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PR3136 PT4 > L07 General Anaesthetics > Flashcards

L07 General Anaesthetics Flashcards

1
Q

What is general anaesthesia (GA) used for?

A

To produce unconsciousness & lack of responsiveness to all painful stimuli

  • i.e. inhibition of sensory & autonomic reflexes
  • i.e. involves a triad of hypnosis, amnesia & analgesia (sleep-inducing, memory loss of painful experience & elimination of pain sensation)
  • Provide conditions for surgical interventions or skeletal muscle relaxation

Endpoint: Keep patients safe & alive upon GA reversal

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2
Q

What are some additional considerations required when a patient undergoes GA?

A

Control of normal physiology w/ mechanical intervention:

  • Maintenance of breathing & O2 levels
  • Maintenance of body temperature
  • Maintenance of heart rate
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3
Q

Describe what the general stages of anaesthesia are.

A

1) Pre-assessment / Pre-medication
2) Induction of anaesthesia
3) Airway management
4) Maintenance of anaesthesia
5) Reversal of anaesthesia
6) Post-operative / Post-anaesthesia care

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4
Q

What constitutes an ideal GA?

A

1) Unconsciousness
2) Analgesia
- To inhibit subconscious reflexes to pain
- Mutually exclusive from amnesia!!
3) Muscle relaxation
4) Brief & pleasant
5) Depth of anaesthesia can be raised & lowered w/ ease
6) Minimal ADR
7) Large margin of safety

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5
Q

What triad of properties should be balanced for an effective GA?

A

Pain relief + inhibition of reflexes + unconsciousness

  • To ensure that induction of GA is rapid & smooth
  • AND analgesia & muscle relaxation are adequate
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6
Q

A single GA agent is sufficient to maintain a balanced anaesthetic effect. True or false?

A

False.
There is NO SINGLE AGENT that has ALL the properties of an ideal GA!
INH + IV GA are the most commonly used combination GA to effect a balanced anaesthetic effect.

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7
Q

Which classes of drugs are most commonly used as a combination for GA?

A

1) Short-acting barbiturates: induce anaesthesia
2) Neuromuscular blocking agents: muscle relaxation
3) Opioids & nitrous oxide: Analgesia

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8
Q

What physiochemical property of inhalant GA determines its duration of onset?

A

Blood solubility.
The higher the blood solubility of INH GA, the slower the onset of anaesthesia.
- GA stays in the blood & more resistant to move into CNS.
- However, faster onset DON’T mean higher GA potency; slower onset DON”T mean low GA potency!!

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9
Q

List some inhalant GA available for anaesthesia.

A

1) Volatile liquids (i.e halogenated hydrocarbons)
- HIDES: Halothane, isoflurane, desflurane, enflurane, sevoflurane
- Needs to be vaporised before inhalation

2) Gases: Nitrous oxide
- Fast onset but poor GA potency

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10
Q

Explain the proposed mechanism of action of inhalant GA.

A

1) Enhance neurotransmission at inhibitory synapses via allosterically increasing GABA receptor sensitivity to action by GABA itself.
- i.e. positive allosteric modulator; reversible in nature

AND

2) Depress neurotransmission at excitatory synapses via blocking glutamate neurotransmitters from acting on NMDA receptors thus preventing NMDA receptor activating
- i.e. negative allosteric modulator

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11
Q

Explain what ‘minimum alveolar concentration’ (MAC) means?

A

Index of inflation anaesthetic potency
- i.e. low MAC = high anaesthetic potency
Defined as the minimum concentration of drug in alveolar air that will produce immobility in 50% of patients exposed to a painful/noxious stimuli.

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12
Q

List all the inhalant GA in decreasing potency.

A 
In increasing MAC:
Halothane = 0.75% (potent)
Isoflurane = 1.2-1.4% (potent)
Enflurane = 1.7% (potent)
Sevoflurane = 2-2.2% (potent)
Desflurane = 6.3%
Nitrous oxide = 105-110%

Concept of MAC values alter with age, condition, concomitant administration of other drugs etc.

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13
Q

To produce therapeutic effects, an inhalation anaesthetic need not reach a sufficient CNS concentration to suppress neuronal excitability. True or false?

A

False.

To produce therapeutic effects, an inhalation anaesthetic MUST reach a sufficient CNS concentration to suppress neuronal excitability.

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14
Q

Which host and drug properties influence the absorption rates of INH GA?

A

1) Concentration of anaesthetic in inspired air
- Higher conc. in inspired air = higher rate of GA uptake in blood

2) Blood solubility of GA
- Higher blood solubility of GA = higher rate of GA uptake in blood = slower onset

3) Blood flow through lungs (i.e. perfusion)
- Faster blood flow thru lungs = higher rate of GA uptake into blood

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15
Q

List all the inhalant GA in decreasing blood solubility.

A 
In decreasing blood solubility:
Halothane = 2.3 
Enflurane = 1.8
Isoflurane = 1.4
Sevoflurane = 0.69
Nitrous oxide = 0.47 (poor)
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16
Q

What factors influence the distribution of INH GA?

A

Determined by regional blood flow:

  • Highly perfused organs such as brain, lungs, liver & heart will receive GA first
  • Anaesthetic levels in highly perfused organs (i.e. central compartment) equilibrate quickly after administration.
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17
Q

How are INH GA eliminated from the body?

