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Emergency Critical Care VTS > Anesthetic Drug Pharmacology > Flashcards

Anesthetic Drug Pharmacology Flashcards

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1
Q

Tranquilizers

A

drugs that reduce anxiety

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2
Q

Sedatives

A

drugs that produce sleep and reduce response to arousal

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3
Q

Analgesics

A

pain relievers

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4
Q

Induction agents

A

used to bring about a state of general anesthesia.

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5
Q

maintenance anesthetic agents

A

commonly inhalent anesthetics, but can also be injectable (also knowna s total intravenous anesthesia - TIVA)

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6
Q

Anticholinergics

Which receptors do they act on?
Where are the receptors located?

A

parasympatholytic drugs act on various muscarinic receptors found in the parasypathetic nervous system.

Receptors can be found in:
* the central nervous system
* salivary glands
* lungs
* sinoatrial and atrioventricular nodes of the myocardium
* smooth muscle of the GI tract

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7
Q

Pathophysiology of anticholinergics

A

Prevent the primary neurotransmitter, acetylcholine, from binding to their receptors, there by reducing the effects of the parasympathetic symptoms.

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8
Q

Common effects elicited by parasympathetic nerouvs system

A
  • bradycardia
  • bronchoconstriction
  • tear and saliva production
  • pupil constriction
  • increased gastrointestinal motility
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9
Q

Two common anticholinergics

A

Atropine
glycopyrrolate

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10
Q

Physiologic effects of anticholinergics

A
  • increase heart rate
  • bronchodilation
  • decreased tear and salive production
  • pupil dilation
  • decreased gastrointestinal motility
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11
Q

Potential side effects of anticholinergics

A
  • arrhythmia
  • sinus tachycardia
  • increase in myocardial oxygen demand
  • increase workload of the heart
  • may thicken airway secretions
  • Should not be used routinely used as part of premedication in most patients.
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12
Q

When to use anticholinergics with caution or avoid use

A

patients with hypertrophic cardiomyopathy

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13
Q

Pharmacokinetics of Aropine

A

Crosses the blood-rain and blood-placental barriers
quicker onset of action
metabolized by hydrolysis
excreted unchanged by kidneys in dogs
metabolized by renal esterase in cats

Peak effects of atropine can be seen within five minutes and duration of action is about 30 minutes

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14
Q

Pharmacokinetics of Glycopyrrolate

A

poorly lipid soluble
does not cross the blood-brain or blood-placental barriers
(use on pregnant patients if anticholingergics are required).
Rapidly cleared and excreted unchanged by the kidneys
Longer onset of action
peak effects at 5-7 minutes
duration of action 60-90 minutes.

Less likely to produce tachycardia
dose-dependent effects similar to atropine
Low doses - may see transient second degree AV block or worsening bradycardia.

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15
Q

Phenothiazines

A

tranquilizers that eert their effect on the central nervous system by blocking dopamine receptors.

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16
Q

Acepromazine
Drug glass
beneficial properties

A

Phenothiazine.

Also has antiemetic and potential antiarrhythmic effects.

Mild effects on vntilation and the rspiratory system.

Significantly reduces the amount of induction and maintenance anesthetic needed

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17
Q

Acepromazine disadvantages

A

Long duration >4 hours
no analgesic properties
inability to reverse
potent cardiovascular side-effects

  • alpha - 1 adrenergic antagonist effects: vasodilation resulting in decreased cardiac afterload and systemic vascular resistence
  • vasodilation - potential hypotension (especially when used with other vasodilating drugs - inhalant anesthetics), or in patients that are hypovolemic, dehydrated or in states of shock

promote hypothermia
temporarily decrease PCV
enlargement of spleen

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18
Q

Contraindications of acepromazine

A

Avoid in patients with liver dysfunction
Weak antihistamine properties therefore should e avoided prior to intradermal allergy skin testing.

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19
Q

Breed predispositions to Acepromazine

A

Some boxer dogs uniquely sensitive and have been reported to have profound cardiovascular depression and syncope

Australian shepherds, mini Australian shepherds, onghaired whippets, collies and several hearding breeds have genetic mutation to their P-glycoprotein pumps within their central nervous system. Known as multidrug-resistant-1 (MDR-1) gene mutation. Alters drug efflux from the central nervous system, resulting in prolonged drug effects.

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20
Q

Benzodiazepines

A

Class of tranquilizers that work by enhancing release of gamma-aminobutyric acid (GABA).

