inhalational agents: history and MAC Flashcards

1
Q

what was surgery like prior to the invention of anesthetic agents?

A
  • surgery was a last, and desperate, resort
  • attempted a wide range of plants (marijuana, belladonna, jimsonweed), hypnosis, and knocking unconscious
  • alcohol: levels needed caused N/V, death rather than sleep
  • opium: strong analgesic but not enough to completely blunt sympathetic stimulation response
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2
Q

when is anesthesiology considered to have begun?

A

1842 w/ the discovery of three agents:

  • nitrous oxide
  • ether
  • chloroform
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3
Q

when and by whom was chloroform discovered?

A
  • 1847

- Dr. James Simpson, British obstetrician

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4
Q

who is Dr. John Snow?

A

first to devote his practice to the administration of anesthetics
-administered chloroform to Queen Victoria during the birth of Prince Leopold

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5
Q

who may have first discovered ether?

A
  • Dr. Crawford W. Long
  • from Georgia
  • first to conceive the use of ether to alleviate pain of surgery, but did not publish his finding
  • not until others took credit for it, claimed he had used since 1841 for minor operations
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6
Q

who first suggested the use of nitrous oxide for anesthesia?

A
  • Horace Wells
  • Connecticut Dentist who had used nitrous oxide successfully during tooth extraction
  • tried to demonstrate technique to a group of Harvard Medical students, but pt. cried out
  • he did not understand the lack of potency of nitrous oxide
  • called “humbug” and driven out of Boston; became addicted to chloroform and committed suicide 1848
  • 1864 finally credited by American dental assoc. and American medical assoc. w/ discovery
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7
Q

who gained recognition first for use of ether?

A

William T.G. Morton

  • dentist and colleague of Wells (N2O)
  • administered ether to Gilbert Abbott at Mass. General, marking first successful public demonstration
  • October 16, 1846- “Ether Day”
  • he called it letheon but later was forced to reveal it was simply diethyl ether
  • able to provide anesthesia during Civil War
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8
Q

what did Morton use to administer the ether?

A

he made a glass inhaler and placed an ether soaked sponge

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9
Q

describe the event on ether day

A
  • October 16, 1846
  • William T.G. Morton, Boston dentist, demonstrated the use of ether during surgery
  • used a glass inhaler containing an ether-soaked sponge to administer the anesthetic to Gilbert Abbott
  • Abbott had a vascular tumor removed by widely known surgeon, John Collins Warren, MD
  • Abbott woke up and denied feeling any pain
  • Warren exclaimed of Morton, “gentlemen, this is no humbug!”
  • known as the “greatest gift ever made to suffering humanity”
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10
Q

Who was Charles Jackson, MD?

A
  • Boston physician and chemist who advised Morton to use ether and claimed to have a large part in the discovery
  • pressed claims for credit all the way to Congress, which upheld Morton as discoverer
  • history of making such claims: also claimed Samuel Morse stole his idea for inventing the telegraph
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11
Q

who is known as the first anesthesiologist and what was his first use?

A
  • Dr. John Snow

- first administered chloroform to Queen Victoria on April 7, 1853

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12
Q

who proposed the use of chloroform as an alternative to ether?

A

James Simpson, MD, an OB in Scotland

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13
Q

why were anesthetics meet religious opposition?

A
  • thought to mock the curse of “primal sin”
  • Genesis 3:16 “Unto a woman, He said, I will greatly multiply the sorrow and thy conception; in sorrow thou shalt bring forth children”
  • Exodus 22:18 “Thou shalt no suffer a witch to live” thought a witch couldn’t handle pain of labor
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14
Q

who finally endorsed the use of anesthetics, rebuffing the minority of priests and ministers who condemned OB anesthesia?

A

Archbishop of Centerbury, John Bird Summer (1780-1862)

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15
Q

who coined the term “anaesthesia”?

A
  • Oliver Wendell Holmes, Sr. (1809-1894)

- from the Greek word “anaisthesia”, meaning “lack of sensation” (1846)

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16
Q

what objections to anesthesia took place?

A
  • American Medical Association (1848)
  • vice president of AMA, John P. Harrison (1849): “pain is curative, the actions of life are maintained by it…”
  • Henry Ward Beecher (famous preacher): “the less pain, the less life capacity; the less pain power, the less life power”
  • Pennsylvania Hospital prohibited use until 1853
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17
Q

describe the ideal anesthetic

A
  • non flammable
  • easily vaporized at ambient temperature
  • potent
  • low blood solubility to assure rapid induction and emergence
  • minimal metabolism
  • compatible w/ epinephrine
  • skeletal muscle relaxation
  • suppresses excessive SNS activity
  • not irritating to airways
  • bronchodilation
  • absence of excessive myocardial depression
  • absence of cerebral vasodilation
  • absence of hepatic and renal toxicity
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18
Q

what were the issues w/ ether?

