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VTS(ECC) Preparation > Anaesthesia & Analgesia > Flashcards

Anaesthesia & Analgesia Flashcards

1
Q

What are the main goals of an anaesthetic drug protocol? What are we aiming to achieve?

A

a. Hypnosis
b. Analgesia
c. Amnesia
d. Muscle relaxation

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2
Q

What is the purpose of multimodal drug protocols? What are the benefits?

A

To lower the amount of each agent used to further reduce the side effects of each agent. When used correctly, this minimises the amount of inhalant anaesthesia required and offers the most cardiovascular stability.

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3
Q

What is neuroleptanalgesia? What are the benefits?

A

Combination of an opiate with a sedative or tranquilizer. Benefits include:
- minimises stress
- offers pre-emptive pain relief as well as preventing peripheral and central sensitization (exaggeration of pain).
- assists with ‘handibility’ of a patient
- promotes smooth induction and recovery
- reduces the amount of induction or maintenance agents required.

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4
Q

What size reservoir bag is appropriate for a 23^kg patient?
a. 1^L
b. 2^L
c. 3^L
d. 5^L

A

B

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5
Q

Delayed recovery, impaired wound healing, increased infection risk, and coagulopathy can result from which of the following?
a. Hypotension
b. Hypothermia
c. Hypocapnia
d. Hypoventilation

A

B

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6
Q

Which induction agent may be beneficial for patients with heart disease because it increases heart rate and cardiac output?
a. Alfaxalone
b. Propofol
c. Fentanyl
d. Ketamine

A

D

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7
Q

A moribund patient that is not expected to survive would be assigned which ASA rating?
a. I
b. II
c. IV
d. V

A

D

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8
Q

A non-rebreathing system would be indicated for which patient?
a. 40^kg German shepherd
b. 12^kg pug
c. 5^kg Yorkshire terrier
d. 55^kg rottweiler

A

C

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9
Q

Which of the following is a partial mu agonist?
a. Buprenorphine
b. Butorphanol
c. Dexmedetomidine
d. Ketamine

A

A

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10
Q

Which induction agent is a neuroactive steroid?
a. Etomidate
b. Propofol
c. Alfaxalone
d. Tiletamine

A

C

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11
Q

A patient with GDV would be assigned which ASA rating?
a. I
b. II
c. III
d. IV

A

D

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12
Q

Flumazenil is which class of drug?
a. Benzodiazepine antagonist
b. Opiate antagonist
c. Alpha-2 antagonist
d. Dopaminergic antagonist

A

A

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13
Q

Which period of time poses the greatest anesthetic risk?
a. Preanesthetic
b. Postanesthetic
c. Induction
d. All times are of equal risk

A

B

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14
Q

Visceral pain is described as which of the following?
a. Easily localized to skin, muscle, joints, or deep tissue
b. Poorly localized, causing aching, cramping, or pressure
c. Chronic pain that lasts despite recovery or healing
d. Nerve pain that results in shooting, burning or tingling pain

A

B

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15
Q

Ketamine belongs to which drug class?
a. NMDA antagonist
b. Sodium channel blocker
c. Alpha-2 agonist
d. Benzodiazepine tranquilizer

A

A

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16
Q

he epidural space in dogs and cats is most accessible between which vertebral spaces?
a. L5–L6
b. L6–L7
c. L7–S1
d. S1–S2

A

C

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17
Q

Which step of the pain pathway interprets impulses in the spinal cord?
a. Transduction
b. Transmission
c. Modulation
d. Perception

A

C

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18
Q

Bladder palpation and potentially bladder expression are important nursing actions for a patient that has received which therapy?
a. Opioid epidural
b. Lidocaine CRI
c. Ketamine CRI
d. Bupivacaine local anesthesia

A

A

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19
Q

Due to lack of evidence-based data, which of the following drugs should not be used as a sole source of pain control?
a. Buprenorphine
b. Hydromorphone
c. Carprofen
d. Tramadol

A

D

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20
Q

The concept of using various agents and techniques to address pain from different angles is called what?
a. Pre-emptive analgesia
b. Multimodal analgesia
c. Preventtive analgesia
d. Critical care pharmacology

A

B

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21
Q

When neurons in the spine have trouble differentiating noxious stimuli from other stimuli, this is called what?
a. Hyperalgesia
b. Allodynia
c. Maladaptive pain
d. Neuropathic pain

A

B

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22
Q

Which drug is often lumped in with NSAIDs but has no true anti-inflammatory effects?
a. Ketamine
b. Lidocaine
c. Acetaminophen
d. Gabapentin

A

C

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23
Q

A state of unease or dissatisfaction, often accompanied by agitation and anxiety, refers to what condition?
a. Delirium
b. Dysphoria
c. Pain
d. Obtundation

A

B

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24
Q

A patient in for neutering would be assigned with an ASA score of?

