Anesthetic induction agents Flashcards
what is the induction step in the anesthesia protocol
- 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)
why don’t we just administer a long-lasting injectible general anesthetic/induction agent?
- 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
why do we use an induction agent and not just start with an inhalant?
- onset of inhalant is often too slow
- we can get to the sweet spot faster with an induction agent
what are the 4 stages/plames a petient experiences during induction of anesthesia
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
Which stages of induction do we want to avoid and why
Stage 2: patient becomes uncomfortable and difficult to deal with
Stage 4: excess CNS depression can lead to death
Stage 3 of induction - the “sweet spot”
- 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
benefits of using an induction agent istead of inhalent alone
- bypass stage II
- transission from consious to unconsious is very smooth
properties of an ideal induction agent
- 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
induction agents vs analgesics
- analgesics alleviate pain and anxiety but do not make patient unconsious
- induction agents produce unconsiousness but may enhance sunsitivity to pain
the intensity of certain adverse effects of induction agents is proportional to the rate of administration…
- faster administration = worse adverse effects
- slower administration = low or no adverse effects
- rapid administration = potentially fatal
what is the best way to obtain balance of effects when inducing anesthesia
- 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
the development of injectible anesthetic
- 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
3 types of injectable general anesthetics
- Barbituates
- Propofol
- Phencyclidines
Barbituates mechanism of action
- inhibit dissociation of GABA from receptors
- keep GABAa open for longer
- inhibits action potentials
what are the problems with using barbituates as induction agents
- can open GABAa in the absence of GABA, producing possible CNS depression due to low theraputic index
- undergo slow metabolism, leading to adverse effects in CNS & CV system and also maked recovery time long
- partial dose can cause intense CNS excitation, including violent seizure-like activity
Why is it a problem that barbituates undergo slow metabolism
- recovery time is long
- can lead to CNS and CV adverse effects including hypotension and respiratory depression
- patients feel “groggy” during recovery
Propofol - a sedative and general anesthetic
- 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
Propofol mechanism of action
facilitates the efefct of GABA at the GABAa receptor in brain - inhibits APs
adverse effects of Propofol
- 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
Main clinical uses of propofol
- induction prior to transefer to inhaled anesthetic - more commonly used than barbituates today
Phencyclidines (e.g. Ketamine) as induction agents
- derived from phencyclidine (PCP)
- inhibits perception of signals associated with senses
- usually cause pseudo-unconsciousness (eyes open, swallowing, hearing, muscle rigidity, hallucinogenic)
mechanism of action of Ketamine (a phencylidine)
- blocks NMDA receptor - main!!
- can also inhibit GABA receptor (close it)
- stimulates sigma opioid receptors (dysphoria)
CNS effects of Ketamine
- pseudo-unconsciousness
- produce some degree of analgesia
- hypothermia
- amnesia
- hallucinations
why should you never give ketamine without pre-medication
- premedication with a benzodiazapine abolishes emergence delirium
- otherwise would cause excitement and very rough recovery
CV effects of Ketamine
- increases heart rate and blood pressure due to SNS stimulation
- advantageous for “shocky” patients
CV effects of the different IV anesthetics
Barbituates: decrease BP
Propofol: decrease BP
Phencylidines: increase HR and BP