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Pharm Test 4 > Inhaled Anesthetics > Flashcards

Inhaled Anesthetics Flashcards

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)
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2
Q

What development made inhaled anesthetics less flammable?

A

Replacing a hydrogen atom with a fluorine atom

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3
Q

What was a main problem with halothane when it was developed?

A

Lots of dysrhythmias

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4
Q

What was the main problem with methoxyflurane when it was made?

A

Free fluorid release causing high output renal failure

also hepatotoxic

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5
Q

What was main problem with enflurane?

A

Generated sz, increase ICP

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6
Q

What is isoflurane an isomer of?

A

Enflurane

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7
Q

Desflurane is completely _____

A

florinated

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8
Q

What was the initial concern with sevoflurane?

A

Free flouride release causing renal failure (like methoxyflurane). HOwever, unfounded results

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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
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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.

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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
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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)
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13
Q

What is glycine?

A

Major inhibitory neurotransmitter in spinal cord and may be site of action for immobility effect

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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

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15
Q

What is the unitary theory?

A

all GA act at same mechanism

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16
Q

What is the degenerated theory?

A

different classes= different mechanisms

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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
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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

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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

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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.

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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
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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

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23
Q

70% nitrous oxide and oxygen significantly ___ ___ for halothane, enflurane, isoflurane, desflurane, and sev

A

reduces MAC

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24
Q

Does N2O provide analgesia?

A

Yes!

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25
Q

What is the concentration effect?

A

Nitrous oxide speeds induction as fresh gas is literally drawn into lung from breathing circuit

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26
Q

What does the second gas effect of nitrous do?

A

Enhances rate of induction

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27
Q

What is diffusion hypoxia?

A

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

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28
Q

What are cardiovascular effects of nitrous oxide?

A
  • 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
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29
Q

What are respiratory effects of nitrous oxide?

A
  • 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
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30
Q

What are cerebral effects of nitrous oxide?

A
  • 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.
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31
Q

What are neuromuscular effects of nitrous oxide?

A
  • 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
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32
Q

What is nitrous oxide’s effect on renal, hepatic and GI?

A
  • 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
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33
Q

Biotransformation and toxicity of nitrous oxide?

A
  • 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
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34
Q

How does nitrous oxide inhibit vitamine b12?

A
  • 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
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35
Q

What are contraindications for nitrous oxide?

A
  • 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
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36
Q

Why do we ask if patient has had recent eye surgery when considering use of nitrous?

A
  • If patient exposed to nitrous w/in 10 weeks after sx for retinal detachment can cause expansion of air bubble in eye, causing blindness
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37
Q

What are drug interactions of nitrous oxide?

A
  • Cannot be used as complete anesthetic (reuiqres high MAC)
  • Decreases MAC requirements of other agents
  • potentiates NMB
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38
Q

What increases anesthetic potency?

A

halogen substitutions

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39
Q

All volatile agents except N2O are __ ___

A

carbon compounds

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40
Q

Which type of halogen has decreased potency, lower weight or higher atmoic weight?

A

Lower weight

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41
Q

Chlorine substitutions lead to ___ ___

A

myocardial depression

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42
Q

What reduces flammability?

A

Florination

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43
Q

Vapor pressure halothane?

BG coeff? MAC?

A

vp: 243

BG: 2.3

MAC 0.74

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44
Q

Vapor pressure enflurane? BG? MAC?

A

VP: 175

BG: 1.8

MAC: 1.68

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45
Q

Vapor pressure isoflurane? BG? MAC?

A

VP: 239

BG: 1.4

MAC: 1.15

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46
Q

Vapor pressure desflurane? BG? MAC?

A

VP: 664

BG: 0.42

MAC: 6.0

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47
Q

Vapor pressure sevoflurane? BG? MAC?

A

VP: 157

BG: 0.69

MAC: 2.05

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48
Q

vapor pressure n2o? BG? MAC?

A

VP: 38,770

BG: 0.47

MAC: 104

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49
Q

What is vapor pressure? Boiling point?

A

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

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50
Q

What is relationship between temperature and vapor pressure?

A

Direct (increase temp, increases vapor pressure)

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51
Q

What is relationship b/w altitude and vapor pressure?

A

Increase altitude, decrease barometric pressur

decrease altitude, increase barometric presure (inverse)

52
Q

When does boiling point occur?

A

When vapor pressure= barometric pressure

53
Q

What is MAC?

