Injectable Anesthetics & Anesthesia Induction Flashcards

1
Q

What are injectable anesthetics?

A
  • majority of these drugs MECHANISM OF ACTION is via potentiation or facilitation of GABA, by their actions at GABA’A’ receptors in the CNS
  • need a high concentration of drug to rapidly reach the site of action (THE BRAIN) for a titratable effect
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2
Q

What are the properties of an ideal injectable anesthetic agent?

A
  • rapid onset of action
  • smooth induction of anesthesia
  • smooth recovery from anesthesia
  • non-irritant to tissues
  • good bioavailability by ALL routes of administration
  • short duration of action
  • non cumulative
  • rapid metabolism
  • no toxic or active metabolites
  • does not cause histamine release
  • minimal cardiorespiratory side effects
  • produces a degree of muscle relaxation
  • produces a degree of analgesia
  • stable in storage
  • stable in solution
  • miscible with other agents
  • inexpensive
  • high therapeutic index (SAFE)
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3
Q

What are the ADVANTAGES of injectable drugs?

A
  • little equipment needed
  • usually easy to administer
  • induction of anesthesia can be rapid & smooth
  • possibly relatively cheap
  • no environmental pollution
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4
Q

What are the DISADVANTAGES of injectable drugs?

A
  • once given, retrieval is impossible
  • patient must be weighed accurately in order to calculate dose
  • when used as the sole anesthetic agent: high dose is necessary to produce sufficient CNS depression to prevent response to surgical stimulus; profound cardiovascular and respiratory depression
  • not well tolerated by: debilitated, hypovolemic, or endotoxemic patients; patients suffering from renal or hepatic disease
  • some drugs have potential for human abuse
  • risk of inadvertent self administration
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5
Q

When do we use injectable anesthetics?

A
  • SEDATION: low doses (sub-anesthetic) can result in profound and reliable sedation ex: “ketamine stun”
  • INDUCTION: MAIN USE; need to be at surgical plane to pass an endotracheal tube into the trachea
  • MAINTENANCE: using the same &/or combination of drugs; “top-ups”; TIVA/PIVA
  • EMERGENCY: to supplement inhalational anesthesia if animal rapidly ‘wakes’
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6
Q

What are the routes of administration of drugs?

A
  • IM: less precision; difficult to titrate effect; best for wildlife anesthesia
  • SUB Q, rectal, oral: too slow; unreliable
  • Intraperitoneal: risk of depositing drug in gut; lab animals
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7
Q

What is IV drug administration?

A
  • ACCURATE, TITRATABLE, RAPID-ACTING
  • injectable anesthetics act in 20-60 secs following injection
  • rapidly achieves surgical plane of anesthesia (Stage 3)
  • bypasses stage 1 & 2 (excitement) w/ correct dose
  • requires restraint & ideally an IV catheter
  • preferred route of administration if possible
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8
Q

What are the pharmacokinetics of IV bolus injection?

A
  • alpha phase: distribution from blood to vessel-rich tissues; heart, brain, lungs, liver, kidneys; lipophilic so uptake into CNS is rapid
  • beta phase: elimination from central compartment (blood); drug leaves the CNS, goes back into blood & animal recovers from anesthetic effects
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9
Q

How does drug movement influence anesthetic recovery?

A
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10
Q

How does the drug concentration in the tissues change during distribution and redistribution over time?

A
  • modern injectable anesthetics have an anesthetic effect lasting 4-10 mins
  • for longer procedures, more injectable drug is given (‘top-ups’) or switch to inhalational drugs
  • recovery from injectable bolus: initially, REDISTRIBUTION - drug from brain to blood & other body systems; ‘hangover effect’ - rapidly metabolized drugs produce little hang over
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11
Q

How are drugs metabolized & excreted?

A
  • anesthetic drugs are handled the same as other exogenous compounds
  • lipid soluble drugs must be converted to water soluble compounds for efficient excretion: PHASE I - oxidation, reduction, hydrolysis; PHASE II - conjugation
  • can produce ACTIVE metabolites: nordiazepam; morphine glucuronide
  • drugs can also be metabolized in other sites as well as the liver: kidney, lungs, gut - PROPOFOL; plasma - REMIFENTANIL, ATRACURIUM
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12
Q

What is CRI?

A

constant rate infusion = not changing rate

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13
Q

What is VRI?

A

variable rate infusion = changing rate

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14
Q

How do we administer drugs to INDUCE anesthesia?