A

1

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25
Q

A patient with well compensated mild mitral valve degeneration would be assigned with an ASA score of?

A

2

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26
Q

A patient with an IRIS stage 3/CKD, diabetes mellitus, other moderate systemic disease would be assigned and ASA score of?

A

3

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27
Q

A dog with haemabdomen secondary to a bleeding splenic mass would be assigned an ASA score of?

A

4

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28
Q

A moribund patient or one that is not expected to survive without surgery is assigned an ASA score of?

A

5

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29
Q

What breeds benefit from surface area dosing?

A

Giant breeds

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30
Q

Why is intravenous induction preferred?

A

Rapid, allows faster airway control

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31
Q

What should be monitored in a patient under anaesthesia?

A
  • HR + ECG
  • Resp + resp effort
  • EtCO2
  • Temperature
  • Pulse + BP
  • Depth
  • Pain
  • MM + CRT
  • SpO2
  • Fluid balance
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32
Q

What are the generic surgical fluid rates for patients under anaesthesia?

A

5ml/kg (Dogs)
3ml/kg (Cats)

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33
Q

How do NSAID’s work?

A

Either partially or completely block cyclooxygenase enzymes 1 & 2 inhibiting prostaglandin formation (prostacyclins, prostaglandins and thromboxane)

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34
Q

What is COX-1?

A

COX-1 is known to be present in most of the tissues in your body. In the gastrointestinal tract, COX-1 maintains the normal lining of the stomach and intestines, protecting the stomach from the digestive juices. The enzyme is also involved in kidney and platelet function.

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35
Q

What is COX-2?

A

Primarily found at sites of inflammation i.e. maccrophages, peripheral sensitisation, may cause gastric ulceration

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36
Q

When may NSAID’s be beneficial and when should they be avoided?

A

Beneficial in healthy pre-operative patients to reduce intra-operative inflammation and to reduce fever. They are to be avoided in critical patients due to risks to the GIT, bone marrow suppression, increased bleeding and renal necrosis.

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37
Q

Salicytes i.e. aspirin have what use in A&A. What patients should not be given aspirin?

A

Potent prostaglandin inhibitor and reduced platelet aggregation and also has anti-pyretic effects. It is poorly metabolised in cats so should be avoided.

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38
Q

Propionic acid derivatives i.e. carprofen and ibuprofen have what use in A&A. What are common side effects?

A

Produce analgesia and also some have anti-inflammatory and antipyretic properties. May cause GI ulceration, vomiting and anorexia but maybe less so than selective COX-2, but may be hepatotoxic

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39
Q

Selective COX-2 inhibitors i.e. firocoxib, meloxicam, carprofen have what use in A&A. What are common side effects?

A

Anti-inflammatory, antipyretic, analgesia, also good for chronic pain/osteoarthritis
Side effects include: vomiting, GI ulceration, diarrhoea, azotaemia and hepatopathy

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40
Q

Why should cats only receive a one off dose of NSAID’s?

A

Lack glucuronyl transferase and therefore have a hard time metabolising NSAID’s

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41
Q

What is pain?

A

Unpleasant sensory event of the peripheral and central nervous systems that is both a cognitive and emotional experience.

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42
Q

What is nociception?

A

The processing of a noxious stimulus
Chemical: acid
Mechanic: cuts, bruises etc
Thermal: heat

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43
Q

Explain the nociceptive pain pathway

A

Injury occurs and nociceptors translate this into an electrical signal (TRANSDUCTION) which is then TRANSMITTED along the length of the neuron to cells in the spinal cord and brain (dorsal horn and dorsal root ganglion). After which secondary neurons receive excitatory or inhibitory inputs from neurotransmitters released by peripheral neurons and neuropathways and the action potential is either transmitted further or inhibited (MODULATION). If transmitted the brain responds making the animal aware of the pain.

