VTS Anesthesia and Analgesia

  1. Primary goal when anesthetizing critically ill patient:
    Keep inhalant concentration as low as possible.
  2. Anesthetic agents with most carfiovascular and respiratory depressants
    Inhalant anesthetics
  3. Balanced Anesthesia (and 4 things it achieves):
    • Concurrent administration of multiple drugs from different classes to achieve:
    • 1. Hypnosis
    • 2. Amnesia
    • 3. Analgesia
    • 4. Muscle Relaxation
  4. Neuroleptanalgesia (and 6 things it achieves)
    • Opioid + Sedative/tranquilizer
    • Works synergistically to:
    • 1. Facilitate handling
    • 2. Decrease stress
    • 3. Decrease induction dose
    • 4. Decrease inhalant concentration
    • 5. Assist with smooth recovery
    • 6. Provides preemptive analgesia
  5. Preemptive analgesia
    Administering analgesic before painful stimulus
  6. Preemptive analgesia prevents:
    Central and peripheral sensitization, which can cause an exaggerated response to pain
  7. Induction agents produce a ______________
    Smooth, rapid transition to general anesthesia
  8. Induction agents that can go IM (2)
    • 1. Ketamine
    • 2. Alfaxolone
  9. Maintenance period:
    • Usually involves inhalant agents
    • May use injectable for short term procedures
    • May also use total intravenous anesthesia (TIVA)
  10. Why is multimodal approach to anesthesia the best?
    Ensures nociceptive stimulation is prevented by using drugs that work at different locations along pain pathway.
  11. Nociceptive pain
    Pain caused by physical damage to body
  12. NSAIDs are best used for treatment of ____________
    Acute, mild-mod. pain associated with inflammation
  13. Primary mechanism of action for NSAIDs
    Blocking prostaglandin formation via inhibition of cyclooxygenase enzymes (COX-1 and COX-2) in arachidonic acid cascade
  14. COX-1 Function
    involved with normal hemostatic functions (renal bloodflow, GI cytoprotective mechanisms, platelet aggregation)
  15. COX-2 Function
    Activated by inflammatory cells, triggers production of inflammatory prostaglandins that contribute to peripheral sensitization and GI ulceration. Serves beneficial homeostatic role.
  16. NSAIDs approved in dogs (7):
    • 1. Carprofen - Rimadyl
    • 2. Deracoxib - Deramaxx
    • 3. Etodolac - Lodine
    • 4. Firocoxib - Previcox
    • 5. Meloxicam - Metacam
    • 6. Tepoxalin - Zubrin
    • 7. Mavacoxib - Trocoxil
  17. NSAIDs have more selectivity for COX-1/COX-2 inhibition. Some have weak COX-1/COX-2 inhibition (which 2?)
    • COX-2
    • COX-1
    • Carprofen, Etodolac
  18. Tepoxalin unique in that it inhibits what?
    COX and Lipoxygenase (LOX)
  19. Lipoxygenase
    Responsible for formation of leukotrienes that further precipitate inflammatory cascade
  20. Which 2 NSAIDs come in injectable and oral, and what are the forms of the rest?
    Carprofen and Meloxicam injectable and oral, others strictly oral
  21. Why don't cats metabolize NSAIDs
    Deficiency in glucuronyl transferase enzymes
  22. NSAIDs approved in cats (2)
    • Meloxicam for 1 time use
    • Robenacoxib for maximum 3 days
  23. Most widely reported NSAID side effects
    • GI toxicity:
    • Gastritis
    • V/D
    • GI ulceration
    • GI perforation in severe cases
  24. When are side effects to NSAIDs most likely to occur
    Inappropriate dosing or use with other NSAIDs or corticosteroids
  25. Why is hydration status important to consider when administering NSAIDs pre-op?
    • Only administer if well hydrated.
