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M1 PDA Block 3 (Tim) > General & local anesthetics > Flashcards

General & local anesthetics Flashcards

1
Q

What are the components of general anesthesia?

A

Amnesia and a lack of response to pain. Unconsciousness is not a required component (eg Ketamine, Midazolam)

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2
Q

What metrics are used to specify the potency of IV and gaseous anesthetics?

A

IV anesthetics have an EC50 related to plasma concentration.

Gas anesthetics have MAC, or minimal alveolar concentration which induces anesthesia. Anesthesia is achieved when the brain reaches MAC (equalized with alveoli).

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3
Q

What are two typical targets of anesthesia? Can you give some examples for each?

A
  1. Activation of inhibitory GABA receptors (eg Sodium thiopental)
  2. Inhibition of excitatory NMDA receptors (eg Ketamine)
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4
Q

Distinguish between inductive and maintenance anesthetics.

A

Anesthetics used for induction need to be fast and pleasant. They are often administered in a single dose (bolus).

Maintenance of anesthesia requires constant administration or long-lived action.

Many anesthetics can serve both functions.

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5
Q

Why may an anesthetic’s duration of action be shorter than its plasma half-life?

A

Although the active site is the CNS, many anesthetics redistribute to fat, leaching out to the plasma over a long interval.

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6
Q

Sodium Thiopental

What class of drug is this?

What is the target?

What is it used for?

What are its side effects?

A

Sodium Thiopental

Barbiturate

GABA receptor (activating)

Induction of anesthesia

Depression of CV (venodilation > hypotension), CNS (severe hangover due to long half-life; decrease ICP), Respiration

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7
Q

Propofol

What is the target?

What are its uses?

What are some additional benefits?

What are some drawbacks?

A

Propofol

GABA receptor (activating)

Induction and maintenance in outpatient setting

Less hangover than ST, reduces nausea and gives “pleasant dreams”

It may elicit pain or excitation on injection, and has worse CV/Resp side effects than ST.

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8
Q

Etomidate

What is the target?

What are its uses?

What are some drawbacks?

A

Etomidate

GABA receptor (activation)

Used in induction of anesthesia in hypotensive patients (low CV and respiratory depression)

Causes pain/myoclonus on injection. Nauseating and potentially suppressive of HPA axis.

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9
Q

Ketamine

What is the target?

For whom is it indicated? Why?

What are its unique side effects?

A

Ketamine

NMDA receptors (antagonism)

Patients with bronchospasm (ketamine is bronchodilatory) and children (experience less delirium)

Nystagmus, salivation, lacrimation, delirium, hypertension & increased ICP.

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10
Q

Midazolam

What is the target?

What is it used for?

Describe its kinetics.

What are its side effects?

A

Midazolam

GABA receptor (activation)

Conscious sedation & anxiolysis as an adjunctive during short surgeries. May be used for induction/pre-op.

Midazolam is activated by hydroxylation–slow induction and long action.

CV & respiratory depression. Contraindicated in Parkinson’s, NMJ diseases, and bipolarism.

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11
Q

Why are gaseous anesthetics generally avoided outside of emergencies?

A

They have very low therapeutic indices and require stricter control.

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12
Q

What are the significance of the following partition coefficients?

Blood:Gas

Brain:Blood

Fat:Blood

A

Blood:Gas is how plasma soluble it is. Lower means faster action and quicker elimination, but a large required dose.

Brain:Blood determines how well it reaches the brain.

**Fat:Blood **affects redistribution kinetics. Higher = longer half-life.

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13
Q

Predict how the following factors may affect gaseous induction.

High partial pressure of inspired air

Low pulmonary ventilation

High pulmonary blood flow

A

Higher partial pressure means a higher dose–this should expedite induction.

Low pulmonary ventilation means slow equilibration–this should slow induction.

High pulmonary blood flow delays equilibration locally, increasing the rate of induction systemically (net increase of gas diffusing from alveoli to blood per unit time)

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14
Q

What determines the arteriovenous concentration gradient of a gaseous anesthetic?

A

It depends on the rate of tissue uptake, which in turn depends on various tissue partition coefficients and perfusions.

For example, the gradient will be greater if all tissue take it up massively. If only the brain does, then the gradient would increase with higher brain perfusion.

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15
Q

In general, what traits of gaseous anesthetics will facilitate fast elimination & recovery?

A

Low blood:gas partition coefficient, low fat:blood coefficient.

Overall, low blood and fat solubilities.

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16
Q

Isoflurane

How blood soluble is it?

What are its uses?

What are its side effects?

A

Isoflurane

It has a moderate blood:gas partition coefficient.

It is widely used for maintenance (can be used for induction) and in conjunction with nitrous oxide.

It is an airway irritant. It can depress respiration (>> hypercapnia). It is also cardiodepressive (arrhythmias and increased ICP).

