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Surgery I > Pre-anesthetic and Induction drugs > Flashcards

Pre-anesthetic and Induction drugs Flashcards

1
Q

name the Phenothiazine Tranquilizers used in vet med

A
  • Acepromazine - widely used
  • Chlorpromazine
  • Promazine
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2
Q

What animals are Phenothiazine Tranquilizers FDA approved for?

A
  • Dogs
  • Cats
  • Horses
  • Extra-label use is common
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3
Q

What is the MOA of Phenothiazines?

A
  • Block D2 dopaminergic receptors in the brain
    • Primary site of action is subcortical receptors in base ganglia, limbic forebrain and reticular activating system
    • Suppress state of arousal and cause lack of motivation for response to external stimuli
  • Block peripheral alpha-1 adrenergic receptors in vasculature
    • structural similarity to other catecholamines
  • Some antihistaminic and anticholinergic activity as well
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4
Q

What are the effects of Acepomazine?

A
  • Antiemetic
  • Vasodilation
    • antiarrhythmic
  • Epinephrine reversal
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5
Q

How does Acepromazine work as an antiemetic

A
  • Act as a direct antagonist to dopamine (D2 receptor) in the CRTZ
  • When given 15 minutes prior to opioids, it diminishes incidence of vomiting from 45% to 18%
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6
Q

How does Acepromazine affect the cardiovascular system?

A
  • Vasodilation (alpha adrenergic-blockade
    • Doses of 0.125, 0.25 mg/kg IV cause 9.4% and 16.8% reduction of mean arterial pressure in anesthetized dogs
  • Heart rate may increase slightly (baroreceptor - mediated response to hypotension)
  • Antiarrhythmic effect
    • decreases sensitivity to catecholamine-induced arrhythmias
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7
Q

What are the effects of Phenothiazine Tranquilizers on the CNS?

A
  • Sedation subsequent to depression of reticular activation system
  • RAS is responsible for wakefulness, serves as a gatekeeper for incoming sensory information, modulates the fight-flight response (SNS) among other functions
  • Decreased spontaneous motor activity is noted with phenothiazines
  • NOT ANALGESIC
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8
Q

How does Acepromazine work as epinephrine reversal?

A
  • There is a paradoxical drop in blood pressure in response to epinephrine (“adrenaline”)
  • Alpha1 - adrenergic blockade so the beta2 - receptor effect predominates revealing vasodilating action of beta-2 adrenergic receptor
    • Occurs with endogenous epinephrine (adrenal release) or administered epinephrine
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9
Q

What are the other effects of Phenothiazine Tranquilizers? why?

A
  • Decreased hematocrit
    • Splenic enlargement due to relaxation of smooth muscle in splenic capsule with sequestration of RBCs in the spleen
  • Antihistamine effect
    • Contraindicated for intradermal skin testing, interferes with wheal and flare response to antigens
  • Hypothermia
    • Effect on central thermoregulatory center
    • Causes loss of body temp control at both low and high ambient temperatures
    • Cutaneous vasodilation also contributes
  • Ptosis and prolapse of third eyelid (dose - related)
  • Persistent penile prolapse (paraphimosis) reported in horses
    • incidence of 2.4% in male horses
    • duration up to 4 hours
    • irreversible trauma can occur
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10
Q

How is acepromazine used in dogs? properties?

A
  • Often combined with opioid analgesics for premedication
  • Hepatic metabolism is slow
    • elimination half-life is 7.1 hours
    • long duration of action
  • Reduce dose in puppies < 3 months of age and in geriatric dogs due to sensitivity to effects
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11
Q

how do cats respond to acepromazine?

A

much less sensitive to the sedative effects

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12
Q

How is acepromazine used in horses? effects? contraindications?

A
  • Slow onset (15 - 30min) before adequate sedation even after IV administration
  • Elimination half-life 3.1hrs
  • Caution in excited animals
    • high levels of endogenous circulating epinephrine may cause hypotensive crisis
  • Contraindications:
    • Shock, dehydration, hypovolemia
      • contributes to ⇣ BP
    • Significant CNS depression
      • long-acting sedation is not reversible
    • Altered liver metabolism
      • Elimination half-life is already lengthy
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13
Q

What happens when there is an Overdose/Adverse Response to Acepromazine? Treatment?

