9. General Anaesthetics Flashcards
general anaesthesia
-a medically induced reversible condition
-unconscious state
-can tolerate painful stimuli
-there is a loss of vegetative or muscular reactions
what are the modes of action of general anaesthesia
Biophysical theory - influences the neuronal membrane fluidity and neuronal function
Biochemical theory- multi receptor activity of GA leads to CNS depression
What are the phases of GA
1)Preanesthetic
2)Excitatory
3) Surgical
4)Paralytic
how are GA classified ?
-via route of admin (inhaled vs injectable)
-via type of anaesthesia induced (associative vs dissociative)
what are the types of GA
-inhalational
-combined (inhaled vs injectable)
-supplemented (GA with other drugs (opioids, anxiolytics, hypnosedatives)
what are the alternatives for GA
neuroleptanalgesia (opioid analgesics and antipsychotics)
analgosedation (analgesics and benzos)
inhaled anaesthetics
-all cause associative type of anesthesia
-pk is influenced by partition coefficient
toxicity - biotransformation and exhalation (pt and staff)
-easy and fast control of level of anesthesia
how are inhaled anesthetics divided
volatile liquids vs anaesthetic gasses
MAC (minimum alveolar concentration)
plasma conc in CNS depends on blood conc which is directly relate to alveolar concentration
-parameter of clinical efficacy
- conc which induces stadium of tolerance in 50% of patients
what are the volatile anaesthetic liquids
-ethers
(halogenated hydrocarbons)
-> ISOFLURANE
->SEVOFLURANE
->DESFLURANE
ISOFLURANE
-weak muscle relaxing activity ,
-highest decrease of peripheral resistance
-Low metabolization
-Strong smell bad in pediatrics
SEVOFLURANE
- Pleasant smell
- Without analgesic effect
DESFLURANE
- PUNGENT SMELL
- Greenhouse gas
- Fast onset and recovery
- Only used for maintenance of anesthesia
what are the anesthetic gases ?
-Nitrous oxide
-Xenon
Nitrous oxide
- Low solubility in plasma
- Increasing conc -> euphoric-> analgesic->anesthetic
- Carrier gas for other inhaled anesthetics
- Can be used for breast feeding females and delivery
Xenon
- NMDA RECEP INHIBITOR
- Minimal influence on CVS
- COSTLY
IV anaesthetics
-can also be given i.m, p.o.intranasally , per rectally
-used for INDUCTION TO GA
-short performances it is used as monanesthesia
-
what are IV anesthetics used for
serious seizures
ICU
C sections
analgesy in refractory pain in oncology
how IV anesthesias classified
barbiturates vs non barbiturates
what are the barbiturates ?
THIOPENTAL
thiopental
-ultra short acting
-used in induction
-used in combo with inhaled GA
-effect onset is no later than 20s -> tissue redistribution
metabolised in liver
-BP and heart output is decreased in HIGH DOSES
what are the non barbiturates?
KETAMINE
PROPOFOL
ETOMIDATE
KETAMINE moa and type
nmda antagonists
dissociative anesthetic
indications of ketamine
GA
resistant bronchospasms
routes of admin of ketamine
iv im transnasally and transbuccaly
pk of ketamine
f depends on route of admin
low plasma protein binding
fast liver metabolism
what are the ae of ketamine
confusion
hallucinations
increased muscle tone
PD -with other GA and muscle relaxants
CI of ketamine
serious hypertension
hyperthyreoisis
acute psychosis
PROPOFOL
moa -alsoteric modulation of gabaa
ind- GA , ICU sedation,
admin route 0IV
Pk -plasma protein binding , rapid CYP metabolism
AE- myoclonus , cough during GA intro , hypotension, hypertriglyceridemia
Interactions- BZD , opioids, analgesics and other GA
CI - hypersensitivity, chronic sedation in pt <16y old
ETOMIDATE
short effect without analgesy
-minimal influence on CVS and respiration
- introduction to GA, diagnostic p. and examinations
opioids used in anesthesiology
ALFENTANIL
SULFENTANIL
REMIFENTANIL
-used for maintenance of anesthesia
Benzos used in anaesthesiology
MIDAZOLAM
DIAZEPAM
used for preperation
what is the course of anesthesia
1) Premedication
2) Induction of GA
3) Maintenance of GA
4) Termination of GA
premedication
anxiolytics – benzodiazepines (midazolam)
* sedatives – benzodiazepines, H1 antihistamines
* analgesics – NSAID, opioids
* reduction of vagus nerve activity- atropine + scopolamine
* prokinetics – metoclopramide
* ↓ gastric acidity – PPI/H2 antagonists
induction of anesthesia
- short acting injectable GA
-can be i.m., p.o. p rect
-rarely in children
-Muscle relaxation-neeeded for INTUBATION (depolarising muscle relaxant suxamethonium )
Maintenance of anesthesia
- inhalational anesthetic (combo of anesthetic, analgesic and muscle relaxant)
e.g. N2O2 +O2 + sevoflurane/isoflurane +opioid +suxamethonium
-TIVA (total IV anesthesia )
- premed- benzos
Induction- fentanyl , propofil
Maintenance – Bristol regime -10-8-6 scheme ( 10 for 10 then 8 for 10 then 6 for rest
-artificial ventilation
Termination of anesthesia
- neostigmine, physostigmine – antagonists of non-depolarizing muscle relaxants
- naloxone – recovery of respiration and vigility (opioid antagonist)
*flumazenil – recvery of vigility (benzodiazepine antagonist)
-Sugammadex- selectively coats muscle relaxants -> fast inhibitor of rocuronium
*! ensuring quality postoperative care
RISKS AND COMPLICATIONS OF GA
- MALIGNANT HYPERTHERMIA -> DANTROLENE
