Anesthesia / analgesia / sedation Flashcards

1
Q

What are the different stages and planes of anesthetic depth

A
  • Stage I = awake (can be sedated / obtunded)
  • Stage II = excitement stage with spontaneous muscle movements
  • Stage III = surgical stage
  • Stage IV = extreme CNS depression, respiratory arrest, eventually cardiac arrest

Stage III divided into 4 planes based on pupils, eye position, jaw tone, etc: target is plane 2 (or 3)

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2
Q

What can be used to reverse opioids in case of dysphoria

A

Butorphanol 0.01-0.05 mg/kg titrated to effect

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3
Q

What is a possible side effect of flumazenil

A

Seizures (mostly in patients known for seizures)

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4
Q

What is the risk with use of PropoFlo 28 in cats

A

Contains benzyl alcohol (benzoic acid) which can be toxic to cats since they have a low liver glucuronic acid conjugation capacity

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5
Q

What sedative / anesthetic can cause adrenal insufficiency

A

Etomidate

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6
Q

What is a possible adverse effect of etomidate in cats

A

Hemolysis due to presence of propylene glycol

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7
Q

Which anesthetic agent can increase intra-ocular pressure

A

Ketamine

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8
Q

What is an induction dose of ketamine (when used in combination with another drug)

A

2-5 mg/kg IV

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9
Q

What anesthetic / sedative agents cause the most splenic relaxation and splenomegaly (and secondary Hct decrease)

A

Acepromazine, propofol, thiopental

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10
Q

What analgesic agent should be preferred in patients with liver failure / PSS

A

Remifentanil (no hepatic metabolism)

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11
Q

What are the classes of neuromuscular blocking agents

A
  1. Depolarizing agents: succinylcholine
  2. Non-depolarizing agents
    - Benzylisoquinolinium agents (atracurium, cisatracurium, doxacurium)
    - Aminosteroidal agents: rocuronium, vecuronium
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12
Q

What is a possible side affect of atracurium? What other benzylisoquinolinium agent can be used to avoid this?

A

Can cause histamine release

Cisatracurium is similar and doesn’t cause histamine release

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13
Q

What metabolism of atracurium and cisatracurium can cause hypotension? What patients are more at risk?

A

Laudanosine (can also cause seizures at high doses)

Patients with liver failure are more at risk due to decreased elimination

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14
Q

How can neuromuscular blocking agents be reversed

A
  • Nondepolarizing agents can be reversed by acetylcholinesterase inhibitors (neostigmine) only if the amplitude of waved on train-of-four monitoring is at least 10% of baseline height
  • Aminosteroidal agents specifically (rocuronium and vecuronium) can be reversed with sugammadex
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15
Q

What opioids can cause histamine release

A

Morphine and meperidine

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16
Q

What dose of naloxone can be used to reverse CNS depression caused by opioids while trying to keep some analgesia

A

0.004 mg/kg IV titrated to effect

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17
Q

What new molecule can reverse the cardiovascular effects of dexmedetomidine without affecting the sedative / analgesic effect

A

Vatinoxan (MK-467) = alpha2-antagonist that does not cross the blood brain barrier

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18
Q

What is the volume of drugs recommended for epidural administration in most cases?

A

0.2 mL/kg (0.1 mL/kg or 0.02-0.05 mL/kg/h when given in catheter) -> blocks until T13-L1

Larger volumes up to 0.4 mL/kg/h can be used cautiously to block more cranial ~T8-T10

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19
Q

What is the mechanism of action of depolarizing / non-depolarizing neuromuscular blocking agents

A
  • Depolarizing: agent binds to ACh receptor and activates it, leading to depolarizing (and initial contraction / fasciculation). The agent is not cleaved by acetylcholinesterase -> stays on the receptor and keeps it open -> persistent depolarization -> flaccid paralysis
  • Non-depolarizing: agent binds to ACh receptor but does not activate it -> competition with ACh -> prevents depolarization
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20
Q

What neuromuscular blocking agents have the least cardiovascular effects

A

Rocuronium / vecuronium > cisatracurium > atracurium

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21
Q

What electrolytic disorder can succinylcholine theoretically cause

A

Hyperkalemia (due to persistent opening of Na / K channels allowing K efflux)