A
  • Extreme sedation and hypotension, acute collapse
  • Treat with adequate fluid therapy to expand circulating blood volume
  • In addition to fluid therapy or if fluids are not effective, use a vasopressor to counteract vasodilation
    • Ephedrine
      • stimulates release of NE from SNS nerve terminals
    • Phenylephrine
      • Direct alpha-1 agonist
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14
Q

Name the benzodiazepines used in veterinary medicine?

A
  • Diazepam (valium)
  • Midazolam (versed)
  • Zolazepam
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15
Q

What is the MOA of Benzodiazepines?

A
  • Benzodiazepine and GABAA receptors are coupled to chloride channel in nerve cell membrane
  • GABA is the neurotransmitter and is inhibitory to neuronal activity
  1. GABAA receptor is activated by GABA causing ion channel to allow Cl- influx
  2. Hyperpolarizes the nerve and decreases neuronal transmission
  3. Benzodiazepines bind to the benzodiazepine receptor (separate from GABA binding)
  4. Potentiate GABA-induced chloride influx into nerve cells
  • Benzodiazepines also interfere with GABA reuptake, prolonging its effect at the neuroeffector junction
  • Benzodiazepines have no intrinsic effect on their own in the absence of GABA
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16
Q

What effects do benzodiazepines have on the CNS?

A
  • Anticonvulsant
  • Anti-anxiety
  • Sedation - variable and species dependent but most species only mild sedation
  • Centrally-mediated muscle relaxation
  • Amnesia
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17
Q

What effects do benzodiazepines have on the cardiopulmonary system?

A
  • Minimal cardiovascular effect
  • vascular irritation may occur when diazepam is administered IV
    • propylene glycol vehicle
  • Minimal respiratory depression
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18
Q

What are the properties of diazepam? uses?

A
  • Propylene glycol carrier due to poor water solubility
  • IV, IM, oral or rectal use
  • Poor bioavailability if given subcutaneously
  • Species-dependent sedation
  • Anticonvulsant in all species
  • Often combined with opioids for premed
  • Often used with ketamine to improve muscle relaxation for anesthesia
  • A good choice in sick or debilitated individuals
  • Elimination half-life 3.2 hrs in dogs
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19
Q

What are the properties of Midazolam? uses?

A
  • More rapid and reliable absorption from IM injection due to higher water solubility properties
    • 90% bioavailability after IM with peak plasma concentration in 15 min
  • Also effective via subcutaneous route and reported to be effective with intranasal administration
  • Commonly given by the IV route as well, often as IV co-induction agent with ketamine, propofol, or other anesthetic induction techniques
  • Shorter acting than diazepam
    • elimination half-life 77 minutes in dogs
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20
Q

What is the antagonist for benzodiazepines?

A
  • Flumazenil
    • rarely used due to wide margin of safety of benzos
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21
Q

Why are opioids used in pre-medication?

A
  • Wide margin of safety
  • Considered “gold standard”
  • Fully reversible with opioid antagonists (naloxone)
  • Often used as part of anesthetic protocol for very sick or debilitated animals
  • Excellent analgesics
  • Good sedatives in many species
  • May produce paradoxical hyperactivity
  • in other species (feline, equine) so used in combination with a sedative like acepromazine of alpha-2 agonist
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22
Q

Why do we use anesthetic premedication?

A
  • Calm the patient and aid in restraint
  • Facilitate the process of IV catheterization
  • Provide analgesia
  • Smooth induction to and recovery from anesthesia
  • Decreases the amount of other anesthetics drugs needed
  • No drug class or combination of drugs should be routinely given to all patients
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23
Q

What are the major classifications of Preanesthetic drugs?

A
  • Alpha-2 Adrenergic Agonists
  • Phenothiazine Tranquilizers
  • Benzodiazepines
  • Opioids
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24
Q

What considerations need to be taken when deciding on preanesthetic drugs for a patient?

