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FNP > General anaesthetics > Flashcards

General anaesthetics Flashcards

1
Q

What are the types of general anaesthetics?

A

Inhalation anaesthetics e.g. ethanol, nitric oxide
Balanced anaesthesia - IV anaesthetics. Adjuncts to anaesthesia, to make it safer.

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2
Q

What is the triad of general anaesthesia?

A

For an operation to take place:
Need for unconsciousness
Need for analgesia
Need for muscle relaxation - loss of reflexes.
General anaesthetics depress CNS activity.

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3
Q

What is the chemical structure of inhalational anaesthetics?

A

Simple, unreactive compounds
Short chain molecules.
No one chemical class

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4
Q

What are examples of inhalational anaesthetics?

A

Halothane
Enflurane
Isoflurane
Desflurane
Sevoflurane
Ethanol
Older - chloroform, fluroxene, diethyl ether.

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5
Q

What is the lipid theory?

A

The concentration of agents required to immobilise tadpoles is inversely proportional to its lipid: water partition coefficient.
Hydrophobicity is important.

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6
Q

What were the observations that led to the lipid theory?

A

When the concentration of anaesthetic in the cell membrane reaches 0.05mM, general anaesthesia is produced.
Anaesthesia occurs when the volume of lipid expanded by 0.4%.
High pressure reverses the anaesthesia - squeezes out the anaesthesia from the membrane.

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7
Q

What were the explanations of the lipid theory?

A

Agents act by volume expansion of the cell membrane.
Or agents act by increasing the fluidity of the cell membrane.
Or through interference with conduction of nerve impulses.

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8
Q

What is the Protein theory?

A

Lipid solubility is merely required for access to proteins - ion channels, receptors, rather than causing anaesthesia.
Anaesthetics may be binding to hydrophobic pockets on proteins - size and shape are important.

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9
Q

What is the evidence for the protein theory?

A

For homologous series of long-chain anaesthetic compounds:
Increased chain length = increased lipid solubility.
But anaesthetic potency stops beyond a certain length - 11 carbon chain.

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10
Q

How is stereoselectivity evidence of the protein theory?

A

Stereo selectivity - molecules have optical isomers - mirror image
Identical lipid solubility but different anaesthetic potency
Binding is important - shape of molecule.

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11
Q

What are the ion channel targets for general anaesthetics?

A

No one single target mediates the effect of any general anaesthetic agent
GABA A receptor, ligand gated ion channel
General anaesthetics acts as Allosteric modulators
Potentiate it so GABA A induces its inhibitory effect
K+ channel are a type of isoform
Increase K+ activation, causes hyperpolarisation, decrease in membrane excitability.

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12
Q

What are the other molecular targets for general anaesthetics?

A

Can also interact with excitatory ligand-gated channels:
NMDA (glutamate receptor), 5-HT3, ACh nicotinic
Show decrease in activity by general anaesthetic agents
Glycine is an inhibitory ligand-gated channel, a target for individual general anaesthetics.

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13
Q

What are the concentration effects of anaesthetics?

A

At low concentration, the ability to form memory is lost first, until there is no ability.
Shortly after concentration increases, consciousness is lost.
As concentration increases, movement is then inhibited.
At concentrations above this, the CVRS response is decreased until it results in death.

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14
Q

What is the therapeutic window for general anaesthetics?

A

The window between inhibiting movement and causing a CVRS response.
An overdose is 2-3x the clinical dose.

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15
Q

What are the stages of anaesthesia?

A
  1. Analgesia
    1. Delirium / the induction phase
    2. Surgical anaesthesia
    3. Medullary paralysis - overdose.
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16
Q

What is analgesia?

A

Drowsiness, reflexes intact and conscious.

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17
Q

What is the induction phase?

A

Excitement, delirium, incoherent speech
Loss of consciousness, unresponsiveness to non-painful stimuli.

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18
Q

What is the dangerous phase of the induction phase?

A

Muscle rigidity, spasmodic movements.
Cardiac arrhythmias
Vomiting - Choking
Aim to move quickly through this phase.

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19
Q

What is surgical anaesthesia?

A

Unresponsive to painful stimuli
Regular breathing
Abolition of reflexes - less tense
Muscle relaxation
Synchronised EEG

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20
Q

What is Medullary paralysis - overdose:

A

Pupillary dilation
Respiration and circulation cease
EEG wanes
Death.

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21
Q

What is a good anaesthetic agent?

A

Potent and fast acting, main determinant is blood: gas coefficient.
How much is given to produce clinical effect.
Lipid solubility is the main determinant of potency.

22
Q

What is MAC?

A

A measure of anaesthetic potency in man
Minimal Alveolar Concentration, expressed as % of inspired air (%v/v).
The concentration of anaesthetic in the alveoli required to produce immobility in 50% of patients when exposed to a noxious stimulus.
This is affected by sex, height and weight, adipose tissue, ginger hair.

23
Q

What is the relationship of MAC and lipid solubility?

A

MAC is inversely proportional to lipid solubility.
The more soluble in lipid, the lower the [anaesthetic] in the patient’s inspired air (%v/v) required to produce anaesthesia.

24
Q

Why should anaesthetics be potent and fast acting?