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22
Q

How is neuromuscular blockade monitored

A

By evoked motor responses to peripheral nerve stimulation (eg. train of four - not as reliable for depolarizing agents)

Adequate recovery of neuromuscular blockade when T4:T1 ratio is at least 0.7

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23
Q

With what neuromuscular blocking agent should anticholinesterases not be used

A

Depolarizing agents (succinylcholine) -> inhibits its degradation and prolongs its action

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24
Q

What is the epidural space delimited by

A

The dura mater (inside) and the boundaries of the vertebral canal = bones, ligaments (outside)

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25
Q

Where does the dural sac end in dogs / in cats

A

In dogs: L6-L7
In cats: L7-S1 (usually goes until S1)

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26
Q

What spinal segment innervates the abdominal wall and peritoneum in dogs

A

T11-L3

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27
Q

List complications of epidurals

A
  • Hypotension - mostly when using local anesthetics due to sympathetic blockade, worse if going more cranial
  • Urinary retention - due to blockade of sacral parasympathetic outflow + effect of morphine
  • Infection
  • Respiratory depression if too large volume (going too cranial) or intrathecal administration
  • Neural damage
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28
Q

What is the recommended fasting time in a patient with no specific concern

A

4-6h (longer fast could be associated with reflux)

Neonates / toys and diabetic patients should be fed some canned food before the procedure

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29
Q

What is the recommended O2 flow rate for rebreathing / non-rebreathing circuits

A
  • Non-rebreathing: 200-400 mL/kg/min
    –> 2-3L/min when rapid changes in anesthetic depth are needed
  • Rebreathing: 20-40 mL/kg/min (minimum 0.5 L/min) - increase when adjusting inhalant dose
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30
Q

The blood/gas partition coefficient of isoflurane is 1.4, sevoflurane is 0.66. Which one will have the fastest onset of action and fastest recovery?

A

Sevoflurane for both (takes less time to attain a given partial pressure and less distributed in tissues so eliminated faster)

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31
Q

What is used to characterize the anesthetic potency of an inhaled anesthetic

A

MAC (minimum alveolar concentration)

32
Q

What is the MAC for isoflurane / sevoflurane in dogs and cats

A

Isoflurane:
- Dogs: 1.3%
- Cats: 1.6%

Sevoflurane: 2.4% for both

33
Q

Name 1 anesthetic agent that can increase ICP and 1 that can decrease it

A

Anesthetic agents increase ICP (isoflurane, sevoflurane)

Propofol can decrease ICP

34
Q

Where is the binding site of local anesthetics located

A

Inside the pore of the Na+ channel (on the S6 segment of the domain DIV of the alpha-subunit) - on the intracellular side

35
Q

In case of inadvertent entry in the subarachnoid space while doing an epidural, what amount of the prepared dose should be administered

A

~1/10th of the dose

36
Q

What is an adverse effect of benzocaine

A

Methemoglobinemia and formation of Heinz bodies (cats ++)

37
Q

List 4 anesthetic considerations in the TBI patient

A
  • Avoid inhalant anesthetics –> loss of cerebral pressure autoregulation, hypoventilation, hypocapnia, increase in ICP at higher doses (at lower doses, vasodilation may improve cerebral perfusion)
  • TIVA recommended
  • Propofol –> hypoventilation and hypotension BUT may be neuroprotective (modulation of GABA receptors and antioxidant effects)
  • Analgesia –> pain can increase ICP
  • Drug options: benzos (& ketamine?) OK, avoid alpha2
38
Q

At what dose of volatile anesthetic can deleterious cerebral effects be seen in the TBI patient?

A

> 1-1.5 MAC

39
Q

How can lidocaine possibly reduce brain injury in the TBI patient?

A

Prevention of Na influx into ischemic neurons

40
Q

List 5 ways to reduce ICP during anesthesia of a TBI patient.

A
  • Temporary hyperventilation (target PaCO2 of 30-35)
  • Hyperosmolar agents
  • Prevention of hyperthermia
  • Head elevation
  • Avoiding jugular vein occlusion
  • Smooth induction and recovery (avoid sympathetic stimulation which could increase ICP)
41
Q

What is the most common period during which peri-anesthetic death can occur?

A

Post-operative - within 3 hours of termination of procedure

42
Q

What are the 5 ASA categories

A

See picture

43
Q

What type of ETT cuff should be prioritized and why?

