Inhaled Anesthetics Flashcards
(127 cards)
1
Q
What are some characteristics desired in the ideal anesthetic?
A
- Rapid induction and recovery (low BG solubility)
- Controllable duration of action
- easy to administer
- no unwanted effects on organs
- no toxic metabolites
- predictable elimination
- useful in all age groups
- adequate muscle relaxation
- pharmacokinetics unaltered by pt pathophys
- high degree speicfic action/function
- levels easily identified and managed- rapid adjustment of depth of anesthesia
- wide margin of saftety (halothane most narrow)
2
Q
What development made inhaled anesthetics less flammable?
A
Replacing a hydrogen atom with a fluorine atom
3
Q
What was a main problem with halothane when it was developed?
A
Lots of dysrhythmias
4
Q
What was the main problem with methoxyflurane when it was made?
A
Free fluorid release causing high output renal failure
also hepatotoxic
5
Q
What was main problem with enflurane?
A
Generated sz, increase ICP
6
Q
What is isoflurane an isomer of?
A
Enflurane
7
Q
Desflurane is completely _____
A
florinated
8
Q
What was the initial concern with sevoflurane?
A
Free flouride release causing renal failure (like methoxyflurane). HOwever, unfounded results
9
Q
What is general anesthesia?
A
State of unsoncsiousness of the brain (hypnosis and sedation), amnesia and immobility
- mechanism may not be same for all three effects
10
Q
What are the assumed sites of action of inhaled anesthetics?
A
CNS (Brain/spinal cord)
- immobility spinal cord mediated
- hypnosis and amnesia in brain
Observations of stereoselectivity supports theory that a mysterious specific protein receptor interaction target molecule is involved.
11
Q
What is the meyer-overton theory?
A
Disproved theory for mechanism of action for inhaled anesthetics
- Absorption of anesthetic molecules expands hydrophobic region- expansion of lipid bilayer beyond critical amt and alters membrane function
12
Q
Potential sites of action of inhaled anesthetics?
A
- Presynaptic voltage gated Na channels
- 2-pore potassium chennels
- TREK nad TASK channels
- Ionotropic and metabotropic receptors
- GABA, Glycine
- Glutamate (NMDA, AMPA, Kainate)
13
Q
What is glycine?
A
Major inhibitory neurotransmitter in spinal cord and may be site of action for immobility effect
14
Q
What do 2 pore potassium channels do?
A
TREK and TASK
Play role in maintaining cell RMP
Make cell membrane +/- negative and decreases excitability
15
Q
What is the unitary theory?
A
all GA act at same mechanism
16
Q
What is the degenerated theory?
A
different classes= different mechanisms
17
Q
What is stage 1 of anesthesia?
A
amnesia/analgesia
- normal pupillary reaction
- changes in respriatory rate
- irregular pulse
- normal BP
- Stage of analgesia/inudction. Dizziness, unreality, lessening sensitivity to touch and pain. sense of hearing increased, response to noises intensified
18
Q
What is stage II of anesthesia?
A
Delirium/excitement
- still pupillary changes
- changing respiratory rate
- pulse irregular and fast
- BP high
***most prone to laryngospasm***
Stage of excitement- variety of reaction involving muscular activity and delirium. VS show evidence of physiological stimulation. Patient may response violently to very little stimulation
19
Q
What is stage 3 of anesthesia?
A
Surgical anesthesia- 4 planes
- no pupil response,
- steady, slow pulse
- normal BP
- Called surgical/operative stage- 4 levels of consciousness. Anesthesia determien which plane is optimal for procedure according to specific tissue sensitivity of individual and surgical site
Each successive plane achieved by increasing concentration of anesthesia
20
Q
What is stage 4 of anesthesia?
A
overdose
- pupils unresponsive
- no respiration
- weak and thready pulse
- low BP
“Toxic” or “danger stage”- NEVER DESIRED. Cadiopulmonary failure and death can occur.
21
Q
Main characteristics of nitrous oxide?