A
  • Type of surgery
  • duration of procedure
  • anticipated complications
  • Postoperative needs
  • age
  • temperament
  • volume status
  • medical condition
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25
Q

Name the alpha-2 adrenergic agonists

A
  • Xylazine
  • Detomidine
  • Romifidine
  • Dexmedetomidine
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26
Q

Name the alpha-2 adrenergic agonists

A
  • Xylazine
  • Detomidine
  • Romifidine
  • Dexmedetomidine
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27
Q

What do alpha-2 adrenergic agonists do? (general)

A
  • Provide sedation
  • analgesia
  • muscle relaxation
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28
Q

What is the MOA of Alpha-2 Adrenergic Agonists

A
  • Bind to and stimulate alpha-2 adrenergic receptors
    • Part of the sympathetic nervous system, alpha-2 receptors are widely distributed throughout the body
    • Receptors are located both pre-synaptically and post-synaptically and have both direct effects and modulatory effects on many systems other than SNS
    • These drugs are not pure alpha-2 agonists but have some alpha-1 and alpha-2 adrenoceptor activity defined for each drug as its alpha-2 : alpha-1 selectivity ratio
      • Alpha-2 adrenergic effects predominate
      • Alpha-2 agonists activate central and peripheral alpha-2 adrenergic receptors
      • Alpha-2agonsits activate both presynaptic and postsynaptic alpha-2 adrenergic receptors
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29
Q

What is the role of alpha-2 adrenoceptor in the sympathetic nervous system?

A
  • SNS regulates many systems within the body
    • part of this regulation involves the modulation of the release of neurotransmitters (nerve terminals) and neurohumoral (adrenal medulla) control
  • Alpha-2 adrenoceptors are inhibitory presynaptic receptors
    • within SNS called “autoreceptors”
  • Norepinephrine (NE) released by nerve binds to alpha-2 receptor and diminishes further release of NE from SNS postganglionic fibers
  • Negative Feedback System
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30
Q

What effect do alpha-2 adrenoceptors have on non-adrenergic nerves?

A
  • can inhibit the release of neurotransmitters such as acetylcholine, serotonin, substance P and other neuropeptides
  • Alpha-2 receptors that inhibit release of a neurotransmitter with which they are not activated are called heteroreceptors
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31
Q

How do alpha-2 receptors contribute to analgesia

A
  • Pain pathway is highly modified within the dorsal horn of the spinal cord. This is a site where many of our analgesics are targeted
  • Presynaptic alpha-2 receptors located on primary afferent C fibers cause decreased release of neurotransmitter from primary pain fibers (heteroreceptors)
  • Postsynaptic alpha-2 receptors are located on spino-thalamic projection neurons in dorsal horn and inhibit ascending nociceptive transmission
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32
Q

What affects do alpha-2 adrenoceptors have on the CNS?

A
  • Sedation
    • alpha-2 receptors in locus coeruleus in the midbrain
  • Analgesia
    • dorsal horn of spinal cord
  • Muscle relaxation
  • Emetic action
    • effect on adrenergic neurons in CRTZ
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33
Q

What are the cardiovascular effects of alpha-2 adrenoceptors

A
  • “Biphasic”
  • Initial increase in blood pressure (peripheral phase)
    • agonist at postsynaptic alpha-1 and alpha-2 receptors in smooth muscle of vasculature
    • These receptors mediate vasoconstriction
  • Bradycardia
    • Reflex response to initial hypertension
    • Increases parasympathetic tone (baroreceptor reflex)
    • May see second degree AV block occasionally
    • Be cautious in use of atropine to treat this
      • increased heart rate may increase hypertension and work of the heart
  • Arrhythmogenic effects are common (bradyarrythmias)
  • Decreased cardiac output (50% reduction is common) due mostly to reduced HR
    • CO = HR x SV
  • After initial BP increase, arterial pressure may decrease over time due a central depression of overall SNS tone (central phase)
  • Cardiac contractility decreases
    • manifestation of decreased SNS influence on the heart
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34
Q

What other side effects are common to alpha-2 adrenoceptors?

A
  • Potentiates central respiratory depression caused by other drugs but very little respiratory depression if used alone
  • Depresses GI and ruminal motility
    • Activation of presynaptic alpha-2 adrenergic receptors in the enteric nervous system inhibit ACh release from cholinergic neurons (heteroreceptor activity)
  • Hypoinsulinemia with possible subsequent hyperglycemia
    • stimulation of alpha-2 receptors inhibits insulin release from pancreatic islet cells
  • Vomition
    • Common in cats (90% of cats with xylazine, 58% of cats with dexmedetomidine)
    • less frequent in dogs (30% xylazine, 10% medetomidine
  • Diuresis
    • Alpha-2 adrenergic receptor stimulation blocks effect of vasopressin (ADH) on kidney
  • Hypothermia
    • Attenuate thermoregulatory control, reduce muscle activity, reduce shivering response, lower CNS shivering threshold
  • Increased intrauterine pressure in cattle
  • Decreased uterine blood flow in all species
35
Q

What is the clinical use of xylazine?