    • Prostaglandins play vital role in regulation of normal renal function by maintaining renal blood flow
  26. Why should NSAID use be avoided with hypoabluminemia
    NSAIDs are highly protein bound
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  31. Why are opioids called the juice of the poppy
    Poppy source of 20 distinct alkaloids of opium
  32. Mechanism of action for opioids:
    • Bind to opioid receptors located at presynaptic and postsynaptic sites in the CNS (brainstem and spinal cord) and peripheral tissues.
    • Block transduction in physical tissues
    • Dampen modulation and perception
  33. Transduction
    Conversion of physical energy into electrical energy by a nociceptor
  34. Modulation
    Amplification or suppression of nerve signals in the spinal cord
  35. Where does perception of pain occur
    Occurs in dorsal horn of spinal cord
  36. 3 types of opioid receptors
    • Mu (Mu-1 and Mu-2)
    • Kappa
    • Delta
  37. Pure agonists
    • Stimulate opioid receptors
    • Predominantly mu receptors ("Pure Mu Agonists")
  38. Agonists/antagonists
    Block one type of receptor while stimulating another
  39. Partial agonists
    Bind to receptor, less efficacious compared to pure agonist
  40. Pure antagonist
    Attach to receptor but do not activate it (reversal agents)
  41. Dogs often sedate/excited when administered opioids and why
    Opioids may cause minor sedation due to CNS depression
  42. Most prominent canine conditions to display sedation when opioids administered
    • Pediatric
    • Geriatric
    • Debilitated
  43. Cats may show sedation/excitement when opioids used under what circumstances and how to avoid
    • May show excitement when opioids used alone or at high doses due to CNS stimulation.
    • Reduced by co-administration of sedative
  44. List of pure agonists opioids (6)
    • 1. Morphine
    • 2. Hydromorphone
    • 3. Oxymorphone
    • 4. Meperidine
    • 5. Methadone
    • 6. Fentanyl
  45. Best opioid option for treatment and prevention of surgical pain
    Pure agonists
  46. Somatic pain
    Skin, tissue, and muscle
  47. Pure agonists are effective against what types of pain
    Visceral and Somatic pain
  48. Effects of pure agonist opioids are ___________
    • Cumulative
    • ^ dose/ ^ frequency = ^ analgesia
  49. Common side effects of pure agonist opioids (4)
    • 1. Vomiting
    • 2. Dose-dependent decrease in respiration (rarely significant unless high dose)
    • 3. Dose dependent decrease in HR and BP (except meperidine)
    • 4. Dysphoria during recovery if given alone or pt in a lot of pain
  50. Pure agonists most likely to cause vomiting in order (3)
    • 1. Morphine
    • 2. Oxymorphone
    • 3. Hydromorphone
  51. Pure agonists lease likely to cause vomiting in order (2)
    • 1. Methadone
    • 2. Meperidine
  52. If vomiting is contraindicated, when should pure agonists be administered
    After induction, as pt will not vomit if induced to general anesthesia
  53. When is vomiting less likely when administering pure agonists
    Less likely if pt already in pain or if drug is given IV
  54. Meperidine effect on HR
    Tachycardia
  55. What breeds are more prone to dysphoria during recovery if administered pure agonist opioid
    Arctic breeds
  56. What can help with dysphoria caused by pure agonist opioids during recovery
    • Low dose sedatives (Acepromazine, Dexmedetomidine)
    • Butorphanol can also act as partial reversal as long as expecting lower pain levels