A
- only inorganic anesthetic gas
- 34x more soluble than nitrogen
- colorless
- sweet smell- some same odorless
- nonexplosive and non flammable but supports combustion
- gas at room temp
- MAC= 105%, low potency
- b/g partition coeff- 0.47
22
Q
We administer nitrous oxide using what kind of technique?
A
Balanced technique- administered with induction agent, skeletal muscle relaxant, opioids, and/or volatile agents
23
Q
70% nitrous oxide and oxygen significantly ___ ___ for halothane, enflurane, isoflurane, desflurane, and sev
A
reduces MAC
24
Q
Does N2O provide analgesia?
A
Yes!
25
What is the concentration effect?
Nitrous oxide speeds induction as fresh gas is literally drawn into lung from breathing circuit
26
What does the second gas effect of nitrous do?
Enhances rate of induction
27
What is diffusion hypoxia?
Rapid transfer from blood and tissues into alveoli, decreases arterial tension of oxygen in the alveoli. MUST administer 100% FIO2 after d/c of N2O
28
What are cardiovascular effects of nitrous oxide?
* Stimulates sympathetic nervous system
* DIrect myocardial contractility depressant
* may unmask undiagnosed myocardial depression in CAD, sever hypovolemia, opioids
* Arterial BP, SVR, CO and HR unchanged or modestly elevated secondary to stimulation of catecholamines (sympathomimetic effect)
* Constricts pulmonary vascular smooth muscle and increases PVR (avoid in Pulm HTN, sleep apnea pt)
* Increases RA pressure
* Associated with higher incidence of epinephrine induced dysrhythmia
29
What are respiratory effects of nitrous oxide?
* Increases respiratory rate
* decreases Vt
* overall decrease in MV
* Minimal change in Ve and resting CO2 elvels
* hypoxic drive markedly depressed
* depression of medullary ventialtion center
* diffusion hypoxia
30
What are cerebral effects of nitrous oxide?
* Increases CBF
* produces mild elevation of ICP
* Increases CMRO2
* may increase motor activity- clonus and opisthotonos- spasm in which head, neck and spine are arched backwards.
31
What are neuromuscular effects of nitrous oxide?
* Does not provide significant muscle relaxation
* may cause skeletal muscle rigidity at \>1 MAC (lab situration, not possible in real life)
* not an MH trigger according to MHAUS
32
What is nitrous oxide's effect on renal, hepatic and GI?
* Decreases renal blood flow by increasing renal vascular resistance
* decreases GFR and urine output
* Hepatic blood flow mildly decreased
* suggest PONV risk increased (activated chemoreceptor trigger zone)
* causes distention of bowel- NOT indicated with bowel obstruction
33
Biotransformation and toxicity of nitrous oxide?
* Almost exclusively eliminated by exhalation
* Irreversibly oxidized cobalt atom in vitamin B12 and inhibits vitamin b12 dependent enzymes
* inhibits methionine synthetas- necessary for myelin formation
* inhibits thymidylate synthetase- necessary for DNA synthesis
* avoid in pregnant patients
* increased incidence of miscarriage in OR personnel
* may alter immune respone to infection
* dose dependent inhibition of leukocytes and chemotaxis for phagocytes
34
How does nitrous oxide inhibit vitamine b12?
* Irreversibly oxidized cobalt atom in vitamine b12 and inhibits vitamine b12 dependent enzymes
* includes methionine synthetase, necessary for myelin formation and thymidylate synthetase, necessary for DNA synthesis
* prolonged exposre \>24 hours, and abuse, can result in bone marrow depression (megaloblastic anemia), peripheral neuropathies, pernicious anemia
35
What are contraindications for nitrous oxide?
* diffuses into air cavities
* anything that has potential for expanding space ie
* air embolism
* pneumothorax
* acute intestinal obstruction
* intracranial air
* pulmonary air cyst
* intraocular air bubble
* tympanic membrane grafting
* diffuses into ETT cuff
* avoid in pt with pulmonary HTN (vasoconstriction)
* limited value in patient requiring high FIO2
36
Why do we ask if patient has had recent eye surgery when considering use of nitrous?
