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Anesthesiology 398 and 466 > Lecture 5 Preanesthetic Medications and Induction Agents Part 1 > Flashcards

Lecture 5 Preanesthetic Medications and Induction Agents Part 1 Flashcards

1
Q

What are Factors To Consider When Selecting A Preanesthetic Medication

A
  1. Species
  2. Health status of the patient
  3. Pain – existing and expected
  4. Temperament
  5. Duration of procedure
  6. Anticipated side effects of drugs administered
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2
Q

What are the 3 types of analgesics for preanesthetics

A
  1. Opioids
  2. Dissociatives
  3. NSAIDS
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3
Q

What are the 2 types of anticholinergic drugs used in preanesthetic

A
  1. Atropine
  2. Glycopyrrolate
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4
Q

What are the 3 types of Neuroleptics, Tranquilizer – Sedative, Amnesic medications for preanesthetics

A
  1. Phenothiazines
  2. Alpha-2 agonists
  3. Benzodiazepines
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5
Q

Should animals be sedated without preanesthetics?

A

“No patient should ever be anesthetized without the benefit of preanesthetic medications.”

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6
Q

What are advantages of using preanesthetics

A
  1. Chemical restraint => ↓ patient & staff stress, easier patient handling for IV catheterization
  2. ↓ stress, ↓ catecholamines => ↓ risk of arrhythmias
  3. ↓ induction & inhalant anesthetic doses => ↓ dose dependent CV/resp depression
  4. Pre-emptive analgesia
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7
Q

What are disadvantages of using preanesthetics

A
  1. Bradycardia – alpha-2 agonists, opioids
  2. Hypotension – acepromazine
  3. Excitement/dysphoria – opioids, benzodiazepines
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8
Q

What are the Mu-, kappa agonists used as preanesthetics

A
  1. Hydromorphone
  2. Fentanyl
  3. Morphine
  4. Methadone
  5. Oxymorphone
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9
Q

What is a Mixed agonist(kappa)/antagonist (Mu) used as a preanesthetic

A

Butorphanol

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10
Q

What is the Partial mu agonist used as a preanesthetic

A

Buprenorphine

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11
Q

What are the reversal drugs used for opoid analgesics

A
  1. naloxone
  2. naltrexone
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12
Q
  1. What type of analgesia do Opioids cause
  2. How much sedation (mild, moderate, heavy)?
A
  1. Analgesia – somatic & visceral
  2. Mild sedation when used alone (normal/healthy patients)
    • Combined with sedative/tranquilizer
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13
Q

What are the mild cardiovascular effects of opoids

A
  1. ↓ HR due to ↑ vagal tone => anticholinergic
  2. Little/no effect on vasculature (histamine release)
  3. Little/no effect on cardiac contractility
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14
Q
  1. What do opoids do to the MAC of inhalant?
  2. Are they respiratory stimulants or depressents
A
  1. ↓ MAC of inhalant** (agonist >> partial or agonist/antag.)
  2. respiratory depression
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15
Q
  1. A full opoid agonist stimulates which receptors?
  2. Does the dose change its analgesic effect?
A
  1. Mu (u) and Kappa (K) receptors
  2. increased dose increases analgesic effect
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16
Q
  1. How do agnoist-antagonist opoids bind to their receptors?
  2. Does it provide more or less analgesia compared to a full agonist?
  3. What happens if you use it with an agonist opoid?
A
  1. Will be an agonist for one receptor and antagonist for the other
    • ex- butorphanol is an agonist at K receptors and antagonist at u receptors
  2. Decreased analgesia vs full agonists
  3. Will increase the dose of full agonist required to achive maximal analgesic effects
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17
Q
  1. How do partial mu agonists bind to its receptor?
  2. Does it provide more or less analgesia compared to a full agonist?
  3. What happens if you use it with a full agonist?
A
  1. will only bind to mu receptors
  2. produces a reduced maximal analgesic effect compared with a full agonist
  3. a large dose of partial agonist will block the receptor actions of a full agonist, moving its dose-response curve to the right and depressing its maximal analgesic effect
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18
Q

