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YEAR 4 - ACC > Anaesthesia - Local Anaesthetics, Pain > Flashcards

Anaesthesia - Local Anaesthetics, Pain Flashcards

1
Q

What is a local anaesthetic?

A

A drug that causes reversible block of nerve impulse in the region which it is applied without affecting consciousness

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2
Q

How do local anaesthetics work?

A

They block the sodium channel in the axon which prevents the transmission of the nerve impulse

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3
Q

What are the different groups of local anaesthetics?

A
  • Esters: procaine, amethocaine (ametop), cocaine, benzocaine, tetracaine
  • Amides: lignocaine, ropivacaine, levobupicaine, mepicaine, prilocaine
  • EMLA (eutectic mixture of local anaesthetics): contains 50:50 mixture of lignocaine and prilocaine; used for topical analgesia

(all the amides have an i before caine whereas esters don’t)

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4
Q

What determines which type of local anaesthetic you use?

A

The speed of its onset and offset

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5
Q

What are the maximum dosages of lignocaine, bupivacaine and prilocaine (with and without adrenaline)?

A

Lignocaine 3mg, with adrenaline 7mg

Bupivacaine 2mg, with adrenaline 2mg

Prilocaine 6mg, with adrenaline 9mg

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6
Q

Why is the dose of local anaesthetic higher if it is mixed with adrenaline?

A

Adrenaline causes local vasoconstriction which prevents systemic absorption - this also increases the duration of local anaesthetic effect

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7
Q

Why is the dose of bupivacaine and bupivacaine with adrenaline the same?

A

Bupivacaine lasts much longer than adrenaline so cannot be increased

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8
Q

When is adrenaline contraindicated in local anaesthesia?

A

Digital or penile blocks
Around the nose/ears
There is risk of local ischaemia (due to vasoconstriction)

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9
Q

What are the side effects of local anaesthetics that contain adrenaline?

A

Palpitations

Hypertension

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10
Q

How do you calculate a safe dose of local anaesthetic?

A
  1. Work out maximum dose in of drug in mg by multiplying maximum dose by patient’s weight
  2. Convert percentage of drug into mg/ml by multiplying it by 10
  3. Find out in ml what the maximum dose you can give is by dividing the mg by the mg/ml

Example:

  1. How much bupivacaine does 1ml of 0.25% solution contain
    1a) Multiply % by 10 and you get the content of the local anaesthetic agent in mg/ml
    1b) Therefore 0.25% bupivacaine contains 2.5mg/ml
  2. What is the safe dose of bupivacaine for this patient
    2a) Multiply weight with safe dose to get the maximum safe dose
    2b) 60kg and 2mg/kg maximum dose = 120mg total dose
  3. How much of 0.25% bupivacaine can be used?
    3a) 0.25% = 2.5mg/ml = 120/2.5 = 48ml maximum
  4. Calculate the same for 0.5% bupivacaine
    4a) 0.5% = 5mg/ml = 120/5 = 24ml maximum
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11
Q

What are the initial features of local anaesthetic toxicity?

A

Neurological toxicity (excitatory signs)

  • Perioral tingling - first sign because the face is highly vascular and is close to the heart
  • Numb tongue
  • Tinnitus
  • Light headedness
  • Anxiety
  • Muscle twitching

Cardiovascular toxicity

  • Tachycardia
  • Hypertension
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12
Q

What are signs of severe local anaesthetic toxicity?

A

Neurological toxicity

  • CNS depression - slurred speech, drowsiness
  • Tonic-clonic seizures
  • Coma

Cardiovascular toxicity

  • Hypotension, bradycardia
  • Heart block
  • Ventricular arrhythmias
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13
Q

How do you treat local anaesthetic toxicity?

A

Intralipid 1.5ml/kg

Control seizures with benzodiazepine

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14
Q

What are the 3 layers of the spinal cord?

Where is CSF present in the spinal cord?

A

Pia mater, arachnoid mater, dura mater from inside outwards

CSF present in subarachnoid space i.e. between pia and arachnoid mater

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15
Q

Where does a spinal block injection occur?

