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Pharmacology Test 2 > Sedatives and IV Anesthetics Part II > Flashcards

Sedatives and IV Anesthetics Part II Flashcards

1
Q

Name a dissociative anesthetic?

A

ketamine

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2
Q

Name a Barbiturate?

A

Thiopental

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3
Q

Name 3 Non- Barbiturates?

A
  • Propofol
  • Alfaxalone
  • Etomidate
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4
Q

Definition of general anesthesia?

A

Drug-induced central (CNS) depression resulting in unconsciousness in which the patient cannot be aroused by painful stimuli, and sensory, motor & autonomic reflex functions are attenuated

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5
Q

Definition of Dissociative anesthesia?

A

Drug-induced dissociation of the thalamocortical and limbic systems
resulting in a catatonic state

The eyes remain open and swallowing reflexes remain functional

Skeletal muscles maintain tone

Sensory input is dissociated from perception

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6
Q

Name the stages of Anesthesia?

A
  1. Analgesia
  2. Excitement phase
  3. Surgical anesthesia
  4. Medullary paralysis
  5. Death
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7
Q

Phase characterized by characterized by voluntary motor excitement and state of analgesia

  • The animal is conscious
  • The animal may urinate or defecate
A

Analgesia

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8
Q

Phase characterized by characterized by involuntary excitation or delirium
Loss of consciousness & voluntary control
Signs of CNS stimulation rather than depression

A

Excitement phase

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9
Q

Phase characterized by plane of surgical anesthetic depth is reached
Consciousness, pain sensation, & most neuromuscular reflexes are
abolished

Respiratory, CV, thermoregulatory function are depressed

  • Light
  • Medium
  • Deep
A

Surgical anesthesia

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10
Q

Phase characterized by characterized by paralysis of vital centers in medulla

A

Medullary paralysis

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11
Q

Phase characterized by respiratory failure and/or CV collapse of resuscitative intervention not immediate

A

Death

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12
Q

MOA of Dissociative anesthetics?

A

Non-competitive NMDA receptor antagonist

Inhibits activation by glutamate of ligand-gated ion channels

Antagonism at glutamate receptor of NMDA subtype

Suppresses central sensitization

In conjunction with opioids

Subanesthetic doses adequate for analgesia

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13
Q

The _____ receptor is thought to be a crucial part of the mechanism of CNS hypersensitisation and dorsal horn wind up–> neuropathic pain

Treats hyperalgesia in response to repetitive afferent stimulation

A

NMDA

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14
Q

What part of the nociceptive pathway does NMDA antagonist fit under?

A

Pain Modulation

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15
Q

Give me an example of a dissociative anesthetic?

A

Ketamine

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16
Q

How is dissociative anesthetics distributed?

A

rapidly distributed to wide array of tissues including the brain

lipid soluble so crosses the BBB

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17
Q

Route of ADM. for dissociative anesthetics?

A

Usually given IV, can be given IM

Acidic pH may cause pain on injection

Readily absorbed from the injection site

decent transmucosal bioavail (~40%)

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18
Q

dissociative anesthetics are metabolized by the _____ and excreted in the ____. What species do we worry about with renal excretion?

A

metab. in the liver

excreted in the urine

Cats have more renal excretion than other species —> CAUTION with renal insufficiency

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19
Q

dissociative anesthetics induction of anesthesia?

A

within a few minutes (3-5)

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20
Q

dissociative anesthetics duration of anesthetic effects?

A

20-45 minutes

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21
Q

dissociative anesthetics recovery?

A

2-10 hours (very long)

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22
Q

What are the 2 duel effects that dissociative anesthetics have on the central nervous system?

A
  1. Depression of the thalamocortical system (sensory perception)
  2. Activation of limbic system, dissociation (emotional/behavioral/memory)
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23
Q

What stages are induced by amnesia and anesthesia through CNS stimulation and catalepsy?

A

Only stages 1 and 2 of anesthesia

Consciousness not lost completely —-> don’t disturb the animal!

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24
Q

Define catalepsy?

A

a medical condition characterized by a trance or seizure with a loss of sensation and consciousness accompanied by rigidity of the body.

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25
Q

With dissociative anesthetics, what is taking place through out the body with catalepsy?

A
  • Muscle tone maintained to hypertonic, need to use in combination with muscle relaxant
  • Pharyngeal and laryngeal reflexes maintained
  • Eyes open, mydriasis
  • Light & sound sensitivity
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26
Q

With dissociative anesthetics, what is taking place through out the body with analgesia at sub anesthetic doses?

