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anesthesia pharm II > inhalational agents: uptake and distribution > Flashcards

inhalational agents: uptake and distribution Flashcards

1
Q

what are the steps in getting the anesthetic agent from the machine to the pt.’s CNS?

A
  • vaporizer
  • circuit
  • alveoli
  • blood/arterial
  • brain
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2
Q

what happens to the partial pressure of an agent as it moves through each step?

A

-decreases w/ each step, so the actual setting on our vaporizer is not what will show on ET concentration (not the amount that makes it to the brain

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3
Q

what moves the agent through from the vaporizer to the CNS?

A
  • series of partial pressure gradients
  • partial pressures between alveolar and arterial equilibrate quickly
  • next, arterial partial pressure equilibrate rapidly w/ brain
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4
Q

alveolar concentrations do not produce unconsciousness directly (not effect site), so what is the significance of using alveolar concentrations?

A
  • can not directly CNS/brain concentrations

- alveolar concentration is a great estimate of CNS/brain concentrations

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5
Q

how can the percentage of anesthetic agent that is first delivered to the circuit from the vaporizer be determined?

A

the vapor pressure of that anesthetic agent divided by atmospheric pressure
ex: isoflurane vp 240/760 gives you approx. 33% delivered

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6
Q

if the vaporizer delivers 33% isoflurane, how is the concentration decreased to MAC of 1.17%?

A

in the circuit, there is fresh gas flow as well as gas being rebreathed that dilutes out

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7
Q

what affects expired concentration of agents compared to inspired?

A

compartments that take the agent out of the alveoli

  • vessel rich group
  • muscle group
  • fat group
  • metabolism
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8
Q

what factors determine partial pressure gradient from MACHINE to ALVEOLI?

A
  • inspired or inhaled partial pressure (P-I)
  • alveolar ventilation (time constant)
  • type of circuit and flow of fresh gas
  • functional residual capacity (FRC)
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9
Q

describe P-I effect on partial pressure gradient from machine to alveoli

A

-a high P-I initially offsets impact of uptake and speeds induction (rise in P-A and thus P-br)
-concentration effect
*the greater the concentration delivered to the circuit, the greater the concentration gradient b/w the vaporizer and the alveoli, and the faster the rise in alveolar concentration to approach P-I
-second-gas effect: “high volume uptake of one gas to accelerate the rate of increase of the P-A of a concurrently administered ‘companion’ gas” (N2O)
-

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10
Q

as equilibrium is achieved and uptake is slowed, P-I must be…?

A
  • reduced to maintain a constant P-br
  • if continue to over-pressurize, will OD; but do not lower below MAC or gradient will shift and gas will come back into alveoli and exhaled out
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11
Q

what should be balanced to maintain a constant alveolar concentration?

A

a balance b/w administration of agent to alveoli and removal of agent from alveoli into the blood (uptake)

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12
Q

how does alveolar ventilation affect partial pressure gradient from machine to alveoli?

A
  • greater alveolar ventilation promotes delivery of anesthetic agent to offset uptake
  • more rapid induction w/ greater alveolar ventilation
  • slower induction w/ decreased alveolar ventilation
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13
Q

how does maintaining spontaneous ventilation w/ inhalation induction protect pt.?

A
  • avoids overdose
  • anesthetic agents impact their own uptake d/t dose-dependent depressant effects on alveolar ventilation (decreased tidal volumes, less alveolar ventilation, pt. will begin to “lighten” back up)
  • if controlled ventilation is used, there is potential for OD d/t loss of protective mechanism
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14
Q

what is a limiting factor to chance of OD w/ controlled ventilation during inhalational inductions?

A
  • PaCO2
  • greater ventilation leads to hyperventilation which decreases PaCO2
  • causes cerebral vasoconstriction and decreased CBF; therefore, reduction in delivery of agent to the brain
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15
Q

what is time constant?

A
  • time required for flow through a container to equal the volume of the container
  • time constant= capacity (L) / flow (L/min)
  • the amount of time, in minutes, required for a 63% turnover of gas within a container
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16
Q

what is the application of time constant?

A
  • the rate of alveolar rise in anesthetic concentration

- how long it takes to change the concentration in a circuit after changing the concentration on the vaporizer

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17
Q

what are the time constants and each percentage of gas turnover w/ each?

A

1: 63%
2: 86%
3: 95%
4: 98%
5: 99.5%

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18
Q

if you have a volume of 5 L capacity w/ flows of 10 L/min, what is the time constant?

A
  1. 5 min

* wash in of new gas greater than 80% after 1 min.

19
Q

what is the most important factor in time constants of gas turnover in the lungs?

A

-minute ventilation

20
Q

what factor of the time constant equation can we adjust to speed up gas turnover?

A

gas flows

*also areas w/ increased CO will have shorter time constants

21
Q

what factors of the type of circuit can affect partial pressure gradient from machine to alveoli?

A
  • volume of gas in the circuit takes away from what is going to alveoli (bigger, less to alveoli)
  • fresh gas flows: higher (5-10 L/min) negates above effect
  • solubility of an agent in rubber/plastic components of the breathing system slows the rise of P-A initially (all to some small degree but esp. Halothane)
22
Q

describe circle system effects

A
  • allows rebreathing of previously exhaled gas
  • exhaled contains lower concentration of agent during the initial uptake phase b/c some is taken out by the body
  • agent concentration coming in the fresh gas from the machine is diluted down by mixing w/ exhaled gas
  • not an issue once equilibrium reached
  • increased stimulation require increased flows
23
Q

describe non-rebreathing circuit (mapleson) effects

A
  • exhaled gas is not rebreathed
  • high flows required
  • concentration of agent in the circuit is very close to the concentration set on the vaporizer dial
  • some agent will be lost to material of the circuit or system (only halothane clinically significant)
24
Q

how does FRC affect partial pressure gradient from machine to alveoli?