* If patient exposed to nitrous w/in 10 weeks after sx for retinal detachment can cause expansion of air bubble in eye, causing blindness
37
What are drug interactions of nitrous oxide?
* Cannot be used as complete anesthetic (reuiqres high MAC)
* Decreases MAC requirements of other agents
* potentiates NMB
38
What increases anesthetic potency?
halogen substitutions
39
All volatile agents except N2O are __ \_\_\_
carbon compounds
40
Which type of halogen has decreased potency, lower weight or higher atmoic weight?
Lower weight
41
Chlorine substitutions lead to ___ \_\_\_
myocardial depression
42
What reduces flammability?
Florination
43
Vapor pressure halothane?
BG coeff? MAC?
vp: 243
BG: 2.3
MAC 0.74
44
Vapor pressure enflurane? BG? MAC?
VP: 175
BG: 1.8
MAC: 1.68
45
Vapor pressure isoflurane? BG? MAC?
VP: 239
BG: 1.4
MAC: 1.15
46
Vapor pressure desflurane? BG? MAC?
VP: 664
BG: 0.42
MAC: 6.0
47
Vapor pressure sevoflurane? BG? MAC?
VP: 157
BG: 0.69
MAC: 2.05
48
vapor pressure n2o? BG? MAC?
VP: 38,770
BG: 0.47
MAC: 104
49
What is vapor pressure? Boiling point?
**Vapor pressure-** pressure created when gas molecules bombard surface of liquid and walls in closed container
**boiling point-** vapor pressure equals barometric pressure
molecules in closed container are distrubuted b/w gas and liquid phase
50
What is relationship between temperature and vapor pressure?
Direct (increase temp, increases vapor pressure)
51
What is relationship b/w altitude and vapor pressure?
Increase altitude, decrease barometric pressur
decrease altitude, increase barometric presure (inverse)
52
When does boiling point occur?
When vapor pressure= barometric pressure
53
What is MAC?
* Minimum alveolar concentration at 1 ATM that produces immobility in 50% of patients exposed to noxious stimuli
* measures potency of IA
* INhalation equivalent of ED50
54
What are factors that do NOT affect MAC?
* Variable stimulus
* species
* sex (Gender)
* duraiton of anesthesia (no conest-sensitive MAC)
* acid-base disturbance
* PAo2 (40-500)
55
Factors decreasing MAC?
* increasing age
* hypothermia
* hyponatremia
* hypotension
* pregnancy (not sure why)
* hypoxemia \<38
* opioids
* ketamine
* benzos
* clniidine
* a2 agonist
* LA
* ETOH (acute)
* lithium
56
Factors increasing MAC?
* Hyperthermia
* CNS stimulants
* youth under 1 yo
* increased pheomelanin production (red hair)
57
What is the equivalent of ED95 for inhaled anesthetics?
* Avoiding movement when no muscle relaxant on board requires 1.3 MAC (similar to ED 95)
58
What is MAC awake?
Concentration that prevents consciousness in 50% of patients is approximately 1/2-1/3 MAC
1/3 MAC- des sevo, iso
1/2 MAC for halothane
60% for N2O
59
What is mac memory?
Concentration of anesthetic associated with amnesia in 50% of patients is significantly less than MAC awake
Never go below mac awake!
60
General characteristics of Halothane?
What is it's chemical structure class?
* Halogenated alkane derivative
* Vapor pressure= 243
* BG coeff- 2.3 (intermediate)
* MAC 0.76
* Non flammable
* Sweet, non pungent
* contains thymol - can make vaporizer sticky
61
One advantage of volatile agents versus TIVA?
More reliable at preventing recall!
62
Cardiovascular effects of halothane?
* Direct myocardial depressant= BP decrease (from decreased CO)
* Dose dependent decrease in CO (SV decreases 15-30%)
* DOES NOT DECREASE SVR
* coronary vasodilator, coronary blood flow decreased from drop in system BP, can cause ischemia
* potection from decreased myocardial oxygen demands
* blunts baroreceptor response to hypotension, no increase in HR
* increased RAP
* increase cutaneous blood flow (watch for hypothermia)
63
Halothane and arrhythmias?
