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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
6 stages of typical GA
``` Premedication Induction Muscle relaxation and intubation Maintenance of anaesthesia Analgesia Reversal ```
26
Stage 1 GA effects
analgesia without amnesia or loss of touch sensation, consciousness retained.
27
Stage 2 GA effects
excitation - excitation and delirium with struggling, respiration rapid and irregular, frequent eye movements with increased pupil diameter, amnesia
28
stage 3 GA effects
surgical anaesthesia - LOC, subdivided into levels/planes of increasing depth
29
stage 3 plane 1 GA features
decrease in eye movements, some pupillary constriction
30
stage 3 plane 2 GA features
loss of corneal reflex
31
stage 3 plane 3/4 GA features
increasing loss of pharyngeal reflex, and progressive decrease in thoracic breathing and general muscle tone
32
Stage 4 GA efffects
Medullary depression - loss of spontaneous respiration and progressive depression of CV reflexes, no eye movements, requires respiratory and circulatory support
33
Which (3) inhalational drugs are potent amnesiacs, potent sedatives, and weak muscle relaxants?
Etodimate, propofol, thiopental
34
Etodimate/propofol/thiopental MOA
GABA A agonists
35
Which (2) inhalational drugs are potent analgesics, weak sedatives, and weak muscle relaxants?
Nitrous oxide, ketamine
36
Which (3) inhalational drugs are potent amnesiacs, potent sedatives, and potent muscle relaxants?
sevoflurane, isoflurane, desflurane
37
What does the depth of anaesthesia induced by an inhaled anaesthetic depend primarily on?
Partial pressure of the anaesthetics in the brain
38
What does the rate of induction and recovery from inhalational anaesthesia depend on?
the rate of change of partial pressure in the brain.
39
4 factors which affect inhalation anaesthesia
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
Define minimum alveolar concentration (MAC)
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
What is the blood:gas partition coefficient in inhalational anaesthetics
Is the measure of solubility in the blood | Determines the rate of induction and recovery of inhalation anaesthesia
42
What are the implications of a lower blood:gas partition coefficient in inhalational anaesthetics
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
Example of inhalational anaesthetic with a low blood:gas partition coefficient
Nitrous Oxide
44
Example of inhalational anaesthetic with a high blood:gas partition coefficient
isoflurane
45
Effect of oil:gas coefficient on inhalational anaesthetics
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
Effect of inhalational anaesthetic solubility in blood on rate of induction and recovery
LOW solubility in blood = fast induction and recovery HIGH solubility in blood = slower induction and recovery
47
2 uses for nitrous oxide
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
How are inhaled anaesthetics eliminated from the body
The major route of elimination of inhalational anaesthetics is via the airways in expired air.
49
4 Factors influencing elimination of inhalational anaesthetics:
ventilation rate blood : gas partition coefficient duration of inhalation extent of tissue equilibration
50
Unwanted CV effects of inhalational anaeshtetics (4)
myocardial depression vasodilatation (isoflurane) hypotension bradycardia / reflex tachycardia
51
Unwanted CNS effects of inhalational anaeshtetics (2)
increase cerebral blood flow and ICP | decreased cerebral vascular resistance
52
Unwanted general effects of anaeshtetics (2)
Postoperative nausea and vomiting (PONV) | Malignant hyperthermia - rare
53
4 examples of IV anaesthetics
Etomidate Ketamine Propofol Thiopental
54
2 IV anaesthetics which can be used as a continuous infusion for total intravenous anaesthesia for short operations
Ketamine and propofol
55
4 features of propofol
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
4 features of etomidate
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
4 features of ketamine
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
2 types of neuromuscular blocking drugs
Non-depolarising (prototype = curare) | Depolarising (prototype = succinylcholine)
59
MOA/effects of neuromuscular blocking drugs
block transmission through the neuromuscular junction (NMJ) at nicotinic receptors, thus decreasing skeletal muscle tone
60
6 non-depolarising neuromuscular blocking drugs
``` Atracurium Cisatracurium Mivacurium Pancuronium Rocuronium Vecuronium ```
61
Depolarising neuromuscular blocking drug
Suxamethonium
62
3 uses of neuromuscular blocking drugs
Endotracheal intubation Surgical procedures Intensive care
63
4 features of suxamethonium
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
features of non-depolarising nm blocking drugs
``` 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
Reversal agent for non-depolarising NM blocker
Anticholinesterases: Neostigmine
66
What is given immediately before the neostigmine during reversal of NM blockage and why?
An anti-muscarinic such as atropine or glycopyrrolate is given to prevent bradycardia or excessive salivation produced by stimulation of muscarinic receptors
67
4 analgesia adjuncts
Opiates: e.g. Fentanyl Alfentanyl Non-opioids: NSAIDs IV paracetamol Patient controlled analgesia (PCA) - postop Spinal and epidural anaesthesia
68
5 summary points for anaesthetics
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

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