Intravenous Anaesthetic Agents

Front 1

What are the 3 goals in anaesthesia?

Back 1

1. Sedation

2. Analgesia

3. Paralysis

Front 2

Name some Benzodiazepines and their functions in anaesthesia

Back 2

1. Midazolam (Versed)

2. Diazepam (Valium)

3. Lorezapam (Ativan)

Function: anxiolysis, sedation, amnesia

Front 3

What is the dosage, clinical effect timing and half life of midazolam?

Back 3

• Dosage: 0.25-0.5mg/kg PO (child), 1-4mg in adults
  

• clinical effect: 20-30 mins
  

• elimination half life: 3 hr
  

Front 4

What is the dosage, clinical effect timing and half life of diazepam?

Back 4

Dosage: 2.5-10 mg

Half life: 20 hr

Front 5

What is the dosage, clinical effect timing and half life of lorezapam?

Back 5

Dosage: 1-4 mg

Front 6

What is the antidote and dosage for the reversal of benzodiazepam effects?

What is it's duration of clinical effect?

Back 6

Flumezanil 0.1mg , every 5 mins

Duration of clinical effect: 1 hour

Front 7

What are the functions of opioids in anaesthesia?

Back 7

• Analgesia
  
• Amnesia
  
• Sedation
  

Front 8

What are the common opioids used in anaesthesia?

Back 8

• Fentanyl
  
• Morphine
  
• Hydromorphone
  
• Meperidine
• remifentanil
  
• sulfentanil
  
• alfentanil
  

Front 9

How do opioids work?

Back 9

agonists to mu, delta and kappa receptors

Front 10

What is the dosage, clinical effect timing and time to peak concentrations of Fentanyl?

Back 10

Dosage: 1 mcg/kg

Clinical effect: 0.5 - 1 hour

Time to peak: 3-5 mins

Front 11

What is the dosage, clinical effect timing and time to peak concentrations of Alfentanil?

Back 11

Dosage: 10mcg/kg

Clinical effect: 12-18 mins

Time to peak: 1.5-2 mins

Front 12

What is the dosage, clinical effect timing and time to peak concentrations of Sulfentanil?

Back 12

Dosage: 0.01mg

Clinical effect: 0.5 - 1 hr

Time to peak: 3-5 mins

Hint 12

***5-10x more potent than fentanyl

Front 13

What is the dosage, clinical effect timing and time to peak concentrations of morphine?

Back 13

Dosage: 0.1mg/kg

Clinical effect: 3-4 hr

Time to peak: 20-30 mins

Front 14

Side effects of opioids

Back 14

- Respiratory depression

(due to low hypoxic drive, increase in apneic threshold)

- Bradycardia

- Urinary retention, constipation

- Muscle rigidity

- Nausea and Vomiting

Front 15

What is the antidote and dosage for opioid overdose?

What is the mechanism?

Back 15

Naloxone, 0.04-0.4 mg every 2 mins

Antagonizes mu receptors

Front 16

What is the antidote to reduce peripheral symptoms of opioids?

Back 16

Methynaltrexone; this does not affect analgesia

Front 17

Name two benefits of using opioids as an anaesthetic

Back 17

• minimal effects on cardiovascular status
  
• ability to decrease stress response to pain
  

Hint 17

Good for haemodynamically unstable patients

Front 18

Name 4 common induction agents

Back 18

• Propofol
  
• Thiopental
  
• Etomidate
  
• Ketamine
  

Front 19

What is the dosage, clinical effect timing and half life of Propofol?

Back 19

Dosage: 2-2.5mg/kg (induction), 0.025-0.2 mg/kg/min (infusion)

Half life: 2-8 mins

Front 20

What are the side effects of propofol?

Back 20

• Potent cardiovascular depressant
  
• Potent respiratory depressant
  
• low cerebral perfusion pressure at high doses
  
• Pain on infusion of propofol
  

Front 21

What are the benefits of using propofol as an induction agent?

Back 21

• Fast onset, titratable, short duration of action
  
• Reduces ICP and cerebral blood flow
  
• Less cognitive disarray
  
• antipruritic + anti-emetic
  

Front 22

What can be added with propofol to reduce pain during bolus infusion?

Back 22

1% Lidocaine

Front 23

What is the dosage of thiopental?