* Decrease SA node depolarization- prone to junctional rhythm
* Decreased conduction AV node/his-purkingje
* caution when epi is injected
64
Halothane respiratory effects?
* Increased rate
* decreased VT
* decreased minute ventilaton, increased resting PACO2
* Apneic threshold rises
* hypoxic drive severely depressed (even at low doses of 0.1 MAC!)
* Potent bronchodilator can reverse asthma-induced bronchospasm
65
Halothane cerebral effects?
* Uncouples cerebral blood flow and metabolism
* increases CBF, ICP, increases IOP while modest decrease in CMRO
* Autoregulation blunted
* can prevent ris in ICP by hyperventilation prior to halothane admin
* cerebral activity decreased
66
Neuromuscular effects of halothane?
Potentiates non depolarizing NM blocking meds
skeletal muscle relaxation 2x less than other volatiles
67
Renal effects of halothane?
Reduces RBF, GFR, nad urine output.
Can limit by preop hydation
68
Hepatic effects of halothane?
* Decreased hepatic blood flow
* hepatic artery vasoconstriciton
* anesthetic induced inhibition of hepatic drug metabolizing enzymes
* metabolism of fentanly, phenytoin, verapamil may be impaired
* minor liver enzyme elevation
* oxidized metabolite- trifluroracetic acid
69
What is the oxidized metabolite of halothane? what does it cause?
Trifluroracetic acid
* Can cause hepatotoxicity
* Mild- 20% develop, self0limited post op hepatotoxicity
* nausea, lethagy, fever, minor increase liver enzymes
* may be due to non-specific drug effect due to changes in hepatic blood flow that impairs hepatic oxygenation
* Halothane hepatitis
* occurs in 1:10,000 to 1:30,000 adults
* extensive hepatic necrosis and death possible
* most likely immune mediated hepatotoxicity- immunoglobulin G antibodies present in 70% diagnosed
70
What is classic presentation of volatile agnet induced hepatitis?
* Fever
* anorexia
* nausea
* chills
* myalgias
* rash
* fever
* arthralgia
* eosinophilia
* followed by juandice 3-6 days later
71
What are risk factors for volatile agent induced hepatitis?
* \>40 yo
* obesity
* female gender
* mexican ethnicity
* genetic susceptibility
* multiple brief procedures within brief duraiton of time
* enzyme induction (alcohol, phenytoin)
72
What causes volatile agent induced hepatitis?
* Cytochrome p450 2EI oxidized each anesthetic (except sevo) to yield highly reactive intermediates that bind coavalently (acetylation) to a variety of hepatocellular macromolecules
* altered hepatic proteins in blood may tirgger immunologic response that causes hepatic necrosis
* blood thinks altered hepatic proteins are foreign and send immune system to attack
73
How much are each of the volatiles metabolized?
* Halothane- 15-20%
* Enflurane- 2.5-3%
* Sevoflurane 2-5% metabolized\<--- not metabolized in same way, doesn't create abnormal hepatic protein. not susceptible to hepatotoxicity
* Isoflurane- 0.2-2% meta bolized
* Desflurane 0.02%
* N2O 0.004%
74
Halothane drug interactions?
* Myocardial depression exacerbated by beta adrenergic blockers and calcium channel blockers
* TCA and MAO inhibitors may cause BP instability
* aminophylline use has resulted in serious ventricular dysrhythmia
75
Halothane contraindications?
* Patient with unexplained liver dysfunction, following halothane exposure
* pre-existing liver dx
* hypovolemia
* aortic stenosis
* patient with pheochormocytoma
* MH- halothane is most potent trigger of all the volatile agents
76
What is isoflurane?
* Halogenated methyl ethyl ether
* Pungent odor- not for peds induction
* non flammable
* MAC 1.2 (1.15 on other ppt)- (high potency)
* BG partition- 1.4 (intermediate solubiltiy)
77
Isoflurane cardiovascular effects?
