General Anaesthetics Flashcards

1
Q

what is anaesthetic?

A

• Anaesthesia = “without sensation”

– reversible loss of awareness of pain

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2
Q

what are the different types of anaesthetic?

A
  • local
  • regional
  • general
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3
Q

what is local anaesthetic?

A

– patient remains conscious
– cheaper, safer
– Used in different ways to give surgeon ability to work on different parts of the body

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4
Q

what is regional anaesthetic?

A

– larger area of the body involved

– Can numb a whole arm

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5
Q

what is general anaesthetic?

A

– Loss/change of consciousness (central effect)
– major surgery can take place
– This is the type you could use to remove appendix/tumours

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6
Q

what is stage 1?

A

– Induction/analgesia
– Reduced responses to pain
– Conscious but drowsy
– Varies dependent on the agent ether»haloethene
The time a patient spends in stage 1 depends greatly on what drug they have been given. Some of the older drugs have a longer period of time within stage 1.

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7
Q

what is stage 2?

A

– Loss of response to stimuli
– Responses to pain preserved
– Gag reflex, coughing can increase
– This can lead to concerns of choking, holding breath, talking, vomiting during the surgery
This is a dangerous phase as you have things a patient may do which would cause harm. We want to minimise the time a patient has in this stage, if you increase the dose you can get to stage 3 quicker.

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8
Q

what is stagw 3?

A

– Surgical anaesthesia
– Regular respiration
– Possibly some reflexes as muscle tone is preserved
– Movement ceases
– Progressive shallowing of breath
this is the level stable steady state where you can do surgey without worrying too much about the patient. As long as you maintain the level of the drug, you won’t have too many issues with the patient. However, if the dose is too large you might get shallowing of patients breath.

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9
Q

what is stage 4?

A

– Anaesthetic overdose
– Medullary paralysis
– Respiration and Vasomotor control ceases
This is an OVERDOSE. Lose the control of the body and the patient will stop breathing. Unless you do something the patient will die.

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10
Q

what are the pharmacokinetics of GA?

A

• We would like rapid induction and rapid recovery
• We would prefer to avoid stage 2 – get them as quickly through this as possible
• We want the, to be in stage 3 in stable state until the surgery is done
• We would prefer the patient not to die in stage 4
• We would prefer to avoid side-effects – help them recover as quickly as possible.
There is no single drug which can achieve all of these goals

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11
Q

what are modern GA?

A

• rapid induction of unconsciousness; i.v. propofol.
o Get to therapeutic levels in plasma very quickly and this will give you rapid indiuction so you get past stage 2 quickly
• maintenance of unconsciousness and production of anaesthesia; inhaled N2O/halothane
• supplementary i.v. analgesic e.g. morphine
• neuromuscular blocker e.g. atracurium – this is for abdo surgery
• Fast induction and recovery (anxiety, hangover), reduces time stage II, homeostatic reflexes remain intact, amnesia not a bad thing to not remember surgery
o This is why sometimes you use i/v for induction and then move to inhaled as this is able to maintain over a longer period of time

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12
Q

how do GA work?

A
–	Alter function of neurones
–	Structures very diverse
o	Argues against unified theory
–	Lipid theory
–	Protein theory
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13
Q

what is lipid perturbation?

A

• Was originally thought to be an effect on lipid alone, but was later interpreted in terms of changing the conformation of membrane proteins by changing the environment in which they are dissolved.
• However, this doesn’t completely work:
o Chain cut-off
o Adding long carbon chains can REDUCE potency
o ?a binding cavity of some sort
• Physical chemistry shows anaesthetics don’t change membranes that much
• Stereoselectivity of anaesthetic actions – membrane action fluidization is not a good explaination
• Some anaesthetics specifically affect certain proteins

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14
Q

what is the protein theory?

A
  • Targets on membrane proteins, the binding sites for the anaesthics are probably situated in the lipid bilayer and the way it works it by dissolving in the bilayer, accessing the protein and then changing the structure and the function of the protein.
  • GABA A = inhibitory ligand gated ion channels
  • Potassium channels open you get hyperpolarisation
  • NMDA are excitatory and general anaesthics inhibit these proteins
  • Volatile anaesthics seems to act on all three receptors these are the ones you inhale
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15
Q

what is the function of GABA?

A

POTENTIATED

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16
Q

what is the fucntion of NMDA>

A

inhibited

17
Q

what is the role of two pore potassium channels?

A

potentiated

18
Q

what is the advantage of inhaled anaesthics?

A
  • Easy to maintain degree of anaesthesia
  • (fast air:blood equilibration) this means you can change conc of the drug very quickly allowing for fast recovery
  • +Rapid emergence from anaesthesia
19
Q

what is a disadvantage of inhaled anaesthics?

A
  • Cumbersome and expensive apparatus
  • -Administered via a mask – psychological effects people might feel suffocated
  • -Atmospheric pollution (scavengers) -
20
Q

what is the metabolism and toxicity of inhaled anaesthics?