  57. What medications can cause hyperthermia in cats
    • 1. Hydromorphone during recovery
    • 2. Morphine
    • 3. Butorphanol
    • 4. Buprenorphine
  58. When should reversal with Naloxone be considered for cats experiencing drug induced hyperthermia?
    In severe cases with an elevated temperature lasting longer than 4-6 hours
  59. Morphine active metabolite
    • Morphine-6-glucuronide
    • Metabolized to this by glucuronidation
    • Longer duration of action than oxy or hydro
  60. Why is morphine less effective in cats?
    Cats have decreased ability to metabolize through glucuronidation
  61. How potent is meperidine when compared to morphine
    Meperidine is 1/8 as potent as morphine
  62. Pure agonist opioid with shortest duration of action
    Meperidine
  63. Does meperidine cause sedation in healthy animals?
    Only causes mild sedation when given alone to healthy animals
  64. What may happen if morphine and meperidine administered rapidly IV?
    • May cause histamine release
    • Avoid in patients with preexisting hypotension
    • Low dose morphine CRI unlikely to cause histamine release
  65. What drugs should meperidine and methadone not be given with and why
    • Monoamine oxidase inhibitors (MAOI) or tricyclic antidepressants
    • Both serotonin reuptake inhibitors
    • When combined, may cause serotonin toxicity
    • Potentially life threatening
  66. Why is Methadone beneficial for treatment and prevention of "wind up" pain?
    NMDA Receptor antagonist
  67. List of Partial Mu Agonist
    Buprenorphine
  68. What receptors does buprenorphine have effect on
    • Partial agonist at mu receptor
    • Little to no effect on kappa receptor
  69. Potency of buprenorphine compared to morphine
    Buprenorphine 30 times more potent than morphine
  70. Potency
    refers to amount of drug required in order to achieve its maximum effect. Does NOT imply anything about analgesic efficacy
  71. Side effects and precautions for buprenorphine
    • 1. Slight respiratory depression
    • 2. Unlikely to cause vomiting
  72. Onset of action time for buprenorphine
    Slow onset of action, peak effect occurring ~30-45 mins post IV/IM administration
  73. Duration of action buprenorphine
    • Dose dependent (6-8 hours)
    • Higher dose = longer duration of action
  74. "Ceiling effect" buprenorphine
    After repeated doses, maximal analgesic efficacy reaches plateau. No further increase in analgesia even though duration of action is prolonged
  75. What kind of pain is buprenorphine best for?
    Best for mild-moderate pain
  76. Can buprenorphine be used transmucosal in dogs?
    • Not recommended
    • Acidic saliva decrease bioavailability to 30-50%
  77. Can buprenorphine be used with pure agonists?
    • Should be avoided, buprenorphine has very high affinity for mu receptors
    • May competitively inhibit pure mu agonist from binding, may need to give higher doses of pure mu agonist
    • Giving buprenorphine afterwards can potentially act as a "reversal" agent
  78. Agonist/Antagonist drugs
    • 1. Butorphanol
    • 2. Nalbuphine
  79. What receptors do Agonist/Antagonists stimulate?
    • Stimulate Kappa receptor
    • Antagonize Mu receptor
  80. What pain are Agonist/Antagonists good at treating
    • Effective at treating mild pain
    • Good for visceral pain, not for somatic pain
  81. Do Agonist/Antagonist provide sedation?
    • Mild sedation in dogs and limited sedation in cats when administered alone
    • Synergistic and profound sedation when combined with sedatives or tranquilizers
  82. Side effects and precautions for Agonist/Antagonists
    • 1. Respiratory depression is minimal
    • 2. Little direc effect on cardiovascular system
    • 3. Vomiting not commonly seen
  83. "Sequential analgesia" with Agonist/Antagonists
    Can be used as reversal agents for pure agonists to partially reverse respiratory depression and sedation while maintaining some analgesic effect
  84. Duration of action for Agonist/Antagonists
    Short (30 min - 1 hour)
  85. "Ceiling effect" with Agonist/Antagonists
    Increase dose or repeated doses prolongs duration of action without increasing intensity of analgesia or sedation
  86. List of opioid antagonists
    • 1. Naloxone
    • 2. Nalmefene
  87. What do opioid antagonists do?
    • Completely reverse the adverse cardiopulmonary, sedation, and analgesic effects of opioids.
