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VTS(ECC) Study > Anesthesia and Analgesia > Flashcards

Anesthesia and Analgesia Flashcards

1
Q

What is the goal of analgesia?

A

Provide a state in which pain is bearable but some protective aspects of pain still remain

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2
Q

Why use multi-modal analgesia?

A

Unlikely that single agent will address whole of the pain - complex pain pathways

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3
Q

When can analgesic therapy be diagnostic?

A

If a patient is particularly stoic or quiet. Often happens in cats.

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4
Q

How do opioids basically function?

A

Have central action to limit input of nociceptive information

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5
Q

Which opioids induce histamine release?

A

Morphine, meperidine, methadone

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6
Q

What are some side effects of opioids?

A

Gastroparesis, ileus
Vomiting, regurgitation, defecation, respiratory depression
Potential for aspiration

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7
Q

Opioids may cause gastric distention due to gastroparesis and ileus. In which disease is this particularly of concern? Why?

A

Pancreatitis. Due to gastric distention stimulating pancreatic enzymes.
Manage with feeding tube and motility therapy if needed

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8
Q

What is one indication of effective opioid pain control in cats?

A

Mydriasis

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9
Q

What is one major indication for the use of remifentanil?

A

Severe liver disease - no hepatic or renal metabolism required

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10
Q

What is one major side effect of remifentanil?

A

Profound respiratory depression

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11
Q

What are the physiologic effects of sudden and complete reversal of analgesia (such as with naloxone)

A

Acute pain, excitement, emergence delirium, aggression, hyperalgesia, catecholemine release leading to death

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12
Q

What does the COX-1 enzyme do?

A

Basal prostaglandin production for normal homeostatic processes - GI mucus production, platelet function, indirectly helps with hemostasis, effect on renal blood flow

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13
Q

What does the COX-2 enzyme do?

A

Found at sites of inflammation - Some basal production of constitutive prostaglandins, triggers production of inflammatory prostaglandins contributing to peripheral sensitization and GI ulceration

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14
Q

Which conditions may be a contraindication for receiving NSAIDS?

A

Renal disease, hypotension, hypovolemia, GI disease, ulceration, liver disease

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15
Q

What is the onset of action for any NSAID?

A

45-60 minutes

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16
Q

Which drugs are an absolute contraindication for co-administration with NSAIDS?

A

Corticosteroids

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17
Q

How long do the analgesic effects of alpha-2 agonists last?

A

30-90 minutes alone, up to 4 hours with opiates

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18
Q

Why should you avoid administration of atipamezole IV?

A

Abrupt hypotension and/or aggression

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19
Q

How long does it take for a transdermal fentanyl patch to provide analgesia?

A

Up to 24 hours in dogs, 6-12 hours in cats

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20
Q

What can alter uptake of transdermal fentanyl patch?

A

Blood pressure, obesity, hair, body temperature

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21
Q

What beneficial effects do NMDA receptor antagonists have?

A

Analgesic, amnestic, psychomitmetic effects, neuroprotective

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22
Q

What adverse effects do NMDA receptor antagonists have?

A

tremors, sedation, increased cardiac output, increased sympathetic tone

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23
Q

How much sodium bicarbonate is added to lidocaine to reduce sting?

A

1-2 parts sodium bicarbonate in 8-9 parts lidocaine

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24
Q

How much sodium bicarbonate is added to bupivacaine to reduce sting?

A

1:30 ratio

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25
Q

What is an absolute contraindication for bupivacaine administration?

A

Life threatening cardiac arrhythmia

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26
Q

What is the maximum safe dose of lidocaine

A

In most species 4mg/kg

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27
Q

What is the maximum safe dose of bupivacaine

A

In most species 1-2mg/kg

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28
Q

What are some contraindications for administration of epidural anesthesia?

A

Pelvic region trauma (loss of landmarks), sepsis, coagulopathy, CNS disease, skin infection at site, hypovolemic shock, severe obesity

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29
Q

Before administration of sedative or anesthesia a physical examination with ECG should be performed. When must an arrhythmia be treated?

A

Frequent, multifocal VPCs, paroxysmal ventricular tachycardia that adversely affects blood pressure or perfusion

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30
Q

What arrhythmias may be seen after administration of opioids?

A

Vagally induced bradycardia or second degree AV block

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31
Q

Why do opioids act as respiratory depressants?

A

Decreased ventialtory response to increasing CO2 concentration

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32
Q

Which opioid has NMDA receptor antagonistic properties

A

Methadone

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33
Q

Which opioid requires a higher dose of naloxone to reverse?