Examples include:
diazepam
midazolam
alprazolam
zolazepam

Provide anxiolysis, mild to moderate skeletal muscle relaxation, amnesia and are effective anticonvulsants

minimal influence on the cardiovascular and respiratory systems

Reversible with flumazenil

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21
Q

Midazolam

A

benzodiazepine

water soluble

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22
Q

diazepam

A

not water soluble
light sensitive
should not be mixed with other agents other than ketamine

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23
Q

Disadvantage of benzodiaepines

A

Does not provide analgesia
does not provide consistent tranquilization.
Some patients may exhibit excitatory effects - dysphoria, disinhibition

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24
Q
A
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25
Q

When to avoid use of benzodiazepines

A

hepatic dysfunction
risk of human buse and addiction
CIV controlled

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26
Q
A
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27
Q

Opioids

A

cause profound analgesia and mild to moderate sedation

works predominantly by influencing mu and kappa opioid receptors within the central and peripheral nervous systems

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28
Q

neuroleptanalgesia

A

occurs when opioids are given in conjunction with a sedative or tranquilizer

profound central nervous system depression and potentially analgesia than when each drug class is given alone.

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29
Q

Side effects of opioids

A

panting in dogs, nausea and vomiting, dysphoria, hypothermia in dogs, hyperthermia in cats, ileus

can ocasionally cause excitement in some species such as cats in high doses

Mild effects of cardiovascular system
increase vagal tone–> results in bradycardia, but minimal effects to blood pressure, systemic vascular resistance and cardiac output unless high doses are used.

can cause respiratory depression

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30
Q

pharmacokinetics of opioids

A

metabolized by the liver –> use with caution in patients with hepatic dysfunction

Agonism of mu receptor can lead to decreased urine production

stimulation of the kappa receptor can incrase urine production due to release of antidiuretic hormone.

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31
Q

Full mu agonists

A

tend to be most likely to cause bradycardia and respiratory depression

morphine
hydromorphone
oxymorphone
methadone
fentanyl
remifentanil

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32
Q

What other receptor does Methadone block?

A

N-methyl-D-aspartate (NMDA)

Also inhibits norepinephrine and serotonin reuptake

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33
Q

partial mu agonist

A

drug that binds to and activates a receptor to produce a biological response that mimics the release of endogenous opioids in the body although the effect is not as robust as full mu agonists.

Buprenorphine only partial mu in vetmed.

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34
Q

Buprenorphine

A

Partial mu agonist.
High affinity for opioid receptor sites - longer duration of effect (8-12 hours) and difficult to reverse with naloxone

Will temporarily prevent full mu agonists from binding

slow onset time of 45-60 minutes

minimal sedation for most; significant bradycardia uncommon

CIII class

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35
Q

Butorphanol

A

agonist-antagonist

kappa receptor agonist
mu receptor antagonist

rapid onset of action but duration is short (<1hr)

Not as efficacious as full mu agonist or partial mu agonists

Provides mild to moderate sedation

CIV class

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36
Q

Alpha-2 Adrenergic agonists

A

Potent sedatives (sleep-producing), effective analgesic that also have muscle relaxant properties.

two drugs: dexmedetomidine and xylazine

mild effects on the respiratory system and ventilation at clinical doses
When administered at higher doses and in combination with other drugs, can cause respiratory depression.

Disadvantages: profound cardiovascular effects

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37
Q

What are the cardiovascular effects of alpha-2 adrenergic agonists?

A

reduced cardiac output
arrhythmias
increased cardiac afterload from increased systemic vascular resistance
increase in blood pressure
overall decrease in oxygen transport to tissues

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38
Q

Why are anticholinergics not recommnded to treat bradycardia from alpha-2 adrenergic agonists?

A

It will increase the myocardial work against increased systemic vascular resistence. Can result in greater hypertension.

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39
Q

Contraindications for alpha-2 agonists

A

Heart disease
patients with hepatic dysfunction

will also result in transient increase in blood glucose and urine output - therefore should be avoided in diabetic patients.

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40
Q

Propofol and Propofol 28

A

GABA agonist

exists preservative free - to be discarded after 6 hours of opening
with preservative - to be used for 28 days.
the preservative is toxic to cats

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41
Q

Advantages of propofol

A

short duration of action
smoothness of induction and recovery
minimal hangover effect

Can be used for TIVA

decreases cerebral blood flow and cerebral metabolic rate of oxygen consumption.
decreases intracranial pressure

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42
Q

pathophysiology of propofol

A

metabolized by the liver and by extrahepatic sites (more stable for patients with hepatic dysfunction)

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43
Q

disadvantages of propofol

A

respiratory depressant
profound cardiovascular effects:
* causes vasodilation and decreased cardiac output
* can lead to hypotension
* Heinz body enemia with repeated does in cats
* risk for allergic reaction
* ability to worsen or trigger pancreatitis beause of its fat emulsion
* pain on injection
* myoclonus (can be minimized with other drugs)

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44
Q

Dose of propofol

A

4-6mg/kg (titrated over 60-90 seconds)

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45
Q

Etomidate

A

propylene glycol-based imidazole derivative, used to induce general anesthesia.

