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Anaesthesia Flashcards

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1
Q

Local anaesthetics are…

A

Drugs that reversibly block the conduction of impulses in the PNS, inhibiting excitation-conduction process in neutrons near the site of administration

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2
Q

LA blocks the…

A

Initiation and propagation of AP by blocking the Na+ channels. The threshold potential is thus not reached, inhibiting depolarisation, and with no impulse conduction the nerve is blocked from signalling a pain response.

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3
Q

In general, LA blocks conduction in…

A

Small-diameter nerve fibres more readily than large fibres, preferentially affecting the pain fibres as these are thinner and more easily penetrated by drugs (motor fibres are thicker=more resistant)

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4
Q

LA agents include

A

-aines

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5
Q

LAs are potentially

A

toxic. Consider age, weight, physical condition and liver function for dosage

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6
Q

Examples of LA amides

A

Bupivacaine, Levobupivacaine, Lidocaine (anaesthesia), Prilocaine, Ropivacaine

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7
Q

Examples of LA esters

A

Cocaine and tetracaine (skin)

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8
Q

List the AEs of LA

A

Allergic reactions and vasoconstriction (these are rare)

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9
Q

List the application techniques of LA

A

Topical/surface, Infiltration, Bier’s block (regional IV), Nerve block, Epidural, Spinal

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10
Q

Topical or surface application

A

LA is applied directly to the target area of skin, nose, throat or urethra.

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11
Q

Infiltration is

A

Performed by injecting the diluted agent into the skin and subcutaneous tissue. Adrenaline is often added to intensify anaesthesia and prevent bleeding as a vasoconstrictor. It is used for minor skin surgery and dental extraction.

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12
Q

Bier’s block is

A

A short procedure of the upper limb where the circulation is blocked by tourniquet (pressure above patient systolic BP) and local anaesthetics are injected into venous vessels distal to the occlusion. Early release of the tourniquet may cause toxicity (inflate for at least 20 mins). It requires full results monitoring. It is not recommended in children due to tourniquet discomfort.

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13
Q

Nerve block is

A

LA injected to a single nerve or a group of nerves. This is usually performed under ultrasound guidance.

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14
Q

Epidural

A

An epidural is an injection of LA into the epidural space. It is commonly used at the thoracic or lumbar region. Insertion of an epidural catheter is completed in a strict sterile procedure. LA is delivered through the catheter. The local anaesthetic in the epidural will slowly be absorbed into the subarachnoid space where it blocks the nerves of the spinal cord. This LA method is commonly used for obstetric, urology and abdominal surgery.
Complications include blockade of the sympathetic nerve fibres and an epidural haematoma.
• Placement confirmation: Resistance test with nervous system (NS) sensation test. The test dose and ultrasound.

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15
Q

Spinal is

A

LA injected into the CSF in the subarachnoid space. This must be performed under strict sterile conditions to avoid infection (e.g. meningitis). LA is injected in close proximity to its site of action, smaller volumes are required, and onset is rapid. There will only be one injection; usually in the lumbar region. The choice of LA is based on the length of the procedure. Common side effects include headache, hypotension and infection.

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16
Q

LA toxicity occurs as a result of

A

A therapeutic error

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17
Q

Clinical manifestations of LA toxicity

A

CNS: agitation, seizures, coma
CV: bradycardia, hypotension, atrial and ventricular dysrhythmias
Resp: resp depression and apnoea

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18
Q

Toxicity management for LA

A

Stop injection, call for help, DRSABCD, manage arrhythmia, provide CV support to suppress seizure, lipid emulsion (mechanism of action unclear but it’s supposed to remove the LA from the target tissue; may have inotropic effect)

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19
Q

General anaesthesia (GA) is

A

A pharmacologically induced reversible state of unconsciousness which is maintained despite the presence of noxious stimuli.

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20
Q

GA strives to achieve the 4 As which are:

A

Awareness (a lack of awareness); amnesia (lack of memory of the event); analgesia; akinesia (lack of overt movement)

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21
Q

GA consists of 4 phases:

A

Induction:(inducing unconsciousness) is performed through either intravenous (IV) injection or via inhalation (or a combination of both)
Maintenance: where there is a level of anaesthesia and homeostasis is achieved and maintained through the procedure
Emergence: the transition from an unconscious state to a conscious state
Recovery: fully conscious

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22
Q

Pre-medications are administered to

A

Reduce patient anxiety, relieve pain, produce sedation and amnesia (to aid a smoother induction of anaesthesia). They also reduce salivary and bronchial secretions.