Back 23

Dose: 3-5 mg/kg

Front 24

Why can't paralytic agents be mixed with thiopental infusion?

Back 24

Thiopental, being very alkaline, may react with paralytic agents (acidic) and lead to IV catheter occlusion

Front 25

What are the side effects of thiopental?

Back 25

• Potent cardiovascular depressant
• Potent respiratory depressant
  
• prolonged cognitive disarray
  

Front 26

What are the advantages of thiopental as an induction agent?

Back 26

It is cerebroprotective, thus recommended in brain surgery cases

Front 27

What is the dosage of Etomidate?

Back 27

0.2-0.5 mg/kg

Front 28

What are the side effects of etomidate?

Back 28

• transient adrenal suppression
  
• pain on injection
  
• myoclonus
  
• high post op nausea vomiting
  

Front 29

What are the advantages of etomidate as an induction agent?

Back 29

• minimal cardio-respiratory depression = good for patients with poor hemodynamic state
  

• Fast onset, titratable, short duration of action
  

Front 30

What is the dosage of ketamine?

Back 30

1-2 mg/kg (IV induction)

3-4 mg/kg (IM induction)

1-2mg/kg/hr (IV infusion)

Hint 30

a dissociative anaesthetic agent

Front 31

What are the side effects of ketamine?

Back 31

• deleterious psychological effects
  
• cognitive disarray
  
• raised ICP
  
• increased salivation
  
• cardiovascular stimulant (avoid in arrhythmia/HTN)
  

Front 32

What are the advantages of ketamine as an induction agent?

Back 32

• potent analgesic
  
• bronchodilator
  
• minimal effects on respiratory drive
  

Front 33

what types of neuromuscular blocking agents are there?

Back 33

Depolarizing vs Non-depolarizing

Front 34

what is the mechanism, onset and duration of succinylcholine?(depolarizing NMB)

Back 34

onset = 30-45 s

duration = 5 mins

Mechanism: agonist to acetylcholine receptors at the NMJ, prevents NMJ repolarization

Front 35

what is phase 2 blockade?

Back 35

prolonged end plate depolarization will lead to conformational changes within the acetylcholine receptor, and slow down recovery

Hence, avoid giving too much!

Front 36

How is succinylcholine removed?

Back 36

It is removed physiologically by pseudocholinsterase.

There's currently no commercially available antidote

Hint 36

dont use acetylcholinesterase inhibitors as it will worsen the NMJ blockade

Front 37

side effects of succinycholine?

Back 37

• Hyperkalemia, esp in burn/denervation injury patients
  
• bradycardia
  
• malignant hyperthermia
  

Front 38

contraindications for succinycholine?

Back 38

• Suspected risk for malignant hyperthermia
  
• history of burn/denervation injury
  
• raised potassium (>5.5 mEq/L)
  
• suspected myopathy
  
• known pseudocholinsterase deficiency
  

Front 39

what is the mechanism of non-depolarizing NMB?

Back 39

competitive antagonism of acetycholine at NMJ receptors, do not cause depolarization of NMJ, unlike succinycholine

Front 40

Rocuronium dosage, onset, duration, indications?

Back 40

Dosage: 0.6mg/kg

Onset: 1-2 mins

Duration: 30-40 mins

Indications: can replace succinylcholine for RSI, as second line

Front 41

Pancuronium onset, duration, indications?

Back 41

Onset: 4-6 mins

Duration: 120-180 mins

SE: tachycardia and HTN

Front 42

Cisatracurium and Vecuronium indications?

Cisatracurium SE?

Back 42

Onset: 2-4 mins

Duration: 30-40 mins

SE: Hypotension

Front 43

What are the antidote for NMBs?

Back 43

acetylcholinsterase inhibitors + anticholinergic drug

Neostigmine 50 mg/kg + Glycopyrrolate 10 mcg/kg

Edrophonium 500 mcg/kg + Atropine 20 mcg/kg

Front 44

What can cause cholinergic crisis in anaesthesia? what is the antidote?

Back 44

excess neostigmine/edrophonium

Antidote= glycopyrrolate/atropine

Front 45

What can cause central anticholinergic crisis in anaesthesia? what is the antidote?

Back 45

excess glycopyrrolate/atropine

Antidote = physostigmine