A
  • Most widely used alpha-2 agonist in large animal practice
    • especially horses
  • Alpha-2:alpha1 = 160:1
  • Elimination half-life in minutes
    • dog 30.1
    • horse 49.5
    • cattle 36.5
  • Rapid onset after IV with 30 minute duration of sedation
  • IM administration, peak plasma levels in 15 minutes
  • Epidural analgesia in large animals
  • analgesic for visceral pain
  • Short term relief of colic pain in horses prior to transport
    • motility and blood flow reduced
36
Q

What is xylazine’s affects on cattle?

A
  • Very sensitive to the sedative effects of xylazine
    • 1/10 equine dose
  • Decreases rumen motility
  • Hypersalivation can occur
  • Predisposes to bloat, regurgitation
  • May cause acute pulmonary edema in sheep due to induction of severe inflammatory response in lung or acute changes in pulmonary hydrostatic pressures
  • To avoid overdose in ruminants a 20 mg/ml form of xylazine is available in contrast to the 100 mg/ml formulation used in equids
37
Q

What are the properties of Detomidine?

A
  • Dormosedan used in horses
  • Injectable and oral gel form available
  • Selectivity ratio is 260:1
  • Longer duration sedation (1hr) compared to xylazine
  • Elimination half-life
    • horse 26-53 min (dose dependent)
    • Cattle 79 minutes)
  • Used for standing sedation, analgesia for colics, and less frequently as premed prior to gen anesthesia
38
Q

What are the properties of Romifidine?

A
  • Developed for use in equine sedation and premedication
    • Use in other species
  • Longer duration of action than xylazine and at higher end of dose range has longer duration than detomidine (up to 2hr)
  • Elimination half-life in horse 138.2 min
  • Less ataxia than xylazine or detomidine
    • sometimes preferred for standing procedures
  • All other effects similar to other alpha-2 agonists
39
Q

What are the properties of Dexmedetomidine?

A
  • Active isomer in the racemic mixture of the drug medetomidine
  • levomedetomidine provided very little of agonist effect of parent drug
  • Selectivity ratio 1620 : 1
  • Used primarily in small animals for sedation or as preanesthetic. Also used extensively in exotics
  • Can be used as a Sedative, analgesic, for restraint, for short term pain control
    • long term pain control as CRI
  • Adverse effects:
    • substantial bradycardia, development of hypertension or signs of poor tissue perfusion
    • Avoid in patients with poor cardiac output, or where increased afterload could be detrimental
40
Q

What are the antagonists for Alpha-2 adrenoceptor?

A
  • May be associated with rapid and occasionally rough recovery due to immediate loss of sedation and analgesia
  • Atipamezole - use with dexmed
  • Yohimbine - use with xylazine
  • Tolazoline - use in Large animals when yohimbine is unavailable
41
Q

What kind of opioid is Buprenorphine? Properties?

A
  • Partial µ - agonist (CIII)
  • Duration of action longer than other opioids (4-8hr)
  • High affinity for µ receptors
    • displace µ agonists
    • More resistant to naloxone reversal
  • Less vomiting, sedation than morphine, hydromorphone
  • ~1 hr to produce maximum effect (IV), clinical efficacy in 10-30 min
  • Oral bioavailability <20% - not effective PO
42
Q

What are the different classes of induction agents capable of producing general anesthesia?

A
  • Phenol derivatives (Propofol)
  • Dissociatives (Ketamine, Tiletamine)
  • Imidazole derivatives (etomidate)
  • Steroid anesthetics (Alfaxalone)
43
Q

How fast are induction agents?

A
  • Rapidly acting
  • high lipid solubility results in rapid arrival in CNS often in one “circulation time” 15-30 sec
44
Q

How do induction agents produce anesthesia?

A
  • Achieving sufficient plasma level which is dependent on:
    • Speed of injection
      • rapid injection = higher concentration in a small quantity of blood passing the brain (rapid IV bolus)
    • Concentration of Drug
      • higher the concentration of drug in solution that is administered the higher the concentration reaching the brain rapidly
      • Not a critical factor in that most drugs are marketed at a precise concentration
45
Q

What does delivery of intravenous anesthesia to the brain depend on?

