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The Patient Y3 Semester 2 > General Anaesthetics > Flashcards

General Anaesthetics Flashcards

1
Q

What is an anaesthetic?

A

Anaesthesia = “without sensation”

reversible loss of awareness

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2
Q

What is local anaesthetic?

A

Local

  • patient remains conscious
  • cheaper, safer
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3
Q

What is a regional anaesthetic?

A

larger area of the body involved

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4
Q

What is general anaesthetic?

A
  • loss of consciousness (central effect)

- major surgery can take place

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5
Q

How many stages of anaesthesia are there?

A

STAGES dependent on dose and with some MOA, the dose will not ramp up instantly into the range that we need for full surgical ANAETHESHIA

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6
Q

What is stage 1 of anaesthesia:

A
  • Pt is conscious but drowsy
  • Reduced responses to pain
  • Amount of time that patient will stay in stage 1 depends on agent used
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7
Q

What is stage 2 of anaesthesia:

A

Dangerous phase - paradoxical things happening

  • gag reflex, coughing increased
  • Responses to pain preserved
  • Loss of response to non painful stimuli

Concerns:

  • Choking
  • Breath holding
  • Talking
  • Vomiting
  • Movement
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8
Q

What is stage 3 of anaesthesia:

A

The desired phase for surgery:

  • Surgical anaesthesia
  • Regular respiration
  • Possibly some reflexes, muscle tone preserved
  • Movement ceases
  • Progressive shallowing of breathing
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9
Q

What is stage 4 of anaesthesia:

A
  • Unless you do something about it your patient will die
  • Overdose
  • Medullary paralysis
  • Respiration and vasomotor control ceases
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10
Q

Pharmacokinetics of General Anaesthesia:

A
  • We would like rapid induction and rapid recovery
  • We would prefer to avoid stage 2
  • We would prefer the patient not to die in stage 4
  • We would prefer to avoid side-effects
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11
Q

is there one single drug for anaesthesia?

A

Therefore, drugs often used in combination

  • different anaesthetics
  • analgesics, muscle relaxants, anxiolytics

Stages of anaesthesia become less apparent

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12
Q

Modern General Anaesthesia drugs used:

A
  • rapid induction of unconsciousness; i.v. propofol
  • maintenance of unconsciousness and production of anaesthesia; inhaled N2O/halothane
  • supplementary i.v. analgesic e.g. morphine
  • neuromuscular blocker e.g. atracurium
  • Fast induction and recovery (anxiety, hangover), reduces stage II, homeostatic reflexes remain intact, amnesia
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13
Q

How do general anaesthetics work?

A
  • Alter function of neurones
  • Protein theories
  • lipid theory
  • Structures very diverse, argues against unified theory
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14
Q

What are the volatile anaesthetics?

A
  • N2O

- Xe

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15
Q

What are the iv anaesthetics:

A
  • Propofol
  • Sodium thiopental
  • Etomidate
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16
Q

What is the protein theory:

A
  • GABAA receptors (inhibitory) (many volatile, IV anaesthetics. Not: xenon, ketamine)

Function POTENTIATED
- NMDA receptors (Ketamine, xenon, volatiles)

Function INHIBITED
- Two pore potassium channels
Function POTENTIATED

  • We have targets on membrane proteins. The binding sites for the anaesthetic located in lipid bilayer and an.
  • May work by dissolving in the bilayer, accessing the binding site on their protein and changing the behavior of the protein.
  • Since these ideas started to crytallise we’ve actually identified. We now know on which proteins some of these drugs work.
17
Q

Types of anaesthetic:

A
  • Inhalational
  • Intravenous
  • Neurolept
  • Dissociative - ketamine
18
Q

Inhalation anaesthetics – pros and cons:

A

Easy to maintain degree of anaesthesia
(fast air:blood equilibration)
+Rapid emergence from anaesthesia

  • Cumbersome and expensive apparatus
  • Administered via a mask – psychological effects
  • Atmospheric pollution (scavengers) – operating staff exposed all day everyday
19
Q

Inhalation anaesthetics – metabolism and toxicity:

A
  • Metabolism unimportant for elimination BUT! Toxic metabolites
  • Fluranes generate fluoride, causes renal toxicity
  • -> Halothane converted to bromide and TFA, hepatotoxic
  • Problem for theatre staff
  • -> liver disease, leukaemia, abortion, birth defects
  • Scavenger systems required
20
Q

How do inhalation anaesthetics enter and leave the body:

A

Enter and leave the body via the lungs
Metabolism generally unimportant for recovery
Pass from gas phase to blood, then to tissues

21
Q

What is the Minimum Alveolar Concentration (MAC)?

