Inhalant Anesthesia Flashcards

1
Q

Purpose of anesthetic vaporizers

A

to deliver a specific amount of inhalant anesthetic to the patient

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2
Q

RVOLTS

basic vaporizer design

A

Resistance
Vaporization method
Output method
Location
Temperature compensated
agent Specifcity

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3
Q

What color is:
1. isoflurane
2. sevoflurane
3. desflurane

A
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4
Q

What are the 2 routes of the inlet gas?

inlet gas = 100% O2 or medical-grade air

A

some goes in the vaporizing chamber (dilute the liquid anesthetic), most bypass and go to patient

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5
Q

Where is the VOC

A

vaporizer always b/w flowmeters common gas outlet

VOC = vaporizer out of circuit

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6
Q

The vapor pressure of inhalant anesthetics are __?__ at room temperature than the partial pressure required to produce anesthesia

A

higher

a vaporizer dilutes saturated vapor by splitting the gas flow that passes through the vaporizer –> splitting ratio (describes variable bypass)

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7
Q

What is the importance of maintaining a constant temperature in the vaporizer? thermo-compensation (TEC)

A

As the liquid anesthetic agent becomes vaporized, its liquid temperature decreases which thus decreases the vapor pressure and the vapor concentration. constant temp avoids vapor output fluctuation

maintained either mechanically or computerized

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8
Q

What is the blood/gas partition coefficient, and what are the values for isoflurane vs sevoflurane vs Desflurane?

A

At equilibiurm (equal volume of alveolar gas in contact with equal volume of capillary blood):

Isoflurane: 1.46 (1 molecule of iso in alveoli and 1.46 molecules of iso in the blood)

Sevoflurane: 0.58 (1 molecule of sevo in alveoli and 0.58 molecules of sevo in the blood)

Desflurane: 0.46 (1 molecule of des in alveoli and 0.46 molecules of des in the blood.

Blood / gas partition coefficient: important determinant of the speed of anesthetic induction and recovery.

Poorly soluble agents (λB/G < 1) generate a high partial pressure,
which creates a steep gradient between Pa and PB. Volatile
anesthetic agents with a low blood–gas partition coefficient

will therefore exert a high partial pressure and produce a more rapid onset and offset of action.

Conversely, soluble volatile anesthetic agents with a low blood–
gas partition coefficient (λB/G > 1) dissolve easily into pulmonary
blood without substantially increasing the partial pressure (Pa).
This leads to a slow onset of anesthesia due to a large fall in PA as the agent leaves the alveolus, decreasing the gradient for further diffusion and a small gradient between PA and PB

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9
Q

What is the minimum alveolar concentration (MAC) of isoflurane vs. sevoflurane vs. desflurane?

A

Isoflurane: 1.4

Sevoflurane: 2.4

Desflurane: 7-10

MAC is the concentration of a vapor in the alveoli of the lungs that is needed to prevent movement (motor response) in response to surgical (pain) stimulus.

End tidal concentration of inhalation anesthetics = ~Palveolar = ~Pbrain

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10
Q

Target organ for inhalant anesthetic drug?

A

The brain

ventilation of the inhalant -> transferred: alveoli into blood -> absorbed: from blood to brain

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11
Q

What determines the direction of flow of inhalation anesthetic gas?

A

Partial pressure gradient

increase in alveolar partial pressure or decrease in solubitlity of anesthetics to blood facilitates induction and mantenance of anesthesia

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12
Q

What is Uptake?

A

uptake of drug by NON-target organs!

aka not the brain, kidneys or liver

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13
Q

What two factors may increase uptake?

factors that offset rise in alveolar partial pressure

A

Increase in solubility of inhalant to blood
- blood = pizza delivery driver, inhalant = your pizza,
- as more inhalant dissolves in the blood (delivery driver eats your pizza), less inhalant available to be delivered to target organ = more uptake!

Increase in cardiac output
- CO = mixer
- higher CO, more blood filtering thru lungs = more inhalant removed from alveoli = less direct delivery of inhalant to only the brain = a slower onset
- lower CO = heart-lung-brain perfusion preserved

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14
Q

Why is clinical onset of anesthesia slower in stressed/excited patients versus sick/debilitated?

A

b/c their CO is quicker = increased uptake

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15
Q

What other factors will decrease the MAC?

A
  • Other drugs that cause CNS depression
  • hyponatremia
  • senesence
  • PaO2 < 40mmHg
  • PaCO2 > 95mmHg
  • Pregnancy
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16
Q

What wave form changes will you see on an EEG (electroencephalogram) with correct inhalation anesthesia?

A

High amplitude, low frequency

lower frequency = lower CNS activity = good
17
Q

When will an inhlanat anesthetic drug increase ICP and why?

A

when the MAC is > 1.0

ICP increases because inhalant anesthetic drugs decrease cerebrovascular resistance/cause vasodilation -> reflex rise in ICP

18
Q

How can long-duration inhalant anesthetic cause severe cardiovascular depression?

A
  • decreases contractility (when >1 MAC // more profound @ high doses)
  • decrease in SVR (dose-dependent dilation)
  • decrease in SV

BP = SVR x CO
CO = HR x SV

19
Q

How do mechanical ventilation and hypercapnia affect cardiovascular system?

A
  • Mechanical ventilation decreases MAP due to increase in intrathoracic pressure and decrease in venous return
  • Hypercapnia: decreases SVR, increases CO, HR, MAP
20
Q

What is the MAC-Sparing Effect?

A

Anesthetic drugs with anesthetic sparing effect decrease the MAC = increased potency

Opioids have this and are commonly used as induction agents or during surgery b/c they allow for less anesthetic gas to be used to achieve a surgical plane of anesthesia.

21
Q

What does sevoflurane degradation in soda lime / baralime (CO2 absorbents) produce?

A

Compound A

nephrotoxic in rats and humans

22
Q

What is Malignant Hyperthermia (MH)? Which gas is the most potent trigger?

A

a skeletal muscular effect of inhalant anesthetic drugs
- life-threatening
- pigs/humans, rare in other species
- Halothane = most potent trigger of MH

Malignant hyperthermia (MH) is a potentially fatal pharmacogenetic disorder of skeletal muscle calcium regulation. Triggered by exposure to certain drugs or stressors, clinical signs include sudden and dramatic rise in body temperature, muscle fasciculation, muscle rigidity, tachypnea, tachycardia, arrhythmia, myoglobinuria, metabolic acidosis, renal failure, and death.

23
Q

Clinical signs of Malignant Hyperthermia

A
  • rapid rise in body temperature (> 40ºC)
  • increase in end-tidal CO2 (> 70 mmHg)
  • muscle rigidity -> significant build-up of lactate -> acidosis