are the 3 advantages and 2 disadvantages?
1. sedative prior to anesthesia
2. seizure control
Advantages:
1. antegrade amnesia [lasts 6 hrs]
2. can be reversed by flumazenil
3. anti-seizure
Disadvantages:
1. respiratory depression [esp to hypercapnia]
2. no analgesia
55
What is the primary use of morphine, fentanyl, and remifentanil in IV anesthetics?
What are the 3 advantages?
What are the 2 disadvantages?
These are opioids used for intraoperative and postoperative analgesia
Advantages:
1. analgesia
2. cardio stability
3. reversed by opioid receptor antag [naloxone]
Disadvantages:
1. nausea
2. respiratory depression
56
What is the primary use of thiopental?
What are the 2 advantages?
What are the 3 drawbacks?
Thiopental is a barbituate used for induction esp. in NEUROANESTHESIA
Advantages:
1. rapid onset
2. cerbroprotective
Disadvantages:
1. no analgesia
2. hypotension
3. slow recovery
57
What is the primary use of etomidate?
What are 3 advantages?
What are 3 disadvantages?
It is used for induction esp in patients with cardio problems or hypotension
Advantages:
1. rapid onset
2. ultra short duration
3. less cardio depression
Disadvantages:
1. nausea/vomiting
2. no analgesia
3. slower elimination
58
What IV anesthetic is:
1. the most common induction agent
2. sedative in the ICU
3. maintenance in short procedures
Propofol
59
If a patient is hypotensive, what 2 barbituates would you consider for IV anesthesia induction agents?
What 2 should you absolutely avoid?
1. etomidate
2. ketamine [esp if they are in shock]
CANNOT use:
1. thiopental
2. dexmedetomidine
60
A patient is really hypotensive so you choice an appropriate induction agent for their IV anesthesia. Now they are having hallucinations, are disoriented, have an increased ICP.
What drug did you give him?
Ketamine
61
If you really want to limit respiratory depression, what IV anesthetics should you consider?
1. ketamine
| 2. dexmedetomidine
62
How do succinylcholine and vercuronium/recuronium differ in terms of advantages/disadvantages?
Succinylcholine:
- Pro = rapid onset [15s], short acting
- Con = malignant hypertension, hyperK, bradycardia
Nondepolarizers:
- Pro = long lasting
- Con = slow onset [1-4min], long lasting
63
How are benzodiazepines [midazolam] administered?
What is the onset of action?
What is duration of action?
What is metabolism/excretion?
1. PO, IV, IM
2. onset of action is 2-4 minutes
3. lasts 1-2 hours [determined by tissue redistribution NOT excretion or metabolism]
4. metabolized in liver, metabolites excreted in urine
64
Describe the mechanism of action of benzodiazepines [midazolam].
They enhance GABA activity by binding to a specific, non-ligand binding site on GABAa receptor in the cerebral cortex.
This increases the FREQUENCY of Cl channel opening.
*benzodiazepines will have no functional effect in the absence of GABA
65
In addition to providing pain relief during general anesthesia, what is the other effect of opioids in balanced anesthesia?
It lowers the MAC of inhalation agents
66
What is the effect of opioids on the cardiovascular system?
No DIRECT myocardial depression, however, they decrease BP via :
1. decreased sympathetic reflex
2. bradycardia
The effect can be significant if combining opioids with other anesthetics
67
What are the 3 major effects of opioids on the brain?
1. analgesia [with mild sedative effect]
2. nausea and vomiting with morphine due to medullary chemoreceptor stimulation
3. physical/psychological dependence with long term or repeated use
68
What is the effect of opioids on respiration?
| If the side effect is life-threatening, what can be given?
Opioids are potent respiratory depressants because they:
1. decrease hypoxic ventilatory drive
2. increase tolerance to hypercarbia
If there is life-threatening respiratory depression in a non-ventilated person, give then naloxone
69
How does the onset of action and duration of action differ from morphine to the other opioids?
Morphine has a slower onset and longer duration of action [4-5hrs]
70
What opioid is 100x more potent than morphine?
How does the onset and duration of action compare to morphine?
What are the 3 preparations?