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23
Q

Pre-medications e.g.

A

Benzodiazepines (anxiolytics/hypnotics/sedatives), analgesics (narcotic/opioids or non-opioids), anticholinergics (to reduce salivation and control bradycardia (atropine)), antiemetics (to reduce nausea and vomiting) and antibiotics (ordered preoperatively to reduce the incidence of wound infection).

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24
Q

Induction agents produce

A

Unconsciousness, which is pleasant, rapid (seconds), and maintains haemodynamics. Includes some resp and circulatory depression

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25
Induction agents e.g.
Thiopentone, propofol, ketamine, midazolam
26
Thiopentone (thiopental)
Enhances or mimics the action of GABA in the CNS and depresses the action of excitatory neurotransmission. Thiopentone is IV administered and has both respiratory and cardiac effects.
27
GABA is
Gamma-aminobutyric acid is the most widely distributed inhibitory neurotransmitter in the CNS. GABA is naturally synthesised in presynaptic neurons, stored in vesicles. Upon neuronal activation, GABA is released from vesicles into the synapse and acts on postsynaptic GABA receptors.
28
Thiopentone action:
Marked respiratory depression, which is dose-dependent, and can be used in conjunction with an inhalation agent. It decreases cardiac output (CO) blood pressure (BP) as the plasma concentration rises. It has a prolonged elimination and is lipid-soluble (fat distribution). It has no analgesic effect.
29
Propofol
Commonly used and works by activating a specific site within the GABA receptor. It shortens channel opening times at the neuronal nicotinic acetylcholine receptor (nAChR) and Na+ channels in the cortex. This causes a rapid induction; suitable for maintenance and sedation; minimal cardiovascular effects with no analgesic properties. The recovery from propofol is more complete, with less “hangover” when compared to thiopental, likely due to its high plasma clearance. It can cause pain at the injection site.
30
Ketamine is
N-methyl-D-aspartate (NMDA) receptor antagonist and interacts with muscarinic acetylcholine receptors (mAChR), voltage-gated Ca2+ channels and opioid receptors. Ketamine’s MOA is complex, but the major effect is likely due to reducing neuronal excitability by blocking NMDA (glutamate) receptors.
31
Ketamine is used in
Induction and maintenance and is a potent analgesic. Referred to as a “dissociative” anaesthetic as it is possible for the patient to remain conscious but with insensitivity to pain and short-term amnesia. It can produce surgical anaesthesia suitable for brief procedures on its own.
32
Ketamine does what to the CV?
It's a CV system stimulant, causes hypertension, tachycardia, ECG changes
33
What can be experienced during emergence after ketamine was used?
Hallucinations and nightmares. Nystagmus is common.
34
Why is ketamine used in paediatric populations?
Because it maintains airway reflexes (only if aged >12)
35
Ketamine is restricted in adults because?
Incidence of hallucinations and dysphoria is much higher than in kids
36
Ketamine is suitable for what kind of procedures?
Short, painful ones (e.g. face lacerations, fracture reduction)
37
Precautions for ketamine
NBM prior with strict vitals and cardiac monitoring and resuscitation equipment nearby. Keep pt in a quiet area, dim lighting and don't stimulate prematurely. Keep parents near kids to make them feel safe
38
Ketamine side effects
Hyper-salivation, emesis, transient laryngospasm, recovery agitation
39
Midazolam (benzodiazepine)
Potentiates the inhibitory effects of GABA in the CNS, resulting in sedative, hypnotic, anterograde amnesic and muscle relaxant effects. It is fast-acting and the patient is typically unconsciousness within 80 seconds. It can cause dangerous cardio-respiratory effects.
40
Volatile agents administration via
Inhalation (via an anaesthetic machine) to pt with a mask or tube by mixing with a carrier gas (air, oxygen)
41
Volatile anaesthetic is
Liquids vaporised to gases via a vaporiser that is inhaled into the lungs and crosses the alveolar-capillary membrane, into circulation, then the brain
42
How volatile agents work
MOA not really understood but probs by binding to the lipid bilayer of nerve cell membranes and cause a small membrane expansion/swelling that distorts ion channels. This enhances inhibitory ion channel activity and inhibits excitatory activity in the brain and spinal cord.