Regarding Butorphanol:

  1. Do you get sedation with it?
  2. Do you get Analgesia?
  3. Is there a ‘ceiling effect’
A
  1. Mild sedation
    • Sedation lasts 1-2 hours, analgesia ~90min.
  2. analgesia
  3. There is a ‘Ceiling effect’
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19
Q
  1. compared to mu agonists, how does butorphanol compare with heart effects?
  2. Respiratory?
  3. Analgesia?
  4. Nausea?
A

Compared to mu agonists, LESS:

  1. Bradycardia
  2. Respiratory depression
    • Panting (seen at higher doses)
  3. Analgesia, MAC sparing
  4. Nausea, no vomiting
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20
Q

How do we use butorphanol in dogs and cats?

A
  1. Alone (dogs) or with sedative/tranquilizer
  2. Non- or mildly painful procedures
    • Imaging, minor surgical procedure
    • Pre-med to avoid vomiting, full agonist to follow
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21
Q
  1. How do we use butorphanol in horses?
  2. Large ruminants?
  3. Small ruminants?
A
  1. Horses
    • With alpha-2 agonist for pre-med
  2. Large Ruminants
    • during/after induction (vocalization)
  3. Ruminants Small
    • as premed + benzodiazepine
22
Q
  1. Regarding Buprenorphine, do you get sedation?
  2. Analgesia?
A
  1. Little sedation,
  2. mild-moderate analgesia
23
Q
  1. How long is the onset of Buprenorphine
  2. How long is the duration?
  3. Is there a ‘Ceiling effect’
A
  1. Slow onset => 30-45min.
  2. Duration => Dogs: 4-10 hours, Cats: 6-12 hours
  3. There is a ‘Ceiling effect’
24
Q
  1. Does Buprenorphine have a weak or strong affinity for mu receptor?
  2. If you give it before surgery, can you easily give other types of opoids?
  3. Can you give it as a pre-med on a painful procedure?
  4. Is it reversable?
A
  1. Strong affinity for mu receptor
    • ‘Sticky’ to mu receptor
  2. is difficult to give them more opiods because the mu receptor is already blocked
    • ‘antagonize’ other opioids, exert ITS effect
  3. Do NOT use as pre-med if painful procedure
  4. difficult to reverse
25
Q
  1. What is the dose for Buprenorphine in small animals?
  2. Compared to mu agonists, how does it affect:
    • Respiration
    • Panting
    • HR
    • Analgesia
    • Nausea
A
  1. 01 - .04 mg/kg
  2. Compared to mu agonists, LESS:
    • Respiratory depression
    • Panting (seen at higher doses)
    • Bradycardia
    • Analgesia (but better than butorphanol), MAC sparing
    • Nausea, no vomiting
26
Q
  1. What is the long acting buprenorphine drug?
  2. Dose?
  3. What limits its use?
A
  1. Simbadol
  2. 0.24mg/kg SubQ, SID
  3. Use is limited by expense ($29/mL)
    • 5.0kg cat => 0.2mg/kg => 0.3mL = $10
    • 30kg dog => 0.2mg/kg => 2.0mL = $60
27
Q
  1. What are the 4 full mu agonists with similar properties and effects?
  2. What severity of pain does it work on?
  3. What are the duration of actions
A
  1. Hydromorphone, Morphine, Oxymorphone, Methadone
  2. Moderate – severe pain
  3. Duration of action:
    • Hydro/oxymorphone: 2-4 hours
    • Morphine, Methadone 4-6 hours
28
Q

Methadone is a full mu agonist and what else?

