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Pharmacology N926 > Inhalational Agents > Flashcards

Inhalational Agents Flashcards

1
Q

3 A’s of anesthesia

A

amnesia, analgesia, areflexia

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2
Q

where in brain are these effects transmitted

A

cerebral cortex, brain stem arousal centers, central hypothalamus, spinal cord

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3
Q

stages of anesthesia

A

stage 1: amnesia and anesthesia. initiation to loss of consciousness. patient able to follow simple commands, protective reflexes remain intact. eyelid reflex intact
stage 2: delirium and excitation. loss of consciousness and lid reflex, irregular breathing pattern, dilated pupils. neurons that inhibit excitation are not functional and can lead to vomiting, laryngospasm, cardiac arrest, and emergence delirium
stage 3: surgical anesthesia. cessation of spontaneous respiration’s, absence of eyelash response and swallowing reflexes.
stage 4: anesthetic overdose. cardiovascular collapse requiring provider intervention

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4
Q

MAC

A

minimum alveolar concentration (%) required to produce anesthesia (lack of movement) in 50% of the population.

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5
Q

circumstances when you may need to increase MAC

A

hyperthermia, drug induced increases in CNS activity, hypernatremia, chronic alcohol abuse

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6
Q

circumstances when you may need to decrease MAC

A

hypothermia, increasing age, alpha 2 agonists, acute alcohol ingestion, pregnancy, hyponatremia

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7
Q

Blood: Gas Solubility Coefficient

A

describes the amount of gas that will dissolve or bind to the blood versus the amount that will diffuse into tissues. “how fast anesthetic gas is delivered to the tissues”. soluble agents remain in the blood longer, so less is released into the tissues during uptake (it will be slower)

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8
Q

Isoflurane solubility coefficient

A

1.4. this means there is 1.4 times more gas soluble in the blood than available to the tissues, or a 1.4:1 ratio

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9
Q

Desflurane Solubility Coefficient

A

.42. this means that only .42 stays in the blood for very molecule that is available to the tissues, or a .42:1 ratio.

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10
Q

Overpressuring

A

administration of a higher concentration of gas than necessary to speed up initial intake. greater effect on high solubility gases.

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11
Q

Oil: Gas Solubility Coefficient

A

indicator of potency. “how efficiently the anesthetic gas can access the tissues to cause its effect” highly lipid soluble drugs tend to be more potent. isoflurane most potent, NO least potent.

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12
Q

how the circulatory system affects uptake

A

increase in CO will create slow uptake. blood spends less time in the lungs, which slows the rise in lung/brain concentration. high solubility gases affected more (Isoflurane)

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13
Q

which agents are not metabolized

A

NO, des, iso

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14
Q

decreases in temperature results in increased

A

potency and solubility.

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15
Q

how does hypothermia affect PK of gases

A

decreases tissue perfusion resulting in slowed induction. can be overcome by increasing gas concentration.
increases tissue anesthetic capacity. tends to slow recovery.

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16
Q

how does hyperthermia affect PK of gases

A

increases CO and anesthetic requirement. also slows induction.

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17
Q

emergence related to solubility

A

the higher the solubility, the slower the emergence. iso>sevo>des>NO

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18
Q

diffusion hypoxia

A

when high concentration of insoluble anesthetics such as NO are delivered, quickly exits lungs during emergence and is replaced by nitrogen resulting in dilution of less soluble gases such as O2 and CO2. deliver 100% O2 for several minutes upon emergence to prevent this phenomenon

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19
Q

emergence phases (not to be confused with stages of induction)

A

phase 1: cessation of anesthetic drugs, reversal of NMB, transition from apnea to breathing, increased alpha and beta waves on EEG.
phase 2: increased HR and BP, return of autonomic responses, responsiveness to pain, salivation, tearing, grimacing, swallowing and gagging, defensive posturing. extubation possible
phase 3: eye opening, response to verbal commands, awake EEG patterns, extubation possible

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20
Q

pediatric related anesthetic considerations r/t PK

A

anesthesia uptake greater in pediatric patients than adults. greater alveolar ventilation/weight ratio. infants have decreased muscle mass, anesthetic agents concentrate more in vessel rich tissue. anesthetic agents less soluble in children than adults. emergence delirium more common in children

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21
Q

how to attenuate emergence delirium

A

dexmedetomidine, fentanyl, ketamine

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22
Q

ether day

A

10/16/1846. WTG morton. removal of jaw tumor at mass gen

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23
Q

Fi

A

inspired gas concentration. determined by FGF rate, breathing circuit volume (includes absorbent and anesthesia bag), circuit absorption

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24
Q

FA

A

alveolar gas concentration. determined by uptake (blood solubility), ventilation, alveolar blood flow, PP between alveolar and venous blood, concentration effect and second gas effect

25
Q

Fa

A

arterial gas concentration affected by ventilation/perfusion mismatching.