A

Classified as a dissociative anesthetics, but there is clinical belief that ketamine provides
significant analgesia.

More somatic analgesia (muscle, skin) than visceral

Short duration of action

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27
Q

Main dissociative anesthetic cardiovascular effects?

A

Centrally mediated CV stimulation

Direct action on myocardium causes myocardial depression, but net effect is CV stimulation

Increased sympathetic tone , Positive inotropic

Decreased parasympathetic tone

↑ CO, CVP, & HR

↑ cerebral blood flow

Some antiarrhythmic action ↑ ICP & IOP

Not recommended for craniotomy or ocular surgery

Not recommended for traumatic brain injury or ocular trauma

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28
Q

Dissociative aesthetic effects on respiration?

A

Safe respiratory profile

Low anesthetic doses stimulate respiration  Bronchodilation

Decreased airway resistance

good for asthmatic patients

Increased airway secretions

Very large doses depress respiration

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29
Q

Dissociative aesthetic effects on GI?

A

Stimulation of salivary secretion

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30
Q

What class is Ketamine?

A

Schedule III non-narcotic controlled substance

31
Q

Does ketamine have excitatory effects?

What happens with lower doses

A

Ketamine in anesthetic doses is known to have excitatory side effects, and causes a hallucinations in people

At lower doses Ketamine does not act on primary pain, but on CNS hypersensitization

32
Q

Can I use ketamine on it’s own for analgesic?

A

Not recommended for use as a sole analgesic

Ketamine is used at subanesthetic doses in combination with opioids in the acute pain setting and has been shown to reduce tolerance to opioids

33
Q

Name another dissociative anesthetic and some general info?

A

Tiletamine

(dissociative) + zolazepam
(benzodiazepine) combined in a fixed ratio

Similar to ketamine + diazepam

L-O-N-G recovery (hours)

Only the zolazepam is reversible

34
Q

Can we use dissociative anesthetics with chemical restraint?

A

Chemical restraint and anesthesia for minor procedures

Rarely ever used alone

35
Q

What makes up kitty magic? When is ketamine commonly used

A

Ketamine + Dexmedetomidine + Buprenorphine = Kitty Magic

ketamine is safe for handling fractious cats commonly used for high volume spay/neuter clinics

36
Q

What is triple drip?

A

Dissociative anesthetics are Part of ‘Triple Drip’ in large animals

Guaifenesin (GG) + Xylazine + Ketamine

Form of total intravenous anesthesia (TIVA)

37
Q

Best dissociative analgesia constant rate infusion drugs?

A

Fentanyl + Lidocaine + Ketamine (FLK)

Morphine + Lidocaine + Ketamine (MLK)

38
Q

Dissociative anesthetics role in acute pain?

A

Reduction of post operative pain hypersensitivity

Reduction of short term tolerance to opioids

Prevention of opioid-induced hyperalgesia (OIH)

Reduction in dose of post operative opioids

39
Q

Advantages of Ketamine?

A 
 ↓ central hypersensitivity to pain
 ↓ chronic pain
 ↓ opioid requirements
 ↓ respiratory depression
 ↑ sense of well-being (human patients)
 Anti-inflammatory role in trauma patient

 Inhibits cytokine production and release both in vitro and in vivo

 Ketamine suppressed LPS-induced TNF-alpha, IL-6, and IL-8 production in human whole blood.

 May be useful for horses suffering from pain or endotoxemia

 Reduced chemotaxis of neutrophils, TNF-α, IL-6

 Minimal hemodynamic effects in healthy animals

 Ketamine has been associated with lower pain scores and better activity post op

 Ketamine associated with improved feeding behavior after surgery

 Useful in the critical care and perioperative setting

40
Q

Disadvantages of Ketamine?

A

 Irreversible

 Can’t be used alone, adjunctive therapy with opioids

 May be inappropriate for patients with certain cardiac disease

 ↑ intracranial pressure

 Contraindicated for traumatic brain injury & space-occupying intracranial/brain disease

 Pain upon IM injection

 Risk of corneal ulceration

 Risk of substance abuse

41
Q

Precautions for ketamine uses?