A
  • flammability
  • prolonged induction
  • delayed emergence
  • PONV high incidence
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19
Q

what brought the development of “modern” inhalation agents?

A
  • with the development of the atomic bomb came discoveries in fluorine chemistry
  • after 1950, all introduced agents (except ethyl vinyl ether) contains fluorine
  • first fluroxene (limited use d/t PONV), then halothane
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20
Q

what were the advantages and disadvantages of halothane?

A

advantages

  • non flammable
  • less pungent
  • less soluble
  • decreased toxicity
    disadvantages: decreased CO and increased arrhythmias (hepatotoxicity)
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21
Q

describe halothane structure

A
  • not an ether, no oxygen
  • an ethane, 2 carbon chain
  • an alkane
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22
Q

after halothane, describe the emergence of newer agents

A
  • Dr. Ross C. Terrell synthesized over 700 fluorinated compounds in an effort to find a better anesthetic than halothane
  • enflurane: methyl ethyl ether; chlorine #347
  • isoflurane: isomer #469 (1970-1980s)
  • desflurane: #653; couldn’t be used in conventional vaporizer d/t its vapor pressure near atmospheric pressure at 669 and low potency making more expensive
23
Q

who invented Sevoflurane?

A
  • Wallin

- there was no perceived need d/t expensive cost and difficult to synthesize

24
Q

what encouraged further development of desflurane and sevoflurane?

A

the advent of outpatient surgery in the 1980s requiring more rapid recovery with a short acting agent

25
Q

what were the effects of increasing fluorination in the agents?

A
  • nonflammable
  • decreased solubility (MAIN advantage)
  • decreased potency (increased MAC)
  • less toxic d/t resistance to degradation
  • decreased percentage metabolized
26
Q

define MAC

A
  • minimal alveolar concentration (partial pressure) of inhaled agent at 1 atmosphere (760 mmHg) that prevents skeletal muscle movement in response to a noxious stimulus in 50% of pts.
  • ED50 or potency
  • MAC can be measure, but what really has the effect on the body is partial pressure
27
Q

how is the ED95 of an agent calculated?

A
  • MAC x 1.3

- 10-30% greater concentration than MAC produces immobility in 90-95% of pts.

28
Q

what portion of the CNS determines MAC?

A
  • spinal cord excitability is decreased resulting in immobility
  • perfusion of the brain alone w/ ordinary circumstances does NOT produce immobility (took up to 3-6x MAC)
  • w/ propofol, the brain determines immobility
29
Q

why use minimal alveolar concentration rather than inspired concentration?

A
  • alveolar reflects the concentration at the cord or the brain most accurately
  • must allow for equilibrium (generally about 10-15 min)
  • dependent on agent: 2-3 time constants
30
Q

what are factors that alter MAC?

A
  • age

- temperature

31
Q

how does age effect MAC?

A
  • *as age increases, MAC decreases about 6% per decade
  • use of nitrous oxide usu. decreases MAC about 60%, but even more in elderly
  • MAC is greatest in pts. less than 1 yr. of age and decreases by nearly 50% in the elderly
  • *greatest to least MAC: infants-children-neonates-adults
32
Q

how does body temperature effect MAC?

A
  • body temperature reduction causes MAC reduction
  • MAC of desflurane decreases almost in half by 10 degree C decrease in temp
  • *MAC of nitrous oxide is not as effected
  • *MAC decreases 2-5% for every 1 degree C drop in temp
  • *consider w/ CABG, use less MAC
33
Q

what factors decrease MAC?

A
  • pregnancy
  • decreased CNS sodium: lethargy (d/t dehydration or absorption of irrigation fluid)
  • depressant drugs
  • other drugs
  • possibly neuraxial opioids
  • PaO2 less than 38 mmHg (but we wont allow this low)
  • BP less than 40 mmHg systolic (we wont allow)
  • cardiopulmonary bypass (decreased temp and metabolic rates)
34
Q

how does pregnancy decrease MAC?

A
  • increased concentrations of progesterone
  • decreases nearly 30% in early postpartum
  • normalizes within 12-72 hrs.
  • typically, moms don’t go for tubal ligations until 2nd day postpartum, so probably normalized
35
Q

what are the effects of depressant drugs on MAC?

A
  • decreased MAC
  • opioids: *non linear synergistic with a ceiling effect (even small dose like fentanyl 3 mcg/kg, causes big decrease in MAC; almost 50% in des from 6.3 to 3.2%, but w/ double the dose only dropped from 6.3 to 2.2%)
  • no amnestic dose of opioids, so w/ ceiling effect, cant totally eliminate MAC needed
  • benzodiazepines: *dose dependent decrease
  • barbiturates and propofol: decrease but redistribution, so effect on MAC doesn’t last long
  • acute ETOH ingestion decreases (but chronic ETOH increases MAC d/t enzyme induction)
  • local anesthetics: lidocaine IV decreases MAC on induction and may prolong if used on emergence
  • N2O: 0.5 MAC of N2O plus 0.5 MAC of isoflurane are additive to 1 MAC of either drug
36
Q

what other drugs decrease MAC?

