Week 3 General Anesthetics Flashcards

1
Q

Stage I-Analgesia

A

subsequent amnesia and inability to feel pain

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2
Q

Stage II- Excitement

A

delirium, combative behavior, elevated BP and resp rate; not common now b/c short-acting anesthetic given before

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3
Q

Stage III- surgical anesthesia

A

reg respiration, skeletal muscle relaxation, decrease in eye reflexes and movements, fixed pupils; loss of motor and autonomic response to pain

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4
Q

Stage IV- Medullary paralysis

A

NOT GOOD; depression of respiratory and vasomotor centers; leads to DEATH

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5
Q

Low blood solubility

A

Leads to faster induction time b/c the drug isnt staying in the blood- also leads to faster elimination

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6
Q

Tissue uptake

A

highly vascularized tissues rapidly reach steady state

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7
Q

Adipose tissue

A

accumulates anesthetics more slowly b/c lower perfusion rate- most anesthetics have high lipid solubility

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8
Q

Meyer & Overton Rule

A

higher lipid solubility the more potent the volatile anesthetic

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9
Q

Potency

A

amt of drug required to produce its effect

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10
Q

Efficacy

A

max strength of the effect of the drug @ saturating concentrations (like Vmax?)

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11
Q

Minimum Alveolar Concentrations (MAC)

A

potency of anesthetics; alveolar concentrations that renders 50% of subjects to strong noxious stimulation’ 1 MAC: Nitrous oxide=100%(not possible), Isoflurane=1.4%(much more potent than NO)

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12
Q

Drug elimination

A

lower blood/gas partitioning coefficient & tissue solubility- faster the elimination; clearance by lungs major route of elimination

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13
Q

Analgesia

A

dorsal horn

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14
Q

Sedation

A

frontal cortex

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15
Q

Hypnosis

A

Thalamus

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16
Q

Immobility

A

Ventral horn neurons (motor neurons)

17
Q

MOA- Inhaled anesthetics-volatiles

A

ion channels are important targets; potentiate GABAa, glycine receptors, K+ channels; inhibit glutamatergic ionotropic receptors and neuronal nAChRs- stop movement

18
Q

MOA- Nitrous Oxide

A

blocks NMDA-R like ketamine; powerful analgesic

19
Q

Organ system effects- volatiles

A

CV- decrease BP; Resp- mucous accumulates, decreased response to hypoxia- must be on ventilator; GI-nausea vomitting; CNS- dec metabolic rate, inc. cerebral blood flow & intracranial pressure; Liver/kidneys- dec blood flow; Uterus- dec contractions

20
Q

Organ system effects- N20

A

CV- no change; Resp- diffusional hypoxia, can diffuse into pneumothorax; GI- nausea/vomiting; CNS- inc cerebral blood flow & intracranial pressure; Liver/kidneys- dec blood flow

21
Q

Volatile anesthetics- malignant hyperthermia

A

mutation in Ryanodine receptor- activated by inhaled anesthetic; leads to uncontrolled release of Ca2+ from sarc retic; succinylcholine can also cause it; Tx- dantrolene (blocks Ca2+ release @ ryanodine receptor), cooling, oxygen, correction of acid-base disturbances

22
Q

Premedication (balanced anesthesia)

A

Midazolam (I.V. benzodiazepine)

23
Q

Induction (balanced anesthesia)

A

Fentanyl (IV opioid), Propofol (IV anesthetic), Curare-like neuromuscular blocker (Pancuronium or Succinyl CoA); tracheal intubation

24
Q

Maintenance (balanced anesthesia)

A

Inhalational Anesthetics (combo)- Sevoflurane (not strong analgesic) + Nitrous Oxide (very good analgesic w/ less side effects)

25
Q

Premedication (Total intravenous anesthesia-TIVA)

A

MIdazolam (I.V. benzodiazepine); Give TIVA if malignant hyperthermia has occured before

26
Q

Induction (Total intravenous anesthesia-TIVA)

A

Remifentanil (instead of fentanyl; shorter acting), Propofol

27
Q

NMJ blockade (Total intravenous anesthesia-TIVA)

A

Rocuronium; tracheal intubation after this

28
Q

Maintenance (Total intravenous anesthesia-TIVA)

A

Remifentanil, Propofol (more to keep asleep?)

29
Q

Benzodiazepines (Midazolam)

A

use prior to induction of anesthesia- reduce anxiety, induce amnesia & sedation; used for sedation for non general anesthesia; used in perioperative period; 15-60 min before anesthesia to produce amnesia; given IV; rapid onset & shorter duration of action

30
Q

Opioids (Fentanyl)

A

induction & maintenance in TIVA; epidural anesthesia together w/ local anesthetics; ICU-conscious and deep sedation; potent respiratory depression; chest wall & laryngeal rigidity-impaired ventilation; dec HR & BP

31
Q

Barbiturate anesthetics (Thiopental)

A

lipophilic rapidly entres & depresses CNS (<1min); short acting b/c it diffuses out of brain rapidly; used during induction of anesthesia & deep sedation; NOT good analgesic; dec cerebral metabolism & blood flow; dec cardiac output & BP; potent respiratory depression

32
Q

Propofol

A

most common for induction & maintenance or day surgery; potentiates GABAa receptors; onset rapid as other barbiturates-recovery more rapid; rare postop vomiting; potent resp depression; dec periperheral resistance; dec intracranial pressure; not a good analgesic

33
Q

Good analgesics

A

Nitrous oxide, Ketamine, Fentanyl

34
Q

Ketamine

A

PCP analog; blocks NMDA receptors; GOOD analgesic; catatonia, amnesia, analgesia w/out loss of consciousness; short procedures; ONLY IV anesthetic that increases HR & cardiac output; minimal effect on respiration; inc intracranial pressure; postop hallucinations

35
Q

Etomidate

A

potentiates GABAa receptors; minimal CV depression; used for someone experiencing shock; causes: vomitting, pain on injection, myoclonus; use as anesthetic induction for pts @ risk of hypotension (elderly)

36
Q

Dexmetodine

A

short term sedation of intubated & ventilated ICU pt or during regional anesthesia; alpha adrenergic receptor agonist (tizanidine); analgesia b/c activation of receptors in spinal cord; hypnosis produced’

37
Q

Increase cranial pressure

A

Volatiles (sevoflurane, desflurane, isoflurane), Nitrous oxide, Fentanyl (in head trauma pts), Ketamine

38
Q

Decrease cranial pressure

A

Thiopental, Propofol, Etomidate,