Lecture 10: Inhalation and IV anaesthetics Flashcards
The triad of anaesthesia consists of?
IV or Volatile agents - Amnesia
Opoids - Autonomic areflexia
Muscle relaxant - immobility
How do volatile agents work?
We don’t know
but…
likely due to GABA modulation in the brain and glycine modulation in the spinal cord
What is MAC?
Minimum alveolar concentraion (%) producing immobility on standard surgical stimulus (forearm incision) in 50% of patients.
More potent agents have a lower MAC (doesn’t inherently mean they are better)
Is not a taget but rather just a dose index to a clinical effect
Dose response curve?
How can you change the dose response curve?
Is very steep and a small increase will heavily increase the effect
This graph will be heavily altered by the use of other drugs
How is dosing measured and monitored?
Finspired —-minute volume—> FA- —-flow—> Blood
We monitor the expired breath and then titrate the amount to reach the aquired amount. Remember we can alter the minute volume as the patient is ventilated.
Pharmacodynamics of volatile agents? (CNS)
- hypnosis, immoblity, amnesia
- decrease CMRO2 (cerebral metabolic rate) = neuroprotective
- Dose dependent increase cerebral BF anf ICP meaning care with neurosurgery
Pharmacodynamics of volatile agents (CVS)
- peripheral vasodilation, lower BP
- HR unchanged
Pharmacodynamics of volatile agents (RS)?
- respiratory depressants - impair ventilatory response to hyoxia and to CO2
- Bronchodilation - (though desflurane is an airway irritant)
Nitrous oxide use, benefit and adverse effects?
Odourless
low potency (MAC 101%)
Rapid onset
analgesic
AE: nausea + vomiting
Isoflurane use, benefits?
Pungent
Pontent (MAC 1.1%)
Itermediate solubility - medium onset speed
very cardiovascular stable
Sevoflurane use, benefits and AE?
Non-pungent and least resp depressant
cheap and good for gas induction in children
intermediate potency (MAC 1.7%)
low sol. - rapid onset
AE: reacts with CO2 so theoretical renal toxicity
Desflurane use, benfits
Intermediate potency (MAC 6%)
rapid onset and offset (ideal for long cases)
Pungent and is known to be an airway irritant
5 types of IV anaesthetic agents
- Barbituates (Thiopentone)
- Phenols (Propfol)
- Imidazoles (etomidate)
- Phencyclidine derivitives (ketamine)
- Benzodiazapines (midazolam)
Mechanism of action of IV agents?
Virtually all except ketamine enchance GABA in the brain and hyperpolarise the neurons shutting the brain down
Ketamine binds to PCP receptor to antaganise glutamate, supressing exitation. Also has an analgesic effect as well
Pharmacokinetics of IV agents?
Highly lipid solubiluty and cross BBB
Drug from IV blous taken up by VRG organs, then leaves these organs as lean tissues take up drug and conc in blood falls
Offest after single IV dose is therefore due primarily to redistribtion (patient may be wide away even though total amount in body is basically unchanged)