General Anesthetics Flashcards
1
Q
what is anesthesia
A
- reversible loss of conciousness
- no concious perception of pain while anesthesia is administered
- stable respiratory and hemodynamic parameters
2
Q
what is the anesthetic triad?
A
- 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
3
Q
patients are afraid of waking up during surgery due to
A
- feeling of pain without being able to communicate
- hear unpleasant conversations
- a recent cane in VA highlighted this issue
4
Q
Monotoring CNS activity while under anesthesia
A
- 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
5
Q
bispectral range guidelines
A
- 100 is awake
- 70 light hypnotic state
- 60 moderate hypnotic state
- 40 deep hypnotic state with EEG suppression
6
Q
general anesthesia
- airway?
- how?
A
- unresponsiveness
- may occur without an artificial airway
- usually done with an inhalation agent
- TIVA also possible
7
Q
regional anesthesia
A
-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
8
Q
local anesthesia
A
-anesthetic agent is placed very superficially for minor surgical procedures
9
Q
sedation
A
- could be considered concious
- cooperative yes
- cognitive abilities diminished (the line between deep sedation and GA is blurry)
- usually achieved with IV agents
10
Q
mechanism of general anesthesia
-sleep cycle
A
- 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
11
Q
dexmedetomidine alpha 2 agonists
A
- increases SW sleep EEG activity
- mimics natural sleep EEG patterns
- may be helpful for ICU sedation to reduce delirium
12
Q
benzodiazapine mode of action
A
- binds the gamma subunit of a GABA receptor
- causes opening of the receptor channel and Cl- influx
- hyperpolarizes the cell, therefore it is inhibitory
13
Q
what are four examples of GABA modulating symptoms
A
- mental alertness
- motor activity
- seizure activity
- CNS control of autonomic function
14
Q
How do gases enter the brain?
A
- 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
15
Q
onset of action of anesthetic gases
A
-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
16
Q
potency of inhaled anesthetics
A
- 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
17
Q
minimum alveolar concentration
- definition
- use
- variables
A
- 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)
18
Q
elimination from the body
A
- currently used inhaled anesthetics undergo almost no metabolism by the body
- they are all pretty much eliminated, unchanged, through the respiratory tract by exhilation
19
Q
volatile anesthetic agents
A
- 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
20
Q
cardiovascular effects of anesthesia
A
- direct myocardial depression
- impaired baroreceptor reflexes
- vasodialtion may be due to a decrease in sympathetic tone from sedation alone
- increased incidence of dysrhythmias
21
Q
respiratory effects
A
- potent bronchodilators
- marked respiratory depressants (not responsive to hypoxia and CO2)
- decreased tidal volume, plus increased respiratory rate, which leads to diminished alveolar ventilation
22
Q
neuromuscular and neurophysical effects
A
- 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
23
Q
isofluorane
A
- 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!!
24
Q
sevofluorane
A
- 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)
25
Q
NO
A
- 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
26
Q
IV anesthesia
- induces what in what time
- mechanism
- cardiovacular effects
- clearing
A
- 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
27
Q
propofol
- effect
- dose
- distribution
- elimination
- off label effect
- caution
A
- 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
28
Q
how do narcotic anesthetics leads to death
A
-blunt your responsiveness to CO2
29
Q
opioids bind to 4 receptors
A
mu
- kappa
- delta
- sigma
30
Q
mu receptors
A
- spura spinal analgesia
- respiratory depression
- physical dependance
- muscle rigidity
31
Q
kappa
A
-sedation, spinal anesthesia
32
Q
delta
A
-analgesia
33
Q
sigma
A
- dysphoria
- hallucinations
- respiratory stimulation
34
Q
ketamine
- what type of agent
- state of consciousness
- what receptor antagonist
- action of glutamate
- binds what receptor
- causes what
- developed to be
A
- 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