A

High-volume low-pressure –> minimize risk of ischémie tracheal injury

44
Q

As a general rule, in the absence of pathology, what should a patient’s PaO2 be based on the FiO2 administered?

A

PaO2 is roughly 5x DiO2

45
Q

What consideration should you remember about monitoring anesthetic depth when a patient has received ketamine?

A

With ketamine, the eyeballs do not rotate

46
Q

Name 3 causes of bradycardia in the anesthetized patient that are not responsive to pharmacological treatment

A
  • Severe hypothermia
  • Cardiac conduction abnormalities
  • Severe myocardial hypoxemia
47
Q

What can be used for treatment of some cases of local anesthetic‐induced collapse and cardiac arrest?

A

Intravenous lipid emulsion

48
Q

True or false: all opioids used in cats can cause hyperthermia

A

True - occurs in about 50% of cats

49
Q

What gene is affected in malignant hyperthermia?

How do you treat this condition?

A

Ryanodine receptor gene mutation, RYR1

Removal of any triggering agent, ventilation with 100% oxygen, administration of dantrolene and aggressive cooling

50
Q

List 5 causes of prolonged anesthetic recovery

A
  • Hypothermia
  • Over-narcotization
  • Hypothyroidism
  • Adrenal insufficiency
  • Hypoglycemia
  • Increased ICP
51
Q

What is the mechanism of action of local anesthesia?

A

Blockade of inward Na+ currents through voltage‐gated Na+ channels, thereby impeding membrane depolarization and nerve excitation and conduction

52
Q

What is the duration of lidocaine as a local anesthetic? Bupivacaine?

What are the doses

A

Lidocaine: 1h
- Epidural: 4mg/kg of 2%
- IV (anesth): 1-2 mg/kg bolus, 50-100 mcg/kg/min CRI
- Max dose 6-10 mg/kg

Bupivacaine: 3-10h
- Epidural: 1mg/kg of 0.5%
- Mac dose 2mg/kg

53
Q

List 5 adverse effects of local anesthetics

A
  1. CNS toxicity
  2. Cardiovascular toxicity
  3. Local neurotoxicity
  4. Myoxicity
  5. Methemoglobinemia
  6. Allergic reactions
54
Q

Explain the difference between full agonist and partial agonist opioids

A

Full agonist: Produce a dose dependent increase in effect until maximum stimulation of the receptor is achieved

Partial agonist: Produce a dose dependent increase in effect, but plateaus at a maximum effect less than that of full agonists

55
Q

What concept is Transcutaneous electrical nerve stimulation (TENS) based on?

A

Gate control theory –> application of a non-noxious (soothing or light rubbing) stimulus can help activate the gate control mechanism, and reduce the pain

56
Q

What is the difference between a competitive antagonist and an irreversible antagonist?

A

Competitive antagonist:
- Decreases potency of agonist
- Efficacy is unchanges
- Can override with higher dose of agonist

Irreversible antagonist
- Decreases efficacy of agonist
- Mildly decreases potency
- Cannot override with higher dose (covalent bond is formed)

57
Q

What is the difference between epidural anesthesia and spinal anesthesia?

A

Epidural anesthesia refers to the administration of drugs (usually a local anesthetic solution) into the epidural (extra­ dural) space

Spinal anesthesia refers to administration of a drug into the suba­ rachnoid space

58
Q

List 5 categories of loco-regional anesthesia

A
  1. Topical anesthesia
  2. Infiltration anesthesia
  3. Regional or nerve block anesthesia
  4. Neuraxial anesthesia
  5. Intra-articular anesthesia
59
Q

What are the most important nerves of the brachial plexus and which spinal segments they rise from?

