inhaled anaesthetics, IV anaesthetics Flashcards
3 components to balanced anaesthetics
- hypnosis/amnesia = IV or volatile agent
- autonomic areflexia = opioids
- immobility = muscle relaxant
mechanisms of anaesthetic uptake
Pi = PA = Pa = Pbr
beginning gases are breathed in and at the end breathed out
relationship between dosage and solubitilty
solubility (=oil:gas partition coefficient)
the more soluble the less dose required in a patient
how do volatile agents work?
increasingly likely that it works through GABA modulation in the brain and glycine modulation in the spinal cord
describe MAC
minimum alveolar concentration producing immobility on standard surgical stimulus in 50% of patients
- a means of describing dose and potency referenced to a standard clinical effect
- NOT a target
(way of describing dose to a standard clinical effect)
what causes the MAC dose-response curve to move
the use of other drugs
e.g. fentanyl (opioid) moves the curve to the left
what increases MAC
- young age
- hyperthermia
- hyperthyroid
- drugs
what decreases MAC
- old age
- hypothermia
- hypothyroid
how is dosing titrated
controlled inhaled fraction of vapour on a vapourizer
measured by level in exhaled gas
does setting 6% on the vapourizer mean the patient has an alveolar concentration of 6%
no, because fraction of drug in the alveolar is determined by the fraction of drug you inspire and the minute volume. At the same time, blood is taking it away around the body
- monitored by ‘end tidal’ agent
(dose titration higher at the beginning)
what do these anaesthetics do to the CNS
- hypnosis, immobility (along with NMBA), amnesia
- decrease CMRO2 (cerebral metabolic rate of oxygen)
- dose dependent increase CBF & ICP
what do these anaesthetics do to the CVS
- peripheral vasodilation, lower BP
- HR unchanged
- modern agents do not affect SV greatly
what do these anaesthetics do to the respiratory system
- respiratory depressant
(impair response to hypoxia and CO2) - bronchodilation
nitrous oxide
- odourless non-flammable gas
- low potency
- rapid onset
- analgesic
(potential adverse effects e.g. nausea & vomiting)
chemical structure of modern agents
methyl ethyl ethers
isoflurane
- relative cardiovascular stability
sevoflurance
- good for gas inductions (children)
- reaction with CO absorber-nephrotoxic by-product (kidney patients)
desflurane
- rapid onset and offset
- good for long cases
types of intravenous agents
- barbiturates (e.g. thiopentone)
- phenols (e.g. propofol)
- imidazoles (e.g. etomidate)
- phencyclidine derivates (e.g. ketamine)
- benzodiazepine (e.g. midazolam)
mechanisms of action for IV agents (include exception)
(like inhalation agents)
enhance GABA transmission (prolong Cl- current)
- hyperpolarisation
ketamine = antagonises NMDA receptor
- suppress excitation - analgesic effect
pharmacokinetics of IV agents
- highly lipid soluble & cross BBB
- offset after a single IV dose is therefore primarily due to redistribution
- metabolism is much slower for most agents (not ketamine)
thipoentone
- very rapid onset (10 seconds)
- often used in emergency Caesarian
- rapid offset by redistribution
- slow clearance
- metabolized in liver
- some decrease in PVR & BP (careful in shocked patients)
- repsiratory depression & loss of airway reflexes
propofol
- moderately rapid onset
- rapid offset by redistribution
- fast clearance (can be used for maintenance)
- metabolised in liver
- significant decrease in PVR & BP
- respiratory depression & loss of airway reflexes
propofol vs thiopentone
- propofol is now the preferred ‘standard’ IV anaesthetic
- wears off quicker
- metabolised faster
- good for day surgery
however both cause CVS instability
Etomidate
- remarkable CV stability
- less respiratory depression
- rapid clearance & good recovery profile
but:
-adrenocortical inhibition (loss of stress hormone production for healing/recovery)
ketamine
- analgesic
- CVS stimulant (good in shocked patient)
- preserves airway reflexes and respiratory drive (e.g. will still cough)
- increases CMRO2, CBF & ICP (not good for neurosurgey)
- dissociative state, emergence slower and complicated by dysphoria
total intravenous anaesthesia and when its used
- when we dont want to give a volatile agent
- avoids inhalation route/complications of vapours
- but expensive and no monitoring agent
- e.g. a pateint who sufferes from post-operative nausea and vomiting (as all volatile agents produce this) TIVA can be given
inhaled anaesthetics work by:
modulating the action of GABA in the brain and glycine in the spinal cord
