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Y4 PPT > B43 - anaesthetics > Flashcards

B43 - anaesthetics Flashcards

1
Q

Local anaesthetic MOA

A

block the voltage-dependent Na+ channels that depolarise the neuron.

progressively interrupt Na+ channel-mediated depolarisation until nerve conduction stops (more than 90% of Na channels)

bind to the Na+ channel at a site on the inner surface of the membrane and hold the channel in an inactivated state

produce reversible blockade of nerve conduction

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2
Q

Factors affecting LA action (4)

A

local concentration of the LA

the size of the nerve fibre
nerve myelination

length of nerve exposed to the LA

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3
Q

Which fibres are affected by LA first?

A

Myelinated Aδ and small non-myelinated C fibres transmitting pain blocked before larger sensory and motor fibres

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4
Q

Which pathways have the longest duration of LA blockage?

A

Pain

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5
Q

2 requirements for successful LA blockage

A

LA penetrates at the nodes of Ranvier and must block at least three consecutive nodes

Unmyelinated nerves must be blocked over a sufficient length and around the full circumference of the nerve

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6
Q

Intrinsic potency, duration of action, and onset of LA is dependent on: (2)

A

Lipophilic-hydrophilic balance

Hydrogen ion concentration (pH and pKa)

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7
Q

Clinically potency, duration of action, and onset of LA is also dependent on: (4)

A

Vasoconstrictor/vasodilator properties
Fiber size, type, and myelination
Frequency of nerve stimulation
Electrolyte concentrations

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8
Q

What is the potency of LA drugs directly related to?

A

lipid solubility

(The lipophilic aromatic group enables the molecule to cross the nerve membrane and bind to the inside of the Na+ channel)

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9
Q

2 implications of LAs with a high pKa

A

more ionised at physiological pH so their speed of onset of anaesthesia will be slower

re-ionise to a greater extent within the cell (at pH 7.4) and produce more effective blockade

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10
Q

What does use dependence in LA mean

A

Use-dependence means that the more the channels are opened, the greater the block becomes.

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11
Q

5 clinical uses of LA

A 
Local infiltration – e.g. for suturing
Topical – e.g. ocular
Nerve blocks – local and regional
Epidural
Spinal
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12
Q

4 common LA drugs

A

Lidocaine
Bupivacaine
Tetracaine
Prilocaine

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13
Q

6 methods of LA administration

A 
Topical
Infiltration anaesthesia
Peripheral nerve block
Epidural anaesthesia
Spinal anaesthesia
Intravenous regional anaesthesia
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14
Q

Method of LA administration in peripheral nerve block

A

Injection of an aqueous solution around a nerve trunk produces a field of anaesthesia distal to the site of injection

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15
Q

Method of LA administration in epidural

A

Injection or slow infusion via a cannula of an aqueous solution adjacent to the spinal column, but outside the dura mater, produces anaesthesia both above and below the site of injection after 15–30 min

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16
Q

Method of LA administration in spinal block

A

Involves injection of an aqueous solution (1.5–2.5 mL) of local anaesthetic alone (often bupivacaine) or with an opioid into the lumbar subarachnoid space, usually between the third and fourth lumbar vertebrae

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17
Q

Indication and method of administration for regionalised LA

A

IV regional anaesthesia involves injection of a dilute solution of LA into a limb after application of a tourniquet

Used for reduction of fractures or removal of ganglia etc

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18
Q

What is duration of action of LAs dependent on?

A

the degree of receptor binding and on their rate of removal from the site of administration, rather than their systemic elimination by metabolism

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19
Q

Why is adrenaline often added into solution for injection w/ LA

A

Most LAs cause vasodilation at the site of injection, which will enhance their removal. Adrenaline -> vasoconstriction

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20
Q

Which LAs have short half lives

A

ester-linked local anaesthetics (e.g. tetracaine)

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21
Q

Which LAs often produce pharmacologically active metabolites?

A

The amide-linked drugs (e.g. lidocaine and prilocaine)

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22
Q

Local SE of LA

A

irritation and inflammation

ischaemia from the use of vasoconstrictor agents – don’t use with adrenaline for ring blocks!!

