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Neuro > General Anesthesia B&B > Flashcards

General Anesthesia B&B Flashcards

1
Q

what factor determines the potency and onset/offset of an inhaled anesthetic?

A

solubility of gas for blood determines onset/offset - need to saturate blood to generate partial pressure (dissolved = no effect)

solubility of gas for lipids determines potency

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2
Q

Describe how blood solubility affects the efficacy of inhaled anesthetics

A

molecules dissolved in blood (higher solubility) = no anesthetic affect

Molecules NOT dissolved = anesthetic affect

Need to saturate blood to generate partial pressure… So more solubility in blood = longer to take effect

measured by the blood/gas partition coefficient (>1 = more likely to be found in blood, <1 = more likely to be found in alveoli/ gaseous form)

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3
Q

You have two inhaled anesthetics, drug A and drug B. Drug A is less soluble in blood then drug B. Which of the drugs will have a faster anesthetic effect?

A

Less soluble in blood = faster rise in partial pressure = faster anesthetic effect

Drug A will have a faster anesthetic affect

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4
Q

halothane has a blood/gas partition coefficient of 2.3, while desflurane has a blood/gas partition coefficient of 0.42 which of these inhaled anesthetics will have a faster onset of action?

A

> 1 = more likely to be found in blood
<1 = more likely to be found in alveoli/ gaseous form

halothane likes to stay in blood —> SLOW induction
desflurane quickly leaves blood —> FAST induction

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5
Q

How is the potency of an inhaled anesthetic measured?

A

via the oil/gas partition coefficient - represents the lipid solubility of the drug, higher = more potent (Meyer-Overton rule)

but in clinical use by the minimum alveolar concentration (MAC): concentration of anesthetic that prevents movement in 50% of subjects in response to pain

MAC = 1/lipid solubility
… this means low MAC = high potency

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6
Q

Isoflurane has an oil/gas partition coefficient of 98 while desflurane has an oil/gas, partition coefficient of 28. Which inhaled anesthetic is more potent?

A

represents the lipid solubility of the drug, higher = more potent (Meyer-Overton rule)

isoflurance is more potent than desflurane

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7
Q

minimum alveolar concentration (MAC)

A

concentration of anesthetic that prevents movement in 50% of subjects in response to pain

MAC = 1/lipid solubility
… this means low MAC = high potency

MAC changes with age (lower in elderly)

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8
Q

what are the common side effects of all inhaled anesthetics? (5)

A
  1. myocardial depression (low CO)
  2. respiratory depression
  3. N/V
  4. increased cerebral blood flow (high ICP)
  5. decreased GFR
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9
Q

what are the special side effects of each of the following inhaled anesthetic?
a. halothane
b. methoxyflurane
c. enflurane

A

a. halothane: hepatotoxicity (massive necrosis), malignant hyperthermia

b. methoxyflurane: nephrotoxicity (renal toxic metabolite)

c. enflurane: seizures

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10
Q

which inhaled anesthetic carries a risk of hepatotoxicity and malignant hyperthermia?

A

halothane; not really used anymore due to side effects

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11
Q

which 2 drugs can trigger malignant hyperthermia and what is this condition associated with?

A
  1. halothane: inhaled anesthetic
  2. succinylcholine: paralytic (for surgery)

—> fever, muscle rigidity/damage (high CK), tachycardia (high K+), HTN after surgery

due to AD mutation in ryanodine receptors in sarcoplasmic reticulum (Ca2+ channel) —> overactive, ATP consumption, heat generation, tissue damage

tx: dantrolene (muscle relaxant)

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12
Q

A pt receives halothane (inhaled anesthetic) for their surgery. After the surgery, they experience fever, muscle rigidity, and a rapid heart rate. BP shows they are hypertensive. What should they be treated with?

