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Pharmacolgy > General Anesthetics > Flashcards

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
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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
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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
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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
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5
Q

bispectral range guidelines

A
  • 100 is awake
  • 70 light hypnotic state
  • 60 moderate hypnotic state
  • 40 deep hypnotic state with EEG suppression
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6
Q

general anesthesia

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

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8
Q

local anesthesia

A

-anesthetic agent is placed very superficially for minor surgical procedures

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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
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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
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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
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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
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13
Q

what are four examples of GABA modulating symptoms

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

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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

Pharmacolgy (12 decks)

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