A
  • Metabolism unimportant for elimination
  • BUT! Toxic metabolites
  • Fluranes generate fluoride when metabolised, causes renal toxicity
  • Halothane converted to bromide and TFA, hepatotoxic
  • Problem for theatre staff - do not want to breath them in often
  • liver disease, leukaemia, abortion, birth defects
  • Scavenger systems required
21
Q

what is the mechanism of action for inhaled?

A
  • Enter and leave the body via the lungs
  • Metabolism generally unimportant for recovery
  • Pass from gas phase to blood, then to tissues
  • And on the way out to the opposite, tissue, blood and breathed out as gas
22
Q

what is the minimum alveolar conc?

A
  • The concentration required to produce anaesthesia in 50% of patients
  • Measures the potency of the anaesthetic
23
Q

what is the blood-gas partition co-efficient?

A
  • A measure of how well the drug dissolves in blood
  • Determines rate of induction and recovery
  • To get rapid induction you don’t want the gas to be very soluble in the blood. If you have high solubility in the blood you will cause a reservoir effect. Meaning you would have to fill up the drug within the blood before it could take effect in the tissue.
24
Q

what is the oil-gas partition co-efficient?

A
  • High oil-partition coefficient confers high POTENCY
  • BUT! Lots of the anaesthetic will dissolve in fat
  • Fat is poorly vascularized – poor blood supply so will take time for Anaesthetic will take a long time to leave this tissue so it has to go from fat  blood  elimination
  • Patient will have a slowly resolving “hangover”
25
Q

what are the two phases of recovering from GA?

A

• Recovery from anaesthesia often has two phases. The first, rapid phase will depend on the blood:gas coefficient as for induction: the lower the blood solubility, the faster the recovery. However, there is a slow phase too. this is due to anaesthetic dissolving in fatty tissues. The patient is likely to be conscious but “groggy” during this part of recovery.

26
Q

what happens if you have a drug witha. high oil partition?

A

• If you have a drug with high oil partition then it will be highly potent but the patient will end up with a hangover as loads of the drug will be left in the fat. They may regain consciousness but they will have a low level of this drug in the fat and make them very groggy. This is more of an issue the fatter the patient is.

27
Q

what are the most common inhaled anaesthics?

A
  • Most common: N2O and isoflurane
  • In the UK, desflurane and sevoflurane becoming popular (£) – many ways better drugs but they are more expensive so less used
  • Ether: explosive, irritant and causes nausea; but cheap (still used in 3rd world countries but not listed in BNF) – bad for patient but has explosive properties
28
Q

what is isoflurane?

A
  • Widely used (but being replaced)
  • No metabolism; little toxicity; not proconvulsive like some of the older drugs
  • £ 2x halothane
  • Hypotension (-ve inotrope, decreases SVR)
  • Coronary vasodilator – myocardial ischaemia recently disputed – steals blood from other areas of the heart
  • Possible worries regarding neurodegeneration from repeated surgeries
29
Q

what is sevoflurane?

A

• Described by many as the “anaesthetic of choice”
• Very rapid induction (very low blood:gas coefficient) it doesn’t dissolve well in blood so it can easily leave the blood as it is saturated at low levels
• Very little metabolism so not much toxicity
BUT!!
• Very high cost (5 x halothane) high volumes needed so very costly
• Some concerns regarding neurodegeneration – problem is repeated surgeries
• Recovery so rapid that post-op pain relief needed – regain consciousness quickly so need opioids to take you through the time after op

30
Q

what is nitrous oxide/

A
  • Entonox’
  • N2O (not NO)
  • Low blood:gas partition coefficient
  • Analgesic at concentrations lower than those which cause unconsciousness – you will never be able to just cause unconsciousness with N2O as you would compromise the levels of oxygen the human was getting
  • It is widely used in childbirth. Nitrous oxide breaks down at high temperatures (like in a car engine cylinder) to release nitrogen and oxygen).
31
Q

what are the advantages of i/v anaesthic?

A
  • Rapid induction
  • No stage II
  • Simple apparatus
  • Pleasant induction
  • No atmospheric pollution
32
Q

what are the disadvantages of i/v?

A
  • Once it’s in, it’s in; level of anaesthesia difficult to control
  • Recovery can be slow:redistribution, metabolism
  • Finite duration (but can infuse)
  • vein damage e.g. thrombophlebitis
33
Q

what is thiopental?

A

• The only barbiturate commonly used in surgery
• Very lipid soluble; crosses BBB very quickly
• Induction dependent on blood flow – usually very good
rapid distribution

34
Q

what is propofol?

A
  • Rapid metabolism – rapid recovery compared to other IV, no hangover
  • Can be continuously infused to maintain anaesthesia without inhaled agent
  • Acts by potentiating GABAA receptors (etomidate very similar mechanism)
  • Day surgery
  • Widely abused by medical personnel
  • “Milk of amnesia”
  • Euphoria, induction of sleep
  • But! Steep dose response curve
  • difficult to monitor dose