Acts through enhancement of the inhibitory neurotransmitter (GABA) and depresses the reticular formation of the brainstem causing hypnosis and unconsciousness

rapid acting; non-cumulative

46
Q

Cardiovascular effects of etomidate

A

no changes to cardiac output, strole volume or myocardial contractility
no appreciable changes to heart rate or MAP
does not sensitize the heart to catecholamine-induced arrhythmias

do not influence the respiratory drive, but can have a brief period of apnea upon induction.

brief period of myoclonus

47
Q

neurologic effects of etomidate

A

decreases cerebral blood flow and cerebral metabolic rate of oxygen consumption.
likely has anticonvulsant properties due to its interactions with GABA complex

48
Q

Pharmacokinetics of etomidate

A

metabolized and distributed by the liver, heart, kidneys and spleen.

Rosses placental barrier but rapidly cleared

49
Q

Side effects of etomidate

A

pain upon injection
inhibition of natural adrenocorticoid production
hemolysis of red blood cells

50
Q

Ketamine

A

Dissociative drug
Analgesic effect by being a NMDA receptor antagonist
bronchodilator
breif analgesia properties
favorable cardiovascular and respiratory effects
CIII controlled

51
Q

Is ketamine used in critical patients with hypovolemia and cardiopulmonary instability?

A

Ketamine is favorable for use in patients with hypovolemia and cardiopulmonary instability.
Ketamine can increase heart rate, cardiac output and blood pressure.

Ketamine can produce apneustic breathing patterin following administration.

52
Q

Is ketamine reversible?

A

No

53
Q

what are the pharmacokinetics of ketamine?

A

Can cause excitement - dysphoria, hallucinations, unpredictable behavior when given higher doses and without concurrent CNS depressing drugs.

Avoid in patients with hepatic dysfunction

It may increase intracranial pressure and cerebral metabolic oxygen consumption when used a lone, but not an issue when iven with other drugs such as benzodiazepines or propofol.

Increases intraocular pressure

My result in seizure like activity, but at other doses may be used to treat refractory seizures

54
Q

Alfaxalone

A

neurosteroid produces a GABA-A agonist effect

55
Q

Properties of alfaxalone

A

smooth inductiion of general anesthesia with minimial hangover

Less respiratory depressant than propofol

Less changes to blood pressure, cardiac output, and systemic vascular resistance.

56
Q

Disadvantages of alfaxalone

A

Cost
6 hour shelf life once opened
potential for rocky anesthetic recoveries

57
Q

Pharmacokinetics of alfaxalone

A

metabolized by the liver and eliminated by the kidney.

58
Q

Inhalant anesthetics

A

Sevoflurane
isoflurane
desflurane

59
Q

Minimum alveolar concentrations (MAC)

A

lowest concentration of inhalant needed to prevent gross motor response in 50% of patients when a painful stimulus is administered

MAC is a measure of drug potency. The more potent a volatile liquid, the lower the MAC

60
Q

Blood-gas partition coefficient

A

ratio of concentration of a compound in a solvent to the concentration in anotehr solvent (e.g. alveoli) at equilibrium.

A measure of drug solubility and lipophilicity.

higher blood gas partition coefficients will have slower onset and recovery than agents with lower blood-gas partition coefficient

61
Q

Factors that can decrease MAC

A

concurrent drug administration
hypothermia
severe hypotension
increased age
hypercapnia
pregnancy
severe hypoxemia

62
Q

Factors that can increase MAC

A

drug use
hyperthermia
young age

63
Q

Effects of inhalant anesthetics on cardiopulmonary systems

A

heart rate not usually affected
can cause vasodilation and decline in mean arterial blood pressure
Depresses cardiovascular system

Depression of respiratory drive is dose dependent

64
Q

Effects of inhalent anesthetics on intracranial pressure

A

dose dependent increases in cerebral blood flow and intracranial pressure.

65
Q

Effects of inhalant anesthetics on other body organs

A

Reduced blood flow to liver, kidneys and reduces glomerular filtration rate and urine output.