A

 Pain with IM injection

 good for use in cats, but less good for IM use in dogs

 Eyes usually remain open

 lubricate often, blink reflex delayed for up to hours

 Respiratory depression seen at high doses

 ‘Rough’ recovery can be seen (usually if used alone)

42
Q

Avoid using ketamine if?

A

 Contraindication for increased ICP or IOP

 Seizures

 Not for use in myelography

 Certain cardiac disease or hypertension

 Hypertrophic cardiomyopathy (HCM) in cats

 Hyperthyroidism

 Pheochromocytomas

 Hepatic insufficiency

 Contraindicated for renal disease or failure in cats

 Other reported adverse effects:

 Muscle tremors and hypertonicity, CNS stimulation & convulsions

 Nausea, vomiting, hyper salivation

43
Q

Review in summary for dissociative anesthetics?

  • Sedation
  • Anesthetic induction?
  • Muscle relaxation
  • Analgesia
  • CV/Resp?
  • Other?
A

 Sedation? Yes Dissociation, used in combination with other drugs

Anesthetic induction? Yes, only induction agent with analgesic properties

Muscle relaxation? No muscle relaxation by itself

Analgesia? Yes, very good Opioid-sparing effect

Cardiovascular/Respiratory effects?

  • Sympathetic stimulation is the main effect!
  • Minimal respiratory depressive effects
  • Bronchodilation

Other? Cataplexy, lack of blinking/ocular exposure

44
Q

Name a drug example of a barbiturate?

A

Thiopental

45
Q

Name the drug examples of non-barbiturates?

A

 Propofol
 Alfaxalone
 Etomidate

46
Q

Anesthetic drugs that potentiate GABA will create a dose-dependent CNS depression: ?

A

Sedation  hypnosis  anesthesia  coma  death

47
Q

Thiopental, propofol, alfaxalone, etomidate are all ____ agonists?

48
Q

What are the Gaba agonists effect on nociception?

A
  • Perception

- Modulation (anticonvulsants)

49
Q

Mechanism of action for injectable anesthetic GABA agonists? Main effects?

A

Several of the induction agents work by potentiating GABAA receptors

Main effects: sedation & hypnosis

50
Q

Barbiturates are thought to ______ the amount of time that GABA remains on the binding site and at higher doses are reported to be able to activate chloride channels without ––– being present

The end result of chloride entry into the cell is hyperpolarization

A

increase

without GABA

51
Q

GABA dependent mechanism may be the cause of _______ effects and the GABA independent mechanism may result in _______

A

anticonvulsant and sedative

anesthesia

52
Q

Absorption of injectable anesthetic GABA agonists

A

 Administered intravenously and orally but IM
and SC injection can cause tissue damage

 Readily absorbed orally

53
Q

Distribution of injectable anesthetic GABA agonists

A

Distribution to all tissues and the rate of
distribution depends on their lipid solubility

More lipid soluble are faster acting (BBB)

54
Q

Metabolism and elimination of injectable anesthetic GABA agonists?

A

 Metabolized by hydroxylation in the liver

 Thiobarbiturates are also inactivated in the brain and the kidney

 Barbiturates are enzyme inducers

55
Q

Duration of action of injectable anesthetic GABA agonists?

A

Duration of action and recovery depends on redistribution and elimination

56
Q

Recovery of injectable anesthetic GABA agonists?

A

slower in thin animals such as greyhounds or emaciated animals


57
Q

Barbituates main effects in the CNS?

A

Sedation, hypnosis, and anesthesia

Poor analgesia unless anesthetized

Anticonvulsant (- intracranial pressure)

Decrease brain metabolism (neuroprotective) sometimes used for head trauma by decreasing metabolic requirements

58
Q

Main effects of Barbiturates in the CVS?

A

Hypotension is mainly due to cardiac depression with lesser contribution from vasodilation

Hypotension may cause reflex tachycardia

Thiobarbiturates may sensitize the myocardium to catecholamine-induced arrhythmias

59
Q

Barbiturates main effects on the respiratory system?

A

 Dose-dependent respiratory depression (especially at anesthetic dose)

 Cats are more sensitive to respiratory depression

 Intravenous injection causes more depression than oral administration

60
Q

What’s significant about deaths by barbiturates?

A

This is of primary importance with these drugs and is likely the most common cause of death, due to inaccurate dosing or poor monitoring.

Best to intubate and monitor closely (pulse oximetry, designated tech, ECG, capnometry etc…)

61
Q

Skeletal muscle effects of barbiturates?