A

malignant hyperthermia: triggered by some anesthetics

—> fever, muscle rigidity/damage (high CK), tachycardia (high K+), HTN after surgery

due to AD mutation in ryanodine receptors in sarcoplasmic reticulum (Ca2+ channel) —> overactive, ATP consumption, heat generation, tissue damage

tx: dantrolene (muscle relaxant)

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13
Q

what are 2 contraindications for use of nitrous oxide as an inhaled anesthetic?

A

NO diffuses rapidly into air spaces and will increase volume

cannot use in patients with pneumothorax or abdominal distention as this can double the cavity size

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14
Q

what kind of drugs are desflurane, sevoflurane, halothane, enflurane, isoflurane, and methoxyflurane?

A

inhaled anesthetics

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15
Q

which barbiturate can be used as a general anesthetic? describe its properties

A

thiopental (Pentothal): binds GABA receptors

HIGH potency (high lipid solubility) + RAPID onset (rapid entry into brain) + ultra SHORT acting (rapidly distributes to muscle and fat)

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16
Q

what kind of drug is thiopental (Pentothal) and what is it used for?

A

barbiturate used for general anesthesia - binds GABA receptors

HIGH potency (high lipid solubility) + RAPID onset (rapid entry into brain) + ultra SHORT acting (rapidly distributes to muscle and fat)

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17
Q

how does the clinical use of midazolam, lorazepam, diazepam, and alprazolam differ when give orally vs intravenously?

A

these are benzodiazepines: bind GABA receptors (increase Cl- influx)

orally = anti-anxiety (anxiolytic)
IV = general anesthesia (sedation, amnesia, anticonvulsant)

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18
Q

name 4 benzodiazepines that can be used for general anesthesia

A

midazolam, lorazepam, diazepam, and alprazolam (”-zolam/zepam”)

bind GABA receptors (increase Cl- influx)

orally = anti-anxiety (anxiolytic)
IV = general anesthesia (sedation, amnesia, anticonvulsant)

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19
Q

what is the treatment for benzodiazepine overdose (ex, midazolam, lorazepam, diazepam, and alprazolam)

A

bind GABA receptors (increase Cl- influx)

Flumazenil is a selective competitive antagonist of the gamma-aminobutyric acid (GABA) receptor and is the only available specific antidote for benzodiazepine (BZD) toxicity

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20
Q

which benzodiazepine is used as general anesthetic for short procedures such as endoscopy?

A

midazolam (Versed) - washes out very quickly

bind GABA receptors (increase Cl- influx)

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21
Q

what is an important consideration when prescribing opioids as general anesthesia or sedatives for procedures? (ex: morphine, fentanyl, hydromorphone)

A

will NOT cause amnesia - the patient will remember everything, so if undergoing a dangerous procedure, should also be given something to cause amnesia

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22
Q

what side effects will patients experience who are given opioids as sedatives or analgesics for procedures? (ex: morphine, fentanyl, hydromorphone)

A

act on opioid (mu) receptors in brain

side effects: decreased respiratory drive, decreased blood pressure, nausea/vomiting, ileus, urinary retention.

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23
Q

what is the effect of opioids bindings Mu receptors? (ex: morphine, fentanyl, hydromorphone)

A

Mu receptors are GPCR, cause increase in K+ efflux which hyper-polarizes the neuron for less pain transmission

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24
Q

which side effects of opioids persist, even after chronic use and tolerance?

A

Constipation and meiosis

25
Q

What are the effects of ketamine?

A

PCP derivative (“angel dust”) - antagonist of NMDA receptors (glutamate)

“Dissociative drug” – patient enters trancelike state, analgesia and amnesia, can increase BP/HR but few respiratory or CV effects

“Emergence reactions” occur afterwards – disorientation, dreams, hallucinations… if given as anesthetic for surgery, co-administer midazolam (benzodiazepine) to mitigate

26
Q

which IV general anesthetic is often co-administered with midazolam (benzodiazepine) to mitigate “emergence reactions,” including disorientation, dreams, and hallucinations?

A

ketamine: PCP derivative (“angel dust”) - antagonist of NMDA receptors (glutamate)

27
Q

what is the effect of etomidate? when is it most often clinically used?

