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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
1. What is the dose for Buprenorphine in small animals? 2. Compared to mu agonists, how does it affect: * Respiration * Panting * HR * Analgesia * Nausea
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
1. What is the long acting buprenorphine drug? 2. Dose? 3. What limits its use?
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
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
1. Hydromorphone, Morphine, Oxymorphone, Methadone 2. Moderate – severe pain 3. Duration of action: * Hydro/oxymorphone: 2-4 hours * Morphine, Methadone 4-6 hours
28
Methadone is a full mu agonist and what else?
NMDA antagonist
29
What are the side effects of Hydromorphone, Morphine, Oxymorphone, Methadone
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
1. How long does it take for Fentanyl to work 2. What route do you usually give it by?
1. Short acting; 15 -30 min., 2. Requires IV catheter, constant rate infusion (CRI)
31
1. What type of drug is fentanyl 2. How much analgesia dose it cause?
1. Full mu agonist 2. Moderate-severe pain
32
What are side effects of fentanyl
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
How do we use Fentanyl
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
What are the 4 types of sedatives/ tranquilizers
1. Acepromazine 2. Alpha-2 agonists 3. Benzodiazepines (BNZ) 4. Dissociatives
35
What are the Alpha-2 agonists used as sedatives/ tranquilizers
1. Small animal- Dexmedetomidine 2. Large animal- primarily horses: * Xylazine * detomidine * romifidine
36
What are the Benzodiazepines (BNZ)
1. Midazolam 2. Diazepam
37
What are the Dissociatives
1. Ketamine 2. Tiletamine in Telazol™ (tiletamine + zolazepam)
38
What type of drug is acepromazine
* Phenothiazine * alpha-1 antagonist
39
1. How much sedation does Acepromazine cause 2. What is the onset? 3. Whats the duration?
1. Mild – moderate sedation 2. Slow onset of action ~20-30 minutes 3. Long duration of action 4-6 hours
40
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?
1. No reversal agent 2. No analgesic effects BUT synergistic effect with opioids 3. Significant ↓ induction dose & MAC of inhalant
41
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
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
What other effects does acepromazine have that is not sedative? (3)
1. Anti-emetic (if administered 15 min. before opioid) 2. anti-arrhythmic effects (↓ sympathetic tone) 3. ↓ opioid side effects such as panting
43
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?
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
Does acepromazine cause seizures?
* 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
1. does Dexmedetomidine have dose dependent sedation? 2. What is the onset 3. What is the duration of action?
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
1. What is the reversal agent to dexmedetomidine? 2. What is Jose's quick hint in using this reversal?
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
1. What does Dexmedetomidine do to cardic output? 2. Why? 3. What types of patients will you use this drug to sedate?
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
Explain the pharmacology of Dexmedetomidine (what receptors it targets and what effects happen because of it)
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
Explain the Biphasic hemodynamic effects of dexmedetomidine (include the time period and which receptors are activated)
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
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?
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
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?
1. Treatment with anti-cholinergic **indicated** 2. Bradycardia and low BP is due to central Alpha-2A sympatholytic effect
52
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?
yes

Anesthesiology 398 and 466 (22 decks)

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