A

Subarachnoid space, below the arachnoid mater, in the CSF

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16
Q

Where does an epidural occur?

A

Epidural (outside dura) space = between dura mater and vertebral canal (in fatty tissue)

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17
Q

Where does the spinal cord end?

A

Lower border of L1

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18
Q

Where does the subarachnoid space end?

A

S1

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19
Q

At what level can you do a spinal block?

A

Below L2, down to S2 (the spinal cord ends at L1 then there is the corda equina so there is less chance of damaging the spinal cord)

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20
Q

What is the route from skin to subarachnoid space?

A

Skin > subcutaneous fat > supraspinous ligament > infraspinous ligament > ligamentum flavum > epidural space > dura mater > arachnoid mater > subarachnoid space

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21
Q

How long is the onset of action and duration of action for a spinal block?

A

Onset: 5-10 minutes

Duration of action: 2-3 hours

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22
Q

How long is the onset of action and duration of action for an epidural?

A

Onset: 15-30 minutes

Duration of action: up to 72 hours

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23
Q

What are signs of a post dural puncture headache?

A

Worse on sitting up

Relieved by lying down

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24
Q

How do you treat a dural-puncture headache?

A

Blood patch - inject patient’s own blood into epidural space to seal

25
Q

What are the benefits of spinal/epidural anaesthesia over general anaesthesia?

A

Less risk of chest infection after surgery
Less effect on respiratory/cardiovascular system
Less chance of VTE
Excellent pain relief post-op and less need for strong analgesia
Less PONV

26
Q

What are some contraindications to spinal/epidural anaesthesia?

A 
Anticoagulant states - risk of pressure damage to the cord from a bleed
Sepsis - risk of infection in CSF
Shock or hypovolaemia 
Raised ICP - risk of coning
Patient refusal/unwillingness
Neurological disease
IHD
27
Q

Define pain

A

An unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage

28
Q

What defines chronic pain

A

Pain lasting for more than 3 months
Pain lasting after normal healing
Sometimes there is no identifiable cause

29
Q

What is the RAT assessment of pain?

A
  1. Recognise
  2. Assess
    2a) Severity
    2b) Type
    2c) Neurovascular assessment in severe pain/trauma
  3. Treat
30
Q

What can be used to assess the severity of pain?

A

1 to 10
Faces pain scale
Visual analogue scale
FLACC score children under 7

31
Q

How can you classify pain?

A

Duration - acute/chronic
Cause - cancer/non-cancer
Mechanism - nociceptive/neuropathic

32
Q

What is characteristic of neuropathic pain?

A 
Burning
Shooting
Numbness
Pins and needles
Not well localised
33
Q

What are some examples of neuropathic pain?

A

Trigeminal neuralgia
Complex regional syndrome
Sciatica

34
Q

What are some signs of acute post-operative pain?

A

CVS - tachycardia, HTN
Resp - reduced vital capacity, reduced FRC, basal atelectasis, respiratory infection
GI - N&V, ileus
GU - urinary retention

35
Q

What is the physiological process of nociceptive pain?

A
  1. Periphery - tissue damage causes cell breakdown and release of chemical mediators that stimulate nociceptors and send a signal to A delta or C nerves then to spinal cord
  2. Spinal cord
    - first order neurons have cell bodies in the dorsal root ganglion
    - at the dorsal horn, the first order neuron synapses with the second, which travels up opposite side of spinal cord via spinothalamic tract to the ventral posterolateral (VPL) of the thalamus
  3. Brain
    - second and third order neurons synapse at the thalamus
    - third order neurons connect to somatosensory areas in post central gyrus of parietal cortex
36
Q

What are the differences between the different nerve fibres responsible for transmitting pain signals?

A

A delta fibres

  • Myelinated
  • Faster transmission
  • Responsible for sharp pain
  • Associated with pulling away from noxious stimuli (afferent portion of reflex arc)

C fibres

  • Not myelinated
  • Slower transmission
  • Responsible for dull, persistent pain
37
Q

How do descending inhibitory pathways modulate ascending pain pathways?