A

 Inhibit sensitivity of the motor endplate to Ach

 Abdominal muscle relaxation not complete

62
Q

Body temp. effects of barbiturates?

A

 Hypothermia due to peripheral vasodilation and reduced basal metabolic rate

 Decreased temperature can lead to delayed recovery, coagulation abnormalities and ventricular arrhythmias

63
Q

Renal effects of barbiturates?

A

 Oliguria and anuria due to decreased blood pressure and resulting reduction in GFR

 Stimulation of ADH (vasopressin)

64
Q

Uterus and fetus effects of barbiturates?

A

 Depression of uterine contractions

 Depression of fetal respiration

65
Q

Name the non barbiturate drugs?

A

Propofol
Alfaxalone
Etomidate

66
Q

Propoflo?

A

Emulsion containing egg lecithin and soybean oil

Ideal for bacterial growth, use or discard within 12-24hr

One of the few white liquids that can go IV

67
Q

Propoflo 28?

A

Benzyl alcohol preservative

Once opened stable for 28 days

Not labeled for cats

68
Q

Pharmacokinetic for both formulations of propofol?

A

 Given IV only (slowly to effect over 20 seconds)

 Rapid onset (< 1 minute), short duration of action

 Widely distributed to all tissues (lipid soluble drug)

 Redistribution to muscle then to fat

 Metabolism is rapid (hepatic and extrahepatic)

 Rapid metabolism allows for repeated dosing/CRI

 Metabolites excreted in urine

69
Q

Main effects on different body systems (CNC, cardiovascular, Respir., Muscle)

A

Central Nervous System
 Dose-dependent CNS depression

Cardiovascular
 Vasodilation w/out reflex tachycardia (cardiac depressant)
 Splenic engorgement can be observed

Respiratory
 Dose dependent respiratory depression
 Rate-dependent apnea (e.g. with rapid administration)

Muscle
 Laryngeal reflexes decreased
 Myoclonic movements on induction
 After induction generally good muscle relaxation

Other
 Appetite stimulation
 Heinz-body anemia (> 5 days repeated use cats)
 Risk of dependence

70
Q

Alfaxalone?

A

Alfaxalone Neurosteroid which is an analog of progesterone

MOA:
 GABA agonist

Does not bind to usual ‘steroid’ receptors (no effect on glucocorticoid, mineralocorticoid, or sex hormones!!)

Approved (Class IV controlled substance) in US 08/2014

71
Q

Alfaxalone compared to propofol?

A

 Similar pharmacokinetics

 Rapid onset, short duration, no accumulation (CRI ok)

 Labeled for IV usage only

 Sometimes used (off label) IM unlike propofol

 Contains no preservative – use within 24h

 In other countries labeled shelf life of 7 days

Similar pharmacologic effects
 Dose dependent CNS depression
 No significant analgesia
 Good muscle relaxation
 Metabolized in the liver (glucuronidation and sulfation)
 Cardiac and respiratory depression similar to propofol
 Myoclonus can be seen during induction (and if given by non-IV routes), possibly some on recovery
 May see increased secretions?

72
Q

Etomidate?

A

 MOA:
Depresses the CNS by enhancing GABA

Indicated in patients with significant cardiac disease

 Has a sedative hypnotic,and anesthetic effects

 No analgesic effect

 Good muscle relaxation during anesthesia

 May cause excitement or myclonic twitching which can be minimized by pretreatment with benzodiazepenes or opioids

Does not have significant cardiovascular effects compared to other IV anesthetics

 Inhibits cortisol synthesis

 Rapid recovery with no accumulation

 Rapid hepatic metabolism

 Metabolites excreted in kidney and bile

 Can be used as induction agent in the dog & cat

 Reported to be better for critical patients

73
Q

Injectable anesthetic GABA agonists clinical uses?

A

Anesthetic Induction

This is stage I and II

Generally characterized by excitement

Ultra short acting barbiturates can be used to shorten induction

Premedications also decrease excitement

Procedural sedation

Emergency anti-convulsants

TIVA

74
Q

Pharmacologic effects propofol and alfaxalone?

A

Pharmacologic Effects Overview

Sedation?
 Full anesthesia

Muscle relaxation?
 Good muscle relaxation

Analgesia?
 None

Cardiorespiratory effects?
Respiratory depression and hypotension, Apnea on induction

Other?
 Myotonia on induction, anticonvulsant

Pharmacology Test 2 (7 decks)

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