* Mild dose dependent myocardial depressant
* occurs with any volatile agent. Overdose can result in CV collapse
* "cardiac stable"- not 100% true since any volatile can cause cardiac collapse with overdose
* CO maintained by rise in HR, partial preservation of baroreceptor reflex (elderly/neonates may see decrease in HR)
* *get response from baroreceptors if surgeon nicks blood vessel*
* Mild B adrenergic stimulation
* increases cutaneous and skeletal muscle blood flow (*dilation*)
* lowers BP via decreased SVR
* lowers LV stroke volume by 15-30%
* Rapid increase in concentration--\> transient increase in HR and BP
* Increased CVP
* Dilates coronaries
78
Why don't you want to use isoflurane during ablations?
* Increases refractoriness of accessory pathways and AV conduction, so isoflurance can interfere with interpretation of EP studies (*they won't be able to find the extra pathway causing dystrhythmias)*
79
What is anesthetic pre-conditioning?
* Happens with every agent, not just isoflurane
* Brief exposure to VA can activate K atp channels- hyperpolarizing effect
* causes negative inotrope/relax vascular smooth muscle
* This dilation protects the heart in subsequent ischemic episodes
* *heart is "primed" to tolerate lack of perfusion/reperfusion better*
* *Good agent to use during anesthesia when there's any interruption to blood flow to the heart*
80
What is coronary steal syndrome?
* With ischemia, normally the local blood vessels dilate in order to bring more blood to that area, which diverts blood flow to the ischmic area preferentially
* concern with isolfurance, is that it dilates ALL coronary vessels, so you're loosing the preferential dilation to the ischemic areas
* concern for decreased perfusion to the already ishemic area
* more of a theoretical concern at this point
81
Isoflurane respiratory effects?
* Tachypnea is less pronounced at \>1MAC compared with other agents
* still has increased RR, decreased TV and MV
* Increased resting PaCO2 *(because of decrease in MV)*
* Blunted response to hypoxia and hypercarbia
* bronchodilator
82
What are cerebral effects of isoflurane?
* Increased CBF, ICP at concentrations \>1 MAC (effects less than halothane and enflurane)
* Effects reversed by hyperventilation
* reduces CMRO2, electrically silent EEG at 2 MAC (thought to provide cerebral protection durign ischemic periods)
* Enhances CSF reabsorption
83
Nueromuscular, hepatic and renal effects of isoflurane?
* NM- relaxes skeletal muscle (*at spinal cord level)*
* Hepatic
* maintains total hepatic blood flow- vasodilator of hepatic circulation
* has beneficial effects on hepatic oxygen delivery
* relatively new finding
* Renal
* decrease RBF, GFR, UOP (*as with all VA)*
84
Metabolism and toxicity of isoflurane (forane)
* slowly metabolized 0.2% to Trifluroacetic acid principal end product
* Hepatotoxicity rare
* Does not produce fluoride ion at clnically sig levels
85
Contraindications for isoflurane? Relative?
* Contraindication- MH
* Relative- very low EF, premie
86
Characteristics of desflurane? (suprane)
* Totally flourinated methyl ethyl ether
* Similar in structure to isoflurane
* Pungent odor- many avoid in asthmatics, but no contraindication
* Vapor pressure clsoe to atmospheric (669), needs special vaporizer
* MAC 6 (low potency)
* BG 0.42 (low solubility)
* Rapid in and out, *even in long cases*
* *has some context sensitive 1/2time but minimal*
87
What is the TEC 6 vaporizer?
* Used for desfulrane
* electrically heated to 39 and pressurized to 1520 mmHg (2atm) to keep in liquid phase
88
Desflurance cardiovascular effects?
* Similar to isoflurane- mild dose dependent cardiac depressant effect
* Decrease SVR nad LV storke volume (15-30%)
* **decreased arterial blood pressure *secondary to decrease SVR***
* **CO remains unchanged** or slightly depressed at 1-2 MAC
* **Baroreceptor reflex intact,** rise in HR
* rapid increase in concentration: transient increase in HR, BP and catecholamine levels (des \>isoflurane)
* **Does not increase, dilate coronary** arterial blood flow
* increased CVP
89
Desflurane respiratory effects?