A

Buprenorphine - may require up to 10x dose

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34
Q

Why does acepromazine cause peripheral vasodilation

A

Alpha antagonist properties

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35
Q

How long does IM administration of acepromazine take to become effective?

A

20-30 minutes

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36
Q

What are the reasons for decreased cardiac output after administration of alpha-2 agonists?

A

Decreased heart rate, myocardial depression, increased afterload (decreased stroke volume)

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37
Q

What are side effects of alpha-2 agonists?

A

Bradycardia, peripheral vasoconstriction, respiratory depression, vomiting, inhibition of insulin release, diuresis

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38
Q

Why must you use ketamine only with extreme caution in patients with underlying heart diesease?

A

Increased myocardial contractility and oxygen consumption. Especially use with caution in HCM

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39
Q

What respiratory effect of ketamine makes it useful for patients with underlying lung disease

A

Bronchodilator effects

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40
Q

Why is ketamine contraindicated in cranial or ocular trauma

A

Raises intracranial pressure and intraocular pressure

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41
Q

What drug may cause seizure like activity when administered as a sole agent in the dog?

A

Ketamine

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42
Q

What is the duration of action of propofol

A

5-10 minutes

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43
Q

Why must propofol be used with caution in hypovolemic patients or those with cardiovascular compromise

A

Acts as peripheral vasodilator, myocardial depressant, cardiovascular depression

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44
Q

What is the required MAP to maintain blood flow to tissues

A

> 60-70mmHg

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45
Q

What PCV is required to maintain oxygen carrying capacity and delivery?

A

> 25%

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46
Q

How much can the PCV drop during anesthesia?

A

3-5%

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47
Q

How much fresh frozen plasma is required to raise albumin by 1g/dL

A

45mL/kg

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48
Q

What adverse effects may be seen from human albumin administration?

A

Polyarthritis, future transfusion reactions, glomerulonephritis, other immune-mediated effects

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49
Q

What changes may need to be made in the anesthetic protocol for a patient with kidney disease

A

Higher fluid rate, monitor urine output, monitor which drugs are excreted via renal metabolism

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50
Q

What changes may need to be made in the anesthetic protocol for a patient with liver disease

A

Monitor glucose, monitor drugs which are cytochrome P450 enzyme dependent, potential for coagulopathy

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51
Q

What is the duration of action of thiopental?

A

10-15 minutes

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52
Q

Which induction agents reduce intracranial and intraocular pressure?

A

Thiopental and propofol

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53
Q

Why is popo-flo 28 contraindicated in cats?

A

Potential for toxicity of benzyl alcohol

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54
Q

Why is propofol used with caution in cats? Under what circumstances?

A

Can cause Heinz body anemia, slower metabolism and excretion. Happens with recurrent administration (>3 days) or CRI administration

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55
Q

What type of drug is alfaxalone

A

Synthetic neuroactive steroid - induction agent

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56
Q

What is the duration of action of alfaxalone?

A

14-50 minutes

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57
Q

Why should you avoid use of etomidate as a single agent?

A

Retching and myoclonus

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58
Q

Why can etomidate cause hemolysis in cats after repeated administration

A

Propylene glycol

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59
Q

What is a major side effect of etomidate?

A

Adrenal dysfunction lasting 24-48 hours

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60
Q

What does ketamine rely on to increase heart rate, blood pressure, and cardiac output

A

Sympathetically mediated catecholamine release

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61
Q

What happens after administration of ketamine to a patient with depleted catecholamine stores?

A

Hypotension and potential for cardiovascular collapse

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62
Q

What type of analgesia does ketamine provide?

A

Peripheral and somatic

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63
Q

How is remefentanil processed?

A

Non-specific estrases in blood and tissue

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64
Q

Which premedications and induction agents cause splenomegaly?

A

Acepromazine, thiopental, propofol

Also decrease PCV

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65
Q

What are some indications for utilizing neuromuscular blockades?

A

Management of increased intracranial pressure, tetanus, drug overdose, seizure,
Surgically - skeletal muscle relaxation, controlled respiratory effort, ocular immobilization, rapid intubation

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66
Q

Why is intermittent bolus dosing preferred to CRI dosing of neuromuscular blocking agents?

A

Control of tachyphylaxis, monitor for accumulation, provision of analgesia and anemia, liming complications of prolonged or excess blockade

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67
Q

Which drugs are benzylisouinoliunium agents?

