Anesthetic induction agents Flashcards

1
Q

what is the induction step in the anesthesia protocol

A
  • to rapidly and smoothly produce a state of unconsciousness
  • usually with an IV general anesthetic
  • short duration (1-3 min)
  • during this breif period the patient is connected yo a machine hat delivers an inhaled anesthetic (for maintenance)
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2
Q

why don’t we just administer a long-lasting injectible general anesthetic/induction agent?

A
  • high risk if patient stops breathing
  • we can’t remove IV anesthetics (chance of overdose)
  • by switching to inhaled anesthetic, we can rapidly reduce the concentration of inhaled anesthetics via artificial ventilation
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3
Q

why do we use an induction agent and not just start with an inhalant?

A
  • onset of inhalant is often too slow
  • we can get to the sweet spot faster with an induction agent
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4
Q

what are the 4 stages/plames a petient experiences during induction of anesthesia

A

Stage 1 - Analgesia: semiconsciousness and amnesia
Stage 2 - Excitement: struggling, delirium, vomitting, urination, combative behaviour
Stage 3 - Surgical Anesthesis: unconsiousness, regular breathing returns and movement ceases
Stage 4 - Medullary Depression: breathing stops, heart stops, death

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5
Q

Which stages of induction do we want to avoid and why

A

Stage 2: patient becomes uncomfortable and difficult to deal with
Stage 4: excess CNS depression can lead to death

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6
Q

Stage 3 of induction - the “sweet spot”

A
  • knocks out cerebral cortex - patient is unconsious
  • vital support systems like breathing and heart function controlled by the brain stem are still active
  • we perform surgery in this stage
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7
Q

benefits of using an induction agent istead of inhalent alone

A
  • bypass stage II
  • transission from consious to unconsious is very smooth
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8
Q

properties of an ideal induction agent

A
  • painless administration
  • high potency and efficacy
  • minimal cardio-respiratory effects
  • minimal abdominal organ toxicity
  • inhibition of gag reflex
  • rapid and predictable onset
  • rapid metabolism for minimal grogginess during recovery
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9
Q

induction agents vs analgesics

A
  • analgesics alleviate pain and anxiety but do not make patient unconsious
  • induction agents produce unconsiousness but may enhance sunsitivity to pain
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10
Q

the intensity of certain adverse effects of induction agents is proportional to the rate of administration…

A
  • faster administration = worse adverse effects
  • slower administration = low or no adverse effects
  • rapid administration = potentially fatal
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11
Q

what is the best way to obtain balance of effects when inducing anesthesia

A
  • use lowest dose possible that still has an effect
  • combine half dose of opioid and half dose of IV anesthetic
  • opioid = analgesia, no anesthesia
  • IV anesthetic = anesthesia, no analgesia
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12
Q

the development of injectible anesthetic

A
  • first IV anestetics were barbituates (e.g. pentobarbital)
  • long-acting drugs like this had high fatality rates
  • newer IV anesthetics are short-acting non-barbituates
  • newer IV anesthetics are used to induce unconsiousness then transfer patient to an inhalant
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13
Q

3 types of injectable general anesthetics

A
  1. Barbituates
  2. Propofol
  3. Phencyclidines
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14
Q

Barbituates mechanism of action

A
  • inhibit dissociation of GABA from receptors
  • keep GABAa open for longer
  • inhibits action potentials
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15
Q

what are the problems with using barbituates as induction agents

A
  1. can open GABAa in the absence of GABA, producing possible CNS depression due to low theraputic index
  2. undergo slow metabolism, leading to adverse effects in CNS & CV system and also maked recovery time long
  3. partial dose can cause intense CNS excitation, including violent seizure-like activity
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16
Q

Why is it a problem that barbituates undergo slow metabolism

A
  • recovery time is long
  • can lead to CNS and CV adverse effects including hypotension and respiratory depression
  • patients feel “groggy” during recovery
17
Q

Propofol - a sedative and general anesthetic

A
  • one of the most popular IV anaesthetics
  • not likely to activate GABAa in the absence of GABA
  • rapidly metabolizes - smooth recovery
  • can be given in smaller doses if needed
18
Q

Propofol mechanism of action

A

facilitates the efefct of GABA at the GABAa receptor in brain - inhibits APs

19
Q

adverse effects of Propofol

A
  • dose dependent depression of respiration and blood pressure
  • if injected rapidly, apnea (temporary pause in breathing) is longer
  • hypotensionn is greater than other induction drugs
20
Q

Main clinical uses of propofol

A
  • induction prior to transefer to inhaled anesthetic - more commonly used than barbituates today
21
Q

Phencyclidines (e.g. Ketamine) as induction agents

A
  • derived from phencyclidine (PCP)
  • inhibits perception of signals associated with senses
  • usually cause pseudo-unconsciousness (eyes open, swallowing, hearing, muscle rigidity, hallucinogenic)
22
Q

mechanism of action of Ketamine (a phencylidine)

A
  • blocks NMDA receptor - main!!
  • can also inhibit GABA receptor (close it)
  • stimulates sigma opioid receptors (dysphoria)
23
Q

CNS effects of Ketamine

A
  • pseudo-unconsciousness
  • produce some degree of analgesia
  • hypothermia
  • amnesia
  • hallucinations
24
Q

why should you never give ketamine without pre-medication

A
  • premedication with a benzodiazapine abolishes emergence delirium
  • otherwise would cause excitement and very rough recovery
25
Q

CV effects of Ketamine

A
  • increases heart rate and blood pressure due to SNS stimulation
  • advantageous for “shocky” patients
26
Q

CV effects of the different IV anesthetics

A

Barbituates: decrease BP
Propofol: decrease BP
Phencylidines: increase HR and BP