A
  • goal is to achieve stage 3 anesthesia & bypass the excitement phase (anesthesia stages 1 & 2)
  • titrate “to effect” in SMALL ANIMALS: consider premedication - 20-80% dose reduction depending on premedication
  • consider physical status of your patient
  • slow injection (60-120 seconds) OR give 1/3 to 1/2 of calculated dose: wait for maximum effect; proceed further w/ increments until desired effect
  • in LARGE ANIMALS - give whole dose: this is for safety purposes - you DO NOT want a partially anesthetized Eq
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15
Q

What is TIVA and PIVA?

A
  • Total IntraVenous Anesthesia (TIVA): one or more drugs can be used; can be slow to change depth of anesthesia
  • Partial IntraVenous Anesthesia (PIVA): use injectable drugs to supplement inhalational anesthesia
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16
Q

What are the different injectable anesthetics?

A
  1. substituted phenols (propofol)
  2. neurosteroids (alfaxalone CD-RTU)
  3. phencyclidine derivative/aryl-cyclohexamines (dissociative) (ketamine)
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17
Q

What is propofol (alkyl phenol)?

A
  • acts on GABA’A’ receptors in the CNS to produce anesthesia
  • induction smooth and rapid: onset 40-90 secs & one dose lasts 5-10 minutes
  • short duration of action depends on REDISTRIBUTION: EXTRA-HEPATIC sites of metabolism - kidneys, lungs, GI tract
  • recovery is fast & smooth
  • used for induction & maintenance (TIVA): minimal accumulation
  • no analgesia
  • occasionally pain upon IV injection
  • no tissue damage if injected perivascularly
  • vehicle is a lipid emulsion (intralipid): will grow bacteria - discard w/in 24 hrs of opening
  • PropoClear - lipid free formulation
  • Propoflo 28 - contains preservative & is labelled for use up to 28 days after opening
18
Q

What is propofol’s effect on the cardiovascular system?

A
  • cardiovascular depression if DOSE DEPENDENT
  • myocardial depression
  • venodilation = decreased BP
  • resets baroreceptor reflex - increases HR with drop in BP does NOT occur
  • AVOID in hypovolemic animals or patients with cardiac disease
19
Q

What is propofol’s effect on the respiratory system?

A
  • respiratory depression is DOSE DEPENDENT
  • post-induction apnea
  • post-induction cyanosis
  • supplement oxygen or pre-oxygenate
  • mild bronchodilation
20
Q

What do you sometimes see on induction or recovery with propofol?

A
  • occasionally in Ca: limb stiffness, paddling movements, opisthotonus, twitching
21
Q

what is propofol recommended for?

A
  • C-SECTIONS
  • CEREBROPROTECTION - reduces CBF & cerebral metabolic rate
  • patients w/ compromised LIVER function
22
Q

How does propofol work in Fe?

A
  • reduced capacity for glucuronide conjugation
  • propofol infusion - recovery from anesthesia is delayed
  • repeated administration over several days: hemolysis & Heinz Body formation; clinical relevance of this has been questioned
23
Q

What is alfaxalone CD-RTU?

A
  • acts on GABA’A’ receptors in the CNS to produce anesthesia
  • induction is smooth & rapid (onset 15-45 secs & 1 dose lasts 5-10 mins)
  • short duration of action depends on REDISTRIBUTION
  • recovery is fast & quality improves w/ premedication
  • used for induction & maintenance (TIVA) - rapidly metabolized: no accumulation
  • no analgesia
  • no pain upon injection
  • no tissue damage in injected perivascularly
  • similar effects to propofol: longer shelf life; clear solution
  • can be administered IM
24
Q

How does alfaxalone act on the cardiovascular system?

A
  • cardiovascular depression is DOSE DEPENDENT
  • hypotension - combination of myocardial depression & some peripheral vasodilation
  • compensation via reflex tachycardia (Baroreceptor reflex)
25
Q

How does alfaxalone act on the respiratory system?

A
  • respiratory depression is DOSE DEPENDENT
  • post-induction apnea
26
Q

What is alfaxalone good for?

A
  • good muscle relaxant
  • produces reliable sedation in Fe when given IM
  • excellent in reptiles (IM)
27
Q

What is co-induction?

A
  • combine alfaxalone OR propofol w/ another agent to minimize the amount required: decrease dog dependent cardiovascular & respiratory side effects
  • typical agents include: benzodiazepines (midazolam or diazepam); ketamine
28
Q

What is Ketamine?

