Ch 25: General Anesthetics Flashcards
General Anesthetics
useful for rendering patients that are unable to experience pain during procedures: surgical obstetric therapeutic diagnostic
General Anesthetic produce an unconscious state
- Depress the CNS
- Depress CV system
- Depress Respiratory System
Depress the CNS
- Loss regulatory mechanisms
a. thermoregulation
b. baroreceptor reactivity - respiratory
- Lose protective mechanisms
a. glottic reflexes
b. position injuries - corneal abrasions
Depress CV system
- Decreased contractility
- Peripheral vasodilation
- Reduced organ perfusion
Depress Respiratory system
- Induced Hypoxemia
2. Cause retention of secretions (pneumonia)
Why do we use general anesthesia?
Patients want to be sleep patients are uncooperative can't use a regional anesthesia produce amnesia produce analgesia promote muscle relaxation
4 stages of general anesthesia
analgesia excitement
surgical anesthesia
medullary paralysis
analgesia
somewhat conscious
excitement
unconscious & amnesic, but agitated & restless
surgical anesthesia
slow, deep breathing, muscle relaxation
medullary paralysis
breathing stops, CV collapse…. need support for life
Inhaled agents
potent rapid induction & recovery muscle relaxant non-irritating to airway no excess CV depression suppresses excessive sympathetic activity
Types of inhaled agents
gases
volatile liquids
gases
traditionally ether & chloroform, now only nitrous oxide (N2O)
volatile liquids
halothane
isoflurane
desflurane
sevoflurane (newest)
Inhaled agent pharmacokinetics
- must reach a therapeutic tissue concentration in the brain
- highly lipophilic
(will get widely distributed throughout body) - Induction & recovery time increased in obese patients (adipose “sink”)
- recovery is based on respiratory, CV. and metabolic rates
pharmacokinetics
drugs moves from machine to lungs, to blood, to CNS circulation, to local sites
Induction time based on:
- conc. of drub, pressure of system, response rate
- solubility of gas, CO, pressure gradient
- solubility into brain tissue, blood flow into tissue, artery to vein pressure difference
reversal of anesthesia
- turn vaporizer to “0” & hyperventilate
- most leaves unmetabolized through lungs
- if needs to be metabolized, liver function is important in recovery time
- circulation effects speed of drug movement
General Perturbation Theory
- works by disrupting membranes
- potency correlated w/ lipid solubility
- similar effects for a variety of chemical structures
- presumable “squeeze” membranes to slow ion flux
- general phenomena throughout brain
Specific Receptor Theory
- bind to receptor sites or ion channels to slow Na+ influx
- related to lipophilicity
- variety of ion channels & receptors (GABA-a & NMDA)
reduced neurotransmission
- may cause strengthened inhibition/ reduced excitation
- a greater effect on excitatory transmission than inhibitory
inhaled agent side effects
- cv depression
- decreased B.P & H.R.
- depressed airway reflexes (cough)
- bronchodilator (good for asthma & emphysema)
- decreased ciliary action (retain secretions)
- reduced ability to speed up respiration following hypoxia & hypercarbia
- may enhance potency
- likely to reduce side effects of either
intravenous agents
used for induction of anesthesia
from stage 1 to 3 quickly
IV agents used
thiopental midazolam propofol ketamine etomidate