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44
Q

What occurs as a result of neuroendocrine activation in response to pain?

A

Activation of the hypothalamic-pituitary-adrenal gland axis which results in catecholamine and pro-inflammatory cytokine release. As a result there is altered immune function and impaired wound healing and wind up if not mitigated.

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45
Q

What is the difference between nociceptive and neuropathic pain?

A

nociceptive pain is the normal processing of pain (i.e. fractures, tissue injury) whereas neuropathic pain is abnormal processing of pain input (cancer, phantom pain).

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46
Q

What is the difference between visceral and somatic pain?

A

Visceral pain is poorly localised and results in cramping and throbbing whereas somatic pain is localised and results in aching and throbbing

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47
Q

What are the 5 main opiate receptors? What are their actions?

A

Mu - analgesia, euphoria, respiratory depression, sedation
Kappa - analgesia, sedation
Delta - analgesia
Sigma - autonomic stimulation, dysphoria, hallucinations
Epsilon - analgesia

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48
Q

What drugs are mu opiates (full agonists)?

A

Fentanyl, methadone, hydromorphone, meperidine, morphine

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49
Q

What is the reversal agent for opiates?

A

Naloxone, nalbuphine (morphine, hydromorphone)

50
Q

What is acepromazine? What are the benefits? when shouldn’t they be used?

A

Phenothiazine derivative that allays fear and anxiety and is a proposed dopamine blocker. It also has the benefit of suppressing the CRTZ to suppress vomiting.
Due to its alpha-blockade properties it can induce hypotension so should be avoided in cardiovascularly unstable patients and should also be avoided in patients with bleeding disorders as it reduces platelet aggregation.

51
Q

What are benzodiazepines? What are the benefits? When shouldn’t they be used?

A

They are used to relieve anxiety, provide muscle relaxation and inhibit GABA receptors. Benefits include muscle relaxation, anxiolysis, anticonvulsant.
They should be avoided in patients with hepatopathy (i.e. PSS, lver disease) as they are highly protein bound and have been associated with hepatotoxicity.

52
Q

What is the reversal agent for benzodiazepines?

A

Flumazenil

53
Q

What are a2 agonists? What are the benefits? When shouldn’t they be used?

A

Work on decreasing epinephrine release producing potent sedation and mild analgesia. The have been shown to reduce induction <80% inhalant anaesthesia by <50%. They are only suitable for healthy patients and shouldn’t be given to patients with cardiovascular compromise.

54
Q

What is the reversal agent for medetomidine and dexmedetomidine?

A

atipamezole

55
Q

What is the recommended treatment for bradydysrhythmias due to a2 agonist administration?

A

If adequate blood pressure then treatment may not be indicated. It is recommended to reverse is cardiac output compromised and avoid anticholinergics unless completely necessary to avoid increasing myocardial work load and O2 demand.

56
Q

What is the reversal agent for xylazine?

A

Yohimbine and tolazoline

57
Q

What are anti-cholinergics used for?

A

Treating sinus bradycardia, AV block and sinus arrest but will only work if the bradycardia is a result of vagal stimulation. Usually given to pediatric patients in premed as they rely on their HR for CO.

58
Q

What is the benefit of using a barbituate as an induction agent? What are the side effects?

A
  • smooth, rapid induction without excitement
  • may be useful for patients with intracranial disease
  • short acting 15-20min
  • side effects: vasodilation, sloughing if goes perivascular, cummulative, induces apnoea if given too quickly.
59
Q

What is the benefit of using ketamine or telazol as an induction agent? What are the side effects?

A
  • dissociative causing catelepsy, amnesia and mild analgesia
  • useful in wind-up pain as block neuronal hypersensitisation
  • good when used with opiod and benzo
  • side effects: tachydysrhytmias, may increase ICP, spastic muscle jerking
60
Q

What is the benefit of using propofol as an induction agent? What are the side effects?

A
  • ultra short acting
  • rapid, smooth induction and causes amnesia
  • used to control refractory seizures
  • side effects: heinz body anaemia in cats, arrhythmias, apnoea, bacterial infection (soy bean emulsion), hypotension
61
Q

What is the benefit of using etomidate as an induction agent? What are the side effects?