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23
Q

Systemic SE of LA

A 
Cardiovascular:
myocardial depression
vasodilatation
hypotension
arrhythmias 
CNS:
agitation 
confusion 
tremors 
convulsions 
respiratory depression
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24
Q

4 types of drugs used in anaesthesia

A

Intravenous anaesthetics
Inhalational anaesthetics
Intravenous opioids
Neuromuscular blockers and reversing agents

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25
Q

6 stages of typical GA

A 
Premedication
Induction
Muscle relaxation and intubation
Maintenance of anaesthesia
Analgesia
Reversal
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26
Q

Stage 1 GA effects

A

analgesia without amnesia or loss of touch sensation, consciousness retained.

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27
Q

Stage 2 GA effects

A

excitation - excitation and delirium with struggling, respiration rapid and irregular, frequent eye movements with increased pupil diameter, amnesia

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28
Q

stage 3 GA effects

A

surgical anaesthesia - LOC, subdivided into levels/planes of increasing depth

29
Q

stage 3 plane 1 GA features

A

decrease in eye movements, some pupillary constriction

30
Q

stage 3 plane 2 GA features

A

loss of corneal reflex

31
Q

stage 3 plane 3/4 GA features

A

increasing loss of pharyngeal reflex, and progressive decrease in thoracic breathing and general muscle tone

32
Q

Stage 4 GA efffects

A

Medullary depression - loss of spontaneous respiration and progressive depression of CV reflexes, no eye movements, requires respiratory and circulatory support

33
Q

Which (3) inhalational drugs are potent amnesiacs, potent sedatives, and weak muscle relaxants?

A

Etodimate, propofol, thiopental

34
Q

Etodimate/propofol/thiopental MOA

A

GABA A agonists

35
Q

Which (2) inhalational drugs are potent analgesics, weak sedatives, and weak muscle relaxants?

A

Nitrous oxide, ketamine

36
Q

Which (3) inhalational drugs are potent amnesiacs, potent sedatives, and potent muscle relaxants?

A

sevoflurane, isoflurane, desflurane

37
Q

What does the depth of anaesthesia induced by an inhaled anaesthetic depend primarily on?

A

Partial pressure of the anaesthetics in the brain

38
Q

What does the rate of induction and recovery from inhalational anaesthesia depend on?

A

the rate of change of partial pressure in the brain.

39
Q

4 factors which affect inhalation anaesthesia

A

Absorption across alveolar membranes
Solubility of the anaesthetic in the blood
Cardiac output – circulation time
Relative concentration of the anaesthetic in the brain and blood at equilibrium

40
Q

Define minimum alveolar concentration (MAC)

A

Measure of POTENCY
Minimum alveolar concentration at which 50% of the population will fail to respond to a single noxious stimuli (e.g. first surgical skin incision)

41
Q

What is the blood:gas partition coefficient in inhalational anaesthetics

A

Is the measure of solubility in the blood

Determines the rate of induction and recovery of inhalation anaesthesia

42
Q

What are the implications of a lower blood:gas partition coefficient in inhalational anaesthetics

A

faster induction and recovery

Partial pressure in the lungs = pp in blood = pp in brain

The higher the solubility the faster it dissolves across the lung membrane thus the less chance to build up a high concentration in the alveoli

43
Q

Example of inhalational anaesthetic with a low blood:gas partition coefficient

A

Nitrous Oxide

44
Q

Example of inhalational anaesthetic with a high blood:gas partition coefficient

A

isoflurane

45
Q

Effect of oil:gas coefficient on inhalational anaesthetics

A

The oil: gas partition coefficient is a good measure of lipid solubility
The potency of an anaesthetic increases as its solubility in oil increases
As Δ(oil:gas) increases, the MAC decreases

46
Q

Effect of inhalational anaesthetic solubility in blood on rate of induction and recovery

A

LOW solubility in blood = fast induction and recovery

HIGH solubility in blood = slower induction and recovery

47
Q

2 uses for nitrous oxide

A

Nitrous oxide is a gaseous anaesthetic that is not sufficiently potent to be used alone

Is used part of a combination of drugs to allow a significant reduction in dosage (with other inhalational anaesthetics or intravenous anaesthetics)

Used for maintenance of anaesthesia

48
Q

How are inhaled anaesthetics eliminated from the body

A

The major route of elimination of inhalational anaesthetics is via the airways in expired air.