43
Inhaled anaesthetics are administered at a specific
Gas concentration (dependent on the agent used)
44
Volatile anaesthetics are used with an
Adjunct analgesic because they may not have useful analgesic actions
45
E.g. of volatile agents
Isoflurane (medium induction, maintenance, pungent) Sevoflurane (fast induction, maintenance, well-tolerated) Desflurance (fast induction, maintenance, low solubility)
46
Nitrous oxide (N2O) is
A good analgesia in sub-anaesthetic concentrations; induction; maintenance as an adjunct in major therapy
47
All volatile agents trigger what
Malignant hyperthermia and is contraindicated in pt who are known or suspected to already have it
48
What is malignant hyperthermia
A rare but potentially fatal condition and is an inherited abnormality in muscle membranes. It is triggered by depolarising neuromuscular blocking agents (e.g. suxamethonium) and volatile agents. It is a syndrome of accelerated metabolism in skeletal muscle, rapid fever, acidosis, perfuse sweating and muscle rigidity.
49
How to deal with malignant hyperthermia
Stop the triggering agent. For active cooling administer dantrolene (antidote); a direct inhibitor of muscle contractions, and possibly an antiarrhythmic agent as well as electrolyte and fluid replacement.
50
Maintenance of anaesthesia requires...
The delivery of pharmacologic agents with the aim to achieve the “4A’s” and haemodynamic stability throughout the surgery.
51
What can have a deleterious effect on maintenance?
Hypothermia
52
How is the maintenance phase achieved?
Using inhaled agents, opioids and muscle relaxants.
53
Alfentanil is an
analgesia that is an opioid adjunct used during induction and/or maintenance
54
Fentanyl and morphine are
analgesia that are opioid adjuncts in GA; severe pain
55
Commonly used analgesic agents:
Synthetic opioids fentanyl, remifentanyl and alfentanil because they are short-acting, facilitate finer titration, and ease emergence at the end of the procedure.
56
E.g. of muscle relaxants (aka neuromuscular blocking agent)
Suxamethonium, pancuronium, atracurium, vecuronium, rocuronium
57
Muscle relaxants are used to...
Prevent muscles from moving when a patient is unconscious and reduce the amount of anaesthetic agent needed.
58
Neuromuscular (NM) blocking agents can be split into two categories...
Depolarising and non-depolarising. Difference is MOA and the need for reversal.
59
Depolarising blocking agents does what?
Mimics (similar structure) the action of ACh. Depolarisation leads to initial muscle twitching (classic feature fasciculation) and the drug will cause persistent depolarisation (paralysis).
60
E.g. of depolarising blocking agents
IV suxamethonium (only one clinically used)
61
What does suxamethonium do?
Acts as an agonist at nicotinic receptors on the motor endplate
62
How to tell if depolarising blocking agent is working
Fasciculation, and when this subsides (usually quickly) the NM blockade follows
63
When are depolarising blocking agent used?
In emergency situations and in rapid sequence intubation. It is short-acting (<5 mins) and doesn't need reversal.
64
How is a depolarising blocking agent metabolised?
By plasma cholinesterase, an enzyme produced by the liver
65
Side effects of depolarising blocking agents?
Malignant hyperthermia
66
E.g. of non-depolarising agents
IV atracurium, pancuronium, rocuronium, vecuronium
67
Non-depolarising blocking agents does what?
Act as a competitive antagonist at the ACh receptors endplate. The nACh receptor antagonists (NM junction) prevent depolarisation.
68
How to choose which non-depolarising blocking agents to use?
The choice of agent is influenced by onset, duration and side effects
69
What do non-depolarising blocking agents require?
Reversal of muscle paralysis and anticholinergic effects such as bradycardia, BP drop and bronchospasm.
70
Non-depolarising agents can typically cause...
Histamine release from mast cells. The effect is not related to the action at nicotinic receptors (and may be immunologic). Reversal is accomplished by agents that displace the drug anticholinesterase to increase ACh (e.g. neostigmine). A combination of neostigmine and atropine can control potential cholinergic effects.
71
What happens in the emergence phase?
The patient begins to return to his/her preoperative state of consciousness
72
How is emergence achieved?
By administering the anaesthetics in appropriate doses according to the anticipated length of procedure, metabolism and excretion.
73