    • Should only be considered with absolute opioid overdose
  88. Why is a partial reversal of an opioid not recommended?
    Difficult to assess when effects of respiratory depression are decreased while some of analgesic effects are still present
  89. Why should you use caution when reversing an opioid?
    • Acute awareness of pain can lead to sympathetic stimulation:
    • 1. Catecholamine release
    • 2. Cardiac arrhythmias
    • 3. Hypertension
    • 4. Detah
  90. How to administer opioid antagonist
    Dilute in saline, titrate IV slowly to effect over 5-10 mins
  91. Naloxone onset time
    • 1-2 mins IV
    • 5 mins IM
  92. Naloxone duration of action
    • 30-60 mins
    • Additional doses may be necessary for complete reversal to avoid re-narcotization
  93. What opioid may be hard to fully reverse?
    Buprenorphine, strong affinity for mu receptors
  94. Nalmefene onset time
    • 1-2 mins IV
    • 5 mins IM
  95. Nalmefene duration of action
    1-2 hours
  96. Types of sedatives/tranquilizers
    • 1. Phenothiazines
    • 2. Benzodiazepines
    • 3. Alpha-2 Agonists
  97. Types of opioids
    • 1. Pure agonists
    • 2. Partial mu agonist
    • 3. Agonist/Antagonist
    • 4. Opioid antagonist
  98. Types of induction agents
    • 1. Barbiturates
    • 2. Dissociatives
    • 3. Propofol
    • 4. Etomidate
    • 5. Alfaxalone
  99. Most commonly used phenothiazine for sedation
    Acepromazine
  100. Other properties besides sedative effects of acepromazine
    • 1. Antiemetic
    • 2. Antihistamine
    • 3. Antiarrhythmic
  101. Side effects and precautions of Ace
    • Does not cause significant respiratory or cardiac depression at clinically significant doses
    • Causes slight decrease in GI motility
    • No analgesia
    • No reversal agent
    • Causes peripheral vasodilation that can lead to hypotension
    • Inhibits platelet aggregation
    • May lower seizure threshold
    • Some european line boxers may be more sensitive, prone to fainting and sudden collapse
  102. Routes of administration for Ace
    • IV
    • IM
    • SG
  103. Acepromazine duration of action
    6-8 hours
  104. Acepromazine with respiratory distress patients
    Low doses of ace may be beneficial
  105. Fort Dodge dose for ace for sedation when used alone
    • 0.5 - 1.1 mg/kg
    • *Manufacturer dose much higher than what is actually required for premedication
  106. Boehringer Ingelheim dose for ace for sedation when used alone
    • Dog: 0.1 - 0.2 mg/kg
    • Cat: 0.2 - 0.4 mg/kg
  107. Premedication dose for ace when combined with other drugs such as an opioid
    0.01 - 0.05 mg/kg
  108. Why can ace cause hypotension
    • Causes blockade of alpha-1 adrenergic receptors
    • Causes peripheral vasodilation
    • Effect dose dependent - usually only at manufacturer dose
  109. What patients should Ace be avoided in due to platelets
    Thrombocytopenia or clotting disorders due to platelet aggregation
  110. Platelet aggregation
    The clumping together of platelets in the blood (thrombus formation)
  111. List of benzodiazepines
    • 1. Diazepam
    • 2. Midazolam
  112. Benzodiazepine properties
    • Anxiolytic 
    • Mild sedation
    • Skeletal muscle relaxation
  113. Anxiolytic properties
    Anti-anxiety
  114. Drugs used as first line anticonvulsant
    Benzodiazepines
  115. Precautions and side effects of benzodiazepines
    • Minimal effect on cardiovascular and respiratory systems at normal doses
    • Provide no analgesia
    • No reliable sedation in young, healthy animals
    • Highly protein bound (90%) - use with caution with hypoalbuminemia or other highly protein bound drugs (NSAIDs)
    • Though to worsen clinical signs of hepatic encephalopathy
  116. Benzodiazepines are best at causing sedation in what animals
    • Pediatrics (<8 weeks old)
    • Geriatrics
    • Critically ill
    • Debilitated animals
  117. What can benzodiazepines cause in young, healthy animals and when is this more likely
    • Hyperexcitability
    • Difficulty handling
    • Aggression
    • If delivered alone or even with opioid
  118. Why is IM/SQ administration of Diazepam not advised
    • Diazepam insoluble in water, prepared in propylene glycol
    • Causes pain when delivered IM/SQ and unreliable absorption
  119. Why must Diazepam be administered slowly IV
    Rapid injection can cause dysrhythmias and thrombophlebitis due to propylene glycol carrier
