Anaesthesia and Pain Flashcards

1
Q

What is Anaesthesiology?

A

Branch of medicine concerned with the administration of medications or anaesthetics agents to relieve pain and support physiological functions during a surgical procedure

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2
Q

What is Analgesia?

A

Suppression of physiological responses to stimuli (usually pain) through hypnosis (suppression of consciousness) and narcosis (dulling of consciousness and paralysis - no movement)

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3
Q

What is Anaesthesia?

A

Practice of administering medications by injection or by inhalation that blocks the feeling pain and other sensations or that produces a deep state of unconsciousness that eliminates all pain and other sensations - allows medical and surgical procedures without distress or discomfort

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4
Q

What is Local Anaesthesia (LA)? How does it work?

A

Administrations of an agent to induce the absence of pain in a part of the body
• Reversibly block the conduction of impulses in the PNS - inhibits excitation-conduction process = blocks the initiation and propagation of action potential = blocks Na+ channels = threshold potential not reached = inhibits depolarisation = no impulse conduction = nerve blocks from signalling a pain response
• Blocks conduction in small-diameter nerve fibres more readily than large fibres
• Pain fibres are affected preferentially because they are thinner and more easily penetrated by these drugs (Motor axons - larger in diameter = relatively resistant)
• Consciousness is not depressed
• Can be injected around a nerve or nerve trunk (e.g. nerve block) to produce a regional anaesthesia (RA) to a large region of the body
Selectivity of LA agents are they only effect neurons located near the site of administration​ and they suppress pain without generalised depression of the nervous system

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5
Q

What are the types of LA? Name some. What are the adverse effects?

A
Amides (-AINES):
• Bupivacaine
• Levobupivacaine
• Lidocaine/ lignocaine (anaesthesia)
• Prilocaine
• Ropivacaine

Esters:
• Cocaine
• Tetracaine (skin)

Adverse Effects: If administered correctly, adverse effects are rare and include allergic reactions; adverse effects from added vasoconstrictors also occur.

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6
Q

What are the techniques of LA? (6) Give a brief summary of each.

A

Topical/ surface - applied directly to the target area of skin, nose, throat or urethra

Infiltration - injecting the diluted agent into the skin and subcutaneous tissue (Adrenaline is often added to intensify anaesthesia and prevent bleeding as a vasoconstrictor) - minor skin surgery and dental extraction

Bier’s Block (regional IV) - Upper limb where 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) - requires full results monitoring *Not recommended in children due to tourniquet discomfort

Nerve Block - LA is injected to a single nerve or a group of nerves - usually performed under US guidance

Epidural - • injection of LA into the epidural space
•Commonly used at the thoracic or lumbar region
• Insertion of an epidural catheter is completed in a strict sterile procedure and LA delivered through the catheter
• Slowly be absorbed into the subarachnoid space - blocks the nerves of the spinal cord
• Commonly used for obstetric, urology and abdominal surgery

Complications: blockade of sympathetic nerve fibres and an epidural haematoma
• No CSF
Placement confirmation: Resistance test with nervous system (NS) sensation test. The test dose and ultrasound

Spinal - • injected into the CSF in the subarachnoid space
• Injected in close proximity to its site of action, smaller volumes are required, and onset is rapid
• Performed under strict sterile conditions to avoid infection (e.g. meningitis)
• Only 1 injection; usually in the lumbar region
• Choice of LA is based on the length of the procedure
Common side effects include headache, hypotension and infection

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7
Q

What is needed to be taken into account to avoid LA toxicity? How can it occur? What are the clinical manifestations? What is the management of LA toxicity?

A

LAs are potentially toxic drugs: patient’s age, weight, physical condition and liver function must be taken into account in determining the drug dosage

* Generally occurs as a result of a therapeutic error: too high a dose of ingested or topically administered local anaesthetic
* Inadvertent venous or arterial injection

Clinical Manifestations:
• CNS: agitation, seizures and coma
• CV: bradycardia, hypotension, atrial and ventricular dysrhythmias
• Respiratory: respiratory depression and apnoea

Toxicity management for LA: stopping injection; call for help; DRSABCD; manage any arrhythmias and provide CV support to suppress seizure
• Administer lipid rescue (20%) - mechanism of action of lipid emulsion for the treatment of LA toxicity is unclear. A “lipid sink” is where the lipid binds the LA to remove it from the target tissue - may have inotropic effect

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8
Q

What is general anaesthetic (GA)

A

Induces reversible state of unconsciousness - maintained despite presence of noxious stimuli
• May be used alone or in combination with LA or RA
**An epidural and GA may be used for major abdominal surgery - allows for the continued use of the epidural for postoperative pain management

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9
Q

What are the 4 A’s that GA strives to achieve?