A
  • minimal cardiovascular effeccts so useful in patients with cardiovascular disease or that are haemodynamically unstable
  • cerebral perfusion maintained better in comparison to other induction agents
  • not to be used as CRI
  • avoid in patients on steroid therapy or adrenocorticol dysfunction
62
Q

What is the benefit of using alfaxalone? What are the side effects?

A
  • produces hypnosis and muscle relaxation
  • rapid and smooth induction
  • side effects: apnoea, vasodilation
63
Q

How do inhalant anaesthetics such as sevoflurane and isoflurane work?

A

absorbed by the body via the lungs and distributed by the blood to the brain. The inhalant passes into a vaporiser and mixes with oxygen then through a breathing circuit to the patients lungs where it is rapidly diffused into blood to the brain.

64
Q

What is MAC?

A

Minimum alveolar concentration.
lowest concentration of an anaesthetic that produces no response to painful stimulus in 50% of patients.
Low MAC = high potency
High MAC = low potency

65
Q

What is MAC influenced by?

A
  • premed
  • CRI
  • blocks
  • hypoxaemia
  • PCV
  • hypothermia
  • hepatic disease
66
Q

Which of sevoflurane and isoflurane is more potent?

A

Isoflurane

67
Q

What are the negative endocrine and metabolic effects of pain?

A
  • immune dysfunction
  • immobility
  • delayed recovery
  • delayed wound healing
  • catecholamine release = increased metabolic demand and O2 consumption
  • increased HR & dysrhythmias
  • increased BP
  • stress hormone release
  • suffering
68
Q

What are the effects of fear and stress amplifying the pain response?

A
  • cortisol release
  • hyperglycaemia
  • catecholamine release
  • sympathetic NS stimulation
    All lead to a catabolic state
69
Q

MAP must be over ______ to ensure adequate coronary, cerebral and renal perfusion.

A

65-70mmHg

70
Q

What is a good sedative protocol for patients with cardiovascular instability?

A

Opiod + Benzodiazepine + ACP (+-)

ACP reduces afterload, calms and reduces arrhythmias. Avoid if hypotensive/hypovolaemic

71
Q

What is a good sedative protocol for patients with respiratory instability?

A

ACP + Propofol + Ketamine (+- benzo)

72
Q

Why are IV drugs preferred in unstable patients?

A

More predictable and titratable. An IVC also allows administration of reversals if required.

73
Q

What is the minimum PCV required for adequate O2 capacity and O2 delivery?

A

25%

74
Q

How much does the PCV typically drop during anaesthesia?

A

3-5%

75
Q

When is colloidal therapy indicated? Why would this be inititated? What are some options?

A

Indicated when TP <35 or albumin <20 in order to maintain normal colloidal osmotic pressure (COP). Without adequate COP fluid leaks into extravascular compartments and oedema forms.
- Human albumin
- Plasma
- vetstarch
- hetastarch (care)

76
Q

When would neuromuscular blocking agents be used in anaesthesia? What are some key points with their use?

A

Used when there is respiratory dysynchrony to improve gas exchange and is of particular use in intrathoracic procedures and ocular surgery.
- PPV must be performed
- No analgesia or anaesthetic properties
- Need to monitor nerve response
- May cause histamine release
- Only partially reverse

77
Q

What are symptoms of sedative overdose?

A

Stupor , depression, ataxia, coma

78
Q

What are symptoms of muscle relaxant overdose?

A

Muscle flaccidity, CNS depression, respiratory depression, cardiovascular effects, anticholinergic syndrome

79
Q

What are the symptoms of narcotic overdose?

A

CNS depression, respiratory depression, cardiovascular depressionGI stasis

80
Q

What is the main course of treatment for overdose of sedative, muscle relaxants and narcotics?

A
  • reversals
  • intubation and ventilation (airway management)
  • diuresis
  • decontamination
  • HR + BP monitoring
  • Vasopressor therapy
  • Intralipids
  • haemodialysis
81
Q

What are immobile post-operative patients at risk of? What is involved in immobile patient care?

A

Atelectasis
Pneumonia
Decubital ulcer formation
Thrombosis

Recumbency change 4-6h, PROM’s and massage at least 4x a day, comfortable bedding, relieve pressure points, assisted standing

82
Q

What does inadequate nutrition in the post-operative patient result in?