  120. What medications will cause precipitate to form with Diazepam?
    • Atropine
    • Acepromazine
    • Barbiturates
    • Opioids
  121. What medication can be mixed with Diazepam?
    Ketamine
  122. How long can Diazepam be stored in plastic?
    Absorbs into plastic and decreases active drug concentration in solutions. Do not store in plastic longer than 2 hours
  123. Midazolam route of administration
    • IV
    • IM
    • SQ
  124. Is midazolam compatible with other drugs?
    Yes
  125. Is Diazepam compatible with other drugs?
    Incompatible with most drugs and solutions
  126. Midazolam is _________  soluble
    Water soluble
  127. Reversal agent for benzodiazepines
    • Flumazenil
    • Competitive blocker of benzodiazepines at the GABA receptors located in the CNS.
    • Antagonizes the sedative and amnesic effects
    • Not commonly used due to cost
  128. How to administer Flumazenil
    • Give IV and titrate
    • Effects usually noted within 2 minutes
  129. List of Alpha-2 Agonists
    • 1. Xylazine
    • 2. Medetomidine
    • 3. Dexmedetomidine
  130. Dexmedetomidine commonly used in ___________
    USA
  131. Medetomidine still available in _________
    Canada
  132. Xylazine commonly used in what type of animals?
    Large animals
  133. Main effects of alpha-2 agonists
    Profound sedation and muscle relaxation
  134. Do alpha-2 agonists provide analgesia?
    Yes, but effects are shorter duration than the sedative effects
  135. Precautions and side effects of alpha-2 agonists
    • Minimal effect on respiratory system
    • Biphasic effect on blood pressure
    • Significant bradycardia (HR decreases by 50% of normal resting rate)
    • Inhibit antidiuretic hormone (ADH) and insulin release
    • Heavily sedated dogs may respond with aggression to touch or stimulus
    • Increase dose will increase duration of action but level of sedation will reach a plateau
  136. alpha-2 agonists biphasic effect on blood pressure
    • 1. Initial activation of peripheral post-synaptic alpha-2 receptors results in vasoconstriction and period of hypertension
    • 2. After central and peripheral pre-synaptic alpha-2 receptors activated, results in sustained decrease in BP due to vasodilation (blocks norepinephrine)
  137. Is bradycardia concerning with alpha-2 agonists
    • Normal physiological response, no need to treat if adequate blood pressure
    • Decrease in sympathetic drive allows vagal tone to predominate
    • Baroreceptor reflex responds to the initial hypertension with reflex bradycardia
    • Decrease in cardiac output results due to decreased HR, but studies show organ perfusion is still adequate
  138. What does inhibition of ADH and insulin release cause with alpha-2 agonists
    Causes diuresis and transitory hyperglycemia
  139. alpha-2 agonists cause what reduction of induction and inhalant concentrations
    • Can cause up to 80% reduction in induction agents
    • 50% reduction in inhalant concentration
    • Micro-doses intra-op can help maintain steady state of anesthesia while keeping inhalant low
