Inhaled Agents #2 Flashcards

1
Q

General anesthesia is defined as:

A

State in which the body is rendered insensible to pain or other stimuli

  • amnesia
  • analgesia
  • immobility
  • unconsciousness
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2
Q

Goal of inhaled anesthesia

A

To produce and maintain a constant partial pressure of inhalational anesthesia in the brain

Accomplish this by production a partial pressure in the alveoli (PA) which produces a partial pressure in the blood (Pa) which in turn produces a partial pressure in the brain (Pbr)

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3
Q

What are the 4 phases of uptake and distribution of inhalation anesthetics?

A
  1. Developing an inspired anesthetic concentration
  2. Development of an alveolar anesthetic concentration
  3. Development of a blood anesthetic concentration
  4. Distribution of the anesthetic agent from the blood to the tissue
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4
Q

What kind of flow do you want with “wash in”

A

Using high flows of delivery gases (5-10L/min) can precisely control the partial pressure of an anesthetic agent

-increasing the flow rate does not change the pp of the anesthetic agent

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5
Q

Concentration effect

A

High concentrations of inspired gases are rapidly removed from the lungs by the blood. This tends to encourage increased inspired volumes of fresh gases at a high concentration, increasing the minute ventilation as a result

-creates a higher concentration gradient which means faster uptake

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6
Q

The rate at which the alveolar partial pressure of an anesthetic rises is determined by what 2 factors?

A
  1. Inspired concentration
  2. Alveolar ventilation

-when alveolar ventilation is high, the partial pressure of the anesthetic in the alveolar increases rapidly

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7
Q

Second gas effect

A

When the first gas (N2O) is used, it is picked up rapidly from the alveoli by the blood. This rapid crossing of N2O into the blood tens to pull the second gas (eg isoflurane) along with it, so that the arterial partial pressure of the second gas rises more rapidly than it would if it were alone in the alveoli

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8
Q

Three factors determine how rapidly anesthetics pass from the inspired gases to the blood

A
  1. Solubility of the agent (blood:gas)
  2. Rat of blood flow through the lungs (cardiac output)
  3. Partial Pressure of the agents in the arterial/venous blood (Pa)
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9
Q

Solubility of agent in blood

A

Expressed as blood:gas partition coefficient. Represents ratio of anesthetic concentration in the blood to the anesthetic.
-concentration of a gas (alveolar) when the 2 are int he state of equilibrium

Blood:gas = anesthetic blood concentration
__________________________________
Anesthetic alveolar concentration

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10
Q

How does cardiac output influence how fast the anesthetic agent will be picked up from the alveoli?

A

The higher the blood flow, the more blood that is exposed to the agent, the faster the agent is picked up front eh alveoli and delivered to the tissues

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11
Q

How does the partial pressure of venous blood change as agent is being administered?

A
  • initially venous pp is very low as most was delivered to the tissues which also had a very low pp
  • with each circulation time more anesthetic is deliver to the tissue and their pp rises, the returning venous blood will also begin to have higher pp as it returns to the lungs
  • as the venous pp risers there is less picked up from the alveoli and uptake decreases
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12
Q

The rate of which the pp in tissues begin to rise depends on what 2 factors?

A
  1. Solubility of the gas in tissues (tissue:blood partition coefficient) Most agents are equally soluble in lean tissue and blood, so their pp are very similar at equilibrium
  2. Tissue blood flow. The higher the blood flow to a particular tissue, the faster the anesthetic is delivered and the faster the pp and concentration will rise in that area
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13
Q

What are the 4 categories of tissue groups?

A
  1. Vessel rich: brain, heart, liver, kidney, endocrine
  2. Muscle: skin and muscle
  3. Fat: adipose tissue (becomes a reservoir to store gases)
  4. Vessel poor; bone, ligaments, teeth, hair, cartilage (will never really get to this point with our gases)
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14
Q

You don’t typically see this stage of anesthesia until emergence?

A

Stage I

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15
Q

Stage I anesthesia

A

Begins with the administration of anesthesia and ends with the loss of consciousness.

Brain gas tension is very low. Dorsal horn activity decreases and there is a decreased synaptic transmission in the spinothalamic tract

  • pupils normal, reactive
  • RR slightly irregular bc gases irritating
  • HR irregular
  • BP normal
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16
Q

Stage II of anesthesia

A

Stage of delirium or excitement

This stage extends from the loss of consciousness to the beginning of surgical anesthesia

The pp of the brain rises and there is blockade of inhibitory neurons, which enhances and facilitates synaptic transmission

Will see increased muscle tone, irregular breathing, jaw clenching, involuntary activity, pupils dilate, blood pressure and HR are elevated

Reflexes still present. Laryngospasm reflexes heightened

  • eyes diconjugate,
  • RR very erratic
  • HR irregular and fast
  • BPhigh
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17
Q

You do not want to stimulate pts during what stage of anesthesia?