Fentanyl is 100x more potent
It has a faster onset and shorter duration of action [it is more rapidly cleared]
1. IV
2. patch [transdermal]
3. lollipop [transmucosally]
71
How does the potency, onset of action, and duration differ for fentanyl and remifentanil?
Remifentanil has the same potency as fentanyl. The difference is that remifentanil is ULTRA short acting [3min]
72
Why is remifentanil ULTRA short acting?
How is it administered?
What type of surgery is it especially useful for?
it has a unique ester structure that can be rapidly hydrolyzed by esterases in the plasma.
It is administered by continuous infusion during surgery, but the short duration allows for rapid wake up after surgery
Useful for neurosurgery
73
What is the use of naloxone?
How should it be delivered?
What negative side effect is there?
Naloxone is a competitive antagonist at the opioid receptor so it is used in opioid overdose to try to reverse the respiratory depression.
*has a short duration of action [30min] due to distribution in tissue. This is shorter than most opioids so you may need continuous infusion.
Negative side effect: it also reverses analgesia so the patient may be in significant pain
74
What are the 3 subtypes of opioid receptors in the brain?
What receptor type do most of the morphine-like agents acts as agonists on?
What are the 2 mechanisms of action of opioids?
Opioid receptors are mu, kappa and delta.
Morphine drugs work on the mu receptor [GPCR] that:
1. inhibits the release of excitatory neurotransmitters pre-synaptically [block Ca channel]
2. inhibit activation post-synaptically by activating hyperpolarizing K channels
75
What IV induction agent is used most commonly with neuroanesthesia?
Why?
thiopental because it:
1. decreases cerebral blood flow
2. decreases cerebral metabolic rate/O2 consumption
3. decreases intracranial pressure
4. protection from transient focal cerebral ischemia
5. anticonvulsant
76
What are the effects of thiopental on cardiovascular system?
| What 3 patients specifically should it be avoided for?
1. rapid decrease in BP due to vasodilation
2. increased HR due to central vagolytic effect
Avoid with:
1. CHF
2. B-blockade
3. hypovolemia
77
How fast is induction with thiopental?
What is recovery time?
What is elimination time?
What procedures should you avoid its use, just based on pharmacokinetics?
Induction is in 20seconds due to rapid distribution of the drug in high flow tissue [brain].
It is this fast because 50% is unionized [lipid soluble] at physio pH
Recovery takes 20-30 minutes and depends on the redistribution to other less vascular tissue [NOT metabolism or excretion]
Elimination is very slow and takes 8-10 hours because the drug leaves the tissue where it was redistributed and goes to the liver
*avoid using in outpatient surgeries
78
What is the mechanism of action of thiopental [a barbituate]?
What are the 2 main ways it is different from benzodiazepines?
1. It acts to enhance GABA activity by binding to non-ligand pocket sites to PROLONG OPEN STATE by slowing dissociation of GABA. [different from benzodiazepines that increase frequency of opening].
2. At high concentrations they can directly activate the Cl channel independent of GABA [also different from benzodiazepines]
3. inhibits glutamate and Ach [contribute to anesthetic vs. sedative effect of benzos]
79
A patient with CHF needs to get anesthesia. What agent is at the top of your list because of the minimal cardiovascular depression associated with it?
Etomidate
* also reduces ICP, CMR, CBF like thiopental
* also has minimal respiratory effects
80
Describe induction, recovery, and elimination of etomidate?
Induction- patient unconscious in less than 1 min
Recovery- rapidly redistributes to lower perfusion tissue in 5 minutes
Elimination- hydrolysis by esterases in the liver in 1-2 hours
81
What is the mechanism of action of etomidate?
Similar to barbituates [thiopental] and benzodiazepines [midazolam], it binds to GABA receptor increasing the receptors affinity for GABA.
At high concentrations, it can directly induce current in the absence of GABA
82
What is the effect of the following on the GABA receptor?
1. benzodiazepine
2. barbituate
3. etomidate
4. propofol
1. binds and increases the FREQUENCY with which the channel opens [GABA dependent]
2. bind and PROLONG open state of the channel [GABA independent]
3. increases GABAr AFFINITY for GABA [at high concentrations, GABA independent]
4. slowing the closing time of GABA receptor
83
What anesthetic is the choice for outpatient surgery? Why?