A
  • composed of residual volume (cant change) and expiratory reserve volume (can ventilate)
  • larger the FRC, the slower the induction of agent
  • neonates have smaller FRC than adults as a % of TLV, more volume changed w/ each respiration, and faster induction than adults
  • don’t want fast induction w/ neonates so don’t over-pressurize as much
25
Q

what factors determine transfer of agent from ALVEOLI to ARTERIAL BLOOD?

A
  • solubility: blood:gas partition coefficient
  • cardiac output (pulmonary blood flow)
  • alveolar-to-venous partial pressure gradient
26
Q

define blood:gas partition coefficient

A

a distribution ratio describing how the anesthetic distributes itself b/w two phases at equilibrium
*at equilibrium, are more particles in the gas phase or blood phase?

27
Q

how does solubility affect rise of P-A toward the P-I?

A
  • the more soluble the agent, the more agent has to be dissolved in blood before the P-a equilibrates w/ the P-A (slow induction)
  • the less soluble agent, minimal amounts of agent must be dissolved before equilibrium is achieved; the rate of rise of P-A and P-a, and induction are rapid
28
Q

what affects partition coefficients (solubility) of agents?

A
  • temperature dependent
  • decreased temperature, increased solubility
  • increased temperature, decreased solubility’
  • *important on emergence when trying to blow off, want less soluble so can come out of blood to alveoli to be exhaled
29
Q

although N2O is more soluble than desflurane, why does it have a more rapid increase in alveolar concentration to inspired concentration?

A

much higher concentrations of N2O are utilized (approx. 70% compared to 6% of desflurane)
*concentration effect

30
Q

how does cardiac output affect transfer of agent from alveoli to arterial blood?

A
  • affects uptake by carrying away agent from the alveoli and preventing rise in P-A
  • increased CO leads to greater uptake/removal of agent from the lungs and slowed induction
  • rate of increase of more soluble agents is affected more by CO; the increase in CO will slow the induction and risk in P-A
31
Q

what is the effect of decreased cardiac output (cardiomyopathy, MI, low EF, etc.)?

A
  • results in increase in P-A (blood not coming by alveoli to uptake agent)
  • further deepens anesthetic depth
  • further myocardial depression
  • induction is quicker; not necessarily desired w/ pathology
  • use a less soluble agents
32
Q

how does alveolar-to-venous partial pressure gradient affect transfer of agent from alveoli to arterial blood?

A
  • during uptake, the VRG will remove anesthetic delivered
  • mixed venous blood returning to lungs has a lower partial pressure of agent
  • gradient b/w alveolar partial pressure and the venous blood is great, encouraging diffusion out of the alveoli
  • as saturation of the VRG increases, the gradient becomes smaller, and P-A rises
33
Q

what are factors determining transfer of agent from arterial blood to brain?

A
  • brain:blood partition coefficient
  • cerebral blood flow
  • arterial-to-venous partial pressure difference
  • causes anesthetic loss
34
Q

what factors help determine tissue uptake?

A

-A= solubility
-Q= cardiac output
-P-A= alveolar partial pressure
P-V= mixed venous partial pressure
-P-a is barometric pressure
*determined by solubility, blood flow, pressure gradients, and tissue

35
Q

how much of cardiac output goes to vessel rich groups?

A
  • 75%

- brain, heart, kidney, splanchnic, liver, endocrine

36
Q

how much of CO goes to the muscle group?

A
  • 18%

- muscle, skin

37
Q

how much of the CO goes to the fat group?

A

-5%`

38
Q

how much of the CO goes to vessel poor group?

A
  • 2% of CO

- bone, ligament, cartilage

39
Q

describe elimination of inhalation agents

A
  • generally is reverse of uptake
  • slower awakening w/ higher soluble, longer duration of exposure (lower soluble agents no affected much by time), and higher concentration
  • elimination via exhalation predominantly (*increase alveolar ventilation)
  • metabolism can speed recovery of halothane
  • reverse pressure gradients
40
Q

how should pressure gradients be reversed to promote elimination?

A
  • turn off vaporizer
  • empty out circuit (increased flows to wash out)
  • increase alveolar ventilation (alveolar gradient drops-agents returns out of blood-agents comes out of brain)
41
Q

how can the rate of elimination be increased?

A
  • eliminate rebreathing (high flows)
  • high fresh gas flows
  • low anesthesia-circuit volume (shorter circuits)
  • low absorption by anesthesia circuits (cant control)
  • decreased solubility (choose in beginning)
  • high cerebral blood flow (don’t hyperventilate)
  • increased alveolar ventilation (assist)
42
Q

what are implications for rapid recovery?

A
  • airway protection/oxygenation (hypoxic drive decrease not dose dependent; very low doses affect)
  • return to normal CV function
  • turnover
  • quicker discharge from PACU
  • quicker return to normal activities
  • decreased amt. of available drug for metabolism/toxicity
  • eliminate enhancement of NMB
  • rapid movement through the 0.1 MAC concentration that causes enhanced perception of pain
  • safety, cost, pt. satisfaction
43
Q

if a less soluble drug leads to more rapid awakening, why not switch over to desflurane before the end of the case?

A

agents have an additive or even synergistic effect regarding return to normal mental function

44
Q

if turning on agent off and starting another, what two agents will cause greatest concentrations at overlap?

A
  • turning off a high blood:gas soluble (tends to hold on)

- turning on a low blood:gas soluble (rapid induction)

anesthesia pharm II (5 decks)

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