A

IV general anesthetic - modulates GABA receptors to block neuroexcitation

induces anesthesia but NOT analgesia! (patient can still feel pain), but has rapid onset so often used for rapid sequence intubation

relatively hemodynamically stable - good for hypotensive patients

side effect: blocks cortisol synthesis (secondary adrenal insufficiency)

28
Q

which 2 IV drugs are used in combination for rapid sequence intubation in the hospital?

A

etomidate (puts patient to sleep) + succinylcholine (paralyzes patient)

both are rapid onset and wash out quickly

29
Q

what are the effects of propofol as an anesthetic?

A

GABA modulator, causes sedation and amnesia

can cause myocardial depression and hypotension

30
Q

what types of anesthetics are used for induction vs maintenance?

A

IV used for induction (ex: propofol, etomidate, ketamine)

inhaled used for maintenance (ex: propofol, sevoflurane, desflurane)

31
Q

what is the drug rocuronium used for?

A

paralytic used for surgery

32
Q

what are the 4 possible functions of an anesthetic drug?

A
  1. analgesia
  2. loss of consciousness
  3. amnesia
  4. muscle relaxation

4 types: inhaled, IV, local, neuromuscular blockers

33
Q

what are the clinical uses and adverse effects of desflurane, isoflurane, and sevoflurane?

A

halogenated volatile general anesthetics used for maintenance of general anesthesia + induction of general anesthesia in pediatrics

adverse effects: N/V, bronchospasm, reduced systemic vascular resistance (SVR), malignant hypothermia

34
Q

for what aspect of anesthesia are desflurane, isoflurane, and sevoflurane used?

A

halogenated volatile general anesthetics

used for maintenance of general anesthesia + induction of general anesthesia in pediatrics

35
Q

what is the mechanism of action and clinical uses (4) of propofol?

A

GABA agonist used as IV anesthetic

causes sedation, induction + maintenance of general anesthesia, antiemetic (low dose)

side effects: decreased SVR, cardiac inotropy, respiratory drive, ability to protect airway reflexes

36
Q

name an IV anesthetic that can be used as an antiemetic at low dose

A

propofol: GABA agonist

causes sedation, induction + maintenance of general anesthesia, antiemetic (low dose)

37
Q

what is the MOA and clinical use of etomidate?

A

GABA agonist used as IV anesthetic for induction of general anesthesia

side effects: burning on injection, N/V, diminished respiratory drive, dose dependent cortisol suppression

38
Q

what is the MOA and clinical uses (3) of ketamine?

A

NMDA receptor antagonist used as IV anesthetic

used for sedation + induction of general anesthesia + adjunct to general anesthesia

side effects: hallucinations, increased ICP

39
Q

what are 2 important side effects of ketamine?

A

NMDA receptor antagonist used as IV anesthetic (sedation + induction)

side effects: hallucinations, increased ICP

40
Q

name an IV anesthetic which may cause hallucinations as a side effect

A

ketamine: NMDA receptor antagonist

used for sedation + induction of general anesthesia + adjunct to general anesthesia

41
Q

what is the MOA and clinical use of dexmedetomidine?

A

alpha2 agonist used as IV anesthetic

induces sedation + analgesia, also used for attenuation of anesthesia

side effects: bradycardia and possible hypotension

42
Q

name an alpha2 agonist used for sedation and analgesia

A

dexmedetomidine: alpha2 agonist used as IV anesthetic

side effects: bradycardia and possible hypotension

43
Q

how would the following factors affect the pharmacokinetics of local anesthetics?
a. lipophilicity
b. pKa
c. protein binding

A

a. high lipophilicity (hydrophobic) = high potency, longer duration, slower onset of action

b. high pKa = slower onset of action

c. high protein binding = longer duration

44
Q

describe how pH affects the pharmacokinetics of local anesthetics

A

local anesthetics are weak bases which are protonated in acidic pH and neutral in basic pH

the neutral form is required to diffuse to site of action, but charged form is required for activity!! - neutral form enters cells then is trapped within as pronated form, which is able to bind Na+ channels from within

the more acidic the extracellular medium (sepsis, local infection, DKA, etc), the higher the proportion of the charged form