A

Stage II

Pts will react in an exaggerated way

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18
Q

Stage III of anesthesia

A

Partial pressure of teh brain (Pbr) further increases giving rise to progressive depression of the ascending (sensorys pathways of eh reticular activity system, producing a suppression of spinal reflex activity or skeletal muscle relaxation

  • return to regular respiration
  • excite to subsides
  • pupils become centered
  • cough, gag, and eyelids reflexes absent

considered “normal” stage of anesthesia. This is where we want to get the pt.

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19
Q

Stage IV of anesthesia

A

Stage of depression

Pp of the brain (Pbr) continues to increase and there is depression of the vital medullary centers which results in a profound respiratory and cardiac depression

  • pupils dilate
  • everything decreases (HR, BP)

*don’t want to get to stage 4

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20
Q

Signs of “light” anesthesia

A
  • increase RR
  • increase BP, HR
  • increase muscle tone
  • swallowing, coughing returns
  • tear formation (abolished at surgical stage)
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21
Q

Signs of “deep” anesthesia

A
  • hypotension
  • diaphragmatic breathing
  • pupils become dilated, lack luster
  • bradycardia
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22
Q

What is an indication that surgical anesthesia is beginning?

A
  • loss of reflexes

- rhythmic respirations

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23
Q

MAC

A

Minimum alveolar concentration

Defined as the partial pressure of an inhalation anesthetic at 1 atm that prevents skeletal muscle movement in response to a surgical skin incision in 50% of the pt population.

Index of potency for inhalation agents

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24
Q

MAC is measures where? Why?

A

In alveoli

The pp of anesthesia in the alveoli and brain are nearly equal at equalibrium

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25
Q

____________ is a reliable indicator of dose and potency of an anesthetic

A

MAC

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26
Q

The _______ the MAC, the more potent the agent and the _______ the blood:gas protection coefficient.

A

Lower

Higher

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27
Q

Factors that decrease MAC

A
  • hypoxia: decreased PaO2 causes narcosis itself
  • anemia: decreased PaO2, decreases MAC
  • hypotension: decreased MAP decreases MAC (bc metabolism lower)
  • drugs: narcotics, sedative, acute ETOH injection, calcium channel blockers
  • pregnancy: due partially to hormone influences
  • age: elderly, decreased CBF, CMRO2

*as we age our MAC goes down 4-6% for each decade past 40

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28
Q

Factors that increase MAC

A
  • age: infants. 1-12 months (not brand new born)
  • hyperthermia (metabolism up)
  • drugs: chronic use of ETOH, barbiturates, narcotics
  • red heads
29
Q

How does temperature affect MAC?

A

Hypothermia: decrease MAC

Hyperthermia >42 degrees C: decrease

30
Q

How does age affect MAC?

A

Young: increase
Elderly: decrease

31
Q

How does ETOH affect MAC?

A

Acute intoxication: decrease

Chronic abuse: increase

32
Q

How does anemia affect MAC?

A

Hct < 10% decreases

33
Q

How does PaO2 affect MAC?

A

< 40mmHg: decrease

> 95mmHg: decrease caused by < pH in CSF

34
Q

How does thyroid function affect MAC?

A

Most sources say no change for both hypo and hyper thyroid

35
Q

How does BP affect MAC?

A

MAP < 40mmHg: decrease - bc no perfusion to brain

36
Q

How do electrolytes affect MAC?

A

Hypercalcemia: decrease
Hypernatremia: increase - caused by altered CSF
Hyponatremia: decrease - caused by altered CSF

37
Q

How does pregnancy affect MAC?

A

Decreases MAC

38
Q

How do drugs affect MAC?

A

-local anesthetics: decrease - except cocaine bc its a stimulant

Drugs that decrease:

  • opioids
  • ketamine
  • barbiturates
  • benzodiazepines
  • verampamil
  • lithium
  • sympatholytics: methyldopa, reserpine, clonidine
  • sympathomimetic: amphetamine - chronic

Drugs that increase
-sympathomimetic: amphetamine - acute, cocaine, ephedrine

39
Q

At what MAC value will 95% of pts not move with incision?

A

1.2 MAC

40
Q

At what MAC will 99% of pts not move in response to incision?

