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Pharmacology Basics > Local Anaesthetics eLFH > Flashcards

Local Anaesthetics eLFH Flashcards

1
Q

What is Phase 1 action potential?

A

RESTING MEMBRANE POTENTIAL:

The Na+/K+/ATPase pump exchanges 3 intracellular Na+ ions for 2 extracellular K+ ions at the expense of a molecule of ATP.

3 Sodium out, 2 Potassium in

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2
Q

What is Phase 2 of the action potential?

A

DEPOLARISATION:

Sodium channels open in response to action potential being initiated at the synapse

  • allowing an influx of sodium ions into the axon.

This causes the membrane potential to rise to +30mV at which point the channels close.
This is depolarisation.

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3
Q

What is Phase 3 of the action potential?

A

REPOLARISATION:

Voltage gated potassium channels open and allow K+ to move down its concentration gradient and move extracellularly.

The Na+/K+/ATPase pump continues its ionic exchange so that the original resting membrane potential of -80 mV is restored.

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4
Q

What aspect of the action potential does local anaesthetic effect?

A

Local anaesthetic agents block the sodium channels of the phospholipid membrane in order to stop propagation of the action potential.

Must attach INTRACELLULARY to work.
Phase 2 Block

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5
Q

LA - how does it act on ion channel?

A

uncharged extracellularly, goes into cell and becomes ionised - this allows it to bind to specific sodium ion and renders it inactive.

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6
Q

How might the physical properties of the nerve affect speed of blockade onset?

A

Speed of blockade onset can be further affected because:

  1. Smaller-diameter neurones are affected prior to larger-diameter neurones
  2. Myelinated fibres are blocked before unmyelinated fibres of the same diameter.
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7
Q

Name the amide LA’s

A

Lidocaine, Ropivocaine, Bupivocaine, Prilocaine

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8
Q

Name the ester LA’s

A

Tetrocaine, Procaine, Cocaine.

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9
Q

Are LA’s acids or bases?

A

Weak bases

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10
Q

Why are LA’s produced as hydrochloric salts?

A

This makes them water soluble.

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11
Q

% plasma protein binding: Bupivicaine

?duration of action

A

95%

Several hours

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12
Q

% plasma protein binding: Lidocaine

?Duration of action

A

70%

90 - 120 minutes

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13
Q

Metabolism of ester LA’s?

A

Rapid hydrolysis by plasma esterases, namely pseudocholinesterase.

> > Production of para-aminobenzoic acid (PABA), which carries a potential for anaphylaxis in a small group of individuals.

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14
Q

Metabolism of amide LA’s?

A

Amide local anaesthetics undergo metabolism in the liver.

Therefore, their metabolism is dependent on both renal function and blood flow and, in turn, affects the elimination half-life.

Amides are then excreted renally, with approximately 5% of the drug remaining unchanged.

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15
Q

Lidocaine:

  • Onset time
  • Duration
  • Uses
A

AMIDE.
- onset: 2 minutes

  • Duration: 20-40 minutes.
  • Its membrane-stabilizing properties have also seen it used as an infusion in GA.
  • CLASS IIB antiarrhythmic agent (VT treatment)
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16
Q

Ropivocaine:
- long or short acting?

  • which enantiomer less toxicity?
  • more or less potent than Bupivicaine?
A

Ropivacaine was developed to provide a long-lasting local anaesthetic with a reduced side-effect profile to rival bupivacaine.

It is available as a pure S-enantiomer preparation, which is of a lower toxicity than the R-enantiomer.

Compared to Bupivicaine: less potent, shorter duration action and less cardiotoxic.

17
Q

Prilocaine vs Lidocaine

A

Prilocaine is another amide local anaesthetic, which is similar to lidocaine, though with a more intermediate duration of action.

It causes less local vasodilatation and is less bound, leading to an increased volume of distribution.

These in turn reduce its propensity to cause central nervous system (CNS) toxicity and cardiotoxicity.

18
Q

Which LA can cause methaemoglobinaemia?

A

PRILOCAINE. (o-toluidine)

19
Q

What type of block is Prilocaine used for?

A

Most commonly Biers block due to short duration of action.

20
Q

How long does it take motor function to return post regional block with Prilocaine?

A

60 - 75 minutes.

21
Q

Why is cocaine linked to cardiac issues?

A

The vasoconstrictive properties of cocaine also effect the coronary circulation and can cause cardiac dysrhythmias and death.

22
Q

How does cocaine exhibit its vasoconstrictive effects?

A

local inhibition of noradrenaline reuptake.

23
Q

What does EMLA contain?

A

EMLA 5% combines 2.5% lidocaine with 2.5% prilocaine and is used for topical anaesthesia prior to cannulation, especially in children.

24
Q

What does Ametop gel contain?

A

4% tetracaine

More popular than EMLA because prilocaine shown to cause local vasodilation.

25
Q

What are the risks of using Bupivacaine?

A

There is an increased risk of cardiotoxicity, which is cumulative and very difficult to treat due to the duration for which it blocks cardiac sodium channels.

26
Q

How does Levobupivacaine compare to Bupivacaine?

A

Levobupivacaine was developed, which is the pure S-enantiomer of bupivacaine, making it far less cardiotoxic.

Its pharmacokinetic properties are comparable to those of bupivacaine, though it undergoes more hepatic metabolism with no unchanged drug excreted.

27
Q

Lidocaine:

  1. Dose
  2. Dose with Adrenaline
  3. speed onset
  4. duration
A

3mg/kg
7mg/kg
Quick onset
Short duration

28
Q

Bupivacaine:

  1. Dose
  2. with Adrenaline
  3. speed onset
  4. duration
A

2mg/kg

2.5mg/kg

Intermediate onset
Long duration

29
Q

Ropivacaine:

  1. Dose
  2. speed onset
  3. duration
A

Ropivacaine

3-4 mg/kg

Quick onset
Intermediate duration

30
Q

Prilocaine:

  1. Dose
  2. with Adrenaline
  3. speed onset
  4. duration
A

Prilocaine

6 mg/kg

9 mg/kg

Quick onset
Short duration

31
Q

What drugs can potentiate LA block?

A

Adrenaline, Opioids, Clonidine, Glucose (intrathecally)

32
Q

How can lidocaine affect myocardial action potential?

A

Lidocaine acts on sodium channels in the myocardium to increase the threshold potential and shorten the action potential. It is used as a treatment for ventricular tachycardia when amiodarone is contraindicated or has been used unsuccessfully.

33
Q

What is the regimen for management of LA toxicity?

A

Intralipid® (20%)

  1. An initial bolus of 1.5 ml/kg over 1 minute. Simultaneously start an infusion of 15 ml/kg/hour
  2. Reassess after 5 minutes. If there is no improvement, repeat the bolus and double the infusion to 30 ml/kg/hour
  3. At 10 minutes, reassess again and repeat the bolus dose, for the last time, with no change in the infusion rate
  4. Do not exceed the maximum cumulative dose of 12 ml/kg
34
Q

Which has a faster onset, Lidocaine or Bupivacaine and why?

A

Lidocaine, with a lower pKa than bupivacaine, therefore has a faster onset due to this higher proportion being unionized.

35
Q

What type of pain fibres are blocked first?

A

Smaller diameter,

and myelinated before unmyelinated.

Pharmacology Basics (25 decks)

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