A

NMDA antagonist

29
Q

What are the side effects of Hydromorphone, Morphine, Oxymorphone, Methadone

A
  1. Moderate – severe analgesia
  2. NO ‘ceiling effect’, dose dependent MAC sparing
  3. CV effects minimal; bradycardia
    • Do not cause myocardial depression or vasodilation (except Morphine & histamine release)
  4. Nausea, Vomiting (except Methadone), defecation
  5. Dysphoria, vocalization, Panting
  6. Respiratory depression
  7. Hyperthermia in cats
  8. Morphine can cause histamine release if given quickly IV
30
Q
  1. How long does it take for Fentanyl to work
  2. What route do you usually give it by?
A
  1. Short acting; 15 -30 min.,
  2. Requires IV catheter, constant rate infusion (CRI)
31
Q
  1. What type of drug is fentanyl
  2. How much analgesia dose it cause?
A
  1. Full mu agonist
  2. Moderate-severe pain
32
Q

What are side effects of fentanyl

A
  1. Moderate – severe analgesia
  2. NO ‘ceiling effect’, dose dependent MAC sparing (up to 65%!!)
  3. CV effects minimal; bradycardia (> other mu agonists)
    • Does not cause myocardial depression or vasodilation
    • No histamine release
  4. No Vomiting, may cause nausea
  5. Less vocalization, panting, can cause dysphoria in non-painful patients
  6. Respiratory depression (> other mu agonists)
    • Monitor EtCO2, IPPV intra-op
    • Monitor SpO2 @ recovery
33
Q

How do we use Fentanyl

A
  1. Induction agent in critically ill SA patients
    • Fentanyl 5-10 mcg/kg IV, Midazolam 0.2 mg/kg IV => intubate
  2. Intra-op and post-op CRI
  3. Other routes/formulations:
    • Fentanyl patch
    • Transdermal formulation
34
Q

What are the 4 types of sedatives/ tranquilizers

A
  1. Acepromazine
  2. Alpha-2 agonists
  3. Benzodiazepines (BNZ)
  4. Dissociatives
35
Q

What are the Alpha-2 agonists used as sedatives/ tranquilizers

A
  1. Small animal- Dexmedetomidine
  2. Large animal- primarily horses:
    • Xylazine
    • detomidine
    • romifidine
36
Q

What are the Benzodiazepines (BNZ)

A
  1. Midazolam
  2. Diazepam
37
Q

What are the Dissociatives

A
  1. Ketamine
  2. Tiletamine in Telazol™ (tiletamine + zolazepam)
38
Q

What type of drug is acepromazine

A
  • Phenothiazine
  • alpha-1 antagonist
39
Q
  1. How much sedation does Acepromazine cause
  2. What is the onset?
  3. Whats the duration?
A
  1. Mild – moderate sedation
  2. Slow onset of action ~20-30 minutes
  3. Long duration of action 4-6 hours
40
Q
  1. Does Acepromazine have a reversal agent?
  2. Does it provide analgesic effects?
  3. What does it do to induction drug doses and MAC of inhalant?
A
  1. No reversal agent
  2. No analgesic effects BUT synergistic effect with opioids
  3. Significant ↓ induction dose & MAC of inhalant
41
Q
  1. Because acepromazine is also an alpha-1 antagonist, what will that do?
  2. What does it do to BP and HR?
  3. Temperature?
  4. How does it rate in sedation vs benzodiazepines and alpha-2 agonists
A
  1. Alpha-1 antagonist => vasodilation
  2. Hypotension, bradycardia
  3. Hypothermia (redistribution of blood from core to periphery)
  4. more reliable/profound sedation than benzodiazepine, but less than alpha-2
42
Q

What other effects does acepromazine have that is not sedative? (3)

A
  1. Anti-emetic (if administered 15 min. before opioid)
  2. anti-arrhythmic effects (↓ sympathetic tone)
  3. ↓ opioid side effects such as panting
43
Q
  1. Do you use the same dose of acepromazine for SQ/IM vs IV administation?
  2. What type of patients do you need to use caution in
  3. dose?
A
  1. Lower dose for IV administration
  2. Caution inL
    • very young
    • geriatric
    • liver dysfunction
    • critically ill patients
  3. 005 - .02mg/kg IM or IV
44
Q

Does acepromazine cause seizures?