A
  • Brain Blood Flow
    • vessel rich tissues
      • Only 10% body mass gets very high CO (75% at rest)
    • Depends on total CO
      • Low CO states can result in more rapid onset of anesthesia
        • less distribution of blood flow to all body tissues
        • blood flow to brain is preserved
        • Higher peak plasma concentration is delivered due to less “dilution” with lower CO
  • Lipid Solubility of drug
    • more lipid soluble agents move into and out of the brain more quickly
      • blood-brain barrier
  • Protein binding
    • only ‘free’ drug can move into brain
      • Propofol is about 98% protein-bound
        • if changes to 96% drug activity has doubled
      • Can improve activity with
        • hypoproteinemia
        • other protein bound drug competition (NSAIDS, antibiotics)
        • Renal Disease (azotemia)
46
Q

How do patients recover from IV anesthetic?

A
  • Depends on decreased CNS drug concentration
    • decreasing CNS conc depends on redistribution of drug away from brain
      • 1 minute Brain level peaks
      • 2 minutes Plasma level is 20% of original concentration
      • Muscle level peaks at 20 min
      • Fat level peaks at 45 - 60
    • Hepatic metabolism
      • after CRI of highly lipid soluble drugs there is a context-sensitive half-life
    • Renal Excretion
      • ketamine in cats only
47
Q

What is anesthetic recovery vs total elimination?

A
  • Recovery occurs faster than whole body elimination
  • blood levels must be reduced below what is required for anesthetic effect for recovery to occur
    • Hangover from lingering drugs can persist with drugs that have a slow metabolic elimination (compared to those with rapid metabolism/clearance)
      • especially true after CRI
48
Q

What is Propofol? use? types? properties?

A
  • IV anesthetic agent
  • Ideal for outpatient procedures - rapid recovery
    • clear awakening, little “hangover”
  • INsoluble in water
  • 2 formulations
    • formulated in emulsion
      • soy & egg lecithin - support bacterial growth
      • No preservatives - limited shelf-life (<24hr)
    • Microemulsion formulation
      • benzyl alcohol preservative - 28 day shelf-life
  • Ultrashort acting induction agent
    • rapid recovery due to redistribution away from vessel-rich tissues
  • NOT cumulative
    • liver metabolism very rapid
      • 60% of clearance
    • extrahepatic sites have yet to be clearly ID (renal? lung?)
49
Q

What is the MOA of Propofol?

A
  • Activate GABA receptors in the CNS (similar to benzos)
    • Specific binding sit on the GABAA receptor, separate from benzo site
  • Depress polysynaptic responses, major inhibitory control in the CNS
  • At low conc - can augment the affinity of the GABAA receptor for GABA and increase the mean chloride channel opening time
    • Increases chloride conductance and hyperpolarizes neurons
  • at high conc - anesthetic - directly increases channel openings, even in the absence of GABA
  • Summary:
    • Increases inhibitory effect of GABA at the GABAA receptor
      • CNS depression
        • sedation/anesthesia
        • muscle relaxation
          • myoclonus can occur
        • little analgesia
          • only through CNS depression
50
Q

What are the cardiovascular effects of propofol?

A
  • transient effects
  • Minimal effect on myocardial contractility
  • short term vasodilation ( ⇣ cardiac preload)
  • mild to moderate hypotension
    • no reflex tachycardia to offset ⇣ BP
  • Reduced CO - dose dependent
  • Slower infusion at induction is safer than rapid bolus
51
Q

What are the respiratory effects of Propofol?

A
  • Depressant
    • decrease in tidal volume and RR
  • May produce apnea
    • more common w/ rapid infusion rate/high doses
    • Be prepared to intubate and ventilate until breathing resumes
52
Q

What are the advantages of Propofol?

A
  • Rapid onset
  • short duration of action
  • rapid smooth recoveries
  • Non-cumulative - unless prolonged CRI
    • Context-sensitive half time increase with CRI
  • Useful for anesthetic induction and/or maintenance by CRI
53
Q

What are the disadvantages of Propofol?

A
  • Moderate Hypotension
  • Respiratory depression (apnea)
  • Poor analgesia (need alternative source)
  • Drug vehicle may support bacterial growth
  • Formulation can cause pain on IV injection
  • Heinz body hemolysis reported with repetitive use in cats
    • more than 3 consecutive days
54
Q

Name the dissociative anesthetics used in vet med

A
  • Ketamine
  • Tiletamine (with zolazepam in Telazol)
55
Q

What is the MOA of Dissociative anesthetics?

