General Anesthetics Flashcards

1
Q

What are the 4 stages of general anesthesia?

A

stage 1: analgesia and amnesia (still responds to commands)

stage 2: delirium (LOC)

stage 3: surgical anesthesia (respiration regular, decreased autonomic reflexes0

stage 4: medullar depression (relative OD! severe CV collapse and respiratory depression)

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2
Q

Within stage 3 (surgical anesthesia) there are 4 planes that are based on what?

A

eye movements, depth of respiration and muscular relaxation

(light surgical, moderate surgical, deep surgical, excessive surgical)

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3
Q

What are the 5 basic goals of general anesthesia?

A

loss of awareness

amnesia

analgesia

blunting of the ANS

skeletal muscle relaxation

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4
Q

What is the general combo of drugs to achieve the 5 goals of anesthesia?

A
  1. general anesthetic - loss of awareness
  2. Benzodiazepine - amnesia
  3. opioid - analgesia and BANS
  4. Neuromuscular blocker - skeletal relaxation
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5
Q

What are the two main routes of delivery for general anesthetics?

A

inhalation of gaseous form

injection IV

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6
Q

Because of the nature of gases, how are drug concentrations expressed for general anesthesia?

A

in terms of partial pressurs = Panesthestic

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7
Q

How does Henry’s Law relate to general anesthesia?

A

of gas molecules that enters a liquid (blood in this case) before equilibrium is determiend by the solubility of the gas in the blood

drugs that dissolve into blood do NOT raise the Panesthetic

this means that the more anesthetic dissolves into the blood, the longer it will take to attain equilibrium and you’ll end up with greater concentrations of it at equilibrium

this means the AMOUNT OF UNDISSOLVED DRUG IN BLOOD is what’s related to clinical effect

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8
Q

What are three factors that affect Parterial?

A
  1. concentration of the anesthetic in inspired air
  2. pulmonary ventrilation rate
  3. transfer of anesthetic form alveoli to blood (solubility of the anesthetic inb lood)
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9
Q

What is the minimum alveolar concentration (MAC)?

A

it’s the dose of anesthetic producing surgical anesthesia in 50% of the patient population

so basically equivalent fo the ED50

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10
Q

Anesthetics with the ____ MAC values are the most potent.

A

lowest

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11
Q

At what MAC is surgical anesthesia usually attained?

A

doeses at 1 MAC value often produces only light anesthesia

for surfical anesthesia you usually need to use 1.3 or 1.5 MACs

(deep anesthesia is at 2 MACs)

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12
Q

What is potency and what is it a function of?

A

potency is the amount of drug necessary to produce an effect of specified intensity

it’s a function of lipid solubility! (oil:gas partition coefficient)

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13
Q

The ___ lipid soluble the anesthetic, the greater its potency.

A

more

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14
Q

In terms of the blood;gas partition coefficient (X blood/X gas)…

the ____ soluble a drug is in the blood, the longer it takes to raise it’s partial pressure in blood.

A

more

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15
Q

While the oil:gas partition determines anesthetic potency, the blood;gas partition coefficient determines….

A

rate of onset

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16
Q

Describe the second gas effect.

A

rapid uptake of the first anesthetic from the elveoli into the blood creates a negative pressure in the alveoli, thus drawing in more of a second inhaled anesthetic agent whos alveolar uptake might otehrwise be slow

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17
Q

Given what we know about the second gas effect, why is Nitrous oxide used first even though it’s not a good anesthetic when given alone?

A

It’s rapidly raken up by the aovleoli and then into the blood

it then creates a second gas effect, so helps the next anesthetics to be taken up faster

this basically decreases the time for both induction and recovery

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18
Q

What is diffusion hypoxia?

A

It can occur during recovery

N2O rapidly goes from the blood to the aovleoli, leaving “no room” for oxygen to enter the lungs - this can lead to hypoxia

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19
Q

If the time course for anesthetic elimination is the “mirror image” of induction, fat soluble anesthetics leave the body the ______.

A

slowest

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20
Q

What are the routes of elimination for anesthetics?

A

lung is the primary route

also through diffusion through skin and mucous membranes

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21
Q

Although biotransformation isn’t really important for terminating the action of inhalant anesthetics, why is it toxicologcially important?

A

halogenated anesthetics will liberate checmially reactive halide ions which can acutely or chronically hamr kidneys, liver and reproductive organs

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22
Q

WHat are the neuromusclar blockers usually given for?

A

to facilitate placement of the endotrachiael intubation tube

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23
Q

What are the 4 main halogenated hydrocarbon inhalation anesthetics?

A

halothane

isoflurane

methosyflurane

sevoflurane

24
Q

What are the CNS effects of halogenated hydrocarbon anesthetics?