A

Have a fast speed of induction it passes the dangerous phase quicker.
It also means there is quicker recovery.

25
Q

How is the depth of anaesthesia controlled?

A

Rate of induction is affected by:
Properties of anaesthetic
Physiological factors

26
Q

What are partition coefficients?

A

How much the anaesthetic wants to be in one compartment compared to another air to blood, blood to tissue.
Inhaled gas goes into blood - blood: gas partition coefficient.
Agent to brain is tissue: blood partition coefficient.

27
Q

How do you increase the transfer of anaesthetics to the alveoli?

A

Can speed up rate of induction by increasing concentration of anaesthetic, and increasing the rate and depth of breathing.

28
Q

What does transfer of anaesthetic to the blood depend on?

A

Blood has a certain capacity (solubility) for the anaesthetic agent.
Anaesthetics must fully saturate the blood before it can leave.
A lower blood: gas partition coefficient increases the speed of induction, they are inversely proportional.

29
Q

What is the ideal solubility of anaesthetic agents in blood?

A

The agent needs a high enough capacity to dissolve in the blood, but low solubility so less molecules are needed to saturate the blood, so it can leave and enter another compartment.
Low capacity increases the speed of induction.

30
Q

What is the transfer of anaesthetic to the blood affected by the heart?

A

The rate of pulmonary blood flow affects speed of induction.
The higher the cardiac output, the faster the transfer from gas to blood.

31
Q

What is the tissue: blood partition coefficient?

A

The anaesthetic agent solubility in the tissue.
Tissue: blood coefficient is 1 for all lean tissue - all tissue except adipose tissue.
Anaesthetic concentration in brain rises fast.

32
Q

What is the tissue: blood coefficient of adipose tissue?

A

> 1 - so has high capacity, or high solubility in the tissue.
This decreases the speed of induction and recovery as the agent accumulates in the tissue if highly lipid soluble.

33
Q

What is the tissue blood flow of anaesthetics?

A

High blood flow to lean tissue, this causes fast transfer.
Blood flow to adipose tissue is lower - it is less vascularised, so transfer is slower.

34
Q

How are inhaled anaesthetics eliminated?

A

Mainly via the lung, related to factors involved in speed of induction.
Liver metabolism is not important for most anaesthetics, except for methoxyflurane and halothane, which have a possibility of toxicity.

35
Q

What are the effects of halothane?

A

Adv - potent, fairly fast
Disadv - possible liver toxicity.

36
Q

What are the effects of enflurane?

A

Adv - Less liver damage.
Disadv - possible seizures

37
Q

What are the effects of isoflurane

A

Adv - rapidly acting, muscle relaxation
Disadv - bad smell

38
Q

What are the effects of sevoflurane?

A

Adv - pleasant odour and rapid recovery.
Disadv - metabolites cause renal damage.

39
Q

What are the effects of nitrous oxide?

A

Or Entonox
Adv - very rapid, effective analgesic, fast rate of induction.
It is a supplement to other general anaesthetic agents, not used alone due to low potency.

40
Q

What is balanced anaesthesia?

A

Using combinations of different drugs for optimal clinical effect with lowest risk.

41
Q

What are IV anaesthetics?

A

Directly into blood
Rapid onset
Short acting
Commonly used for induction
Can be used along for short procedures.

42
Q

What is the mechanism of action of IV anaesthetics?

A

Interact with specific ligand-gated receptors.
Potentiation of GABA A receptor action
Antagonism of NMDA receptor.

43
Q

How do IV anaesthetics interact with GABA A receptors?

A

Specifically increase GABA A receptor activation
Positive allosteric modulators.
Thiopental, etomidate, propofol, midazolam (benzodiazepine).

44
Q

How do IV anaesthetics interact with NMDA receptor?

A

Ketamine
Dissociative anaesthetic - lasts 10-20 minutes
No loss of consciousness, but everything else - sensory loss, analgesia, paralysis, surgical anaesthesia.
Through antagonism of NMDA receptor.

45
Q

What are adjuncts to general anaesthetics?

A

Premedication
Muscle relaxants
Anti-emetic

46
Q

What is premedication?

A

Benzodiazepines
Opioids
Antimuscarinics

47
Q

What are benzodiazepines?

A

Benzodiazepines for reducing anxiety, amnesia, sedation
e.g. loraxepam, midazolam

48
Q

What are opioids?

A

Opioids - pain relief
Morphine, fentanyl, pethidine

49
Q

What are antimuscarinics?

A

Facilitate intubation and ventilation
Dry up secretion, and smooth muscle relaxation.
If gaseous anaesthetic, alveoli wall crossed more easily as no mucous.
Atropine, hyoscine, glycopyronium.

50
Q

What are muscle relaxants?

A

Relax deep, abdominal, tracheal and diaphragm muscles, without need for deeper anaesthesia.
Benzodiazepines
Neuromuscular blockers e.g. tubocurarine, Pancuronium, gallamine, suxamethonium

51
Q

What are anti-emetic adjuncts to general anaesthetics?

A

Decrease peri-operative nausea (before and after anaesthesia).
e.g. metoclopramide

FNP (12 decks)

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