49
Q

4 Factors influencing elimination of inhalational anaesthetics:

A

ventilation rate
blood : gas partition coefficient
duration of inhalation
extent of tissue equilibration

50
Q

Unwanted CV effects of inhalational anaeshtetics (4)

A

myocardial depression
vasodilatation (isoflurane)
hypotension
bradycardia / reflex tachycardia

51
Q

Unwanted CNS effects of inhalational anaeshtetics (2)

A

increase cerebral blood flow and ICP

decreased cerebral vascular resistance

52
Q

Unwanted general effects of anaeshtetics (2)

A

Postoperative nausea and vomiting (PONV)

Malignant hyperthermia - rare

53
Q

4 examples of IV anaesthetics

A

Etomidate
Ketamine
Propofol
Thiopental

54
Q

2 IV anaesthetics which can be used as a continuous infusion for total intravenous anaesthesia for short operations

A

Ketamine and propofol

55
Q

4 features of propofol

A

Does not accumulate
Continuous infusion can be used for total intravenous anaesthesia or for sedation of adults in intensive care
Has now largely replaced thiopental as an induction agent
More rapid recovery and less hangover effect than occurs with thiopental

56
Q

4 features of etomidate

A

Etomidate has a rapid onset of action after intravenous injection
Its action is terminated by rapid metabolism in plasma and the liver by esterases
Duration of action is about 6–10 min with minimal hangover
Less effect on CVS so may be preferred in shocked patients

57
Q

4 features of ketamine

A

Believed to act by blocking activation of the NMDA receptor
IV has slower effect than thiopental (1-2 min)
Produces an effect, known as ‘dissociative anaesthesia’, in which there is a marked sensory loss and analgesia, as well as amnesia, without complete loss of consciousness
produces analgesia that outlasts anaesthesia

58
Q

2 types of neuromuscular blocking drugs

A

Non-depolarising (prototype = curare)

Depolarising (prototype = succinylcholine)

59
Q

MOA/effects of neuromuscular blocking drugs

A

block transmission through the neuromuscular junction (NMJ) at nicotinic receptors, thus decreasing skeletal muscle tone

60
Q

6 non-depolarising neuromuscular blocking drugs

A 
Atracurium
Cisatracurium
Mivacurium
Pancuronium
Rocuronium
Vecuronium
61
Q

Depolarising neuromuscular blocking drug

A

Suxamethonium

62
Q

3 uses of neuromuscular blocking drugs

A

Endotracheal intubation
Surgical procedures
Intensive care

63
Q

4 features of suxamethonium

A

Very polar and must be given IV – does not cross blood brain barrier
Onset of action within 1 min
Rapidly hydrolysed by pseudocholinesterase
Very short duration of action (about 3–12 min)
Initial depolarisation of the motor endplates prior to blockade, which results in muscle fasciculation

64
Q

features of non-depolarising nm blocking drugs

A 
Not absorbed orally and must be given IV
Different onset of action and duration
Rocuronium 2-3 min onset
Pancuronium 4-5 min onset
Recovery of muscle action depends on the rate of clearance of the drug from the plasma
65
Q

Reversal agent for non-depolarising NM blocker

A

Anticholinesterases: Neostigmine

66
Q

What is given immediately before the neostigmine during reversal of NM blockage and why?

A

An anti-muscarinic such as atropine or glycopyrrolate is given to prevent bradycardia or excessive salivation produced by stimulation of muscarinic receptors

67
Q

4 analgesia adjuncts

A

Opiates: e.g.
Fentanyl
Alfentanyl

Non-opioids:
NSAIDs
IV paracetamol

Patient controlled analgesia (PCA) - postop

Spinal and epidural anaesthesia

68
Q

5 summary points for anaesthetics

A

Many GAs are multimodal (or ‘balanced’)
IV anaesthetic agents for induction
Inhalational volatile anaesthetics for maintenance
Additional opiates or other analgesic adjuncts for analgesic effect
Use of neuromuscular blocking agents and reversal agents

Y4 PPT (10 decks)

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