Anesthetics Flashcards

1
Q

Nitrous oxide

A
  • inhaled general anesthetic
  • low blood solubility –> fast on/off set
  • potent analgesic: 20%
  • weak anesthetic due to low lipid solubility
  • few negative features: no cardiac arrhythmias, seizures or hepatic/renal toxicity
  • rarely ever used alone, not safe to do so
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2
Q

Halothane

A
  • inhaled general anesthetic
  • prototype halogenated hydrocarbon
  • high lipid solubility = potent anesthetic
  • weak analgesic, use with nitrous oxide or other potent analgesic

concerns:

  • relaxes smooth muscle so not good for delivery of baby
  • malignant hyperthermia (therapy: dantrolene)
  • hepatic necrosis

Effects during stage 3 surgical anesthesia:

  • CV - hypotensive, neg inotroph, depresses baroreceptor with gradual sympathetic activation, bradycardia, can induce re-entrant cardiac rhythms, increased cardiac sensitivity to epinephrine-induced cardiac arrhythmias
  • increased response to skeletal muscle relaxants - reduces need for muscle relaxant. this is a problem for neurologic patients (myasthenia gravis)

Post surgical effects:

  • recovery is slow so Stage II delirium may occur
  • hepatotoxicity due to metabolites (bromide)/preservatives
  • post-op shivering/heat loss
  • -> Halothane has been replaced by newer halogenated hydrocarbons
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3
Q

Dantrolene

A

therapy for malignant hyperthermia, a rare congenital condition. First the facial muscles become rigid, then the muscles throughout the body become rigid, activated skeletal muscle increases hyperthermia –> tissues become damaged

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4
Q

Enflurane

A
  • inhaled general anesthetic
  • more stable than halothane
  • less neg inotropic effect on the heart
  • lower incidence of severe cardiac arrhythmias
  • greater decline of skeletal muscle tone
  • no malignant hyperthermia or hepatic necrosis

Post surgical effects:

  • at doses greater than MAC, EEG signs of seizures, avoid in epileptics
  • metabolized to free F- but not sufficient to cause renal toxicity
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5
Q

Isoflurane

A
  • inhaled general anesthetic
  • less soluble in blood than halothane and enflurane which means faster on/offset
  • less neg inotropic action, dilates coronary arteries, less sensitization of the heart to epinephrine-induced arrhythmias
  • not a convulsant
  • enhances relaxation of skeletal muscle

Concerns:

  • irritating to respiratory tract - IV induction overcomes this
  • hypotension during stage III surgical anesthesia
  • respiratory depression and decreased ventilatory response to hypoxia or hypercarbia often necessitates assisted ventilation
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6
Q

Desflurane

A
  • inhaled general anesthetic
  • blood solubility similar to nitrous oxide, therefore fast on/offset
  • very potent - MAC: 6
  • no serious cardiac arrhythmias
  • no malignant hyperthermia
  • 0.02% metabolized means fewer toxic metabolites to cause renal or hepatotoxicity
  • no seizure like effects
  • sensitizes skeletal muscle to relaxants
  • pungent odor and is irritating to the respiratory tract, induce with IV
  • circulatory effects resemble isoflurane
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7
Q

Sevoflurane

A
  • inhaled general anesthetic
  • low blood solubility –> rapid on/offset
  • potent: MAC 2%
  • less irritating to the respiratory tract

Problems:

  • 3% of a dose is metabolized but while plasma F increases, there are no reports of kidney or liver toxicity
  • was degraded in carbon dioxide absorbers (inhalation apparatus) to olefin which is nephrotoxic. nowadays, new inhalation apparatuses are used that won’t cause this.
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8
Q

Thiopental

A
  • IV general anesthetic
  • Barbiturate aka derivative of barbituric acid
  • placed in alkaline solution, must be injected slowly
  • short duration after single dose
  • potent anesthetic but poor analgesic
  • mechanism: potentiate the inhibitory effects of GABA

Effects during stage 3 surgical anesthesia:

