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Inhalation Agents Flashcards

1
Q

ideal inhalation agent

A
  • poorly soluble
  • non-pungent
  • non-flammabe
  • inexpensive
  • easy to produce
  • potent
  • environmentally safe
  • no hepatic metabolism
  • not a trigger for malignant hyperthermia
  • no emetogenic effects (all Vas do)
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2
Q

MAC

A

alveolar concentration at which 50% of patients wiil move to noxious stimuli

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3
Q

prevents movement in 95% of patients on incision

A

1.5 MAC (with no other meds)

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4
Q

1 MAC Halothane

A

0.76%

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5
Q

1 MAC Isoflurane

A

1.15%

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6
Q

1 MAC Sevoflurane

A

1.85%

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7
Q

1 MAC Desflurane

A

6.0%

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8
Q

1 MAC Nitrous Oxide

A

104%

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9
Q

MAC awake

A
  • voluntary response to command
  • usually 1/3 MAC
  • Iso (38%), Sevo, Des
  • MAC awake for N2O 64% (about 2/3)
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10
Q

MAC aware

A
  • concentration at which patient can remember events/ loses ability to learn
  • below MAC awake
  • varies for different agents
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11
Q

MAC- BAR

A
  • average alveolar concentration which blunts autonomic response to noxious stimulus
  • 2.2 MA for Sevo
  • addition of Fentanyl decreases MAC BAR by 50%
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12
Q

site of action of IA

A

cell membranes in the CNS

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13
Q

goal of inhalational anesthesia

A

achieve a constant and optimal brain partial pressure (as reflected by PA/ET gas)

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14
Q

PA (ET gas) is used as an index of…

A

-depth of anesthesia
-recovery from anesthesia
-anesthetic equal potency (MAC)
(1 MAC of all IAs are equipotent, but they have their own individual potencies)

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15
Q

determinantes of PA

A
  • input minus uptake

- delivery into the alveoli (input) minus loss of drug into the blood (uptake)

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16
Q

INPUT

A
  • inhaled partial pressure
  • alveolar ventilation and FRC
  • characteristics of the anesthetic breathing system
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17
Q

UPTAKE

A
  • solubility of the anesthetic in the blood
  • cardiac output
  • alveolar to venous PP differences (A-vD)
18
Q

overpressure

A
  • high initial Pi to help achieve the desired PA more rapidly, accelerating the rate of rise of PA to PBr
  • Pi should be decreased as A-vD decreases to avoid overdose
19
Q

How does hyperventilation effect the rate of rise of PBR?

A
  • delays the rate of rise of PBr
  • (no breathing= no uptake)
  • (hypoventilation= delay in PBr)
20
Q

IAs effect on ventilation

A

-dose dependent depression of ventilation

21
Q

Spontaneous Ventilation under GA (IA)

A

-delivery of IA is decreased as spontaneous ventilation is decreased (protective against excessive anesthetic)

22
Q

Mechanical Ventilation under GA (IA)

A

-no decrease in ventilations as PA approached FI (no feedback, may easily become too anesthetized)

23
Q

characteristics of the breathing system that will increase the rate of rise of PA

A
  • volume of the external breathing system
  • solubility of the inhaled anesthetic in to the components of the breathing system
  • FGF
24
Q

as potency decreases, oswald….

A
  • oswald coefficient decreases

- (decreased potency correlates to decreased solubility)

25
Q

increased solubility is _____________ proportional to the rate of rise of PA toward the PI

26
Q

intermediately soluble

A

Isoflurane

27
Q

poorly soluble

A

Sevo, Des, N20

28
Q

soluble

A

(no modern inhaled anesthetics)

29
Q

95% equilibration of partial pressures b/w blood and tissue phases

A

3 time constants

30
Q

Brain: Blood equilibration time

A
  • 5-15 minutes for volatiles (TCs 2-5 minutes)
  • 2 minutes for poorly soluble
  • 5 minutes for intermediately soluble
31
Q

time constant formula

A

capacity/flow

32
Q

cardiac output and uptake

A
  • inc CO= inc uptake= slow rise in PA, slow inhalation induction
  • dec CO= dec uptake= fast rise in PA, rapid induction
33
Q

AvD

A
  • difference between alveolar and venous pressure

- reflects tissue uptake of IA

34
Q

AvD depends on…

A
  • solubility of the agent in the tissue
  • tissue blood flow
  • arterial-tissue partial pressure differences

(uptake and equilibration within the vessel rich group is rapid- 3 TC, 5-15min)

35
Q

titration of IA based on…

A
  • patient response
  • interactions with other medications
  • degree of stimulation
36
Q

IA reversible effects on CNS

A
  • immobility (reversible, spinal cord mediated)

- amnesia (higher centers)

37
Q

Meyer-Overton Hypothesis

A
  • the MAC of a volatile anesthetic is inversely proportional to it’s lipid solubility (oil: gas coefficient)
  • MAC is inversely related to potency
38
Q

5 Angstrom Theory

A

-proposes that anesthetics exert their effects on two different sites separated by a distance of 5 angstroms (maximal potency is achieved with a molecule 5 carbons long)

39
Q

Multisite Theory of Narcosis

A

-inhaled anesthetics act by effects at multiple sites

40
Q

Unitary Theory of Narcosis

A

-anesthetics act on no more than 2 or 3 sites to produce a specific effect

Pharmacology (9 decks)

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