A

Delayed wound healing, bacterial translocation. Thes prolong hospital stay and increase morbidity.

83
Q

What are portosystemic shunts?

A

Vascular anomalies that connect portal circulation with systemic circulation and are classed as intrahepatic or extrahepatic

84
Q

What are the clinical signs of PSS?

A

GI signs (vomiting and diarrhoea)
CNS disturbances
Small stature
PICA
Urolithiasis
Heaptic dysfunction

85
Q

How are PSS patients stabilised medically?

A

Cathartics to increase gastric transit time
Antibiotics to reduce ammonia producing bacteria
Low protein diet to lower ammonia production
Anticonvulsants to prevent CNS disturbances
IVFT to stabilise acid-base and electrolyte disturbances

86
Q

What is the general meaning of hepatic encephalitis?

A

Build up of ammonia and toxins which cause neurological signs

87
Q

Why may patients with PSS require plasma?

A

They are often hypoproteinaemia/hypoalbuminaemic and may have coagulopathy after fluid administration due to haemodilution

88
Q

What are the surgical options for PSS?

A

Complete or gradual attenuation of the shunting vessel. Gradual attenuation preferred to avoid portal hypertension

89
Q

What are the surgical options for PSS?

A

Complete or gradual attenuation of the shunting vessel. Gradual attenuation preferred to avoid portal hypertension.
- Ameroid ring constrictor (ARC) or cellophane band

90
Q

What are the 3 most common post-operative complications following PSS surgery?

A
  1. Portal hypertension
  2. Coagulopathy
  3. Neurologic abnormalities
91
Q

What is portal hypertension?

A

Increased blood flow after attenuation of the shunting vessel causing congestion particularly to the abdominal organs. Signs of which include: ascites, organ oedema, intestinal fluid loss, haemorrhage, abdominal pain, melena, hypovolaemia.
If unable to be treated with crystalloids, colloids etc may need surgery to remove occlusion device

92
Q

How much does the portal vein supply O2 requirements and hepatotrophic factors of the liver?

A

50%

93
Q

When are seizures likely to occur during the post-operative period in PSS patients? What is the incidence of seizures in these patients?

A

<72 hours, 5-12% incidence in dogs and <37% incidence in cats

94
Q

What is the mortality of PSS patients?

A

EHPSS with slow attenuation 5.5-7.1%
IHPSS 12.5%

95
Q

Why is analgesia imperative in the post-operative thoracotomy patient?

A

Pain impairs ventilation
Pain increases catecholamine release
Pain activates the stress response -> thrombosis and SIRS
To avoid post thoracotomy pain syndrome

96
Q

What are the steps taken in recovering a post-operative thoracotomy patient with respiratory changes?

A

Remove fluid
Provide oxygen
Assess pain
Reverse medication suppressing ventilatory drive

97
Q

What are common causes of hypoxaemia in post-operative thoracotomy patients?

A

Hypoventilation
Lung oedema
ALI
ARDS
Reduced lung compliance
Increased pulmonary resistance

98
Q

What is the complication rate of thoracotomy patients and what are the likely cmplications?

A

Overall complications 36-47%
- surgical approach related 22-77%
- thoracotomy tube care related 22%
- complications due to primary disease

99
Q

What is the lethal triad?

A

Metabolic acidosis
Hypothermia
Coagulopathy

100
Q

When is damage control surgery performed?

A

uncontrolled haemorrhage leading to the lethal triad: metabolic acidosis, hypothermia and coagulopathy

101
Q

What are the 3 stages of damage control surgery?

A

Initial surgery <90min to control haemorrhage then ICU resusitation and nursing care to correct fluid disturbances, O2 debt and coagulopathy <24hr. Finally a definitive repair surgery is performed 24-48h from DC1.

102
Q

Arachidonic acid pathway simplified

A

Injury > arachidonic acid release > LOX and COX pathways > COX = 1 & 2 which activates prostacyclins, prostaglandins and thromboxane > vascular tone, platelet aggregation & pain.

103
Q

COX-3

A

Similar to 1 & 2 in terms of inflammation and pyretic nature. Acetaminophen has been shown to inhibit.