Aside from muscle relaxants, anaesthetic agents are
Rarely actively reversed.
74
Antidotes for analgesia:
None for inhaled agents (cos they depend on timely discontinuation). Naloxone for opioids
75
Naloxone (narcan) can cause
Hyper-alertness and re-narcotisation
76
Pt recovery phase:
Careful extubation and patient vitals must be monitored closely postoperatively.
77
Naloxone is a
Pure opioid antagonist acting at mu and kappa receptors
78
Naloxone does not
Produce analgesia or any of the other effects caused by opioid agonists
79
Naloxone reverses
Resp and CNS depression caused by OD with opioid agonists
80
Endogenous analgesia produced by
CNS
81
Endogenous analgesia work on
Peripheral nerves
82
E.g. of endogenous peptides
(Opioid peptides) endorphins, enkephalins and dynorphins
83
Opioid peptides interact with
Opioid receptors to inhibit perception and transmission of pain signals
84
Non-opioid analgesics are
Drugs that relieve pain without causing the loss of consciousness and are used for acute and chronic pain as well as neuropathic or bone pain
85
Opioid analgesics are
The most effective pain relievers available and are used for moderate to severe pain.
86
How do non-opioid analgesics work?
Relieve pain by mechanisms largely or completely unrelated to opioid receptors and include non-steroid anti-inflammatory and paracetamol. They do not cause respiratory depression, physical dependence, or abuse.
87
Aspirin works as an...
Analgesic, antipyretic, anti-inflammatory and anti platelet drug.
88
How does aspirin work
As a nonselective NSAID, it prevents the synthesis of prostaglandins by non-competitively inhibiting both forms of cyclo-oxygenase (COX) 1 and COX 2.
89
Common AEs of aspirin:
Dyspepsia, vomiting, gastrointestinal (GI) ulceration or bleeding, asymptomatic blood loss, increased bleeding time, headache, dizziness and tinnitus (common with high doses).
90
How does paracetamol work
The paracetamol analgesic effect is not fully determined, however, it may be related to inhibition of central prostaglandin synthesis and modulation of inhibitory descending serotonergic pathways
91
Common AE of paracetamol
Hepatotoxicity
92
E.g. of opioids
Codeine, fentanyl, morphine, hydrocodone, hydromorphone, methadone, oxycodone, oxycodone with naloxone, pethidine, tramadol
93
Opioid analgesics relieve what degree of pain
Moderate to severe
94
How do opioid analgesics relieve pain
By inhibiting pain signal transmission from the periphery to the brain (by inhibiting afferent pain transmission, activating descending pathway, and inhibiting excitation of the sensory nerve terminals in the periphery)
95
What are the opioid receptors and where are they found?
Mu, kappa and delta, found throughout the CNS and peripheral tissues
96
Opioids cause
Altered pain perception and emotional responses to pain. They can cause drowsiness, mental clouding, anxiety reduction, respiratory depression, constipation, urinary retention, orthostatic hypotension, vomiting, miosis and cough suppression.
97
Opioids are widely distributed in which system
Limbic system
98
Opioids are well absorbed with
PO, IM, subcut, or IV
99
CNS effects of opioids:
Analgesia, CNS depression, dec rebased mental and physical activity. resp depression, nausea, vomiting, pupil constriction
100
GI effects of opioids:
Slow motility, constipation, bowel and biliary spasm
101
Opioids can be used for acute and chronic pain especially in:
acute myocardial infarction, biliary or renal colic, burns, other traumatic injuries, postoperative states, cancer, treatment of GI disorders, abdominal cramping, diarrhea as well as treatment of severe, unproductive cough.
102
SEs of opioids
Nausea and vomiting, dyspepsia, drowsiness, dizziness, headache, orthostatic hypotension, itch, dry mouth, miosis, urinary retention, constipation.
103
Precautions of taking opioids for pt with the following conditions or taking meds for these conditions:
Increased hypotension, resp depression, coma. Existing resp depression, chronic lung disease, liver or kidney disease, prostatic hypertrophy. Increased intracranial pressure and hypersensitivity to opioids
104
When can antidepressants or anti-epileptics be used as pain relief?
Antidepressants (e.g. low dose tricyclic antidepressants, duloxetine) or anti-epileptics (e.g. gabapentin, pregabalin, carbamazepine) can be used but only after other methods have been tried and usually only for neuropathic pain.

Medications (10 decks)

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