A

Action potentials travel down from the brain to the dorsal horn of the spinal cord
Activated interneurons release inhibitory neurotransmitters e.g. noradrenaline and serotonin
This modulates the ascending pathway

38
Q

What is the mechanism of action of tramadol?

A

It binds to u-opioid receptors

It prevents the reuptake of noradrenaline and serotonin

39
Q

Who should you not give codeine to?

A

Children
Breastfeeding women

It is a prodrug so it is metabolised to morphine by CYP450 enzymes - if it is metabolised too quickly there will be a fast release of morphine which can lead to overdose

40
Q

How do you manage acute nociceptive pain?

A

Reverse WHO ladder - start at the top and step down as pain improves

41
Q

What are COX1 and COX2 responsible for?

A

COX1 - responsible for maintenance of normal homeostatic mechanisms in bronchi, kidneys, platelets and gastric mucosa. In gastric mucosa, when activated it leads to prostaglandin production which is cytoprotective

COX2 - responds to inflammation by producing prostaglandins

42
Q

Name some selective COX2 inhibitors

A

Parecoxib

Celecoxib

43
Q

What is the purpose of intra-operative opioids?

A

Suppress response to laryngoscopy

Reduce surgical pain

44
Q

What drugs are given at the beginning of anaesthesia?

A

Fentanyl
Remifentanil
Alfentanil

They have a more rapid onset (5 minutes) and higher potency than morphine (30 minutes)

45
Q

How can patients administer their own analgesia post-op?

A

Patient Controlled Analgesia System (PCAS)
Syringe pump containing analgesic (usually morphine) is connected to IV cannula
1mg/ml delivered if they press button every 5 minutes
There is a lock out window

46
Q

What is the disadvantage of the PCAS? How can this be avoided?

A

When they go to sleep and they stop pressing the button, they might wake up with pain

To counteract tell the patient to give themselves some continuous doses before they go to sleep

47
Q

Which local anaesthetic is used for peripheral nerve blocks?

A

Lignocaine (lidocaine)

48
Q

Which local anaesthetic is used for spinal blocks?

A 
Heavy bupivacaine (i.e. bupivacaine + glucose) 
In spinal blocks, the local anaesthetic is injected into the CSF, so it needs to be heavier that the CSF in order for it to settle with gravity. If it were lighter than CSF, it would go to the brain and patient would stop breathing.
49
Q

Which local anaesthetics are long/short acting?

A

Short acting: lignocaine and prilocaine

Long acting: bupivacaine, ropivacaine

50
Q

What is a colloid?

A

A gelatine-based fluid

51
Q

What is the difference in distribution between colloids, crystalloids and dextrose infusions?

A

Colloids stay in the intravascular compartment for longer

Crystalloids distribute very quickly into intracellular and interstitial compartments (60% interstitial)

Dextrose distributes mostly (60%) intracellularly

52
Q

What is the issue with giving too much colloid?

A

Since it stays in the intravascular compartment for longer, too much colloid haemodilutes the patient and interferes with coagulation pathways

53
Q

Why should you not give dextrose to a head injury patient?

A

Most of the dextrose infusion goes intracellularly, which would increase the ICP

54
Q

What are a human’s fluid and electrolyte requirements per day?

A

Water: 25-35 ml/kg
Na+: 1 - 2 mmol/kg
K+: 0.5 - 1 mmol/kg
Cl-: 1 - 2 mmol/kg

55
Q

What is the risk of administering too much saline?

A

Hyperchloraemic acidosis

as well as tissue oedema and cardiac failure

56
Q

What fluid is best if you need to administer large volumes?

A

Hartmann’s

57
Q

How should total parenteral nutrition be administered?

A

Via a central vein because it is strongly phlebitic

58
Q

Which drugs slow the rate of healing?

A 
NSAIDs - slows bone healing
Steroids
Immunosuppressants
Chemotherapy drugs
Smoking
59
Q

What VTE prophylaxis should a patient undergoing an elective hip replacement have?

A

Both mechanical and pharmacological prophylaxis

Compression stockings
LMWH started 6 hours post-surgery and continued for up to 35 days post-op

YEAR 4 - ACC (11 decks)

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