Anesthesia, NMB, and Local Flashcards

1
Q

Define: blood:gas ratio

A

How much of the drug is bound to protein in the blood (inactive): how much of the drug is free molecules (active)

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2
Q

Define: MAC

A

minimal alveolar anesthetic concentration (aka potency): concentration of inhaled drug as a percent of inspired air at which 50% of the population will be TKO’d

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3
Q

Characteristics that will increase MAC/decrease potency

A

hyperthermia, red hair, hypernatremia, increased NTs

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4
Q

Characteristics that will decrease MAC/ increase potency

A

hypothermia, old age, opioids, hyponatremia, lipid soluble, pregnancy/postpartum

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5
Q

What can you do to increase uptake and distribution of an anesthetic

A
  • increase partial pressure of drug in inspired air
  • increase alveolar ventilation
  • decrease functional residual capacity
  • decrease blood solubility
  • decrease CO
  • 2nd gas effect
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6
Q

define: second gas effect

A

give one gas to decrease lung volume, give a second less potent drug to maintain anesthesia

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7
Q

examples of inhaled anesthetic

A

NO2, Halothane (fluranes)

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8
Q

examples of “fluranes”

A

isoflurane, desflurane, sevoflurane

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9
Q

CNS effects of inhaled anesthetics

A

dose dependent depression of EEG, sensory/motor potentials, cerebral metabolism rates; increase in cerebral blood flow > ICP

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10
Q

CVS effects of inhaled anesthetics

A

decrease in systemic resistance and mean arterial pressure, redistribution of blood flow, Iso and Des increase HR

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11
Q

Respiratory effects of inhaled anesthetics

A

decreased tidal volume and reflex to hypoxia; increased respiratory rate and relaxation of smooth muscle

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12
Q

Neuromuscular effects of inhaled anesthetics

A

relaxed skeletal muscle, malignant hyperthermia

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13
Q

Thiopental and Methohexital

  • class
  • mechanism
  • use
A
  • Barbituate
  • GABA agonist, NMDA-glutamate antagonist
  • hypnosis/sedation with rapid onset/short duration > induce anesthesia
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14
Q

Propofol

  • mechanism
  • use
  • side effects
  • consideration
A
  • GABA agonist, alpha2 antagonist
  • sedation and hypnosis, antiemetic
  • propofol infusion syndrome: met acidosis, heart failure, rhabdomyolysis, hyperkalemia, renal failure
  • allergies to soy and egg
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15
Q

Etomidate

  • mechanism
  • use
  • side effects
A
  • GABA agonist
  • elderly or minimal cardiac reserve
  • pain on administration, PONV, involuntary myoclonic movement, decreased cortisol
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16
Q

Ketamine

  • mechanism
  • use
  • side effects
A
  • no idea, dissociative anesthesia
  • cardiovascular stimulation, people who are bleeding out/hypotensive
  • dilerium, hallucinogen, nightmares, nystagmus, salivation, lacrimation
17
Q

Dexmedetomide

  • mechanism
  • use
A
  • a2 agonist, natural sleep

- morbidly obese patients

18
Q

Succinylcholine

  • class
  • mechanism
  • side effect
A
  • depolarizing NMB
  • binds to ACh receptors, ACh agonist
  • dysrhythmia, sludge, malignant hyperthermia, hyperkalemia
19
Q

‘Curoniums’

  • class
  • mechanism
  • reversal
A

nondepolarizing NMB

  • blocks ACh receptors
  • AChE inhibitors
20
Q

what is unique about Atracurium

A

histamine release > hypotension and tachycardia

21
Q

what is unique about pancuronium

A

can’t use with renal insufficiency

22
Q

what is unique about rocuronium

A

can be reversed by sugammadex

23
Q

Reversal of NMBs

A

AChE inhibitors (edrophonium, neostigmine, pyridostigmine) and anti-muscarinics (glycopyrrolate)

24
Q

Local anesthetics

  • active form
  • mechanism of action
A

weak base: nonionized form travels across the membrane, ionized form is active within the cell. Blocks the binding site of the inactivated sodium channel

25
Q

Two types of local anesthetics with examples

A

esters (procaine, cocaine, benzocaine) and amides (lidocaine, bupivacaine, and mepivacaine)

26
Q

Which nerves are the most sensitive to local anesthetics

A

nerves with the smallest diameter, most myelination, and fastest firing rate: Type B > Type C > Adelta > Agamma and Abeta> A alpha

27
Q

Nerve type responsible for sharp pain

A

Adelta

28
Q

Nerve type responsible for dull pain

A

C

29
Q

What factors influence the absorption of a local anesthetic

A

most absorption in highly vascular tissue, lipid solubility, presence of alpha1 agonists

30
Q

How do you keep the local anesthetics from spreading into systemic circulation

A

administer with an alpha 1 agonist

31
Q

which anesthetic comes with it’s own alpha agonist

A

cocaine: it is a norepi reuptake inhibitor, thus more norepi in nerve terminals, more alpha stimulation

32
Q

where does metabolism of local anesthetics take place

A

esters: tissue esterases
amides: liver amidases

33
Q

special considerations of local anesthetic metabolism

A

esterases have high phenotypic variation, there are slow and fast metabolizers-> watch your patient
amides need a properly functioning liver

34
Q

Local anesthetic, systemic toxicity

A

nervous toxicity, cardiovascular toxicity, methemoglobinemia

35
Q

LA early CNS toxicity

A

excitation: decreased inhibition, talkativeness, sensory disturbance, restless, tremor

36
Q

LA late CNS toxicity

A

depression: lethargy, hypotension, bradycardia, decreased respiratory rate, seizure

37
Q

LA cardiotoxicity

A

Bupivacaine: reduced cardiac conductivity, excitability, contractility, arrhythmia, hypotension, bradycardia

38
Q

Local toxicity for LAs

A

Neuronal injury, transient neurologic symptoms (lidocaine), allergies (esters)