A

Neuromuscular blockade agents, atracurium, cisatricurium, doxacurium, mivacurium

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68
Q

How long does atracurium take to show effects? Duration of action?

A

Blockade in 3-5 minutes, duration of 20-30 minutes (1-2 hour recovery after CRI)

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69
Q

What is laudanosine?

A

Byproduct of metabolism of atracurium and cisatricurium - causes hypotension and seizures

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70
Q

What are adverse effects of atracurium and cisatricurium?

A

Histamine release, laudanosine production - especially in hepatic insufficiency

71
Q

What maintenance agent may increase duration of action of atracurium?

A

Sevoflurane

72
Q

Which nerves are used to monitor neuromuscular blockade?

A

Facial, ulnar, tibial, and superficial peroneal

73
Q

What are indications that neuromuscular blockade agents are wearing off?

A

Decreased chest wall compliance, increased resistance to ventilation, greater PIP with no change in tidal volume

74
Q

When are neuromuscular blockade reversal agents contraindicated?

A

When no evidence of muscle response seen

75
Q

What are some reversal agents for neuromuscular blockade agents?

A

edrophonium, neostigmine

76
Q

Why are neuromuscular blockade agents administered with an anticholenergic?

A

Due to accumulation of acetylcholine that occurs

77
Q

Which anticholenergic is administered with neostigmine? Why?

A

Glycopyrrolate, same onset and duration of action

Onset - 7-10 minutes, DOA 60-70 minutes

78
Q

Which anticholenergic is administered with edrophonium? Why?

A

Atropine, same onset and duration of action

Onset - 1-2 minutes, DOA 60 minutes

79
Q

Why is tepoxalin a unique NSAID?

A

Also inhibits lipoxygenase along with COX

-Produces leukotrienes that precipitate inflammatory cascade

80
Q

Why do cats not metabolize NSAIDs as well as dogs?

A

Deficient in glucuronyl transferase enzymes

81
Q

Why must you use caution when administering NSAIDs to patients with hypoalbuminemia

A

They are highly protein bound

82
Q

What are the 3 opioid receptors?

A

Mu, kappa, delta

83
Q

Pure agonists

A

Stimulate receptors

84
Q

Agonist/antagonists

A

stimulate one receptor, block another

85
Q

Partial agonists

A

Partial binding of a receptor

86
Q

Pure antagonists

A

Bind to, but do not stimulate, a receptor

87
Q

What is unique about the effect of meperidine on the heart rate compared to other opioids

A

Causes tachycardia, not bradycardia

88
Q

What is morphine-6-glucuronide? Why is it important?

A

Active metabolite of morphine. Makes it longer acting in dogs and less effective in cats because they cannot use glucuronidation metabolism.

89
Q

Which opioids should be avoided during administration of MAOI inhibitors or tricyclic antidepressants? Why?

A

meperidine and methadone. Buprenorhpine. Serotonin syndrome possible

90
Q

What is the duration of action of fentanyl?

A

15-20 minutes

91
Q

What is the onset of action of buprenorphine?

A

30-45 minutes after IV or IM administration

92
Q

Which opioids have a ceiling effect?

A

Buprenorphine and butorphanol

93
Q

What is a ceiling effect?

A

Analgesic effects do not increase past a certain dose but side effects and duration of action might

94
Q

Which opioid has highest affinity for mu receptor

A

Buprenorphine

95
Q

What is nalbuphine?

A

An antagonist/agonist opioid similar to butorphanol

96
Q

What type of pain is butorphanol and nalbuphine good for?

A

Visceral pain

97
Q

What receptor does butorphanol agonize? Antagonize?

A

Agonistic effect on kappa receptor, antagonistic effect on mu receptor

98
Q

What is the duration of analgesia from butorphanol and nalbuphine?

A

Dogs 1-2 hours

Cats 2-4 hours

99
Q

What is the onset time of naloxone? Duration of action?

A

1-2 minute onset IV, 5 minute onset IM, 30-60 minute duration of action

100
Q

What is the onset time of nalmefene? Duration of action?

A

1-2 minute onset IV, 5 minute onset IM, 1-2 hour duration of action

101
Q

Which sedative may inhibit platelet aggregation?

A

Acepromazine

102
Q

Which breed of dog is more sensitive to acepromazine?

A

European boxers. May cause fainting and collapse

103
Q

Which sedative class should be avoided in severe liver disease?

A

Benzodiazepines - may worsen clinical signs in hepatic encephalopathy

104
Q

Why must you use caution with benzodiazepines in patients with hypoalbuminemia?

