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
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)
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
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
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’
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
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
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
9
Q
How does drug movement influence anesthetic recovery?
A
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
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
12
Q
What is CRI?
A
constant rate infusion = not changing rate
13
Q
What is VRI?
A
variable rate infusion = changing rate
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
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
16
Q
What are the different injectable anesthetics?
A
- substituted phenols (propofol)
- neurosteroids (alfaxalone CD-RTU)
- phencyclidine derivative/aryl-cyclohexamines (dissociative) (ketamine)
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