  140. What causes most predictable sedation?


    C. Alpha-2 agonists
  141. When is sedation unlikely to occur with alpha-2 agonists
    • If pt. is frightened, stressed, or excited prior to or after administration
    • Leave in a quiet environment 20 mins pre and post-administration to allow for maximum affect
  142. How long should patients be left in a quiet environment for maximum sedative effect of alpha-2 agonists
    20 minutes before and after administration
  143. alpha-2 agonists reversal agent
    • Atipamezole
    • Competitively binds to and inhibits alpha-2 receptors and reverses both sedative and analgesic effects
  144. How should atipamezole be administered
    • Give IM
    • Can be diluted in saline and titrated to effect IV in emergency
  145. List of anticholinergics
    • 1. Atropine
    • 2. Glycopyrrolate
  146. Anticholinergic mechanism of action
    Block the action of acetylcholine at muscarinic receptors of parasympathetic nervous system
  147. Anticholinergics treat:
    • 1. Sinus bradycardia
    • 2. Atrioventricular block
    • 3. Sinoatrial arrest
  148. When will Anticholinergics increase HR with bradycardia
    Only when bradycardia due to vagal stimulation. Bradycardia due to hypothermia will not respond to anticholinergics
  149. Anticholinergic of choice during sinoatrial arrest
    Atropine, fastest onset time
  150. What Anticholinergic has fewer tendencies to cause severe tachycardia and cardiac arrhythmias
    Glycopyrrolate
  151. Why should Anticholinergics only be used in premed if deemed necessary?
    • Tachycardia can be just as detrimental to heart. Can lead to:
    • 1. Increased cardiac workload
    • 2. Increased myocardial 02 consumption
    • 3. Decreased cardiac output and 02 delivery (due to decreased filling time)
    • 4. Increased potential for cardiac arrhythmias
  152. What patients require Anticholinergics in their premeds?
    Pediatric patients <12 weeks
  153. Why do pediatrics <12 weeks require Anticholinergics in their pre-meds?
    Rely on HR rather than contractility to maintain cardiac output
  154. Cases where Anticholinergics should be considered for a pre-med
    • Brachycephalic patients
    • Procedures involving head/neck or eyes
    • Patients with pre-existing bradycardia
  155. Precautions and side effects for Anticholinergics
    • Suppresses salivation, glycopyrrolate more so, but neither prevents it
    • Secretions present increase in viscosity so increased risk of mucous plug in endotracheal tube (especially in small dogs and cats)
    • Both capable of producing arrhythmias (arrhythmogenic) where initial arrhythmia worsens before the increase in HR
  156. Arrhythmogenic
    Drug capable of producing arrhythmias
  157. List of dissociatives
    • 1. Ketamine
    • 2. Telazol
  158. What else are dissociatives referred as
    cyclohexamines
  159. What pain are dissociatives good for
    • Good for somatic analgesia
    • Block central neuronal hypersensitization ("wind up") in dorsal horn of spinal cord
    • Should not be used as sole analgesic agent, contribute good multimodal pain management in CRI
  160. dissociatives mechanism of action
    • Do not produce "true" anesthetic state
    • Appear to cause dissociation between thalamus and limbic systems of brain
    • Sub-anesthetic dose act as N-methyl-D-aspartate (NMDA) antagonists
  161. Which dissociative has longer duration of action
    Telazol
  162. Telazol made up of:
    dissociative agent tiletamine and benzodiazepine zolazepam
  163. Side effects and precautions of dissociatives
    • Primary effect on cardiovascular system is depression of myocardial function
    • Secondary stimulation of sympathetic nervous system (indirect effect)
  164. Why should ketamine never be administered alone?
    • Can produce:
    • Muscle and limb rigidity
    • Increased intracranial pressure
    • Increased intra-ocular pressure
    • Potential seizures due to CNS stimulation
  165. What is ketamine typically administered with?
    Benzodiazepine such as diazepam
  166. What can secondary stimulation of sympathetic nervous system by dissociatives  lead to?
    • Increased HR
    • Increased BP
    • Increased cardiac output
  167. dissociatives contraindicated in
    Depleted catecholamine stores (severe trauma, stress, shock)
  168. Why are dissociatives contraindicated in depleted catecholamine stores?
    Because when all catecholamines used up direct depressant effects on cardiovascular system predominate