A
  • clonidine and dexmetomidine (Precedex) decrease MAC by decreasing CNS catecholamines and by hyperpolarizing of CNS cell membranes
  • some beta blockers
  • some calcium channel blockers
  • adenosine
37
Q

what are factors that increase MAC?

A
  • red hair d/t excess pheomelanin production
  • drug induced increases in CNS catecholamine levels (cocaine, ketamine, amphetamines)
  • hyperthermia
  • hypernatremia
  • chronic ETOH d/t enzyme induction
38
Q

what factors do not alter MAC?

A
  • gender
  • duration of anesthesia (except for isoflurane, which decreases d/t accumulation b/c of increased solubility)
  • body mass
  • PaO2 greater than 50 mmHg
  • PaCO2 less than 80 mmHg
  • hematocrit less than 10%
  • SBP greater than 40 mmHg
39
Q

define MAC awake

A

the average of the concentrations immediately above and below those permitting voluntary response to command

  • usually exceeds MAC amnesia, which is hard to measure, so if at MAC awake, know amnesia is covered also
  • gives an idea of how good an amnestic agents is (if wider range between MAC and MAC awake)
40
Q

what affects MAC awake?

A
  • decreases w/ age (but MAC also decreases, so the ratio of the two doesn’t change)
  • inhalation agent
41
Q

what type of anesthetic use are high incidence of recall and why?

A

highest types of case for recall is an opioid, N2O case since MAC awake is 68% and cant give any more than 70%
-very smaller range between MAC awake and MAC (larger ratio or percentage of MAC) and can easily not be above MAC awake

42
Q

what is MAC awake for desflurane, isoflurane, and sevoflurane?

A

1/3 (34%) of their MACs

43
Q

what is the MAC awake for halothane?

A

55% of MAC

44
Q

what is the MAC awake for N2O?

A

64% of MAC

  • not as good an amnestic
  • must supplement for amnesia
45
Q

what is the importance of the ration of MAC awake / MAC?

A
  • higher the ratio, the faster recovery
  • higher the ratio, the poorer the amnestic value
  • *low dose opioids (fentanyl 2-3 mcg/kg) minimally affects MAC awake, but does decrease MAC; this increase the ratio, causing quicker awakening, but poorer amnesia (MAC is decreased closer to MAC awake)
46
Q

does MAC awake ensure ability to protect airway?

A

NO, MAC awake does not ensure return of esophageal sphincter tone or return of pharyngeal function
**sphincter tone is impaired at very low concentrations

47
Q

at what MAC ensures patient airway safety?

A
  • *concentrations of inhaled agent may require levels of less than 0.1 MAC for patient safety
  • *blow all gas off
48
Q

define MAC TE

A

MAC that allows tracheal stimulation

  • no coughing or bucking during suctioning of pharynx
  • no movement or coughing within 1 minute of extubation
  • no breath holding or laryngospasm after extubation
  • *equal to or exceeds MAC (Sevo 2.9-3.2%, 50% more than MAC)
  • *much greater for children
49
Q

when does MAC TE matter?

A
  • important for pediatrics where only inhalation agents are used prior to laryngoscopy
  • when wanting to extubate deep
  • if cuff is deflated, and start to cough, probably in stage II and if extubate, will laryngospasm
  • inflate cuff and allow to wake up
50
Q

define MAC BAR

A
  • minimum alveolar concentration that Blocks Autonomic Response (B-A-R) to surgical stimulus
  • exceeds MAC
51
Q

why should you be careful w/ decreasing MAC and MAC BAR w/ opioids?

A
  • opioids don’t decrease MAC awake

* fentanyl 1.5-3 mcg/kg decreases isoflurane MAC BAR to 0.4 MAC w/ 0.6 MAC of N2O, approaching MAC BAR

52
Q

with 60% N2O, what is MAC BAR of desflurane and isoflurane?

A

1.3 MAC (w/ 0.6 MAC N2O, total 1.9 MAC)

53
Q

with 67% N2O, what is MAC BAR of sevoflurane?

A
  1. 45 MAC (w/ .67 MAC N2O, total 2.2 MAC)

* fentanyl of 3 mcg/kg alone decreases it by 83%

54
Q

why is MAC BAR essential in children?

A

usu. don’t have agents like opioids to block autonomic responses, so much more MAC is required to achieve MAC BAR
- adults have many other drugs that decrease stimulation (opioids, NMB, beta blockers, etc.)