A
  • Effects NMDA receptor-ion channel complex
    • neurotransmitter -glutamate
    • 1° excitatory neurotransmitter of CNS
  • Non-competitive NDMA receptor antagonist
    • Binds to the pore of the NMDA receptor channel
    • Prevents influx of calcium into the cell
56
Q

What are the pharmacokinetics of ketamine?

A
  • Termination of effect due to redistribution
  • Undergoes hepatic metabolism to norketamine, an active metabolite with less potency
  • Cats eliminate unchanged ketamine via the kidney
57
Q

What are the CNS affects of Ketamine?

A
  • Anesthesia with amnesia
  • Analgesia and Catalepsy
    • trance-like state characterized by loss of sensation, loss of consciousness with body rigidity
  • Dissociates the cortex from lower centers
    • out of body experience
  • Both excitatory & depressant effects
  • May produce seizure discharges seen on EEG
  • Increase cerebral blood flow, intracranial pressure
    • Prior administration of benzodiazepine reduces effect
  • Hallucinogenic, vivid dreaming, dysphoria
  • As sole induction agent produces both unsatisfactory muscle relaxation and poor calming effects
  • Almost always combined with benzos or alpha-2 adrenergic agonist
58
Q

What are the cardiovascular effects of ketamine?

A
  • Secondary to increase SNS tone
    • increase HR
    • increase BP
    • increase cardiac contractility
    • increase CO
    • Increased myocardial work
  • Endogenous catecholamine release
    • plasma catecholamine levels rise
    • Ketamine inhibits norepinephrine reuptake into nerves
59
Q

What are the respiratory effects of ketamine?

A
  • Does not cause significant respiratory depression
  • Ventilatory response to elevation in PaCO2 remains intact
  • Bronchodilator
  • Airway reflexes are maintained
  • apneustic ventilation pattern
    • prolonged inspiratory time with inspiratory breath holding before rapid exhalation
    • Despite abnormal pattern
    • PCO2 and minute ventilation is normal
    • Glutamate plays a role in rhythmicity of brainstem respiratory pattern generator
60
Q

What other effects are common with ketamine use?

A
  • increased salivation
  • muscle rigidity
  • Increased intraocular pressure
  • Increased intracranial pressure
  • fetal depression
    • negative effect shown on fetal outcome if used for C-sections in SA patients
61
Q

What are the clinical uses of ketamine?

A
  • Chemical restraint (IM)
  • Minor sx as part of multi-drug combo approach with various sedative/analgesic agents
  • Anesthetic induction (IV) all species
  • In IV combination s to produce anesthetic induction or short term anesthesia
    • Midazolam/ketamine (many species)
    • Xylazine/Ketamine (LA species)
  • Low dose CRI is an effective analgesia supplement
    • subanesthetic dose can produce profound analgesia
    • prevent or minimize central sensitization and wind-up in the nociceptive pathway
62
Q

what is the recovery quality of Ketamine?

A
  • Dysphoric rapid emergence common in dogs
  • slow disoriented recovery in cats
  • animals may benefit from additional tranquilization in recovery
63
Q

how long does ketamine last?

A
  • Variable, depending on dose/route
    • PO 6-10
    • IV 0.5 - 2
    • nasal 6-10
    • IM 3-10
  • Rapidly absorbed via many routes
  • Most species, recovery due to redistribution & metabolism
    • In cats, urinary excretion of unchanged drug
64
Q

What is Etomidate?

A
  • Non-barbiturate, imadazole-derivative anesthetic agent
  • Commercial formulations contains purified R(+) sterioisomer only
  • Not water soluble - in a 35% propylene glycol diluent
    • may cause pain on injection
    • can cause intravascular hemolysis
      • may not be clinically significant, but can result in hemoglobinemia and hemoglobinuria
65
Q

What is the MOA of Etomidate

A
  • GABA-agonist
  • Sedation - hypnosis - anesthesia
  • Binding sit identified on B subunit
66
Q

What are the cardiovascular Effects of Etomidate

A
  • Minimal CV effects
  • Very little effect evident even in the presence of severe CV disease
  • No change in HR, SV, CO, BP
  • No change in SNS tone
  • Highest therapeutic index (LD50/ED50) of the IV induction agents
    • therapeutic index = 26
67
Q

What are the CNS effects of Etomidate?