45
Q

sort the following types of nerve fibers as easiest to block with local anesthetics to hardest to block:
A fibers
B fibers
C fibers

A

B fibers = small, myelinated —> easiest to anesthetize

A fibers = large, myelinated —> middle of the road

C fibers = small, unmyelinated —> hardest to block (minimal Na+ channels)

46
Q

injection of local anesthetics where produces greater blood concentration? injection where produces lease blood concentration? [mnemonic]

A

Injection of local anesthetics into very vascular areas leads to greater blood concentrations than the same dose injected into less vascular areas - remember with ICE BALL

Intercostal - greatest max blood concentration
Caudal
Epidural

BrAchial plexus
Lower Legs - least max blood concentration

47
Q

why is epinephrine sometimes mixed with local anesthetics?

A

epinephrine = vasoconstrictor —> slows absorption at injection site to increase blood availability (does not help long-acting agents)

also increases HR, allowing for immediate recognition of intravascular injection —> STOP INJECTING (build up in cardiac muscle —> lethal via arrhythmias)

48
Q

which type of local anesthetic has a shorter duration of action, esters or amides? which is more likely to cause an allergic reaction

A

esters have a shorter duration of action

… also more likely to cause allergic reactions - PABA metabolite can cause hapten formation —> IgE mediated anaphylaxis

49
Q

what occurs in Local Anesthetic Systemic Toxicity (LAST)

A

inadvertent IV injection or systemic absorption of local anesthetics —> bind/inhibit Na+ and Ca2+ channels

build up in cardiac muscle —> lethal via arrhythmias

neurologic signs first, followed by cardiac signs (HTN/tachycardia —> hypotension/bradycardia —> ventricular dysrhythmias)

50
Q

in what state of activity do local anesthetics bind Na+ channels?

A

active or inactive (NOT resting)

cross membrane as neutral, become protonated and trapped within, and bind intracellular aspect of channel

lipophilic, have pKa’s above neutral pH

51
Q

how are esther vs amide local anesthetics eliminated?

A

esthers: plasma pseudocholinesterase breaks down to PABA (4-aminobenzoic acid) and derivatives

amides: metabolized by cytochrome P450 in liver, water soluble metabolizes excreted by kidneys

52
Q

name a local anesthetic used for dental procedures

A

procaine, aka Novocain - has quick onset; esther

53
Q

name a local anesthetic used for emergency C-sections

A

chlorprocaine - short acting with quick onset; esther

54
Q

name an esther local anesthetic that is potent, long-acting, and has a low therapeutic index

A

tetracaine: esther local anesthetic that is potent, long-acting, and has a low therapeutic index

55
Q

name a topical local anesthetic that is associated with risk of methemoglobin

A

benzocaine: esther local anesthetic

methemoglobin causes “chocolate blood”, treat with methylene blue + oxygen

56
Q

name a local anesthetic that is antiarrhythmic at low dose

A

lidocaine: amide, given IV

57
Q

ropivicaine vs bupivicaine

A

both are amide local anesthetics

ropivicaine: long-acting, less cardiotoxic

bupivicaine: very long acting, very cardiotoxic

58
Q

which amide local anesthetic has the lowest pKa, and is thus quickest acting?

A

mepivicaine: low pKa = quick acting

59
Q

sort the following local anesthetics into either esther or amide:
a. procaine
b. mepivicaine
c. lidocaine
d. chlorprocaine
e. benzocaine
f. ropivicaine
g. bupivicaine
h. tetracaine

A

esthers have 1 “i”: procaine, chlorprocaine, tetracaine, benzocaine

amides have 2 “i”: lidocaine, ropivicaine, bupivicaine, mepivicaine

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