Propofol because it has rapid induction like thiopental and etomidate, but the recovery is substantially faster allowing earlier ambulation
Also, it decreases nausea/vomiting post-op
84
What is the effect of propofol on cardiovascular system?
1. decreases SVR, contractility and preload
2. does NOT change HR
Overall effect is hypotension [even more than thiopental]
85
How do thiopental and propofol differ in how they lower cerebral blood flow?
Propofol decreases CBF by dropping BP
Thiopental cerebral vasoconstricts.
[thiopental is thought to be more cerebro-protective]
86
Which drug is such a profound respiratory depressant that it results in apnea at induction doses?
propofol
87
Describe the induction, recovery and elimination of propofol.
Induction- unconscious in 30 seconds, due to rapid distribution to high flow tissue
Recovery - tissue redistribution in 2-8 minutes for induction dose [if maintenance, frequent redosing is necessary]
Elimination- 30 to 60 minutes as it is rapidly metabolized in the liver and excreted in urine
88
What is the mechanism of action of propofol?
Increases GABA receptor channel being open by slowing the closing channel time
89
What IV anesthetic can be used for sedation, induction and maintenance in procedures like dressing changes, endoscopy or plastics that will make the person have dissociative anesthesia?
What is dissociative anesthesia?
```
Ketamine produces dissociative amnesia where the patient experiences
1. disconnection from the environment
2. catatonia
3. amnesia
4, analgesia
```
[they appear consciuous but they cannot process sensory info]
90
What is the ONLY IV anesthetic that produces cardiac stimulation with increased HR, CO and BP?
Who should you avoid using this drug with?
Who would it be EXCELLENT to use on?
Ketamine should be avoided with:
1. severe CAD
2. uncontrolled HTN
It is perfect for hypovolemic patients
91
You give a patient an IV anesthetic and are monitoring them. They have increased ICP and CBF. The patient has disturbing psychomimetic side effects upon emergence with:
- disorientation
- sensory/perceptual illusions
- vivid dreams post op
What drug did you give?
What should you have premedicated the patient with to avoid the psychomimetic side effects?
Ketamine [which has a chemical structure similar to PCP]
Pre-medication with benzodiazepine is advised
92
Describe the induction, recovery and elimination of ketamine.
Induction: 1-2 minutes
Recovery: similar to etomidate and thiopental in that it redistributes to peripheral tissue in 10-15 min, but amnesia/analgesia continue longer periods of time
Elimination: hepatic metabolism
93
What is the mechanism of action of ketamine?
1. Antagonizes the excitatory NMDA glutamate receptor
2. MAY have a specific receptor
It dissociates the thalamus from the limbic cortex so sensory input does not result in awareness [dissociative anesthesia]
94
What IV anesthetic is a highly selective a2 adrenergic receptor agonist that is used as an adjunct to reduce MAC and opioid requirements? It has analgesic and sedative properties but cannot achieve true surgical anesthesia
Dexmedetomidine :
- substantial analgesia
- sedative for intubated in ICU
95
What is the effect of dexmedetomidine on cardiovascular system?
How does the effect differ if it is a rapid infusion or large bolus vs. slow&low dose?
although highly specific for a2, it can act as an agonist on a1 receptors so the response is biphasic:
1. Rapid infusion/bolus = transient hypertension with reflex bradycardia [a1 effect]
2. slow/low = a2 sympatholytic causes hypotension and further bradycardia
96
An obese patient needs to receive anesthesia. What drug can you give that will preserve the patients response to hypercapnia?
Dexmedetomidine because it preserve respiratory response
97
What is the loading dose, recovery and elimination of dexmedetomidine?
Loading dose: slow infusion over 10 min to avoid hemodynamic swing
Recovery : redistribution to peripheral tissue in 10-15 minutes for a single dose [infusion is longer]
Elimination: biotransformation in the liver in 4 hours
98
What are the 3 locations in the body where dexmedetomidine shows effect?
What is the mechanism of action?
1. Brain - works on a2 adrenergic receptors in the nucleus ceruleus inhibiting NE release --> sedation
2. Spinal cord: inhibits release of substance P and inhibits firing of nociceptive neurons --> analgesia
3. peripheral vasculature: presynaptic a2 mediates negative feedback inhibiting NE release which direct effect on a1 so transient HTN followed by hypo