66
Q

Neuromuscular blocking agents
classifications

A

depolzarizing
non-depolarizatin

does not have any anesthetic, sedative, anti-anxiety or analgesic effects

67
Q

Depolarizaing neuromuscular blocking agents

A

Act as Ach receptor agonists in that they bind to the AcH receptors and generate an action potential.
Because depolarization agents are not metabolized by acetylcholinesterase, the binding of this drug to the receptor is prolonged, resulting in extended depolarization of the muscle endplate. As the muscle relaxant continues to bind to the acH receptor, the endplate cannot repolarize, resulting in muscle relaxation

68
Q

Non-depolarizing neuromuscular blocking agents

A

competitive receptor antagonists - bind to acetylcholine receptors but do not induce ion channel openings and block acetylcholine from binding resulting in muscle relaxation

69
Q

neuromuscular blocking agents pathophysiology

A

alter the binding of acetylcholine to the nicotinic receptors, resulting in skeletal and respiratory muscle paralysis

70
Q

Succinylcholine

classification and side-effects

A

depolarizing neuromuscular blocker

side-effects: muscle soreness, hyperkalemia, malignant hyperthermia, increased intracranial pressure
no reversal agent

71
Q

non-depolzaring neuromuscular blocking agents

A

atracurium, cisatracurium, pancuronium, vecuronium, rocuronium

each has different duration of effect and side effect

72
Q

inihibiting non-depolarizing neuromuscular blocking agents

A

Non-depolarizing neuromuscular blocking agents can be antagonised by acetylcholinesterase inhibitors such as edrophonium or neostigmine

73
Q

use of acetylcholinesterase inhibitors

A

avoid residual neuromuscular blockade and critical respiratory events such as hypoxemia and aspiration during anestehsia recovery

Reversal agents result in acetylcholine release at both niotinic and muscarinic sites

74
Q

Side effects of acetylcholinesterase inhibitors

A

bradycardia
bronchoconstriction
nausea
vomiting
diarrhea
abdominal cramping
rarely cardiac arrest

Atropine = drug of choice to treat adverse effects from AcH inhibitors

75
Q

Types of opioids: agonist

A

The opioid drug binds to the receptor producing maximum stimulation at the receptor

76
Q

Types of opioids: partial agonist

A

The opioid drug binds to the receptor but produces only weak stimulation - has a ceiling effect

77
Q

Types of opioids: Agonist/antagonist

A

have agonist or partial agonist activity at one or more types of opioid receptors and have the ability to antagonize the effects of an agonist at one or more types of opioid receptors

78
Q

Types of opioids: Antaonist

A

The opioid drug binds to the receptor producing no stimulation but effectively blocks the receptor to the other opioids

79
Q

Types of opioids: NMDA antagonist

A

Inhibits the action of N-methyl-D-aspartate receptors. Helps decrease wind up pain.

80
Q

Opioid receptors: Mu receptors

A

Analgesia, euphoria, sedation, respiratory depression, constipation.

81
Q

Opioid receptors: Delta receptors:

A

hallucinogenic effects and decreased gastrointestinal secretions

82
Q

Opioid receptors: Kappa receptors:

A

dysphoria via reduction in dopamine release

83
Q

What are the four phases of pain pathway?

A

Transduction: the processes by which tissue-damaging stimuli activate nerve endings
Transmission: the relay function by which the message is carried from the site of tissue injury to the brain regions underlying perception.
Modulation: neural process that acts specifically to reduce activity in the transmission system.
Perception: the subjective awareness produced by sensory signals.

84
Q

Pain Pathway interventions: Nociception

A

Can be in inhibited by local anesthetics, opioids and NSAIDS

85
Q

Pain Pathway intervention: Transmission along peripheral nerve

A

inhibited by local anesthetics and alpha 2 agonists

86
Q

Pain pathway interventions: spinal cord sensitization

A

inhibited by opioids, NSAIDS, NMDA antagonists, alpha 2 agonists and local anesthetics

87
Q

Pain pathway interventions: conscious perception

A

Inhibited general anesthetics, opioids and alpha agonists.

88
Q

Effects of opioids: Sedation

A

CNS depression or excitement (in cats)

89
Q

Effects of opioids: termoregulation

A

hypothermia mostly, but come can show hyperthermia in cats.

90
Q

Effects of opioids: chemoreceptor trigger zones

A

can see nausea and vomiting. Seen more commonly with morphine.

91
Q

Effects of opioids: depression of coughing reflex

A

used as an antitussive
e.g. codeine or butorphanol

91
Q

Effects of opioids: mydriasis or miosis

A

Depending on CNS depression or stimulation.