A

Awareness (a lack of awareness)
Amnesia (lack of memory of the event)
Analgesia
Akinesia (lack of overt movement)

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10
Q

What are the 4 phases of GA?

A
  1. Induction (induce unconsciousness): performed through either IV or inhalation (or combination of both)
    1. Maintenance: level of anaesthesia and homeostasis is achieved and maintained through the procedure
    2. Emergence: transition from an unconscious state to a conscious state
    3. Recovery
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11
Q

What are pre-medications used for?

A

administered to reduce patient anxiety, relieve pain, produce sedation and amnesia (to aid a smoother induction of anaesthesia). They also reduce salivary and bronchial secretions:
• Benzodiazepines (anxiolytics/hypnotics/sedatives)
• Analgesics (narcotic/opioids or non-opioids)
• Anticholinergics (reduce salivation and control bradycardia (atropine))
• Antiemetics (reduce nausea and vomiting)
• Antibiotics (ordered preoperatively to reduce the incidence of wound infection)

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12
Q

What are the 2 types of inducing agents?

A

Intravenous: produce unconsciousness - pleasant, rapid and maintains haemodynamic - Induce transition from awareness to an anaesthetised state within seconds (include some respiratory and circulatory depression)

  • Thiopentone (thiopental)
  • Propofol
  • Ketamine
  • Midazolam/ benzodiazepine

Inhalation: Volatile Agents

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13
Q

How does Thiopentone work?

A

Enhances or mimics the action of GABA in the CNS and depresses the action of excitatory neurotransmission (IV administered); Respiratory and cardiac effects:
○ Respiratory depression (dose-dependent) can be used in conjunction with an inhalation agent.
○ Decreases CO and BP as plasma concentration rises
○ Prolonged elimination and is lipid-soluble (fat distribution)
○ No analgesic effect
**Gamma-aminobutyric acid (GABA): most widely distributed inhibitory neurotransmitter in the CNS; 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

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14
Q

How does propofol work?

A

commonly used and works by activating a specific site within the GABA receptor
○ Shortens channel opening times at the neuronal nicotinic acetylcholine receptor (nAChR) and Na+ channels in the cortex = rapid induction = suitable for maintenance and sedation
○ Minimal cardiovascular effects with no analgesic properties
○ Recovery more complete, with less “hangover” (cf to thiopental) - likely due to high plasma clearance
Can cause pain at the injection site

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15
Q

How does Ketamine work?

A

N-methyl-D-aspartate (NMDA) receptor antagonist and interacts with mAChR, voltage-gated Ca2+ channels and opioid receptors
○ Complex MOA; major effect likely due to reducing neuronal excitability by blocking NMDA (glutamate) receptors
○ Used in induction and maintenance and is a potent analgesic
○ “dissociative” anaesthetic - patient remain conscious but with insensitivity to pain and short-term amnesia
○ Can produce surgical anaesthesia suitable for brief procedures on its own

	○ CV system stimulant (HTN, tachycardia, ECG changes) and hallucinations and nightmares may be experienced during emergence
	○ Used in paediatric population as airway reflexes are maintained
	○ High incident of hallucinations and dysphoria which restricts its use in adults, but a lower incidence in children makes it suitable for minor paediatric surgery. Nystagmus is common

	○ Indications for use in children is that they must be aged >12 months as there is an increased risk of airway complications in children aged <12 months, especially <3 months
	○ Suitable for short, painful procedures (e.g. face lacerations, fracture reduction)
	○ Pt has to remain nil by mouth prior with strict vitals and cardiac monitoring and resuscitation equipment nearby

	○ Nurse in a quiet area with minimal noise, dim lighting and do not stimulate prematurely. Parents should be next to the child so they feel safe. Side effects include hypersalivation, transient laryngospasm, emesis and recovery agitation
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16
Q

How does midazolam/ benzodiazepine work?