A
  • 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
Q

What are factors that do NOT affect MAC?

A
  • Variable stimulus
  • species
  • sex (Gender)
  • duraiton of anesthesia (no conest-sensitive MAC)
  • acid-base disturbance
  • PAo2 (40-500)
55
Q

Factors decreasing MAC?

A
  • increasing age
  • hypothermia
  • hyponatremia
  • hypotension
  • pregnancy (not sure why)
  • hypoxemia <38
  • opioids
  • ketamine
  • benzos
  • clniidine
  • a2 agonist
  • LA
  • ETOH (acute)
  • lithium
56
Q

Factors increasing MAC?

A
  • Hyperthermia
  • CNS stimulants
  • youth under 1 yo
  • increased pheomelanin production (red hair)
57
Q

What is the equivalent of ED95 for inhaled anesthetics?

A
  • Avoiding movement when no muscle relaxant on board requires 1.3 MAC (similar to ED 95)
58
Q

What is MAC awake?

A

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
Q

What is mac memory?

A

Concentration of anesthetic associated with amnesia in 50% of patients is significantly less than MAC awake

Never go below mac awake!

60
Q

General characteristics of Halothane?

What is it’s chemical structure class?

A
  • 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
Q

One advantage of volatile agents versus TIVA?

A

More reliable at preventing recall!

62
Q

Cardiovascular effects of halothane?

A
  • 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
Q

Halothane and arrhythmias?

A
  • Decrease SA node depolarization- prone to junctional rhythm
  • Decreased conduction AV node/his-purkingje
  • caution when epi is injected
64
Q

Halothane respiratory effects?

A
  • 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
Q

Halothane cerebral effects?

A
  • 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
Q

Neuromuscular effects of halothane?

A

Potentiates non depolarizing NM blocking meds

skeletal muscle relaxation 2x less than other volatiles

67
Q

Renal effects of halothane?

A

Reduces RBF, GFR, nad urine output.

Can limit by preop hydation

68
Q

Hepatic effects of halothane?

A
  • 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
Q

What is the oxidized metabolite of halothane? what does it cause?

A

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
Q

What is classic presentation of volatile agnet induced hepatitis?

A
  • Fever
  • anorexia
  • nausea
  • chills
  • myalgias
  • rash
  • fever
  • arthralgia
  • eosinophilia
  • followed by juandice 3-6 days later
71
Q

What are risk factors for volatile agent induced hepatitis?

A
  • >40 yo
  • obesity
  • female gender
  • mexican ethnicity
  • genetic susceptibility
  • multiple brief procedures within brief duraiton of time
  • enzyme induction (alcohol, phenytoin)
72
Q

What causes volatile agent induced hepatitis?

A
  • 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
Q

How much are each of the volatiles metabolized?

A
  • 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
Q

Halothane drug interactions?

A
  • 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
Q

Halothane contraindications?

A
  • 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
Q

What is isoflurane?

A
  • 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
Q

Isoflurane cardiovascular effects?

A
  • 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
Q

Why don’t you want to use isoflurane during ablations?

A
  • 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
Q

What is anesthetic pre-conditioning?

A
  • 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
Q

What is coronary steal syndrome?

A
  • 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
Q

Isoflurane respiratory effects?

A
  • 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
Q

What are cerebral effects of isoflurane?

A
  • 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
Q

Nueromuscular, hepatic and renal effects of isoflurane?

A
  • 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
Q

Metabolism and toxicity of isoflurane (forane)

A
  • slowly metabolized 0.2% to Trifluroacetic acid principal end product
  • Hepatotoxicity rare
  • Does not produce fluoride ion at clnically sig levels
85
Q

Contraindications for isoflurane? Relative?

A
  • Contraindication- MH
  • Relative- very low EF, premie
86
Q

Characteristics of desflurane? (suprane)

A
  • 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
Q

What is the TEC 6 vaporizer?

A
  • Used for desfulrane
  • electrically heated to 39 and pressurized to 1520 mmHg (2atm) to keep in liquid phase
88
Q

Desflurance cardiovascular effects?

A
  • 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
Q

Desflurane respiratory effects?

A
  • 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
Q

Desflurane cerebral effects?

A
  • Increase CBF and CRMO2 decreased
    • effect not usually seen until >1 MAC
  • Can lower ICP with hyperventilation
  • in neuro anesthesia, stay <1 MAC
91
Q

Desflurane neuromuscular effects?

