General anesthesia

Question 1

Ketamine produces what effect?

Answer 1

Dissociative anesthesia

Question 2

What is MAC?

Answer 2

Stands for minimum alveolar concentration (alveolar-lungs). This is concentration at which 50% of people don’t respond to a surgical stimulus- IE the concentration at which the gas works for half of the population.

Question 3

What are the goals of general anesthesia?

Answer 3

To produce a state of unconsciousness, unresponsiveness, amnesia, immobility (is this talking about the white house?) and autonomic stability in the anesthetic state.

Question 4

T/F Modern general anesthesia tends toward using a combination of drugs, taking advantage of the best aspects of each.

Answer 4

True

Question 5

What would be some characteristics of an ideal surgical anesthetic treatment?

Answer 5

A smooth and rapid induction- they go under quick
Once they’re under, they’re unconscious and don’t remember the surgery.
Essential physiological functions are maintained while undesired reflexes are blocked
The skeletal muscles are relaxed (so they’re not flailing all over the place) but the respiratory muscles are still working as they should
The perception of sensory stimuli should be blocked and when you stop administering the drug, the patient comes out of it smoothly, quickly, and with no lasting effects.

Question 6

There are a lot of things that we want to have happen in the ideal surgical anesthetic treatment. Can it all be done with one drug? What are some things we use to get the job done?

Answer 6

It can’t be done with just one drug.
We use antimuscarinics to minimize salivation and to block vagal stimulation
We use analgesics for preoperative pain relief, sedation and amnesia
We use NO or opioids to reduce the anesthetic requirement and/or provide analgesia
Anti-nicotinic’s are used to paralyze skeletal muscle

Question 7

For us dentists, do we want to put someone under all the way? Why or why not?

Answer 7

Not really- most of what we do doesn’t warrant general anesthesia.

Question 8

What is the Meyer-Overtone correlation?

Answer 8

These two dudes noted a very strong correlation between solubility in olive oil and anesthetic potency.

Question 9

At what point does anesthesia begin?

Answer 9

It begins when the anesthesia reaches a critical concentration in membrane lipids.

Question 10

Why is general anesthesia dependent on the concentration of the drug the membrane lipids?

Answer 10

If the drug is in the membrane lipids then the drug can act on membrane proteins.

Question 11

What membrane proteins are likely targets of general anesthetics? Why?

Answer 11

Ligand activated ion channels
If you block the influx or efflux of ions you can depolarize or hyper polarize cells so that action potentials occur or do not occur.

Question 12

Why would GABA receptors be an attractive target for general anesthetics?

Answer 12

GABA receptors are also found in the membrane, but they are found in the brain.
GABA is an inhibitory neurotransmitter. GABA lets Cl- in and this hyper polarizes the membrane. Barbiturates can bind the GABA receptors and activate the inhibitory effects of GABA. It’s like super inhibition now.

Question 13

Which is more sensitive to anesthetics- synaptic transmission or actions potentials? Why?

Answer 13

synaptic transmissions

Effects have have been observed at both the pre and post synaptic terminals

Question 14

The thalamocortical loop and the reticular activating formation are thought to be critical for maintaining consciousness.

Answer 14

Cool fact Jordan.

Question 15

The limbic system is involved in memory. Inhibition of this system is likely to be involved in anesthetic induced amnesia.

Answer 15

Yet another cool fact.

Question 16

Pain pathways involve the spinal cord. The limbic system is for memory. There are a couple places dealing with consciousness. What does this imply for achieving general anesthesia?

Answer 16

It makes sense that we might need a combination of drugs to get the job done.
It also looks like we need to depress several brain pathways in order to achieve general anesthesia.

Question 17

The blood:gas partition coefficient. What is it and what does it mean?

Answer 17

This coefficient just tells us the solubility of an anesthetic agent in the blood.
The coefficient is the number we get when measuring the concentration of the drug when the drug is in equilibrium between being in the drug and being a gas.
If the anesthetic likes being a gas more than being in the blood, this means that the drug has a rapid onset as well as rapid clearing.

Question 18

The lower the blood:gas coefficient, the _______ the onset and the ______ the recovery.

Answer 18

faster

faster

Question 19

The higher the blood:gas coefficient, the _______ the onset and the ______ the recovery.

Answer 19

slower

slower

Question 20

Ideally, you want a drug that you don’t need a lot of in order to have an effect. Then you want a drug that has a low blood:gas coefficient so that you have a fast onset and a speedy recovery. NO has a MAC of 104% and blood:gas coefficient of 0.47. Tell me about how NO works.
Compare NO to desflurane which has a MAC of 6% and a blood:gas coefficient of 0.45

Answer 20

NO likes being a gas more than being in the blood, so it has a fast onset and fast recovery. However, its MAC (minimum alveolar concentration) is 104%, so it takes a lot of NO to get the desired effect.

On the other hand, desflurane has a low MAC at 6% and a low blood:gas coefficient. So you don’t need a lot of desflurane to get the desired effect. It has a rapid onset as well as a speedy recovery. This is a good anesthetic.

Question 21

Does NO produce full surgical anesthesia? Why or why not?

Answer 21

Nope
the MAC is 104%- you have to breathe pure NO in order to achieve that and bad things will occur in your life if you do that.

Question 22

Some anesthetics have volatile characteristics. Watch out for them.

Answer 22

You got it

Question 23

What do barbiturates do? Where are they acting?

Answer 23

They act as CNS depressants by potentiating the activity of the GABA receptor. (remember how they activate the inhibitory effects of GABA by increasing Cl- influx?)

Question 24

Just to be clear, what does the GABA receptor do?

Answer 24

Barbiturates bind to the GABA receptor and activate chloride channels in the post synaptic membrane. This hyper polarizes the membrane making it more difficult to get an action potential going.

Question 25

Why have intravenous anesthetics become more popular?

What is a major adverse effect to intravenously administered barbiturates?

Answer 25

Well, if you inject the drug directly into a vein it gets to the brain very quickly.
There is reduced cardiac depression.
There is no risk of malignant hyperthermia
There is no occupational exposure to volatile anesthetics
A single injection can be used to induce anesthesia

The down side is the potential for respiratory depression.

Question 26

What intravenous barbiturate is often used in dental outpatient procedures? (I assume this means things like wisdom teeth extractions)

Answer 26

Methoxhexital

Question 27

What does ketamine produce?

Answer 27

Dissociative anesthesia.

Question 28

What is dissociative anesthesia?

Answer 28

It is anesthesia (caused by ketamine) that is characterized by analgesia and amnesia, but doesn’t affect respiratory function. The patient doesn’t appear to be anesthetized- they can open their eyes and swallow, but they don’t process any information.

Question 29

Do I sometimes feel like I have dissociative anesthesia during my lectures?

Answer 29

Yes, I can breathe, open my eyes and swallow, but I often don’t process anything that’s being said

Question 30

Nice work, you’ve made it through.

Answer 30

Now go upstairs and hook yourself up to the NO to take the edge off ;)