A

Highly protein bound

105
Q

Which of the sedative drug classes provides most reliable sedation?

A

Alpha-2 agonists

106
Q

Describe biphasic effect of dexmedetomidine

A

Initially peripheral post-synaptic alpha-2 receptors activated - vasoconstriction and hypertension (increased SVR)
Then - central and peripheral pre-synaptic alpha-2 receptors activated - sustained decease in BP due to vasodilation

107
Q

Why do alpha-2 agonists cause hyperglycemia?

A

Inhibition of insulin release

108
Q

Why do alpha-2 agonists cause bradycardia?

A

Decreased sympathetic drive allows vagal tone to predominate, hypertension leads to a reflex bradycardia due to baroreceptor response, causing an overall decreased cardiac output

109
Q

Why are anticholenergics contraindicated after alpha-2 administration?

A

Increases myocardial workload and oxygen demand and may cause arrhythmia without improvement in CO

110
Q

How do anticholinergics work?

A

Block acetylcholine at muscarinic receptors of parasympathetic nervous system

111
Q

When are anticholinergics indicated?

A

Sinus bradycardia from increased vagal tone, AV block, sinoatrial arrest

112
Q

What are risks of tachycardia

A

Increased cardiac work, increased myocardial oxygen consumption, decreased CO and O2 delivery, increased potential for arrhythmia

113
Q

What is unique about neonatal anesthetic protocol?

A

Require anticholenergics in premedication

Rely on HR rather than contractility to maintain CO

114
Q

What is another word for cycloheamines?

A

Dissociatives

115
Q

What do dissociatives do?

A

Disassociation between thalmus and limbic systems of brain

116
Q

Which disassociative drug causes increased bronchial secretion and hypersalivation?

A

Ketamine

117
Q

How do cats process ketamine?

A

Unchanged in the urine - use caution in severe renal disease

118
Q

Why doesn’t propofol cause reflex tachycardia after decreasing myocardial contractility and systemic vascular resistance

A

Suppresses baroreceptor response

119
Q

Which induction agent has minimal effect on cardiovascular system?

A

Etomidate

120
Q

Which induction agent requires a physiologic dose of steroids to be given?

A

Etomidate

121
Q

Alfaxalone causes dose dependent hypotension due to?

A

Myocardial depression and peripheral vasodilation - offset by reflex tachycardia

122
Q

Vapor pressure

A

Ability of a liquid to evaporate

Noted as percentage of barometric pressure at sea level

123
Q

Solubility

A

Amount of inhalant vapor dissolved within solvent at equilibrium

124
Q

Partition Coefficient

A

Ratio of solubility in solvent

125
Q

What is the route of partial pressure gradients between air and brain

A

inspired air, alveolar air, blood, brain

126
Q

Minimum Alveolar Concentration (MAC)

A

Concentration of inhalant that prevents gross purposeful movement in 50% of patients exposed to noxious stimulus

127
Q

Surgical MAC

A

Surgical MAC = 1.5xMAC

128
Q

2 major considerations in anesthetic protocol for c-section

A

Analgesia for mother with least cardiovascular depression

Delivering viable neonates while minimizing negative effects of drug

129
Q

What are special considerations about physiology of pregnant patients?

A

Susceptible to hypotension, increased SV and HR, relative anemia, blunted response to change in BP from decreased baroreceptor activity
Higher minute volume

130
Q

What type of pain do A Delta fibers convey

A

Fast localized sharp pain

131
Q

What type of pain do C fibers convey

A

Slow poorly localized dull pain

132
Q

Visceral pain

A

From viscera or organs
Well regionalized but difficult to locate
Aching, cramping, longer duration than somatic pain

133
Q

Somatic pain

A

From muscles, skin, and skeletal structure

Superficial or deep

134
Q

Superficial Somatic Pain

A

minor wounds/cuts, etc - sharp well defined localized pain of short duration

135
Q

Deep Somatic pain

A

Deep - From ligaments, tendons, bones, vessels, muscles. Dull, aching, poorly localized, longer acting than superficial somatic pain. Fractures, muscles, sprains, etc

136
Q

Neuropathic pain

A

From nervous system damage

May be peripheral or central

137
Q

Three components of endogenous central analgesia system

A

Periaqueductal grey matter, nucleus raphe magnus, nociception-inhibitory neurons within spinal cord

138
Q

Where in the CNS do benzodiazepines act

A

Limbic, thalamic, hypothalamic

139
Q

How are benzodiazepines metabolized?