A

1.3 MAC

41
Q

_________ allows for potencies to be compared among anesthetics

A

MAC

42
Q

MAC-awake

A

The minimum alveolar concentration at which 50% of subjects will respond to the command “open your eyes”

43
Q

This end-tidal concentration is usually associated with a loss of recall

A

1/3 MAC

This is the MAC value that pts will start to wake up

44
Q

Standard deviation of MAC is roughly

A

10%

45
Q

MAC-BAR

A

Blocked Adrenergic Response
1.5 MAC

Represents the MAC necessary to block adrenergic response to skin incision

-blocking sympathetic outflow that would happen during incision

Won’t see:

  • Changes in plasma norepinephrine
  • Changes in HR
46
Q

MAC intubation

A

Similar to MAC-BAR in that its values exceeds the anesthetic requirements for surgical incision

MAC needed to intubate

47
Q

MAC desflurane

A

6 - 6.6

48
Q

MAC isoflurane

A

1.15 - 1.2

49
Q

MAC sevoflurane

A

2 - 2.2

50
Q

T/F: MAC values for different inhaled anesthetics are additive

A

True

51
Q

One limitation of MAC is__________

A

Ability to determine adequacy of anesthesia

-MAC should only be used as an overall guide to depth of anesthesia

52
Q

What are ways an anesthesia provider can estimate the pt’s anesthetic depth?

A
  • VS
  • muscle rigidity
  • reflexes
  • knowledge of MAC values and what affects them
53
Q

Pharmacokinetics of inhaled agents has 3 steps:

A
  1. Uptake: absorption from alveoli into system circulation
  2. Distribution: cardiac output and blood flow
  3. Elimination: exhaled unchanged by lungs or minimal metabolized in liver
54
Q

Do anesthetic gases absorb into the plastic of the anesthesia circuit?

A

YES

55
Q

How does alveolar ventilation affect rate of induction?

A
  • Increased alveolar ventilation promotes input of inhaled anesthetics to offset uptake by the blood
  • hyperventilation increases induction
  • hypoventilation decreases induction
56
Q

Is controlled or spontaneous ventilation better for induction?

A

Spontaneous is better bc pt is pulling gases in rather than us trying to push gases in

57
Q

How does cardiac output influence rate of induction?

A

Cardiac output influences uptake into the pulmonary arterial blood and therefore PA by carrying away more or less anesthetic from the alveoli

  • High CO (fear) results in more rapid uptake, such a that the rate of rise in PA and the induction of anesthesia is slowed
  • Low CO (shock) speeds the rate of increase of the PA bc there is less uptake from the blood to oppose input
58
Q

How does a right-to-left intracardiac or intrapumornay shunt affect induction?

A

It slows the rate of induction

Bc blood bypassing the lungs

59
Q

How does a left-to-right intracardiac or intrapumornay shunt affect induction

A

Generally not observed and not clinically significant

60
Q

You must maintain the PA of any volatile agent for ________ minutes before assuming the Pbr is similar

A

10-15 minutes

AKA: at least 3 time constants (?)

61
Q

How can you determine the amount of inhaled anesthetics tissue uptakes?

A

PA - PV
Difference between pp of alveolar and venous pp

When end-tidal is delivering back what you’re giving

62
Q

Which tissues equilibrium rapidly to Pa?

A

Highly perfused tissues

63
Q

T/F: Emergence from anesthesia is the inverse of induction

A

True

64
Q

___________ or use of ________ _________ __________ low enought to permit rebreathing of anesthetic will lead to transfer of anesthetics back into the tissues delaying pt recovery (emergence)

A

Hypoventilation

Fresh gas flows

65
Q

What is diffusion hypoxia?

A

Can occur during emergence

  • When N2O is abruptly discontinued
  • N2O still in the body rapidly diffuses across capillary/alveoli membrane diluting the O2 concentration to a point we’re it can cause the PaO2 to drop and hypoxia develops
  • can be avoided by administering 100%O2 for 5-10 minutes after the N2O has been stopped
66
Q

Factors that influence the rate of emergence

A
  • duration of procedure - longer gases running, the more concentration will build up in fat. Will slow emergence
  • temperature of the pt
  • physical condition of pt - not doing well, will be slowed down
  • obesity - may initially wake up, but then as agent is mobilized from fat stores may re-anesthetize themselves
67
Q

How does emergence differ from induction?

A
  • absence of a concentration effect during recovery
  • tissue concentration of inhaled agents serve as a reservoir to maintain PA when the pp gradient is reversed
  • metabolism: potentially impacts the rate of decrease in the PA at the collection of anesthesia. This is of clinical significance in the highly lipid-soluble agents
68
Q

Context sensitive half-time

A

Explains why the longer you run the drug, the longer it takes them to wake up.

-pharmacokinetics of elimination of inhaled anesthetics depends on the length of administration (“context”) and the solubility of the inhaled anesthetic in blood and tissues