  • little serious effect on the heart or vasculature in the absence of hypercarbia or hypoxia
  • reduces cerebral blood flow and intracranial pressure, good for neurosurgery

Recovery/Toxicity:

  • post-op shivering, pain
  • contraindicated in variegate or acute intermittent porphyria, otherwise will experience irreversible demyelination/nerve damage
  • post surgical muscle pain when combined with depolarizing blocker like succinylcholine
  • liver metabolism, cross tolerance with ethanol
  • ion trapping for overdose – alkalinize the blood or urine
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9
Q

Benzodiazepines

A
  • IV general anesthetic
  • Diazepam, Lorazepam, Midazolam
  • antidote = flumazenil
  • causes sedation, reduction of anxiety, and amnesia
  • used alone when analgesia is not required
  • not analgesic
  • severe CV and resp depression when combined with opioids
  • used to control seizures brought on by local anesthetic techniques
  • mechanism: potentiate the inhibitory effects of GABA
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10
Q

Flumazenil

A

antidote for benzodiazepines (diazepam, lorazepam, midazolam)

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11
Q

Propofol

A
  • IV general anesthetic
  • more rapid in action than barbiturates
  • not an analgesic, may be antiemetic
  • metabolized in the liver and extra hepatic pathways; half life is less than thiopental so cleared faster
  • more neg inotropic effect on the heart than thiopental
  • allergic reaction associated with vehicle
  • expensive
  • mechanism: potentiate the inhibitory effects of GABA
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12
Q

Picrotoxin aka PTX

A
  • neurotoxin

- agonist to GABA receptor

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13
Q

Etomidate

A
  • IV general anesthetic
  • sedative/hypnotic, not analgesic
  • high safety index
  • widely used in emergency settings for Rapid Sequence Induction of anesthesia: give etomidate and muscle relaxant like succinylcholine or rocuronium to relax the oropharynx, larynx, and diaphragm (for rapid incubation of patients)
  • minimal CV and resp depression
  • very short duration of action
  • causes nausea and vomiting if pt did not fast (which is often the case if used in emergency situations)
  • pain on injection of glycol formulation
  • myoclonus (rigidity of skeletal muscle)
  • suppresses corticosteroid synthesis
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14
Q

Ketamine

A
  • IV general anesthetic
  • drug of abuse
  • causes dissociative anesthesia, sedation, immobility, amnesia, and analgesia
  • mechanism of action: inhibits the NMDA type glutamate receptor
  • may increase muscle tone
  • good for trauma surgery since BP and resp are well maintained and heart rhythm is stable
  • can be used to treat chronic pain (reflex sympathetic dystrophy - pain, swelling, vasomotor dysfunction of an extremity)
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15
Q

Droperidol + Fentanyl

Brand name: Innovar

A

Neuroleptic/Opioid combo

Neuroleptic (Droperidol) = tranquilizing, adrenergic blocker having antiemetic and anticonvulsant effects

Opioid (Fentanyl) = short acting meperidine derivative 50-100 times more potent than morphine

Can be used alone or together

Problems:

  • abuse potential
  • Droperidol lasts longer than the fentanyl, may need booster to get analgesic effect of the opioid, which can lead to overdose with Droperidol
  • can use for chest wall spasms. treatable with succinylcholine
  • respiratory depression can be severe - must avoid in asthmatic, myasthenia or PD patients
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16
Q

Opioids

A
  • morphine, meperidine, fentanyl, sufentanil, alfentanil
  • causes resp depression, hypotension, post-op nausea and vomiting
  • antidote: naloxone
  • amnesia is poor so may give benzodiazepine too to produce retrograde amnesia
17
Q

Cocaine

A
  • ester local anesthetic

- upper resp tract, vasoconstrictor, toxic, abuse potential

18
Q

Procaine

A
  • local anesthetic
  • prototypic ester local anesthetic: all other ester LA’s are compared to procaine in terms of their duration of action and potency
  • low potency
  • short duration, slow onset
  • infiltration block
19
Q