* Increase RR
* decreased TV
* Overall decrease in minute ventilation, increased resting PaCO2
* blunts hypercarbic and hypoxic response
* profound apnea at 1.5-2 MAC
* \>6% can be irritating to airways, salivation, breath-holding, coughign and laryngospasm
* seen mainly at onset/offset of desflurane, not maintenance
90
Desflurane cerebral effects?
* Increase CBF and CRMO2 decreased
* effect not usually seen until \>1 MAC
* Can lower ICP with hyperventilation
* in neuro anesthesia, stay \<1 MAC
91
Desflurane neuromuscular effects?
* Potentiastes NM blocking agents
* dose dependent decrease in response to TOF and tetanic PNS
92
Renal effects desflurane? Hepatic
* Decrease RBF, GFR, UOP
* No evidence of hepatic injury following its use
93
Contraindications of desflurane? Relative contraindication?
* Contraindication of desflurane- MH
* Relative- anyone that can't tolerate temporary SNS increase. Also asthmatics because of pungent odor.
94
Desflurance biotransformation and toxicity?
* Metabolized \<0.1%
* Serum and urine inorganic fluoride levels essentially unchanged from preanesthetic levels
* Carbon monoxide results from degradation of Des by dried out CO2 absorbents
* high flows on weekend, turn on des on 1st case Monday, increase CO
95
Order of carbon monoxide concentrations with VA?
Des\> enf & Iso \> Halo & Sevo
96
Characteristics of sevoflurane?
Chemical structure type?
* Fluorinated methyl isopropyl ether
* Non-pungent, sweet odor- ideal for peds
* BG- 0.65
* Fast on/off (if short procedure)
* if longer procedure, will act like isoflurane
97
CV effects sevoflurane?
* Mild dose dependent cardiac depressant effect
* SVR, ABP decline slightly
* SV decrease similar to Iso and Des (15-30%)
* Little rise in HR
* only sig \>1.5 MAC
* No evidence of coronary steal
* **Only** common agent that **does not increase CVP**
* **NO** SNS RESPONSE!
98
Sevoflurane Respriatory effects?
* Increased RR and decreased TV, Decreased MV
* Bronchdilator
* minimal airway irritation
* best among current anesthetics, best choice asthmatics
* Decrease in response to CO2 with increased PaCO2
* profound apnea at 1.5-2.0 MAC
99
CNS effects Sevoflurane?
* Decreased cerebral metabolism o2 consumption \> halothane
* increased CBF \< halothane
* increased ICP
* not usually seen until \>1 MAC
* Response to CO2 and autoregulation maintained at 1.5 %
minimal "luxury perfusion" best inhaled agent for neuro.
Less concerning for neuro is \<1 MAC
100
What can sevoflurane "release"?
* **Compound A** is formed when sevo interacts with soda/baralyme, especially at low flow
* not a metabolite
* Compound A is not nephrotoxic alone, but undergoes bioactivation through gluthathione conjugation and metabolism of its conjugates to produce reactive thiol that MAY mediate renal toxicity
* hasn't really been proven in humans, only in rats
* Don't use soda/barlyme with sevo. keep flows \>2L/min
* **Another concern is free fluoride ion release**
* not found to be clinical sig in humans
101
Neuromuscular, heaptic effects of sevoflurane?
* NM- dose dependent potentiation of NDMR
* Hepatic blood flow maintained similar to isoflurane
102
Metabolism and toxicity of sevoflurane?
* Inorganic fluoride level increases- no reproted nephrotoxicity
* metabolized in liver P450 2-5% **DIFFERENT** metabolite from other VA, no concern for halothane hepatitis
* does not get metabolized into trifluroacetylated liver proteins
103
Sevoflurane contraindications?
* MH
* Relative: impaired kidney function. no strong evidence
104
Characteristics of Enflurane?
* Halogenated methyl ehyl ether
* Mild, sweet, ethereal odor,
* nonflammable
* MAN 1.7
* BG 1.9
* Vapor pressure 175
* isomer of isoflurane
105
Enflurance adverse effects?
