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Local Anaesthetics Flashcards

1
Q

Do all local anaesthetics have a benzene ring?

A

Yes.

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2
Q

Is the benzene ring lipophilic or hydrophilic?

A

Lipophilic

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3
Q

Are local anaesthetics weak acids or weak bases?

A

Weak bases.

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4
Q

State how local anesthetic stability is enhanced commercially.

A

Addition of hydrochloric acid which lowers its pH and prolongs the shelf life

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5
Q

Should local anaesthetic be water soluble?

A

Yes. It makes the drug highly ionised until injected into the body

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6
Q

What does the pKa of a local anesthetic determine?

A

Onset of action

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7
Q

Local anesthetics with a pKa closer
to 7.4 will have a quicker onset of
action. Name two local anaesthetics that have a higher pKa but very rapid onset

A

Procaine and chloroprocaine

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8
Q

What is the primary determinant of the duration of action for local anesthetics?

A

The degree of protein binding

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9
Q

Name two proteins found in blood that bind to local anesthetics

A

Albumin and A1 acid glycoprotein

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10
Q

Which route of administration of local anesthetic leads to higher peak plasma levels of local anesthetic in order. 6

A

Intravenous, intercostal, caudal, epidural, upper extremities(brachial plexus), lower extremity (sciatic/femoral)

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11
Q

State how the vascularity of the site of injection of the local anesthetic is related to the peak plasma levels, toxicity and duration of blockade.

A

Peak plasma: High
Toxicity: High
Duration of blockade: Short

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12
Q

What is the pH value of most local anaesthetic formulations and what is the implication of that?

A

pH 4-6: Means the agent are present in a poorly lipid soluble ionic form

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13
Q

State why is it important to add sodium bicarbonate to local anaesthetic preparations.

A

It is important to remember that most local anaesthetic formulations are in an ionic form which is less lipid soluble, so the addition of sodium bicarbonate raises the pH of the solution and increases the percentage of unionised local anaesthetic molecules thus the speed of onset

Note: Also decrease pain by increasing the pH.

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14
Q

State the most useful application of epinephrine addition to local anesthetic formulation.

A

it is a common practice to include epinephrine in the small or “test” dose which precedes the injection of any large amount of local anesthetic

Note: The addition of epinephrine to the test dose lends an increased sensitivity to intravascular injection when compared to aspiration before
injection.

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15
Q

Is the duration of action of local anaesthetics affected by the addition of epinephrine?

A

Nope

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16
Q

State why epinephrine addition is important in local anaesthesia.

A
  1. The addition of epinephrine to local anesthetics also leads to local vasoconstriction, less systemic uptake of the local anesthetic, and a decreased
    risk of toxicity
  2. Can be used to determine what level of local anaesthetic is toxic before administering larger doses
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17
Q

Does epinephrine affect the clinical effects of short acting local anesthetic agents?

A

Yes, by reducing systemic absorption

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18
Q

Does epinephrine potentiate the analgesic action of local anaesthetics?

A

Yes. Through alpha 2 receptor activity

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19
Q

State why esters anaesthetics are more allergic than amides.

A

They are broken down into para amino benzoic acid which is a known allergen

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20
Q

Name two preservatives for local anaesthetic agents that can trigger anaphylaxis.

A

Methylparaben and sulfites

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21
Q

Can local anaesthetic work in acidic tissues?

A

Nope, that is why they do not work at the site of infection.

Lower pH keeps the drug ionised which reduces lipid solubility and thus the entry into the nerve.

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22
Q

List the benefits of adding epinephrine to local anaesthetic solution

A

It is useful to detect intravascular injection, to increase duration of the blockade, and to prevent systemic absorption and toxicity

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23
Q

What is the most versatile widely used local anaesthetic?