A

Metabolized in liver to active metabolites which are conjugated and excreted unchanged in urine

140
Q

Why is diazepam injectable recommended to be administered via central venous line?

A

Propylene glycol vehicle. Irritant to blood vessels after repeat or continued administration

141
Q

What can propylene glycol toxicity cause? (especially toxic in cats)

A

Metabolic acidosis, hyperosmolality, neurologic abnormalities, organ dysfunction

142
Q

Which benzodiazepine can be administered rectally?

A

Diazepam

143
Q

Which injectable benzodiazepine can be administered orally?

A

Midazolam

144
Q

Which injectable benzodiazepine is water soluble?

A

Midazolam

145
Q

When is a benzodiazepine most likely to cause reliable sedation?

A

In the already very ill or when administered along with an opioid

146
Q

What can happen after oral diazepam administration in cats?

A

Fulminant hepatic failure from acute hepatic necrosis

Very rare

147
Q

Is midazolam or diazepam shorter acting?

A

Midazolam - makes it easier to titrate to effect for CRI

148
Q

Adverse effects of long term administration of benzodiazepines?

A

Dysphoria, excitement, delayed awakening. Rarely seizures, or acute benzodiazepine withdraw

149
Q

Why should you avoid the use of flumazenil or sarmazenil in healthy animals in stable condition?

A

Marked excitement and dysphoria

150
Q

Where are opioid receptors primarily located?

A

CNS and gut

151
Q

Why is tachypnea sometimes noted after opioid administration?

A

Excitation and/or alteration of thermoregulation center

152
Q

What is wooden chest?

A

Rare complication after opioid administration due to spasm of chest wall. Makes ventilation difficult.

153
Q

Which opioids are contraindicated in patients with mast cell diseases?

A

Morphine, meperedine, methadone - due to histamine release

154
Q

Urine retention is possible after administration of which type of drug? Why?

A

Opioids. Bladder atony.

155
Q

How are most opioids metabolized?

A

Most undergo hepatic conjugation and metabolite excretion in urine

156
Q

In addition to respiratory depression, what is another respiratory side effect of some opioids?

A

Bronchoconstriction

157
Q

What is important to monitor with morphine CRIs?

A

Efficacy and side effects - long half life and active metabolite means that plasma concentrations may increase over time

158
Q

What is the duration of effect of morphine?

A

4-6 hours

159
Q

What is duration of effect of methadone?

A

4-6 hours

160
Q

Which is more lipid soluble? Morphine or methadone?

A

Methadone

161
Q

What is the duration of effect of hydro and oxymorphone?

A

4 hours

162
Q

What is the duration of action of nalbuphine?

A

30-60 minutes

163
Q

How does tramadol work?

A

Has slight mu binding but more likely from interference with seretonin storage and norepinephrine reuptake

164
Q

When is codine appropriate for analgesia?

A

Moderate long term pain management when oral route can be utilized

165
Q

What does stimulation of presynaptic alpha-2 adrenoceptors in the CNS accomplish?

A

Decreased release of norepinephrine

166
Q

How do Alpha-2 agonists cause sedation?

A

inhibition of noradrenic neurons in upper brainstem

Increases stage II and III sleep - decreased REM sleep

167
Q

How do alpha-2 agonists cause analgesia?

A

Stimulation of receptors in dorsal horn of spinal cord and brainstem
Inhibits nociceptive neurons

168
Q

After administration of alpha-2 agonists what happens to cerebral blood flow?

A

Decreases - ensure adequate oxygenation

169
Q

Why are alpha-2 agonists considered arrhythmogenic?

A

Due to older alpha-2s not being selective - xylazine had affinity for alpha-1 as well - sensitized heart to catecholamine-induced arrhythmias

170
Q

What effect do alpha-2 agonists have on respiratory system?

A

Little. May decrease RR but maintain minute ventilation. Maintains arterial CO2 and O2 pressure

171
Q

What effect do alpha-2 agonists have on urine excretion

A

ADH release is inhibited, promotes diuresis and natriuresis

172
Q

What effects to alpha-2 agonists have on the gastrointestinal system?

A

Decreased salivation, gastroesophageal sphincter pressure, esophageal, gastric, and small intestinal motility, and gastric secretion

173
Q

What other receptors do the alpha-2 agonists effect?

A

Imidazoline receptors

174
Q

How long do alpha-2 antagonists take to take effect?

A

5-10 minutes

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