A

Phencyclidine derivative
- is a DISSOCIATIVE ANESTHETIC AGENT - interrupts information reaching higher centers of the brain
- different from GABA’A’ agonist drugs: cataleptoid state w/ slow nystagmus; muscle rigidity w/ higher doses, maintains cranial nerve reflexes - gag, swallow, & palpebral & central eye positions in Ca & Fe (no ventral-medial rotation)
- racemic mixture: S(+) & R(-) isomers; S(+) isomer is 2-4x more potent

29
Q

How is ketamine used in vet med?

A
  • popular in vet med (high margin of safety)
  • slow onset (30-90 secs) & longer duration (20-30 mins)
  • USED FOR INDUCTION & MAINTENANCE & ANALGESIA - will accumulate
  • can be administered: IM, IV, SQ, TM
  • profound ANALGESIA: somatic > visceral; wind up pain (NMDA antagonist)
  • sub-anesthetic doses can be used for reliable SEDATION
  • neither anti- nor pro-convulsant
30
Q

What is the mechanism of action for ketamine?

A
  • NMDA receptor antagonist (analgesic effects)
  • CNS voltage dependent NA+, K+, Ca2+ channels
  • depression of CNS acetyl choline receptors
  • some action at GABA’A’ receptors
  • depression of nociceptive cells in the dorsal horn of the spinal cord
31
Q

Side effects with ketamine?

A
  • muscle rigidity (catatonia): ALWAYS combine with a muscle relaxant (benzodiazepine OR a2-agonist)
  • AVOID in FE w/ compromised renal function: excreted as the active metabolite (norketamine) via kidneys
  • auditory and visual stimuli are disturbed during recovery to cause ‘emergence delirium’
  • USE WITH OTHER DRUGS TO REDUCE SIDE-EFFECTS: alpha2 agonists, benzodiazepines, acepromazine
32
Q

What effects does Ketamine have on the cardiovascular system?

A
  • healthy animals = indirect mild cardiovascular stimulation: sympathomimetic effects last for 2-15 mins; increase in cardiac work & myocardial oxygen consumption; AVOID in FE w/ hypertrophic cardiomyopathy
33
Q

What might you see in critically ill patients OR those that are catecholamine depleted with the use of ketamine?

A
  • may see mild myocardial depressant effects
34
Q

What effects does Ketamine have on the respiratory system?

A
  • minimal respiratory depression
  • bronchodilation
  • laryngeal & pharyngeal reflexes are preserved
  • irregular or periodic breathing patterns -> apneustic breathing
35
Q

What behavioural side effects might you see with Ketamine?

A
  • can cause rough recoveries (head shaking, vocalization, dysphoria, salivation)
36
Q

What are the major goals of combining other drugs with ketamine?

A
  • decrease the amount of ketamine needed
  • eliminate unwanted side effects (improve recovery quality)
  • produce good skeletal muscle relaxation
  • improve visceral analgesia
  • prolong the period of anesthesia/ immobilization
37
Q

What is ketamine/diazepam (“Ket-Val”)?

A
  • IV induction agent in: Ca, Fe, neonatal foals, Eq, calves, & cattle
  • slow onset (30-90 secs)
  • short acting & rapid recovery
  • MINIMAL CARDIOVASCULAR SIDE EFFECTS
  • MINIMAL RESPIRATORY SIDE EFFECTS: induction apnea can occur
  • DO NOT USE FOR C-SECTIONS: diazepam accumulates in neonates
  • less side effects than a2/ketamine
38
Q

What is a2 agonist + ketamine?

A
  • xylazine + ketamine
  • dexmedetomidine + ketamine + opioid
39
Q

What is xylazine + ketamine?

A
  • good combination in large animals (Eq, cattle; IV)
  • reliable for wildlife immobilization (IM)
  • analgesia, muscle relaxation, & narcosis
  • potent cardiopulmonary depression
  • not recommended for routine use in Fe & Ca
40
Q

What is dexmedetomidine + ketamine + opioid?

A
  • “kitty-magic”
  • wildlife or game ranch animals
  • supportive care (provide O2)
  • monitor closely
  • a2 reversible (atipamezole)
41
Q

What is induction apnea?

A
  • usually observed after a rapid bolus of IV induction agent
  • apnea or hypoventilation result in: poor uptake of maintenance inhalant anesthetic; poor transition to maintenance phase (stable plane) of inhalant anesthesia
  • once IV induction agent is redistributed - animal wakes up
  • assist ventilation until spontaneous ventilation returns (ensure plasma inhalant concentration is adequate)
  • once induction agent wears off, inhalant plasma concentration should be enough to keep patient anesthetized
  • apnea can be avoided by titrating to effect