26
Q

Fa less than EtCO2 would predict

A

venous admixture, alveolar dead space, non uniform distribution (type of surgery, pt position, HPV)

27
Q

most likely targets of anesthetic gas

A

NMDA receptors, tandem pore potassium channels, VgNa channels, glycine receptors, GABA receptors.

28
Q

meyer overton theory

A

has been disproven but, says lipophilicity equates to potency.

29
Q

CNS effects of inhalation agents (except NO)

A 
CMRO2 decreased. 
CBF increased (dose dependent)
in general, inhalational agents do not stop response of cerebral vascular responsiveness to CO2
30
Q

uncoupling

A

combination of effects happening in brain. greater with sevo

31
Q

electroencephalogram and inhalational agents

A

burst suppression happens at 1.2 MAC of des, 2 MAC with iso and sevo

32
Q

evoked potentials

A

inhalational agents decrease amplitude (height of response) and increase latency (how often its recurring. in the setting of ischemia, decreased amplitude and increased latency occurs

33
Q

Emergence Delirium in children common offenders

A

sevo and des. r/t being insoluble, in quick-out quick.

34
Q

cardiovascular effects of inhalational agents (except NO)

A

reduce CO and CI, dose dependent.
reduction of free intracellular Ca2+ contractile state.
as MAC hours increase, slight increase in CI and HR
reduced MAP secondary to SVR reduction

35
Q

volatile agents and NO induce HR changes VIA

A

SA note antagonism (decrease in HR)
modulation of baroreflex activity (decreased BP)
SNS activity (blunting)

36
Q

reverse robin hood

A

if you have compensation for mild cardiac ischemia, blood goes to vasodilator areas versus vasocontricted areas. (Iso)

37
Q

preconditioning

A

heart is exposed to cascade of intracellular events that protect it from ischemic and repercussion insult

38
Q

sensitization

A

mostly specific to halothane. increase sensitization to catecholamines.

39
Q

pulmonary circulation effects r/t inhalational agents

A

NO causes slight increase in PVR, worse in pts with pHTN
volatile agents decrease pulmonary artery pressure r/t vasodilation
HPV mildly depressed. (Iso affects this most, but all gases guilty of this)

40
Q

respiratory effects of inhalational agents

A

fast shallow breaths in the setting of just gas.
bronchodilation on induction (sevo most, des least)
in the case of a spasm, deepen anesthesia

41
Q

renal effects of inhalational agents

A

auto regulation of renal circulation remains relatively intact.
decreased SVR means decreased GFR.
des has least impact on renal function

42
Q

hepatic effects of inhalational agents

A

halothane hepatitis is biggest concern

43
Q

sevo and metabolism

A

undergoes greatest metabolism (5-7%) and metabolites are toxic to kidneys but usually not a problem

44
Q

neuromuscular effects of volatile agents

A

produce dose dependent skeletal muscle relaxation. additive effects on non depolarizing NMB’s. can be reduced to 25-50% of dose compared to TIVA

45
Q

The Ideal Anesthetic Agent

A 
non irritating to respiratory tract
rapid induction and emergence
chemically stable (non flammable)
produce amnesia, analgesia, areflexia
potent (diffuse across tissues quickly)
not metabolized and excreted by respiratory tract (want to breathe it out like it was breathed in)
free of toxicity and allergic reactions
minimal systemic changes
uses standard vaporizer
affordable
46
Q

MH Triggers

A

volatiles and succ (not NO)

47
Q

four physical properties affect how agents work

A 
vapor pressure (as long as liquid is present, VP independent of volume)
boiling point (temperature at which vapor pressure exceeds atmospheric pressure in an open container
partial pressure (daltons law)
solubility (tendency of a gas to equilibrate with a solution aka blood) (henrys law)
48
Q

des chemical properties

A

only Fl attached to O molecule

49
Q

iso chemical properties

A

halogenated methyl ethyl ether. isolated Cl molecule

50
Q

sevo chemical properties

A

fluorinated methyl isopropyl ether. F3C and CF3 attached

51
Q

halothane chemical properties

A

F’s, one Cl and one Bromide. no ether

52
Q

movement of anesthetic from machine to patient is facilitated through

A

fresh gas flow, pressure, temperature

53
Q

isoflurane

A

most potent, most soluble, slowest onset and recovery. reverse robin hood in hypotensive patients. minimal cardiac depression, preserved carotid baroreceptors. most consistent agent.

54
Q

desflurane

A

avoid in patients with reactive airway disease. rapid increases in this agent lead to increased HR and BP. if you overpressurize with this agent, worrisome increase in HR occurs and you have to attenuate with esmolol

55
Q

sevoflurane

A

preferred for inhalational induction. use calcium hydroxide absorbent.

56
Q

NO

A

NMDA receptor antagonist. analgesic properties. good for CV stability but increases risk of PONV.

57
Q

NO contraindications

A

methionine synthase pathway deficiency. PONV, first trimester pregnancy, increased ICP, pHTN, prolonged surgery

58
Q

MH tx

A

dantrolene or ryanodex. with ryanodex, need supplemental mannitol

Pharmacology N926 (16 decks)

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