104
Q

Gastrointestinal side effects of NSAIDs

A

The protective mechanisms such as increased mucous production during injury, enhanced blood flow and the release of PG to promote wound healing. Thus NSAIDs can induce gastric ulceration and prevent GI ulceration repair.
Aspirin (and other NSAIDs) can directly affect the gastric mucosa and allow gastric acids to penetrate into the cells lining the stomach

105
Q

Renal effects of NSAIDs

A

Normally when there is low perfusion and reduced GFR the JGA releases PGs to vasodilate the afferent arteriole. NSAIDs block this thus vasoconstriction prevails in hypovolaemic patients or those with poor perfusion > ARF
* Carprofen, tepoxalin & ketoprofen shown to have little effects on the kidneys unless OD

106
Q

Hepatic effects of NSAIDs

A

Idiosyncratic reaction: hepatocellular injury and increased liver enzymes
The liver metabolises NSAIDs by conjugation of glycin or glucuronic acid
* may be genetic in labs

107
Q

Coagulation effects of NSAIDs

A

Balance between thromboxane and prostacyclin crucial for normal coagulation, and some NSAIDs are shown to impair platelet aggregation and may result in increased thrombosis and/or bleeding (ketoprofen, aspirin, carprofen)

108
Q

Which NSAID is shown to reduce severity of early structural changes and histological lesions in osteoarthritis

A

Carprofen

109
Q

Long term NSAIDs may impair bone healing after fracture, true or false

A

True

110
Q

Drug interactions with NSAIDs

A
  • DO NOT GIVE WITH OTHER NSAIDS AND CORTICOSTEROIDS
  • may reduce effectiveness of furosemide
  • avoid with aminoglycosides
  • incompatible with other highly protein bound drugs
111
Q

Purpose of muscle relaxants

A

Reduce skeletal muscle tension without abolishing voluntary motor control at the level of the cortex, spinal cord, brain stem or all three areas

112
Q

How do opiates work

A

Interact with specific receptors in CNS, PNS, GIT, SM and urinary tract > inhibition of adenyl Cyclades activity > activation of receptor-operated K currents, suppression of voltage gated calcium currents > hyper polarised cell membranes, decreased neurotransmitter release and reduced pain transmission.

113
Q

What is contraindicated to give with morphine and why?

A

Monoamine oxidase inhibitors (MAOIs) as exhibit signs of of opioid overdose even within therapeutic range.

114
Q

Opioids that are weak serotonin reuptake inhibitors and may lead to serotonin toxicity

A

Fentanyl, meperidine, tramadol, methadone, dextromethorphan and can occur when given with monoamine oxidase inhibitors (MAOIs)

115
Q

Treatment of narcotic overdoses

A

Provide adequate ventilation
Give naloxone 0.01-0.04mg/kg
+- gastric decontamination

116
Q

Before a patient goes to surgery

A

Stabilise their respiratory, cardiovascular and pain state and evaluate them globally
Get a minimum database (lactate, lytes, BG, PCV/TP, smear, coags as minimum)
Ensure PCV of at least 20%

117
Q

Post-operative recovery period

A

Generally the most dangerous time for a patient where they should be monitored exceptionally closely
- airway and breathing; cuffed tube until swallowing, watch effort etc
- oxygenation and ventilation; maintain SpO2 above 95%, give supplemental O2, monitor ETCO2
- cardiovascular status; ensure adeq preload, HR, SV etc to ensure adequate DO2, give antiarrhythmics if needed, positive inotropes if indicated, blouses
- analgesia; ensure not painful
- hypothermia; correct

118
Q

How to prevent nosocomial infections in post operative patients

A

Ensure both the patient and their environment is clean
Discard soiled bedding
Bathe patients as required
PPE and good hygiene
Mobility care

119
Q

Immobile patients are at risk of

A

Decubital ulcers
Pneumonia
Atelectasis
Ileus
Thromboses

120
Q

Addressing a hypotensive patient under anaesthesia

A
  1. Reduce inhalant anaesthesia
  2. Fluid blouses
  3. Positive inotropes
  4. Stop inhalants and switch to TIVA
121
Q

Normal MLK dose

A

Morphine 3.3ug/kg/min
Lidocaine 50ug/kg/min
Ketamine 10ug/kg/min

VTS(ECC) Preparation (21 decks)

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