Inhalation/intravenous anaesthetics . Flashcards
Anaesthesia changed with the introduction of what drug? But why don’t we use this now!?
Diethyl ether. You can only achieve the triad of anaesthetics with extreme side effects
What is the ‘triad’ of anaesthesia today; aka, what is wanted/needed out of an anaesthetic
The patient wants hypnosis/amnesia
The surgeon wants them to be immobile
We also don’t want autonomic areflexia (to stop pain)
How do we counteract the issue of side-effects with drugs?
‘Balanced Anasthesia’, using individual drugs for different parts of the triad.
eg; IV for sleep, opiods for pain, and muscle relaxants for immobility.
How is it that we get rid of the drugs once inhaled?
We have to breathe them out! Inhalation Anasthetics don’t get metabolised,
What is the mechanism of uptake for anaesthetics?
These are gases inhaled at certain pressures.
Inhlaed → alveoli → arterial blood → brain
As the pressure of the gas is lower at the end, there is a diffusion gradient towards the brain! Then eventually this reverses and we breath it out!
What is the hypothesis on how the volatile anaesthetics act?
Theory: Their potency is inversly proportional to their Lipid Solubility
“The more lipid soluble, the less agent required”
It was thought that the drug had a distortion effect on the lipid bilayer BUT not all lipophilic volatile agents produce anaesthesia. Clearly lipid-solubility is not the only factor.
What We DO Know: Through GABA modulation (brain) and glycine modulation (spinal cord)
What is MAC? What does 1 MAC equal?
“a means of describing dose and potency referenced to a standard clinical effect”.
1 MAC= minimum alveolar concentration (%) producing immobility on standard surgical stimulus in 50% of patients
NOT a target, but a standard reference point.
The more potent the agent, the _____ the MAC.
Lower. The MAC will produce the SAME RESPONSE but will be at a different percentage for each drug.
How can the dose-response curve be shifted?
The MAC for each drug is calculated in the absence of any other drugs. As soon as you combine drugs, the MAC shifts.
SO although the MAC for desflurane is 6%, this will lower in the presence of another drug, this allows us to use less drugs and still be confident the patient is asleep.
How do we measure/titrate dose?
We can control the Fi vapour on the vaporizer
But even though we can control the Fi via the vaporizer, does that mean that the setting 6% will give the patient an alveolar conc of 6%?
NO. Because when you give a drug, you can only control the [inspired] fraction, but the blood flow at the alveoli carries the drug away, so there is a dynamic balance between the arrival of the drug and it being taken away via the blood.
So sometimes we need to give a higher percentage!
What is the neural pharmacodynamics of inhaled anaesthetic drugs?
- Hypnosis, immobility and amnesia
- Decrease CMRO2 (Good)
- Dose dependant increase Cereba;BF and InterCranialPressure: so be careful in neurosurgery!
What are the pharmacodynamics of inhalation anaesthetics relating to the CVS
- Peripheral vasodilation →lowers BP
- HR and SV unchanged
What are the respiratory pharmacodynamics of inhalation anaesthetics?
- Respiratory depressant (impairs response to hypoxia and CO2) not a biggie bc we can mechanically ventilate
- Bronchdilators (good thing)
Info on Nitrous Oxide (laughing gas)
- Odourless non-flammable gas
- Low potency (MAC 101%)
- Rapid onset
- Analgesic but not on it’s own!
- Some adverse effects; and doesn’t do much!
All the modern agents are _____, but nowadays the H’s are increasingly _______. Why?
All the modern agents are Methyl ethyl ethers, but nowadays the H’s are increasingly Fluoradised.
Why do we use a number of modern inhalation agents?
Because they have specific roles
These are all types of intravenous anaesthetic agents. These all do the same thing, so why do we use so many?
They usually have different characteristics that make them useful in different situations.
Are the intravenous drugs mechanism of action the same or different to inhalation agents.
It is thought they have the same mechanism, but like inhalation agents this is not well understood!
Thiopentone, propofol, etomidate and midazolam ⇒ increase GABA at the GABA receptor (makes cell less responsive)
Ketamine ⇒ Suppresses Glutamate
Pharmacokinetics of intravenous anasthetics? Why is it that a patient may wake up even though total drug in the body hasn’t changed much?
Highly lipid soluble and cross BBB
Drug from IV bolus taken up initally by well perfused areas; eg brain, then redistributes to less perfused areas (fat, muscle), and drug concentration falls.
Offset after a single IV dose is therefore primarily due to redistribution
