Nervous System (Block 6): Conlay Lectures On Anesthesiology

Front 1

Name the 4 stages of anesthesia. Give important characteristics of each.

Back 1

I - Analgesia: ends with loss of consciousness (defined by pt's loss of ability to open eyes on command)

II - Delirium: begins with LOC and goes through two planes (decorticate and decerebrate), period of autonomic imbalance; ending with rhythmic respiration and re-established autonomic balance

III - Surgical anesthesia: 4 planes, beginning wiht onset of rhythmical respiration and return of eyes to fixed position, ends with vasomotor/resp collapse

IV - Arrest

Front 2

Place these symptoms in order when undergoing anesthesia:
numbness in feet, visceral analgesia, circumoral numbness, loss of color vision, numbness in hands, loss of consciousness

Why is there an order?

Back 2

circumoral numbness
numbness in hands
numbness in feet
loss of color vision
visceral analgesia
loss of consciousness

parts of the cerebrum (ie homonculus) that have more activity receive more blood flow, meaning they get more anesthesia and these are areas that go to sleep first!!!

Front 3

at which stage of anesthesia is the risk of death greatest?

Back 3

stage II (delirium)

Front 4

Stage II happens at induction and emergence. what does this mean?

Back 4

this means that the autonomic imbalance and discortcate/discerebrate that occurs entering anesthesia also happens coming out of anesthesia

Front 5

of the 4 planes of stage III (surgical anesthesia) - light, moderate, deep, profound - which stage (s) equal surgical anesthesia?

Back 5

moderate & deep (the middle two!)

Front 6

Anesthetic drugs all seem to end up modifying the __________ loop activity, either through specific neurons or through interneurons that feed into the loop.

Back 6

thalamocortical

Front 7

how do the theories of meyer-overton, the membrane lipid/protein theory, and theory of proteins in ion channels all come together to show how anesthetics work?

Back 7

potency of anesthestic of an alcohol increases as length of chain increases (bc inc in fat solubility). the more lipid soluble an anesthetic is the easier it crosses membranes and the more rapid its onset. the lipid solubility changes membrane conformation around proteins in ion channels (leading to failure of synaptic transmission) and its really these proteins that are affected by anesthetics.

Front 8

what is the Meyer-Overton Rule/

Back 8

anesthetic potency is proportional to lipid solubility

Front 9

what is the pressure reversal phenomenon?

Back 9

in a low pressure place like colorado, it takes much less anesthetics to induce coma (compared to hyperbaric or deep sea situation with high pressure --> need much MORE anesthetic)

this happens possibly because its easier for anesthetics to disrupt membrane macromolecules and cause expansion beyond a critical volume against environemnt with less atmospheric pressure(like colorado)

Front 10

IV anesthetics are inactivated by ________, whereas inhalation anesthetics are inactivated by ________.

Back 10

redistribution; exhalation

Front 11

what are the risks of anesthesia (4)?

Back 11

-failure to maintain airway
- allergic rxn
-cardiac dysrhytmias
- malignant hyperthermia (hereditary condition in which certain anesthetics (e.g., halothane) cause high body temperatures and muscle rigidity)

Front 12

how do local anesthetic agents differ in the way they block things?

Back 12

sympathetic blockade --> sensory blockade --> motor blockade

broad spectrum of neural blockade to block diff types of neurons for diff purposes

Front 13

describe the structure of local anesthetics (think mermaid!)

Back 13

all have hydrophobic head, connected by an intermediate alkyl chain to a hydrophilic tail.

(mermaid's head is out of the water while her tail is in the water). her body is the alkyl intermediate, which is what provides the different classes of local anesthetics.

Front 14

what are the 2 classes of local anesthetics? give examples of each. which is used more and why?

Back 14

amino-esters (cocaine, procaine, 2 chloroprocaine, tetracaine) & amino-amides (lidocaine)

amides are used more because allergies are rare for them. since ester's structure is related to PABA, there's a lot of allergies.

Front 15

what does charged vs. uncharged form have to do with local anesthetic action?

Back 15

only uncharged form can cross lipid membrane, but once it crosses, it ionizes and the charged form can bind to the Na channel receptor and prevent depolarization (to cause anesthesia)

Front 16

what's the relationship bw pH and local anesthetic action

Back 16

in an acidic environment (like local abscess), too much H+ leads to more number of charged speciees, so the compounds can't get across the neural membrane (so no neural blockade can occur) ==> patient can't be anesthetized effectively

Front 17

what determines the duration of anesthetic blockage of a Na channel?

Back 17

the higher percentage of anesthetic binding to the Na channel receptor proteins, the longer the duration the block

Front 18

what are 2 receptor sites that can local anesthetics can bind to and blodck conduction?

Back 18

external (outside axon): tetrodotoxin, saxitoxin

internal (inside axon): clinically useful local anesthetics

Front 19

what is the "frequency-dependent block" concept?

Back 19

The higher the discharge rate of a neuron, the more rapidly and more intensely it will be blocked.

In other words, when cell is firing rapidly, the channel is open more often. So more anesthetic can get through.

Front 20

how can you use the stereospecificity of LA's to clinical advantage?

Back 20

The body likes R isomers.

Heart sodium channels are more selective. Neurons don’t differentiate between S and R enantiomer, but the heart does. So you can give S to produce anesthesia (similar to that of R), but less cardiotoxicity (than R)

Front 21

talk about local anesthetic toxicity.

Back 21

there are 3 types:
- local (neurolysis caused by drug itself -- lidocaine & cauda equina --or something in the preserving solution-- 2 chloroprocaine)
- systemic (CNS, cardiovascular)
- allergic (like from aminoesters)

Front 22

how do local anesthetics cause CNS toxicity like seizures?

Back 22

blockade of inhibitory pathways leads to unopposed neuronal pathways (and convulsions). higher doses block facilitory pathways also, leading to CNS depression. hypoxia lowers seizure threshold resulting in seizures occurring at lower doses!

Front 23

Tell me about these two things:
1. Therapeutic Concentration vs Toxic Concentration

2. Maximal Dose

Back 23

1. Important to know therapeutic conc vs. toxic concentration is not that far apart.
2. You have to know maximal dose is based on where you administer bc absorption differs based how vascularized the area is.