A

Lidocaine

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24
Q
A
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25
What is the maximum dose of lignocaine for single use?
With epinephrine:7 mg/kg Without epinephrine: 3 mg/kg
26
What is the pKa and protein binding of lignocaine?
7.9 and protein binding 64%
27
State 6 uses of lignocaine
Topical Epidural Spinal Biers block Infiltration Peripheral nerve block
28
What is the single maximum dose of bupivacaine?
2 mg/kg
29
List 4 advantages of bupivacaine
High potency Relatively low toxicity Long duration of action Safe in obstetrics
30
What is the pKa and protein binding of bupivacaine
pKa:8.1 protein binding: 96%
31
Which route of administration of bupivacaine leads to severe cardiotoxicity
Intravenous That is why it is also contraindicated for Biers block
32
List three clinical uses of bupivacaine
Neuraxial anaesthesia both spinal and epidural Peripheral block Infiltration
33
T/f: low concentrations of bupivacaine mostly produce sensory block.
True
34
What is an alternative for bupivacaine?
Ropivacaine: Low Cardiac toxicity Other:Levo bupivacaine (S enantiomer) Note: Both used in Europe for spinal
35
What is the usual concentration of bupivacaine used?
0.25-0.5% Remember: 0.5% contain 5 mg/ml
36
Name a clinical use of lignocaine that require the lowest concentration
Biers block
37
Name a clinical use of lignocaine that requires the highest concentration
Topical anaesthesia 2-10% Followed by spinal 2-5%
38
Name a local anaesthetic that is also an antiarrhythmic
Lidocaine
39
Name a local anaesthetic that is a potent vasoconstrictor.
Cocaine Note: It sensitises adrenergic receptors
40
Name a life threatening complication of cocaine
Myocardial infarction
41
State why adrenaline addition is contraindicated when cocaine is the preferred local anaesthetic.
Cocaine sensitises adrenergic receptors leading to increase in heart rate and blood pressure so addition of adrenaline will lead to severe hypertension which is detrimental
42
What is the main use of tetracaine and amethocaine?
Ametop cream for venepuncture and as eye drops Note: High potency and toxicity
43
What is the maximum dose for tetracaine and amethocaine?
1 mg/kg Concentration:0.5-2%
44
Does cocaine have a long duration of action?
Nope only 20-30 minutes Also tetracaine and amethocaine
45
Name a vasoconstrictor added to local anaesthetic solution.
Adrenaline 1:80 000 Or 1:200 000
46
Does adrenaline prolong the duration of action of bupivacaine and ropivacaine?
Minimally but the effect is great for short acting local anaesthetics such as lidocaine
47
State 4 benefits of adding adrenaline to local anaesthetic solution.
Local vasoconstriction minimising systemic absorption of the drug thus reducing the toxicity Enhance the analgesic effect of local anaesthetics Decreases bleeding Prolongs duration of local anaesthetic with short duration
48
List 6 contraindications for addition of adrenaline to local anaesthetic solution
• Nerve blocks in areas that lack collateral blood supply, e.g. digits, eyes, penis • Intravenous regional anaesthesia (Bier's blocks) • In patients with unstable angina, dysrhythmias and uncontrolled hypertension • Utero-placental insufficiency • Patients on tricyclic antidepressants & MAOIs as it may promote hypertension and /or dysrhythmias.
49
State two benefits of adding sodium bicarbonate to a local anaesthetic solution
Increases the speed of onset of the drug Decreases pain sensation
50
State the dose of sodium bicarbonate added in local anaesthetic solution
• 1 ml NaHCO3- 8,5 % added to 10 ml lignocaine. • 0,1 ml NaHCO3- 8,5 % added to 10 ml bupivacaine (precipitates if too alkaline
51
State why dextrose is added to the local anaesthetic during spinal anesthesia
Local anaesthetic solutions are slightly hypobaric (at body temperature) when compared to central spinal fluid (CSF), and will tend to move upwards in the CSF away from the gravitational pull. Dextrose is added to the solution to make it “heavy” or hyperbaric. The solution will then sink in relation to the CSF. Note: This allows the anaesthetist to manipulate the distribution of the LA with the knowledge of spinal curvatures and strategic positioning of the patient.
52
State why esters anaesthetic are more likely to cause true anaphylactic reaction
When ester anaesthetic are metabolised they form para amino benzoic acid which triggers hypersensitivity and anaphylaxis
53
Is anaphylaxis to local anaesthetics common?