Tetracaine

A
  • ester local anesthetic
  • 16x more potent than procaine and has longer duration of action
  • used for spinal block, topically for the eye, toxic because of slow metabolism
20
Q

Lidocaine

A
  • prototypic amide local anesthetic

- good to use lidocaine or other amide local anesthetics for people with allergies to LA’s

21
Q

Edrophonium

A
  • reversible AChE inhibitor
  • increase force of muscle contraction; useful in treating myasthenia graves, glaucoma, and overdose with competitive neuromuscular blocking drugs
  • toxic effects: depolarization block, SLUDGE
22
Q

Neostigmine

A
  • reversible AChE inhibitor
  • increase force of muscle contraction; useful in treating myasthenia graves, glaucoma, and overdose with competitive neuromuscular blocking drugs
  • toxic effects: depolarization block, SLUDGE
23
Q

Nerve gases (Soman, Sarin, etc)

A
  • irreversible AChE inhibitor
  • increase force of muscle contraction; useful in treating myasthenia graves, glaucoma, and overdose with competitive neuromuscular blocking drugs
  • toxic effects: depolarization block, SLUDGE
  • antidotes: atropine, pralidoxime
24
Q

Botulinum toxin (Botox)

A
  • irreversible AChE inhibitor
  • increase force of muscle contraction; useful in treating myasthenia graves, glaucoma, and overdose with competitive neuromuscular blocking drugs
  • toxic effects: depolarization block, SLUDGE
25
Q

Curare and Semisynthetic Alkaloids

A
  • prototype competitive neuromuscular receptor blocker (AchR)
  • slower on/offset of action than newer agents
  • induces histamine release (newer agents don’t)
  • blocks ganglia (newer agents don’t)
26
Q

Mivacurium (Benzylisoquinolines)

A
  • competitive neuromuscular receptor blocker (AchR)
  • little muscarinic or ganglionic AchR block
  • metabolized by cholinesterases
  • short duration of action
  • good substitute for succinylcholine
27
Q

Pancuronium

A
  • prototype steroid neuromuscular receptor blocker (AchR)
  • blocks muscarinic AChR –> tachycardia
  • long duration like curare (problem) but more potent
28
Q

Rocuronium

A
  • steroid neuromuscular receptor blocker (AchR)
  • fast on/offset
  • good substitute succinylcholine
  • antidote: Suggamedex; chelates Rocuronium and terminates its action
29
Q

Succinylcholine

A
  • competitive neuromuscular receptor blocker (AchR)
  • also has intrinsic activity for the AchR –> danger, hyperkalemia for burn or other severely traumatized patients (trauma patient, in particular burn patient, and you give succinylcholine - they may have receptors not only at the muscle endplate but also all along the muscle surface. This is called denervation hypersensitivity. Succinylcholine activates all the receptors release of potassium in the blood. High potassium levels can causes cardiac arrhythmias, which can be fatal.)

2 phases of block:
Phase 1: depolarization block excitation, precedes flaccid paralysis
Phase 2: desensitization block

  • primary advantage: short duration due to metabolism by cholinesterase’s
  • drug of choice to arrest laryngospasm
  • stimulates autonomic ganglia
  • stimulates cardiac muscarinic AChR
  • slight histamine release

Drugs can interact with systems in 2 ways: 1. affinity (must bind to the receptor) 2. intrinsic activity (activates receptor then depolarization blockade)
Succinylcholine has both affinity and intrinsic activity. Curare only has affinity.
Problem: doing eye surgery, produce muscle paralysis with succinylcholine. It is short duration so you must give repeated dose which may activate/contract those muscles, could cause damage.

30
Q

Diazepam

A
  • centrally acting spasmolytic

- potentiates GABA-A receptor response in CNS and spinal cord

31
Q

Baclofen

A
  • centrally acting spasmolytic
  • mimics GABA effect on GABA-B receptors which increases potassium permeability to hyperpolarize nerve terminals and decrease the release of excitatory transmitters
32
Q

Progabide

A
  • centrally acting spasmolytic