92
Q

Effects of opioids: respiratory depression

A

Dose dependent
Can also be due to decreased respiratory responsiveness to chemoreceptors in the brainstem.
Help respiratory function depending on the case (e.g. thoracotomy)

93
Q

Effects of opioids: cardiovascular system

A

Bradycardia but responsive to anticholinergics

Morphine can cause rapid histamine release and can cause vasodilation and hypotension if given IV

Generally though, opioids have minimal effects on cardiac output, cardiac rhythm.

94
Q

Effects of opioids: GI system

A

defecation and bowel movements, but can also lead to constipation (especially long term)

95
Q

Morphine

A

Full opioid agonist that works on Mu, Kappa and Delta receptors.

Natural narcotic

Duration: 3-4 hours

Use with caution when giving IV because of histamine release
poor lipid solubility so in epidural space 12-24 hours.

96
Q

Fentanyl

A

Pure mu agonist, with 100x potency compared to morphine.

Fast onset (approx 5 minutes) and short duration of action (approx 30 minutes) - makes it ideal for CRI

Common effects include apnea and bradycardia (monitor HR and RR) with high doses

Lipid soluble therefore can be administered as patches. 24 hours in dogs and 12 hours in cats for full effect. Last up to 72 hours.

97
Q

Methadone

A

Synthetic mu agonist with 1.5x the potency of morphine.

Duration of time is 2-4 hours

Can give TM in cats

Can cause more dysphoria but less likely to vomit

More affinity to NMDA and alpha 2 adrenergic receptors so can help with wind-up pain.

98
Q

Oxymorphone

A

Synthetic mu opioid and 10x the potency of morphine.

Less likely to make patients vomit

Good for patients with respiratory considerations because less likely to cause any panting.

99
Q

Hydromorphone

A

Less to cause panting

100
Q

Remifentanyl

A

50x potency of morphine
Faster acting than Fentanyl

Unique because it is metabolized by non specific plasma

Independent in kidney and liver metabolism.

101
Q

Buprenorphine

A

Semisynthetic partial mu agonist with partial to no effect on Kappa receptor.

Higher affinity for mu receptors, so can displace morphine if administered at the same time, but cannot elicit maximum clinical response therefore only used to treat mild to moderate pain.

Duration 6-12 hours depending on dose and route of administration.

102
Q

Butorphanol

A

Agonist/antagonist

good sedation when used in conjunction with acepromazine or benzodiazepine.

Works at Kappa receptors - 5x potency at kappa receptor than morphine

Antagonizes mu receptor.

Also has antitussive properties.

103
Q

Naloxone

A

Mu antagonist
higher affinity to mu receptors
reverses opioids
duration of action 20-40 minutes
Onset within 1 minute

Quick onset - naloxone should be titrated to effect to avoid adverse effects
May need additional doses

Theoretically PVC can be seen

Can be used to reverse agonist and agonist/antagonist drugs but will not reverse buprenorphine.

104
Q

Ketamine

A

NMDA antagonist
increase HR/BP due to indirect stimulation of cardiovascular system

Increases intracranial pressure

Cats increase sensitivity - hallucinaations, ataxia, hyperflexia (administer with muscle relaxant)

Good somatic analgesia but poor visceral analgesia

105
Q

Local anesthetics pathophysiology

A

Reversibly bind to sodium channels and block impulse in nerve conduction

Sensation disappear in the order of: pain, cold, warmth, touch, deep pressure

Sensory blockade will usually persist longer than motor blockade

106
Q

Meditomidine, dexmeditomidine, xylazine

A

Alpha 2 agonist
sedation and hypnosis, analgesia and muscle relaxation.

Metabolized in liver and excreted by kidneys

Cardiovascular effects - spike in arterial blood pressure and reflex bradycardia - can see dysrhythmias

Can see pale mucous membranes

emesis in cats

Contraindicated in cardiac cases, renal failure and obstructed urinary tracts as it tends to lead to increase urine output

107
Q

Lidocaine vs bupivicaine

A

Lidocaine duration of effect is 1-2 hours

Bupivicaine is cardiotoxic should not be delivered IV, duration 2-6 hours

108
Q

Diazepam/ketamine

A

can cause cardiopulmonary depression
Prolonged effects in patients with hepatic or renal dysfunction
Cardiovascular effects include:
- tachycardia
- increased blood pressure
- increased cardiac output
- increased myocardial oxygen consumption
Good analgesic properties
muscle relaxant

108
Q
A
108
Q
A
109
Q
A

Emergency Critical Care VTS (21 decks)

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