Nope Mostly people experience numbness from the local anaesthetics anf tachcardia from the epinephrine that entered the blood and think it is true allergy.
54
Name two local anesthetics that cause methenoglobinemia
Prilocaine anf benzocaine Note: They are common ingredients in local anesthetic sprays
55
56
What is the treatment of methemoglobinemia?
Infusion 1-2 mg/kg methylene blue
57
The patiebt who receieved spinal anesthesia presented with transient hypesthesias, paraesthesia and motor weakness of the leg and buttocks, what is the most likely diagnosis and an agent used?
Transient neurological symptoms: Resolves in 3 days Typically caused by ligocaine but bupivacaine and tetracaine can cause it.
58
Which system is affected first in local anaesthetic toxicity?
CNS
59
List 4 earliest signs of local anesthetic toxicity
Lightheadedness(confusion) Perioral or tongue numbness Metallic taste Other: Slurred speech, tinnitus and visual dysfunction especially when the levels are very high
60
List three clinical features of the depressive phase of local anaesthetic toxicity
Loss of consciousness and coma Respiratody arrest with apnoea Seizures
61
List two features of the excitatory phase of LA toxicity
Muscle twitching Convulsion
62
State the treatment of LA induced seizures
Hyperventilation, benzodiazepines or small doses of thiopental or propofol
63
State the commonest risk factor of local anesthetic toxicity.
High dose infusion of local anaesthetic>4mg/kg
64
State two earliest CVS features of LA toxicity
Tachycardia and hypertension
65
T/F: Cardiovascular effects of bupivacaine and ropivacaine can be observed without promontory central nervous effects when systemic toxicity occurs
True
66
List 4 CVS clinical features that are found in the terminal phase of LA tocivity
Peripheral vasodilation leading to severe hypotension Sinus bradycardia and cardiac arrythmias due to reduction in myocardial automatacoty and shortned refractory period Decreased contractility and conduction defects
67
3 features of intermediary phade of LA toxicoty
Myocardial depression Decreased cardiac output Hypotension
68
After how long from the onset of CNS toxicity does cardiovascular toxicity occur in Local anesthetic toxicity?
When the plasma concentration is 2-4 X that required for a seizure to occur.
69
Is it hard to reverse cardiovascular toxicity from bupivacaine?
Yes very hard: The V tachycardia is very resistant Note: Supportive treatment may require cardiopulmonary bypass until the local anaesthetic can be cleared
70
What is the recommended treatment of local anaesthetic toxicitu?
Intralipid 20%: IV bolus 1.5-2 mg/kg of a 20% solution over 1 minute and repeat every 3-5 minutes Note: Start infusion at 0.25 ml/kg/min theb increase to 0.5 if necessary
71
State why propofol cannot be used for treatment of local anaesthetic toxicity even though it has the same composition as intralipid?
Large bolus of propofol lead to vasodilation thus hypotension and cardiac depression Do not forget the possibility of propofol infusion syndrome
72
73
What is the maximum dose of intralipid?
8 ml/kg
74
State the recommended dose for intralipid infusion.
IV bolus 1.5 ml/kg of 20% lipid emulsion then run 0.25 ml/kg/min for 30-60 minutr Repeat the bolus dose for persistent asystole and increase infusion rate for hypotension
75
State a complication caused by infusing 5% lidocaine through spinal microcatheters
Permanent neurologia damage in a form of cauda equina syndrome Mechanism: Pooling of the concentrated local anaesthetic solution around nerve fibers
76
Lidt 6 uses of local anaesthetics
IV placement Epidural Spinal placement Pain management Lido for propofol pain To infiltrate the incision site
77
State two factors that influence the peak blood levels of local anaesthetics
Site of injection Dose administered
78
Rank the site of administration of local anaesthetics based on the peak blood levels in descending order
Intravenous>Tracheal>Intercostal>caudal>epidural>branchial plexus>sciatic plexus>subcutaneous injection
79
Outline the phenomenon of differential conduction blockade by local anaesthetics
Sympathetic nerve fibers are more easily blocked than pain and temperature fibers which are easily blockef than motor, pressure and proprioceptive fibers This is why some patient have incomplete motor and pressure blockade while they have sympathetic and pain fiber blocmade
80
T/F: Small unmyelinated fibers are easily blocked as compared to larger myelinated ones.
False but it they are the same type the smaller ones are easily blocked

Anaesthesia (11 decks)

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