A

potentiates the inhibitory effects of GABA in the CNS, resulting in sedative, hypnotic, anterograde amnesic and muscle relaxant effects
○ Fast-acting and the patient is typically unconsciousness within 80 seconds
○ Can cause dangerous cardio-respiratory effects

17
Q

How do volatile agents work? MOA? What are some examples? When is it contraindicated?

A

liquids vaporised to gases via a vaporiser can be administered (via an anaesthetic machine) to patients (via a mask or tube) by mixing with a carrier gas (air, oxygen)
○ Anaesthetic gas is inhaled into the lungs and crosses the alveolar-capillary membrane, into circulation, and then reaches the brain
○ MOA of inhaled agents is not well understood; thought that volatile agents bind to the lipid bilayer of nerve cell membranes = small membrane expansion/swelling = distorts ion channels = enhances inhibitory ion channel activity and inhibits excitatory activity in the brain and spinal cord
○ Administered at a specific gas concentration (dependent on agent used) and depth of anaesthesia can be controlled by adjusting this concentration
○ May not have useful analgesic actions = used in combination with an adjunct analgesic

Examples of volatile agents include:
1. Isoflurane (medium induction, maintenance, pungent)
2. Sevoflurane (fast induction, maintenance, well-tolerated)
3. Desflurane (fast induction, maintenance, low solubility)
Other inhaled: Nitrous oxide (N2O) (good analgesia in sub-anaesthetic concentrations; induction, maintenance as an adjunct in major surgery)
All volatile agents are triggers of malignant hyperthermia. The use of volatile agents is absolutely contraindicated in patients who are known or suspected to have malignant hyperthermia

18
Q

What is malignant hyperthermia?

A

rare but potentially fatal condition and is an inherited abnormality in muscle membranes
• Triggered by depolarising neuromuscular blocking agents (e.g. suxamethonium) and volatile agents
• Syndrome of accelerated skeletal muscle, rapid fever, acidosis, perfuse sweating and muscle rigidity
• In an anaesthetic emergency, the appropriate response is to stop the triggering agent
• For active cooling administer dantrolene (antidote); direct inhibitor of muscle contractions, and possibly an antiarrhythmic agent as well as electrolyte and fluid replacement

19
Q

What is Maintenance?

A
  • If no further agents were given following induction, the patient would soon awaken
  • Requires the delivery of pharmacologic agents with the aim to achieve the “4A’s” and haemodynamic stability throughout the surgery
  • Hypothermia can have a deleterious effect on maintenance
  • Achieved using inhaled agents, opioids and muscle relaxants
20
Q

What is the purpose of muscle relaxants?

A

prevent muscles from moving when a patient is unconscious and reduce the amount of anaesthetic agent needed (e.g. suxamethonium, pancuronium, atracurium, vecuronium, rocuronium)

21
Q

Neuromuscular (NM) blocking agent (muscle relaxant) produces —– muscle relaxation needed to facilitate intubation (negate gag reflex), allow mechanical ventilation and prevent ——-. NM blocking agents fall into two categories (The difference is in the MOA and the need for reversal) - (expand on each)

A

Neuromuscular (NM) blocking agent (muscle relaxant) produces skeletal muscle relaxation needed to facilitate intubation (negate gag reflex), allow mechanical ventilation and prevent reflexes. NM blocking agents fall into two categories (The difference is in the MOA and the need for reversal): depolarising and non-depolarising

1. Depolarising: Mimics (similar structure) the action of acetylcholine (ACh)
• IV suxamethonium (only one clinically used) - acts as an agonist at nicotinic receptors on the motor endplate. Depolarisation = initial muscle twitching (classic feature fasciculation) = persistent depolarisation (paralysis)
• Clinicians observe for fasciculation, and when this subsides (usually quickly) the NM blockade follows
• Short-acting agent (<5 mins) and does not need reversal
• Used in an emergency situation and in rapid sequence intubation
• Metabolised by plasma cholinesterase (enzyme produced by the liver)
• Side effects: malignant hyperthermia

2. Non-depolarising: competitive antagonist at the ACh receptors endplate; nACh receptor antagonists (NM junction) prevent depolarisation
• Choice of agent is influenced by onset, duration and side effects and require reversal of muscle paralysis and anticholinergic effects (bradycardia, BP drop and bronchospasm)
• IV atracurium, pancuronium, rocuronium, vecuronium
• Typically cause histamine release from mast cells
• 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)
• Combination of neostigmine and atropine can control potential cholinergic effects