A

Nerves:
Supras­capular
Subscapular
Axillary
Musculocutaneous
Radial
Median
Ulnar

Formed from the ventral branches of C6, C7, C8, T1

60
Q

Name and briefly describe 2 thoracic blocks

A
  1. Intercostal nerve block - injection of a local anesthetic solution adjacent to several contiguous intercostal nerves
  • Palpate rib as far dorsally as possible so that nerve is targeted as proximally as possible
  • Advance needle through the skin onto lateral aspect of the rib and walk it off caudally into the intercostal space (avoir entering pleural space)
  • After negative aspiration, slowly infuse 0.5-1ml of anesthetic
  • Repeat at two sites cranial and two sites caudal to the initial rib
  1. Intrapleural regional anesthesia: deposition of a local anesthetic solution into the pleural space that exists between the parietal and visceral pleurae
  • Over‐ the‐needle catheter is connected to a syringe filled with 2–3 mL of saline via a three‐way stopcock
  • Advanced onto the lateral aspect of the seventh or eighth rib at its midpoint
  • Needle is then ‘walked off’ the cranial border of the rib until it can be advanced through the intercostal space
  • Nega­tive interpleural pressure aspirates the saline
  • infuse local anesthetic from preloaded syringe on three was stopcock
  • After removal of the catheter, patient is positioned with the operative side down for at least 10 min, allowing the local anesthetic to pool and block the underlying intercostal nerves
61
Q

What space is blocked by the TAP block?

A

Space between transversus abdominis and internal abdominal oblique muscles

62
Q

What group of spinal nerves supply:

  1. The pelvic limbs
  2. Abdominal wall and peritoneum
  3. Thorax
A
  1. L3-S1
  2. T11-T13 & L1-L3
  3. T2-13
63
Q

Describe the approach to an epidural

A
  • Patient placed in sternal recumbency
  • Needle is advanced between the dorsal spinous processes of L7 and S1 (medial sacral crest) (should not be any resistance), then through the supraspinous and inter­ spinous ligaments (resistance will be noted)

–> Hanging drop: if a drop of saline is placed in the hub of the needle, as the needle penetrates into the epidural space it will usually be aspirated into the space

–> Loss of resistance: if pressure is being applied to the plunger
syringe, a sudden loss of resistance to injection will be appreci­ated when the needle punctures the ligamentum flavum and enters the epidural space

64
Q

Why are inhalant anesthetics avoided for anesthesia in the respiratory pstient (ie on MV in the ICU)?

A
  • They inhibit hypoxic pulmonary vasoconstriction
  • They may be associated wth immunosuppression
65
Q

What PCV is required for adequate O2 delivery in the anaesthetized patient (according to SACCM…) ans what happens to PCV during GA?

A

> 25%

PCV can decrease by 3-5% during GA

66
Q

What is the difference between metabolism of benzylisoquinolium and aminosteroidal NMB agents?

A

Benzylisoquinolium degredation is independent of enzymatic function - inactivated in the plasma

Aminosteroidal - undergoes hepatic metabolism and renal elimination

67
Q

What is your approach to the hypotensive GA patient?

A
  1. decrease inhalant anesthetic
  2. Administer fluid boluses while being conscious of total volume administered and patient underlying disease
  3. If patient is also bradycardia, administer anticholinergic (atropine, glyco) or sympathomimetic (ephedrine)
  4. Inotrope and/or vasopressors
  5. Discontinue inhalant anesthetic and transition to TIVA
    Ex: mu-agonist in combination with ketamine or lidocaine
68
Q

What nerves are blocked in a coccygeal epidural?

What is the lidocaine dose?

A

Pudendal
Pelvic
Caudal

0.1-0.2 ml/kg od 2% lidocaine

69
Q

List 5 contraindications of epidurals

A
  • Trauma over the pelvic region and loss of landmarks
  • Sepsis
  • Coagulopathy
  • CNS disease
  • Skin infection
  • Hypovolemic shock
  • Severe obesity
70
Q

What are 2 essential safety features to have on every anesthetic machine?

A
  1. An in-circuit manometer
  2. A safety pop-off valve
71
Q

What is an acceptable leak for a ventilator?

A

300 ml/min

72
Q

True or false: Maropitant decreases MAC in cats and dogs

A

True

73
Q

What is the baseline anesthetic fluid rate for dogs and cats?

A

Dogs: 5ml/kg/h

Cats: 3 ml/kg/h

74
Q

List 4 anesthetic machine causes of hypercapnia

A
  • Excessive dead space and CO2 rebreathing
  • Exhausted CO2 absorbant
  • One-way valve not functioning
  • Inadequate O2 flow
75
Q

List 5 adverse effects of hypothermia in the anesthetic patient

A
  • Delayed drug metabolism
  • CV dysfunction
  • Cerebral depression
  • Impaired perfusion
  • Increased O2 consumption
76
Q

What is a neuroleptanalgesic?

A

An opioid combined with an anxiolytic drug