A
  • Decreased cerebral blood flow
  • Decreased cerebral O2 consumption
  • Decreased intracranial pressure
68
Q

What is Myoclonus? why does Etomidate cause it?

A
  • Involuntary muscle contractions
  • Disinhibitory effect on extrapyramidal (involuntary) motor activity
  • Incidence decreased with prior administration of benzos or adequate premedication
  • Incidence may be decreased by low dose incremental “pretreatment” with etomidate
    • “split-dose induction”
69
Q

How does Etomidate cause Adrenocortical Suppression?

A
  • Inhibits 11 - B - hydroxylase
    • Enzyme necessary for synthesis of cortisol and aldosterone
  • Adrenal suppression lasts for 5-8 hrs after single IV bolus
  • Contraindication for repeated use or CRI sedation
  • Contraindicated in animals with Hypoadrenocorticism (Addison’s)
70
Q

name the steroid anesthetics

A
  • alphaxalone
  • alphadolone
71
Q

What is Saffan?

A
  • mix of alphaxalone and alphadolone
  • alphaxalone was most active portion
  • alphadolone improved solubility
  • Cremophor EL vehicle caused allergic reaction involving histamine release
    • contraindicated in dogs due to severe release
    • cats experienced edema +/- hyperemia of paws and ears with occasional laryngeal or pulmonary edema
72
Q

What is Alfaxan?

A
  • Modern formulation - Alphaxlone only
  • formulated inside a cyclodextrin ring which opens to release drug as a result of pH change post-injection
73
Q

What is the MOA of alfaxalone?

A
  • GABA agonist
  • Binding site on B-subunit
74
Q

what are the uses of alfaxalone?

A
  • sedation, hypnosis, anesthesia
  • IV as anesthesia induction
  • IM for sedation
75
Q

What are the effects of Alfaxalone?

A
  • minimal hypotension (dose dependent)
  • increase in HR
  • Slight increase in cardiac index (secondary to ⇡HR)
  • Mild respiratory depression (dose dependent)
  • No tissue irritation when used IM
  • Excellent muscle relaxation
76
Q

How is Alfaxalone cleared from the body?

A
  • Rapid metabolic clearance
  • Hepatic metabolism
    • BOth Phase I (cytochrome P450) and Phase II (glucuronidation and sulfation) pathways
  • Elimination half-life
    • dogs 34 minutes
    • cats 43 minutes
77
Q

What are the available formulations of alfaxalone?

A
  • Preservative-free formulation
    • opened bottles discarded within 24 hours of initial use
  • Multi-dose formulation
    • 28 day shelf-life
    • Ethanol, chlorocresol, and benzethonium chloride as preservative
78
Q

What are the inhibitory receptors for pain?

A
  • Opiate - spinal and supraspinal (some peripheral)
  • GABA (gamma-aminobutyric acid) - peripheral, spinal, and supraspinal
  • Serotonin (many different subtypes and locations - some inhibit pain, some enhance pain transmission
  • Alpha-2 (NE): binds presynaptically to decrease neurotransmitter release - spinal and supraspinal
79
Q

how are opioids metabolised?

A

Primary hepatic metabolism (Phase I and/or Phase 2)

80
Q

What effects other than analgesia do Mu opioids have?

A
  • Dose-dependent respiratory depression
    • clinical significance minimal in healthy animals
    • Caution in animals w/ preexisting respiratory comprimise
      • head trauma (cerebral edema)
      • respiratory disease
      • other respiratory depressants (inhalant anesthetics, propofol)
  • Bradycardia - parasympathetic mediated
  • Cardiac Output - minimal effects
    • proportional increase in Stroke volume relative to bradycardia
    • high doses can lead to mild/moderate decrease in CO
  • Vascular Effects:
    • Primary hypotensive effects when combined with propofol, inhalants, acepromazine
  • hypothermia
81
Q

What effects do mu agonists have on the urinary system?

A
  • Urinary retention - increases tone of sphincters and inhibit micturition
  • Decreased urine production - mech unknown
  • Not commonly recognized clinically in animals
82
Q

what are the adverse effects of morphine

A
  • bradycardia
  • hypothermia
  • dysphoria
83
Q

Why should buprenorphine not be given with Mu agonists?

A
  • Partial agonist with high affinity for receptors.
    • will displace mu agonists
    • more resistant to naloxone reversal

Surgery I (37 decks)

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