10 - Anaesthesia Flashcards
what system is involved in the sleep/wake cycle and is a target of anaesthesia/
reticular activating system
what are the 5 stages of anaesthesia?
- preparation
- induction
- maintenance
- early recovery
- delayed recovery
what is the biggest concern when anaesthetising diabetic pts?
hypoglacaemic episode
what are the 3 types of anaesthesia?
- local
- general
- combined
in what type of anaesthesia is consciousness not impaired?
local
what are the 3 types of local anaesthesia?
- topical
- field
- regional - spinal/epidural
what is the triad of general anaesthesia?
- hyponosis - IV agents
- analgesia - opiates and non opiates
- muscle relaxation - depolarising and non- depolarising
when is propofol typically used in anaesthesia?
induction
the potency of anaesthetic agents is related to what?
their lipid solubility
order these anaesthetics from most to least potent:
* isoflurane
* halothane
* N2O
* sevoflurane
* deslurane
- halothane
- isoflurane
- sevoflurane
- desflurane
- N2O
what pain pathways is the area targeted by anaesthetic drugs?
descending pain pathways
what receptors do opiates act on?
mu receptors
list 3 natural opiates
morphine
dihydro-morphine
codeine
give an example of an opiate analogue
tramadol
give 4 examples of synthetic/semisynthetic opiates
- pethidine
- fentanyk
- alfentanyl
- remifentanyl
mu 1 receptors are primarily involved in what?
analegesia
mu 2 receptors are primarily involved in what?
respiratory depression
mu3 receptors are primarily involved in what?
vasodilation
what can be given in cases of opiate over dose?
naloxone
how should naloxone be administered and why?
- via infusion
- very short half life
why should naloxone not be given as a bolus?
can result in pulmonary oedema
at what stage of anaesthesia are neostigmine and glycopyrolate used?
recovery
what is role of glycopyrolate in the recovery stage of anaesthesia?
offsets bradycardia caused by neostigmine
why should pts fast before elective surgeries/
empty stomach reduces the risk of stomach contents refluxing into oropharynx and then being aspirated into the traceha
before being put under general anesthesia the pt will breath 100% O2 for a few minutes - why is this?
gives them a reserve of O2 for the perikod between losing consciousness and being successfully intubated and ventilated - in case there are issues establishing an airway
what premedications can be given before a pt is put under general anaesthesia?
- benzos - relaxes muscles and reduces anxiety
- opiates - reduces pain and hypertensive response to laryngoscope
- alpha2-adrenergic agonists - sedation + pain
- antacids - reflux, pregnancy, hiatus hernia
- antibiotics - surgical implant, endocarditis
- anticholinergics
what is the theory of general anaesthetic action?
enhance inhibitory signals or blocking excitatory signals
how are anaesthetic agents administered in the induction phase?
IV or inhalation
list 4 IV options for general anaesthetic
- propofol
- ketamine
- sodium thiopentone
- etomidate
what are 4 inhaled options for general anaesthetics?
- sevoflurane
- desflurane
- isoflurane
- nitrous oxide
what is the mechanism of inhaled anaesthetics?
- diffuse across lung tissue
- enter blood
- enter brain
- recovery via exhalation
what is the mechanism for IV anaesthetics?
- bolus of drug injected directly into blood
- travels to brain
- ultimate recovery by elimination
what drug is commonly used for TIVA?
propofol
why may inhalation induction be chosen over IV?
- IV access is difficult to obtain
- difficulty maintaining airway
- pt preference, eg,. children
what is the duration of action of IV anaesthetics? what is used to prolong this?
- duration = 5-10 minutes
- prolonged using mixture of inhaled anaesthetics
maintenance of anaesthesia is achieved through what?
inhalation of a carefully controlled mixture of:
* oxygen
* nitrous oxide
* volatile anaesthetic agent
or through continuous infusion of propofol through an IV catheter
how do muscle relaxants work?
preventing ACh from binding to receptor
what are the two categories of muscle relaxants?
depolarising - suxamethonium
non-depolarising - rocuronium
atracurium
what is used to reverse the effects of muscle relaxants at the end of surgery?
cholinesterase inhibitors - neostigmine or sugammadex (non-depolarising muscle relaxants)
antimetics are often given at the end of the procedure to prevent post-operative nausea and vomiting - give 3 examples
ondansetron - avoid in pts with prolonged QT interval
dexamethasone - caution in diabetics and immunocompromised
cyclizine - caution in heart failure and elderly
what are some significant risks of anaesthesia?
- accidental awareness
- aspiration
- dental injury
- anaphylaxis
- cardiovasc events
- malignant hyperthermia
- death
what is malignant hyperthermia?
potentially fatal hypermetabolic response to anaesthesia that causes:
* hyperthermia
* increased CO2 production
* tachycardia
* muscle rigidity
* acidosis
* hyperkalaemia
what increases the risk of malignant hyperthermjia?
- volatile anaesthetics - isoflurane, sevoflurane, desflurane
- suxamethonium
- genetic mutations - autosomal dominant
how is malignant hyperthermia treated?
dantrolene - interrupts muscle rigidity and hypermetabolism by interferring with Ca2+ movement in skeletal muscle
a pt is having surgery. identify why the following anaesthetic agents are used in combination:
* propofol
* isoflurane
* fentanyk
* atracurium
* suxamethonium
* atropine/glycopyrrolate
* neostigmine
- propofol - IV rapid induction
- isoflurane - inhalaed for maintenance
- fentanyl - opiod analgesic
- atracurium - muscle relaxant
- suxamethonium - muscle relaxant
- atropine/glycopyrrolate - muscarinic antagonist to prevent/treat bradycardia and reduce salivary secretions
- neostigmine - reverse NMJ blockade
what is the mechanism of action of propofol?
GABA agonist - increases inhibitory effect
what is the volume of distribution of propofol?
- 60L/kg
what is the MOA of isoflurane?
- reduces gap junction channel opening times
- alters tissue excitability
- induces muscle relaxation
what is the MOA of fentanyl?
- agonist of mu opioid receptor
- inhibits adenylate cyclase
- = downregulation
- hyperpolarises cell and inhibits nerve activity
what is a typical dose of fentanyl?
0.05mg/mL IV
what is the MOA of suxamethonium?
- depolarising neuromuscular blocker
- mimics ACh but not rapidly hydrolysed
wh
what is the MOA of atracurium?
- non-depolarising neuromuscular blocker
- antagonist of ACh sp. at nicotinic receptors
what is the MOA of neostigmine?
- inhibits AChE
- prolongs action of ACh
- increases muscular contraction and reverses muscle relaxants
what is hte MOA of atropine/glycopyrrate
- antagonise muscarinic receptors
- inhibit cholinergic transmission
- decreases bradycardia risk from neostigmine
what is the MOA of mannitol?
- increases blood plasma osmolarity
- increases flow of water from tissues
- decreases ICP
