General Anesthetics

Question 1

what is anesthesia

Answer 1

• reversible loss of conciousness
• no concious perception of pain while anesthesia is administered
• stable respiratory and hemodynamic parameters

Question 2

what is the anesthetic triad?

Answer 2

• hypnosis: sedation
• analgesia: pain relief
• muscle relaxation: done with a muscle relaxant or high levels of inhalation agent (just becaseu a patient may move in response to a painful stimulus does not mean that they are awake

Question 3

patients are afraid of waking up during surgery due to

Answer 3

• feeling of pain without being able to communicate
• hear unpleasant conversations
• a recent cane in VA highlighted this issue

Question 4

Monotoring CNS activity while under anesthesia

Answer 4

• in 1966 the FDA approved a device that processes real time EEG data
• bispectral index was created
• this is a unitless scale used to assist in determining the point of conciousness

Question 5

bispectral range guidelines

Answer 5

• 100 is awake
• 70 light hypnotic state
• 60 moderate hypnotic state
• 40 deep hypnotic state with EEG suppression

Question 6

general anesthesia

• airway?
• how?

Answer 6

• unresponsiveness
• may occur without an artificial airway
• usually done with an inhalation agent
• TIVA also possible

Question 7

regional anesthesia

Answer 7

-where a dose of local anesthetic is placed near large nerves to render a specific portion of the body paralyzed and insensitive to pain and movement

Question 8

local anesthesia

Answer 8

-anesthetic agent is placed very superficially for minor surgical procedures

Question 9

sedation

Answer 9

• could be considered concious
• cooperative yes
• cognitive abilities diminished (the line between deep sedation and GA is blurry)
• usually achieved with IV agents

Question 10

mechanism of general anesthesia

-sleep cycle

Answer 10

• surrently unknown
• thought to involve modulation of GABA and Ach receptors in the brain by the inhaled or IV substances
• most are GABA agonists
• block decending neuronal arousal pathways
• does not mimic natural sleep patterns

Question 11

dexmedetomidine alpha 2 agonists

Answer 11

• increases SW sleep EEG activity
• mimics natural sleep EEG patterns
• may be helpful for ICU sedation to reduce delirium

Question 12

benzodiazapine mode of action

Answer 12

• binds the gamma subunit of a GABA receptor
• causes opening of the receptor channel and Cl- influx
• hyperpolarizes the cell, therefore it is inhibitory

Question 13

what are four examples of GABA modulating symptoms

Answer 13

• mental alertness
• motor activity
• seizure activity
• CNS control of autonomic function

Question 14

How do gases enter the brain?

Answer 14

• patient breaths a mixture of gases
• partial pressure of the anesthetic gas builds in the alveoli
• anesthetic gas enters blood through the caps and is transported to all of the high flow organs first
• anesthetic gass diffuses into the brain

Question 15

onset of action of anesthetic gases

Answer 15

-directly proportional to the RISE of partial pressure (gaseous tension) of the gas in the brain ; not the concentration (or amount) of gas in the brain

Question 16

potency of inhaled anesthetics

Answer 16

• directly proportional to their lipid solubility
• these are a small component of the totla gase being inhaled by the patient (30%oxygen, 1-5% anesthetic, the rest is air or nitrous oxide)
• if a gase is more potent, then you use a lower concentration and vice verse

Question 17

minimum alveolar concentration

• definition
• use
• variables

Answer 17

• the alveolar concentration in a patient population in which only 50% of patients will respond to a specific surgical stimulus
• allows comparison of potencies between different inhaled gases
• many variable: patient age, temperature, other drugs on board)

Question 18

elimination from the body

Answer 18

• currently used inhaled anesthetics undergo almost no metabolism by the body
• they are all pretty much eliminated, unchanged, through the respiratory tract by exhilation

Question 19

volatile anesthetic agents

Answer 19

• liquids at or near room temp
• changed to a gas form in a very precise way via a vaporizer and administered to the patient via a mask or breathing tube in very carefully controlled amounts

Question 20

cardiovascular effects of anesthesia

Answer 20

• direct myocardial depression
• impaired baroreceptor reflexes
• vasodialtion may be due to a decrease in sympathetic tone from sedation alone
• increased incidence of dysrhythmias

Question 21

respiratory effects

Answer 21

• potent bronchodilators
• marked respiratory depressants (not responsive to hypoxia and CO2)
• decreased tidal volume, plus increased respiratory rate, which leads to diminished alveolar ventilation

Question 22

neuromuscular and neurophysical effects

Answer 22

• decreased muscle tone
• may induce muscle weakness
• conscious awareness
• therefore little movement in response to pain
• decreased cerebral oygen consumption, the brain is asleep, increased cerebral blood flow

Question 23

isofluorane

Answer 23

• most commonly administered anesthetic in the world
• clinically used concentrations: 0.5-2.5% of inspired gas
• noxious to inhale awake
• potent vasodilator
• may cause tachycardia at higher concnentrations
• inexpensive!!

Question 24

sevofluorane

Answer 24

• much less potent thatn isofluorane
• clinically used concentrations: 1-6% of inspired gas
• not noxious to breath whie awake
• excreted via inhalation very rapidly
• most commonly used for peds patients and/or anesthesia for short procedures (may induce emergent dilerium)

Question 25

NO

Answer 25

- true gas - not very powerful - used in 50-70% concentrations and this does not cause general anesthesia (MAC is 105%) - will diffuse quickly into closed air-filled spaces within the body, rapidly expanding the size within that space

Question 26

IV anesthesia - induces what in what time - mechanism - cardiovacular effects - clearing

Answer 26

- when given as an IV bolus will induce rapid loss of consciousness - mechanism is unknown but most are GABA agonists - myocardial depression and or vasodilation leading to hypotension - rapidly redistribute away from the brain so that consciousness may begin to return in 5 to 10 minutes if no other drugs administered

Question 27

propofol - effect - dose - distribution - elimination - off label effect - caution

Answer 27

- rapid loss of conciousness when given IV - typical dose is 1 to 3.5 mg/kg given as a bolus or continuous infusion - rapid redistribution, so patient may wake up soon afterward if no other drugs given - rapid elimination from body, return to pre-anesthetic baseline quickly - no hangover - inherent anti-emetic effect - use cautiously if patient is hypovolemic becaues blood pressure may drop

Question 28

how do narcotic anesthetics leads to death

Answer 28

-blunt your responsiveness to CO2

Question 29

opioids bind to 4 receptors

Answer 29

mu - kappa - delta - sigma

Question 30

mu receptors

Answer 30

- spura spinal analgesia - respiratory depression - physical dependance - muscle rigidity

Question 31

kappa

Answer 31

-sedation, spinal anesthesia

Question 32

delta

Answer 32

-analgesia

Question 33

sigma

Answer 33

- dysphoria - hallucinations - respiratory stimulation

Question 34

ketamine - what type of agent - state of consciousness - what receptor antagonist - action of glutamate - binds what receptor - causes what - developed to be

Answer 34

- dissociative agent: has an effect on the thalams to interpret sensory impulses from the reticular activating system to the cerebral cortex - the patient may appear conscious but unable to respond to sensory input - has been demonstrated to be an N-methyl-d-aspartate receptros antagonist (NMDA to alter the action of the neurotransmitter glutamate) - throughout the body glutamate is involved with the preception of pain responses - binds to mu opioid receptors - can cause hallucinations, hypertension, altered motor function, amnesia, bronchodilation - was developed as a safer PCP-like agent