* Myocardial depression
* sensitizes heart to dysrthmic effects of epi
* abolished hypoxic drive
* marked respiratory depression at 1 MAC, paco2 60 mmHg
* decreased mucociliary function
* increased CSF, and resistance to CSF outflow
* **no reason to use in nuero**
* EEG changes, tonic-clonic sz
* excaerbated by high concentration, hypocapnia, repetitive auditory stim
* **Hyperventialtion NOT recommended, because of increase risk for sz!!**
106
Metabolism and toxicity of enflurane?
* Low metabolism (2-5%)
* Fluoride production much less than methoxyflurane
* induces deflurination, may be clinically sig in rapid acetylators
* detectable renal dysfunction unlikely
107
Enflurane contraindicaitons?
* Avoid in pt with preexisting kidney dx or impairment
* avoid in pt with suspected or known sz disorder
* avoid in pt with increased ICP
* triggering agent for MH
108
OSHA and waste gas policies?
* No worker should be exposed to \> 2ppm halogenated agents in O2 or air
* no \> 0.5ppm halogenated agents if used with nitrous oxide
* No \> 25 ppm N2O
* highest level found b/w anesthesia machine and wall
* *these numbers are arbitrary and don't know full implications of highly concentraed, brief doses*
109
What are characteristics of xenon?
* Inert, odorless, nonexplosive gas
* BG partition= 0.115
* MAC 63-7%
* Does expand closed air spaces \< N2O
* CV stability, blunt SNS response to pain, analgesia, hypnosis
* costly
* limited pt experience
110
Who was Horace Wells?
Dentist that used N2O on his own tooth extraction in 1846
111
Who was Long?
* Used diethyl ether for cyst removal but did not report finding
112
Who was William TG Morton?
* Successfully demonstrated ehter as anesthetic at Mass General
* Within a month of demo. ether gained widespread use in other US cities
113
What was chlorofom?
* Used in UK
* Pleasant odor
* nonflammable
* known hepatoxin
* severe CV depressant
* high incidence of death with administration
* difficult to administer
* *Queen Victoria used in childbirth*
114
What was the first halogenated hydrocarbon anesthetic?
Fluroxene
withdrawn d/t organ toxicity
115
Who synthesized N2O?
* Priestly 1776
116
What is Xenon?
* Inert gas, odorless, nonexplosive
* BG= 0.115
* MAC 63-71%
* Does expand closed air space
CV stability, blunts SNS response to pain, analgesia, hypnosis
Costly
limited patient exposure
117
What anesthetics are pungent and therfore not good to use for inhalational anesthetic (especially in peds)?
Desflurane
Isoflurane
118
Which anesthetics do you not want to use in renal patients?
* Sevoflurane (not proven, just theoretically can lead to renal failure from free flouride release)
* Enflurane
119
Which drugs are direct myocardial depressants?
Halothan
N2O
(as a note, all anesthetics are myocardial depressants, these 2 are noted on ppt as being "direct")
120
Which is the best VA to use in asthma?
Sevoflurane
121
Which VA blocks baroreceptors?
Halothane
| (isoflurane is PARTIAL)
122
Which VA are coronary artery dilators?
Halothane
Isoflurane
123
Which VA decrease SVR (and therefore BP decrease from decrease SVR)
Isoflurane and desflurane \>sevoflurane
124
Which VA have SNS activation?
* Isoflurane (Beta activation, however, so see skeletal muscle dilation, dilations coronary, and decrease in BP!!, decrease in LV stroke volume! )
* N2O
* Desflurane (only at high concentration i.e. overpressure)
Hint to remember- **SNS is activated in a BIND** (beta activation- isoflurane, n2o, desflurane)
125
Which drugs do you avoid in neuro?
* Halothane
* Enflurane
* N2O
"HEN"
126
Which drugs increase arrhythmia risk with epi?
* Halothane
* Enflurane
* N2o
"hen"
127
Which drugs decrease hepatic blood flow?
* Halothane
* Enflurane
* N2O