A
  • NO!
    • (Tobias et al, JAAHA, 2006) - Retrospective study of use of Ace in dogs with seizure history => NO seizures reported within 16 hours of Ace administration
    • human drug ‘chlorpromazine’ at high doses can cause seizures in people, so people may have been confused
    • It was said in older textbooks that it does but this is no longer true
45
Q
  1. does Dexmedetomidine have dose dependent sedation?
  2. What is the onset
  3. What is the duration of action?
A
  1. Potent sedative + analgesia
    • Dose dependent sedation – mild => profound
  2. Rapid onset (~5 minutes)
  3. Short duration of action (~30-60 minutes, depending on dose)
46
Q
  1. What is the reversal agent to dexmedetomidine?
  2. What is Jose’s quick hint in using this reversal?
A
  1. Atipamizole
  2. You use the same mL of antipamizole to reverse what you used for dexmedetomidine to sedate! (helpful in emergency situations)
    • If you are using the 0.5mg/ml concentration of dexmedetomidine and the 5.0 mg/mL concentration of atipamizole, which I am pretty sure there are no other concentrations on the market but always good to double check!
47
Q
  1. What does Dexmedetomidine do to cardic output?
  2. Why?
  3. What types of patients will you use this drug to sedate?
A
  1. 40% ↓ CO
  2. reflex bradycardia due to vasoconstriction
  3. Reserve for healthy or very painful, fearful, aggressive patients (this is my favorite drug to use on the meanies, really knocks them out!)
    • Add Ketamine 1.0 – 2.0 mg/kg IM if unhandleable
48
Q

Explain the pharmacology of Dexmedetomidine (what receptors it targets and what effects happen because of it)

A

There are 3 alpha receptors that are Transmembrane G protein coupled receptor and the G-proteins couple to effector mechanisms

  • Alpha-2A in locus ceruleus (brain) =>
    • inhibition => sedation, anxiolysis, sympatholytic properties
  • Alpha-2B in vasculature => excitatory =>
    • vasoconstriction
  • Alpha-2B & 2C in dorsal horn of spinal cord =>
    • inhibit nociception
49
Q

Explain the Biphasic hemodynamic effects of dexmedetomidine

(include the time period and which receptors are activated)

A
  1. Initial hypertension (10-30 minutes) response due to peripheral α-2-B stimulation with vasoconstriction
    • INITIALLY, bradycardia is a baroreceptor mediated response due to ↑ BP
  2. Subsequent hypotension (after 30-60 min) due to bradycardia and peripheral vasodilation because:
    • there is a central α-2-A stimulation => ↓ norepinephrine causes hypotension due to bradycardia & peripheral vasodilatation
    • ↓ sympathetic outflow slows HR in latter phase
50
Q

During the initial first hour of dexmedetomidine administration there is a Bradycardia (HR < 50 dogs, <80 cats) with a normal to high BP

  1. Should you treat with an anti-cholinergic to increase the HR?
  2. Why or why not?
A
  1. Treatment with anti-cholinergic contra-indicated
  2. Severe hypertension w/o ↑cardiac output
    • You will increase the HR but the BP will go really high to about 180-220 MAP without increasing CO
    • It will increase myocardial work because there is vasoconstriction for the heart to work against
    • Will lead to decreased cardiac perfusion which will then lead to ventricular arrhythmias
    • Could have kidney failure, retinal detachment from the increase BP
51
Q

After about one hour of dexmedetomidine administration there is a Bradycardia (HR < 50 dogs, <80 cats) with Low BP

  1. Should you treat with an anti-cholinergic to increase the HR?
  2. Why or why not?
A
  1. Treatment with anti-cholinergic indicated
  2. Bradycardia and low BP is due to central Alpha-2A sympatholytic effect
52
Q

If you had a dog with a HR of 50 with a MAP of 60 that was given dexmedetomadine, do you treat with an anticholinergic?

Anesthesiology 398 and 466 (22 decks)

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