A

The concentration in the alveoli required to produce anaesthesia in 50% of
patients

Measures the potency of the anaesthetic

22
Q

What is Blood-gas partition coefficient?

A
  • A measure of how well the drug dissolves in blood
  • Determines rate of induction and recovery
  • We want it to be low
23
Q

Oil-gas partition coefficient:

A
  • High oil-partition coefficient confers high POTENCY (see previous slide)
  • BUT! Lots of the anaesthetic will dissolve in fat
  • Fat is poorly vascularized
  • Anaesthetic will take a long time to leave this tissue
  • Patient will have a slowly resolving “hangover” as lots of the drug will dissove in fat
  • This will be worse the fatter the patient (and the more fat soluble the drug)
24
Q

Recovery from anaesthesia:

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.

25
Q

Individual inhalational anaesthetics?

A
  • Most common: N2O and isoflurane
  • In the UK, desflurane and sevoflurane becoming popular (£)
  • Ether: explosive, irritant and causes nausea; but cheap
26
Q

Characteristics of isoflurane:

A
  • Widely used (but being replaced)
  • No metabolism; little toxicity; not proconvulsive
    £ 2x halothane
  • Hypotension (-ve inotrope, decreases SVR)
  • Coronary vasodilator – myocardial ischaemia recently disputed
  • Possible worries regarding neurodegeneration
27
Q

Characteristics of sevoflurane:

A
  • Described by many as the “anaesthetic of choice”
  • Very rapid induction (very low blood:gas coefficient)
  • Very little metabolism

BUT!!

  • Very high cost (5 x halothane)
  • Some concerns regarding neurodegeneration
  • Recovery so rapid that post-op pain relief needed
28
Q

Nitrous oxide:

A
  • ‘Entonox’
  • N2O (not NO)
  • Low blood:gas partition coefficient
  • Analgesic at concentrations lower than those which cause unconsciousness
  • Trauma and obstetrics; chloroform alters uterine activity
  • Low potency; even at 80:20% with O2, no loss of consciousness
  • Thus 70:30% used as adjunct
  • Recovery – rapidly leaves blood and tissues, passes out through lungs
  • Dilutes O2 in lungs for a few minutes transient hypoxia (large amounts N2O leave blood rapidly)
  • Extra O2 at end of anaesthesia
29
Q

Home Office Guidance on nitrous oxide:

A

“A customer who looks over 25 attempts to buy several containers of whipped cream canisters containing nitrous oxide from a shop at 11pm. they are not buying anything else.
The cashier asks the customer why they are buying whipped cream. The customer hesitates in replying and when they do, they seem intoxicated, slurring their words
In this scenario the cashier should consider not selling the goods”

30
Q

Contraindications for N2O:

A
  • Early pregnancy, pernicious anaemia, scuba diving

- Major problem as a greenhouse gas (~300x CO2)

31
Q

Intravenous Anaesthetics Advantages:

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

Intravenous Anaesthetics Disadvantages:

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

Thiopental DRUG:

A
  • The only barbiturate commonly used in surgery
  • Very lipid soluble; crosses BBB very quickly
  • Induction dependent on blood flow
  • Rapidly redistributed into tissues
  • -> liver, kidneys, brain (fast blood flow)
  • -> muscle
  • Slowly distributes into fat (slow blood flow)
  • Rapid decline in blood levels (redistribution) then drops slowly
  • metabolism and fat distribution
  • Rapid awakening, long hangover
  • No repeated doses i.e. to maintain anaesthesia
  • blood –> plateau becomes elevated – accumulation
    ve inotrope; increases HR and cardiac O2 demand

Pooling of blood in periphery
–> hypotension in hypovolaemic patients

Resp depression (used in euthanasia, lethal injections)

34
Q

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

35
Q

Ketamine:

A 
- “Dissociative” anaesthetic
analgesia, amnesia 
but patient still partly conscious
- Non-competitive antagonist NMDA receptors
- Little effect on respiration, - blood pressure
- Heart rate increased
- Very safe for emergency situations
- RTAs, battlefield surgery
- High abuse potential
- Olney’s lesions
36
Q

Neurolept Anaesthesia:

A
  • Combination of a “neuroleptic” (“major tranquillizer” i.e. antipsychotic) and opioid
  • Effects similar to ketamine
  • Not used very frequently on humans
  • > common in veterinary medicine
  • > used in tranquilizer guns eg. Large Animal Immobilon (elephant tranquilizer)

The Patient Y3 Semester 2 (21 decks)

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