  169. Why does ketamine increase risk of mucous plugs in ET tubes?
    Causes hypersalivation and increased bronchial secretions
  170. Why were anticholinergics used with ketamine in the past?
    To counteract increased salivation and bronchial secretions
  171. Why is the use of anticholinergics in conjunction with ketamine no longer recommended?
    Together they can cause severe tachycardia and increase in myocardial 02 demand
  172. Ocular considerations with ketamine use
    • Palpebral and corneal reflexes remain intact
    • Eyes remain in central position until dissociative effects are gone
    • *Very important to lube eyes*
  173. What is common during recovery if ketamine is the only agent on board?
    • Emergence delirium. Signs include:
    • Vocalization
    • Hallucinatory behavior
    • Ataxia
    • Hyperreflexia
    • Hyperthermia
    • Increased muscle activity
  174. How does metabolism of ketamine differ between cats and dogs?
    • In cats it does not undergo hepatic metabolism, excreted unchanged in urine
    • Use in caution with severe renal disease
  175. Canine considerations when recovering from telazol
    Dogs tend to have rough recoveries because zolazepam has shorter duration of action that tiletamine
  176. Feline considerations when recovering from telazol
    Zolazepam has longer duration of action in cats so they tend to have a smoother recovery
  177. Propofol drug class
    Propofol is it's own drug class
  178. Propofol administration route
    Only IV, does not work IM or SQ
  179. Propofol-28 contains what preservative?
    • Benzyl alcohol so gives it a 2 day shelf life
    • High dose benzyl alcohol has not been studied so should not be used as CRI
  180. Propofol shelf life once opened
    No preservative, only good 6-8 hours once open
  181. Propofol metabolism
    • Rapid recovery and clearance
    • Exceeds hepatic blood flow so indicates other tissues (kidney and lungs) take part in metabolism
    • Good choice for pt. with hepatic disease
  182. Propofol causes decreases in what body functions?
    • Decrease in:
    • Cerebral blood flow
    • Intracranial pressure
    • Cerebral metabolic 02 requirements
    • Good choice for patients with head trauma
  183. Precautions and side effects for Propofol
    • Significant respiratory depression
    • Apnea and hypotension common if administered too fast
    • Excitatory response can occur if given without premed
    • Decrease in myocardial contractility and systemic vascular resistance which can lead to significant hypotension
    • Impairs baroreceptor reflex response to hypotension
  184. How to administer propofol to avoid apnea and hypotension
    Give 1/4 - 1/3 of initial dosage over 10-20 seconds, titrate rest to effect if need be
  185. Signs seen with excitatory response to propofol
    • Muscle twitching and rigidity
    • Paddling
    • Possible opisthotonos
  186. Opisthotonos
    Spasm of the muscles causing backward arching of the head, neck, and spine
  187. What happens when Propofol impairs baroreceptor reflex response to hypotension
    • Prevents compensatory increase in HR in critically ill or systemically challenged patients
    • Use in caution in patients with hypovolemia, pre-existing hypotension, and significant cardiac disease
  188. Why are CRIs and consecutive uses (more than 3 days in a row) of propofol not recommended in cats?
    Cats have decreased ability to metabolize phenol compounds
  189. Prolonged use of propofol in cats can induce (one time dose does not cause):
    • Oxidative injury to RBC
    • Heinz body formation
    • Diarrhea
    • Anorexia
    • Malaise
    • Prolonged recovery
  190. Malaise
    A general feeling of discomfort, illness, or uneasiness
  191. Alfaxalone drug class
    Neuro-active steroid anesthetic
  192. Alfaxalone produces:
    good hypnosis and reasonable muscle relaxation
  193. Precautions and side effects of Alfaxalone
    • Dose dependent hypotension may be seen due to myocardial depression and peripheral vasodilation
    • Minimal respiratory depression
    • Excitement may be seen on recovery if it is sole agent on board
    • Provides no analgesia
  194. Dose dependent hypotension in alfaxalone is offset by:
    reflex tachycardia
  195. Route of administration for alfaxalone
    • IV in cats and dogs
    • IM also, less effective unless it is administered deep into the muscle
    • No histamine release or pain on injection associated with this drug
  196. Alfaxalone shelf life
    Does not contain preservative, open bottle should be discarded within 7 days
Author
anubis_star
ID
353637
Card Set
VTS Anesthesia and Analgesia
Description
VTS Anesthesia and Analgesia
Updated