17
Q

Desflurane

How blood soluble is it?

What are its uses?

What are its side effects?

A

Desflurane

It is very volatile and has poor blood solubility.

It is used for maintenance in outpatient settings. It also promotes skeletal muscle relaxation.

Its side effects match isoflurane, but it is a worse irritant (hence, not used for induction)

18
Q

Sevoflurane

How blood soluble is it?

What are its uses?

What are its side effects?

A

Sevoflurane

It has a very low blood:gas partition coefficient.

It is used for both induction and maintenance in wide settings.

It has milder respiratory irritation, but may have nephrotoxic metabolites (fluoride ion, “compound A”)

19
Q

Nitrous Oxide

How blood soluble is it?

What are its uses?

What are its side effects?

A

Nitrous Oxide

It is very insoluble in blood.

It is an effective carrier gas for other inhaled anesthetics. It is a weak anesthetic alone.

It is commonly abused, is a negative inotrope, but has minimal respiratory depression besides displacing oxygen at the concentrations used clinically. This high concentration is presumably also why it is contraindicated in pneumothorax.

20
Q

All local anesthetics target what aspect of nerves?

Name some example applications/formulations.

A

The axonal voltage-gated sodium channels.

Topicals (sprays/drops), local injection, nerve block, epidural and spinal anesthesia.

21
Q

Why is it important for local anesthetics to be weak bases?

A

They must be protonated to act on the channel. However, since they generally act intracellularly, they must be uncharged in some fraction to penetrate.

22
Q

Sort these channel states by anesthetic affinity: Unactivated, Activated, Inactive.

What implications does this have for mechanism of action?

A

Activated (open) > Inactive > Unactivated.

Local anesthetics prefer positive membrane potentials and nerves that fire more frequently.

23
Q

Why are local anesthetics less effective during infection or inflammation?

A

The slightly decreased tissue pH reduces the amount of uncharged anesthetic, reducing its penetration and action.

24
Q

Why might cocaine be co-administered with epinephrine?

A

Vasoconstrictors are often co-administered with vasoconstrictors to increase their depth and duration, and to avoid systemic toxicity.

Though, cocaine is already a potent vasoconstrictor alone.

25
Q

Order the following nerve types by their sequence of blockage: Motor neuron, nociceptor, fine touch, crude touch/pressure, cold, warmth

Justify this ordering.

A

Pain > Cold > Warmth > Touch > Deep Pressure > Motor

Anesthetics have stronger response to unmyelinated and small fibers. C fibers are small and unmyelinated, while alpha fibers are large and myelinated.

Not sure why cold comes before warm though–aren’t warm C-fibers?

26
Q

What side effects are seen with local anesthetics, and in what order?

A

First, CNS stimulation occurs (twitches and tremors), followed by CNS depression (drowsiness, coma). CV toxicity follows (decreased inotropy and chronotropy). Death usually occurs due to respiratory or cardiac arrest.

27
Q

How are ester anesthetics inactivated, and what are their special considerations?

How are amide anesthetics inactivated, and what are their special considerations?

A

Esters are inactivated by plasma esterases. They have higher incidences of hypersensitivity.

Amides are inactivated by liver enzymes. So, use caution in patients with liver disease.

28
Q

Cocaine

Is it an ester or amide?

What are its uses?

A

Cocaine

Ester.

It is used for anesthesia of the upper respiratory tract. It is also a potent vasoconstrictor and blocks NET.

29
Q

Procaine

Is it an ester or amide?

What are its uses?

A

Procaine

Ester.

Infiltration anesthesia, otherwise outdated.

30
Q

Tetracaine

Is it an ester or amide?

What are its uses?

A

Tetracaine

Ester.

It is used for spinal, topical, and ophthalmic anesthesia, but not for nerve block. It is a “better” procaine.

31
Q

Benzocaine

Is it an ester or amide?

What are its uses?

A

Benzocaine

Ester.

It is used as a topical for wounds and ulcers. It has very low water solubility, limiting its rate of absorption (safe!)

32
Q

Lidocaine

Is it an ester or amide?

What are its uses?

A

Lidocaine

Amide.

It has very broad uses–topical, nerve block, etc. This the one we’ll probably see most often.

33
Q

Bupivicaine

Is it an ester or amide?

Compare it to lidocaine.

A

Bupivicaine

Amide.

It is more specific for sensory neurons, but is more cardiotoxic. The S-enantiomer is preferable (less toxic).

34
Q

Ropivacaine

Is it an ester or amide?

Compare it to bupivicaine.

A

Ropivacaine

Amide.

It is even more motor-sparing, but less cardiotoxic. Suitable for epidural and regional anesthetic. Marketed as either racemic or just S-enantiomer

M1 PDA Block 3 (Tim) (13 decks)

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