A
  • Potentiastes NM blocking agents
  • dose dependent decrease in response to TOF and tetanic PNS
92
Q

Renal effects desflurane? Hepatic

A
  • Decrease RBF, GFR, UOP
  • No evidence of hepatic injury following its use
93
Q

Contraindications of desflurane? Relative contraindication?

A
  • Contraindication of desflurane- MH
  • Relative- anyone that can’t tolerate temporary SNS increase. Also asthmatics because of pungent odor.
94
Q

Desflurance biotransformation and toxicity?

A
  • 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
Q

Order of carbon monoxide concentrations with VA?

A

Des> enf & Iso > Halo & Sevo

96
Q

Characteristics of sevoflurane?

Chemical structure type?

A
  • 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
Q

CV effects sevoflurane?

A
  • 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
Q

Sevoflurane Respriatory effects?

A
  • 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
Q

CNS effects Sevoflurane?

A
  • 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
Q

What can sevoflurane “release”?

A
  • 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
Q

Neuromuscular, heaptic effects of sevoflurane?

A
  • NM- dose dependent potentiation of NDMR
  • Hepatic blood flow maintained similar to isoflurane
102
Q

Metabolism and toxicity of sevoflurane?

A
  • 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
Q

Sevoflurane contraindications?

A
  • MH
  • Relative: impaired kidney function. no strong evidence
104
Q

Characteristics of Enflurane?

A
  • Halogenated methyl ehyl ether
  • Mild, sweet, ethereal odor,
  • nonflammable
  • MAN 1.7
  • BG 1.9
  • Vapor pressure 175
  • isomer of isoflurane
105
Q

Enflurance adverse effects?

A
  • 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
Q

Metabolism and toxicity of enflurane?

A
  • Low metabolism (2-5%)
  • Fluoride production much less than methoxyflurane
    • induces deflurination, may be clinically sig in rapid acetylators
  • detectable renal dysfunction unlikely
107
Q

Enflurane contraindicaitons?

A
  • 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
Q

OSHA and waste gas policies?

A
  • 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
Q

What are characteristics of xenon?

A
  • 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
Q

Who was Horace Wells?

A

Dentist that used N2O on his own tooth extraction in 1846

111
Q

Who was Long?

A
  • Used diethyl ether for cyst removal but did not report finding
112
Q

Who was William TG Morton?

A
  • Successfully demonstrated ehter as anesthetic at Mass General
  • Within a month of demo. ether gained widespread use in other US cities
113
Q

What was chlorofom?

A
  • 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
Q

What was the first halogenated hydrocarbon anesthetic?

A

Fluroxene

withdrawn d/t organ toxicity

115
Q

Who synthesized N2O?

A
  • Priestly 1776
116
Q

What is Xenon?

A
  • Inert gas, odorless, nonexplosive
  • BG= 0.115
  • MAC 63-71%
  • Does expand closed air space <n2o>
    </n2o><li>CV stability, blunts SNS response to pain, analgesia, hypnosis</li><li>Costly</li><li>limited patient exposure</li>

</n2o>

117
Q

What anesthetics are pungent and therfore not good to use for inhalational anesthetic (especially in peds)?

A

Desflurane

Isoflurane

118
Q

Which anesthetics do you not want to use in renal patients?

A
  • Sevoflurane (not proven, just theoretically can lead to renal failure from free flouride release)
  • Enflurane
119
Q

Which drugs are direct myocardial depressants?

A

Halothan

N2O

(as a note, all anesthetics are myocardial depressants, these 2 are noted on ppt as being “direct”)

120
Q

Which is the best VA to use in asthma?

A

Sevoflurane

121
Q

Which VA blocks baroreceptors?

A

Halothane

(isoflurane is PARTIAL)

122
Q

Which VA are coronary artery dilators?

A

Halothane

Isoflurane

123
Q

Which VA decrease SVR (and therefore BP decrease from decrease SVR)

A

Isoflurane and desflurane >sevoflurane

124
Q

Which VA have SNS activation?

A
  • 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
Q

Which drugs do you avoid in neuro?

A
  • Halothane
  • Enflurane
  • N2O

“HEN”

126
Q

Which drugs increase arrhythmia risk with epi?

A
  • Halothane
  • Enflurane
  • N2o

“hen”

127
Q

Which drugs decrease hepatic blood flow?

A
  • Halothane
  • Enflurane
  • N2O

Pharm Test 4 (4 decks)

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