A

decrease brain metabolic rate

increase cerebral blood flow

Bad: increases ICP

25
Q

What are the CV effects of the halogenated hydroarbon inhalation anesthetics?

A
  1. decrease myocardial contratility
  2. decresed stroke volume
  3. leads to lower aterial blood pressure
  4. sensitizes myocardium to catecholamines, so increases automaticity
26
Q

Halignant hyperthermia occurs with all inhalation anesthetics except____

but especially common with _____

A

doesn’t occur with nitrous oxide

most commonly seen with halothane

27
Q

What are the advantages to using halothane?

A

it’s very potent (MAC from .7 to .9)

rapid induction and recovery

among the least expensive volatile anesthetics

doesn’t irritate the larynx so you don’t get laryngospasm

28
Q

What are the disadvantages to using halothane?

A

inadequate analgesia and muscle relaxation

depresses myocardium and baroreceptor reflexes (decreases CO and BP)

sensitizes myocardium to catecholamines (increases automaticity)

increases cerebral blood flow and intracranial pressure

respiratiory depression

29
Q

What are the two major toxicities seen with halothane?

A

potential for acute or chronic hepatic toxicity = halothane hepatitis

malignant hyperthermia (potentially fatal)

30
Q

What’s the treatment for malignant hyperthermia?

A

cool the patient

treat with dantrolene which blocks Ca2+ release from SER in muscle cells

31
Q

What are the benefits to using isoflurane over halothane?

A

it’s equally potenta nd induction is in les than 10 minutes

unlike halothane, it doesn’t sensitize the myocardium to catecholamines and you have less hepatotoxicity and renal toxicity because of its lower rate of metabolism

32
Q

What are the disadvantages to isoflurane?

A

it can cause arrhythmias (although rare)

pungent odor

potential for malignant hyperthermia

33
Q

What halogen anesthetic is the newest approved in north america and is “almost perfect”?

A

sevoflurane

34
Q

What inhalation anesthetic is the ONLY one that’s actually a gas?

A

nitrous oxide

35
Q

What are the advantages to nitrous oxide?

A

low blood solubility, so rapid onset

littl effect overall on cardiovascular system

can be used for the second gas effect to hasten anesthesia produced by more potent, but more soluble inhalaiton anesthetics

does have mild to moderate analgesic activity

36
Q

What are the disadvantages to Nitrous Oxide?

A

it’s MAC is 104%!!

So you can’t use it as a sole anesthetic agent

doesn’t have any muscle relaxing effect

37
Q

Do IV anesthetics work faster or slower than inhalants?

A

they work faster

38
Q

Injectables are best suited for _____ of anesthsia and for ___ operative procedures

A

induction of anesthsia

short operations

39
Q

Why can’t you use intravenous anesthetics as the sole anesthetic for surgeries?

A

they’re not good enough as muscle relaxation

40
Q

What are the 5 general classes of injectable anesthetics?

A

barbiturates

benzodiazepines

propofol

ketamine

opioids

41
Q

What are two examples of barbiturates used for injectable anesthesia?

A

thiopental (pentothal)

methohexital (brevital)

42
Q

What is the mechanism of action for the barbiturates?

A

they facilitate GABA induced Cl- entry into neurons, leading to CNS depression

43
Q

What are two examples of Benzodiazepines used for injectable anesthetic?

A

Midazolam (versed)

Disazepam (Valium)

44
Q

What is the mechanism for the benzos?

A

same as the barbiturates actually

facilitates GABA-induced Cl- entry inot neurons, leading to CNS depression

45
Q

Why are benzodizepines more attractive than the barbiturates?

A

they have less cardiovascular and respiratory depression than the barbiturates

46
Q

What is the most important fuction of the benzos?

A

their amnestic action

47
Q

What abuse drug is katamine most similar to?

A

phencyclidine (PCP)

48
Q

What does a “dissociative” anesthetic like ketamine do?

A

makes the patient unaware of environment and not feel pain

the patient will appear awake with eyes open

49
Q

What are the pharmacological effects and benefits of ketamine?

A
  1. anesthetic, analgesic, amnestic, and sedative

airway reflexes and respiration maintained

cardiofascular system not depressed - actually stimulated, making it idal for patients with unstable CV function

50
Q

What is the likely mechanism of action for keramine?

A

NMDA glutamate receptor blocker

51
Q

What is the prinicple brawback for ketamine?

A

the occurrence of emergence reactions like delirium and hallucinations “bad trips” basically

52
Q

What are the three main opioids used for aneshtesia?

A

fentanyl

sufentanyl

alfentanil

53
Q

Why are opioids good for patients with compromised mycoardial function?

A

because opioids lend to hemodynamic stability, (in addition to analgesia and anesthesia)

54
Q

What’s the main issue with opioids?

A

respiration has to be maintained artificially and may be depressed into the post-op period

55
Q
A