A

1) INH GA are excreted almost entirely through the lungs via expiration.
- Minimal hepatic metabolism; however, some metabolites can be toxic!

2) Factors that determine uptake also determine rate of elimination
- If blood flow to brain is high, INH GA levels will also drop rapidly when administration is stopped.

Nephrotoxic: Inorganic fluorides of isoflurane, enflurane & sevoflurane
Hepatotoxic: Halothane

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18
Q

What are the clinical indications relating to the use of nitrous oxide?

A

1) Analgesia for dentistry & during delivery (due to high analgesic properties when used alone)
2) GA (possibly as an adjunct to other volatile liquid INH GA due to low potency / high MAC)
- Supplement analgesic effects of primary anaesthetic

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19
Q

What are some important clinically significant properties of halothane?

A
  • Volatile liquid, non-flammable & non-irritating
  • Potent (MAC 0.75%)
  • Medium onset & recovery due to highest blood solubility of 2.3
  • However, little or no analgesia until subconsciousness supervenes
  • Relaxes skeletal muscle & potentiates skeletal muscle relaxants
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20
Q

What are some possible side effects of halothane?

A

1) Dose-dependent respiratory depression

2) Depression of cardiac output:
- Resulting in bradycardia, arrhythmia, hypotension & dysrhythmia

3) Halothane-associated hepatitis

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21
Q

Which drug is contraindicated when a patient is administered with halothane as INH GA?

A

Epinephrine / Adrenaline

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22
Q

What are some important clinically significant properties of isoflurane?

A

Similar to halothane

  • Volatile liquid, non-flammable & non-irritating
  • Potent (MAC 1.4%)
  • Medium onset & recovery due to relatively high blood solubility of 1.4
  • Pungent smell
23
Q

What are some possible side effects of isoflurane?

A

1) Depression of systemic vascular resistance:
- Resulting in bradycardia, arrhythmia, hypotension & dysrhythmia

2) Nephrotoxicity (due to inorganic fluoride metabolite)

24
Q

What are some important clinically significant properties of sevoflurane?

A
  • Volatile liquid, non-flammable & non-irritating
  • Potent (MAC 2%)
  • More rapid onset & recovery due to very low blood solubility of 0.69, amongst volatile halogenated hydrocarbons
25
Q

What are some possible side effects of sevoflurane?

A

1) Depression of systemic vascular resistance:
- Resulting in bradycardia, arrhythmia, hypotension & dysrhythmia

2) Nephrotoxicity:
- Due to inorganic fluoride metabolite via hepatic metabolism
- When exposed to CO2 adsorbents in anaesthetic machines, sevoflurane becomes unstable & degrade in to potentially nephrotoxic metabolites.

26
Q

Which drug is contraindicated when a patient is administered with sevoflurane as INH GA?

A

CO2 adsorbents

27
Q

What are some important clinically significant properties of nitrous oxide?

A
  • Non-flammable, odourless gas
  • Rapid onset & recovery (due to poor blood solubility of 0.47)
  • Lack potency (due to MAC 105-110%)
  • Gives analgesia & amnesia, BUT NOT complete unconsciousness or surgical anaesthesia (i.e. subconscious pain reflexes may still be active!
  • No muscle relaxant effects
28
Q

What are some possible side effects of nitrous oxide?

A

Postoperative nausea & vomiting

29
Q

Which type of GA induces unconsciousness?

A

IV GA

30
Q

Intravenous general anaesthetics can keep a patient asleep for long periods of time. True or false?

A

False.

IV GA only induces unconsciousness, BUT unable to keep one asleep for long.

31
Q

What is one important consideration with regards to the use of IV GA in patients?

A

Need to ensure mechanical ventilation are in place!

- Most IV GA depresses respiration!

32
Q

What are the advantages of using a combination of INH GA & IV GA?

A

1) Permit reduced dosage of INH GA
2) Produces effects that cannot be achieved by IV GA alone
- IV GA to induce; INH GA to maintain

33
Q

List all examples of IV GA available.

A 
KEMPT: 
Ketamine 1.5 mg/kg 
Etomidate 0.2-0.3mg/kg
Midazolam 0.02mg/kg (for anxiolysis as well)
Propofol 2-4mg/kg
Thiopentone / Thiopental 4-7mg/kg
34
Q

Describe the pharmacokinetic profile of thiopental.

A

Barbiturate with extremely high lipid solubility

A:

  • Enters brain easily & rapidly w/ rapid onset of action (unconsciousness w/in 10-20s after IV)
  • Ultra-short acting barbiturate w/in 10-20min when injected alone / w/o INH agents
  • Duration of action depends on its clearance

D:

  • Redistributes to less vascularised tissues
  • Large Vd due to high lipophilicity
  • Extensively bound to plasma protein as well

M:

  • Slow hepatic metabolism into active metabolite (pentobarbital)
  • Accumulation of pentobarbital results in prolongation of clinical action, leading to liver cirrhosis if unchecked

E:

  • Less than 1% excreted unchanged
  • Small amt of free drug can be excreted by glomerular filtration
  • Potentially reabsorbed in tubules
35
Q

Describe the mechanism of action of thiopental.

A

Potentiates GABA-A-mediated Cl- currents by binding allosterically at the barbiturate site of GABA-A receptors, leading to CNS depression via enhancing neurotransmitters at inhibitory synapses.

36
Q

Describe the mechanism of action of propofol.

A

Potentiates GABA-A-mediated Cl- currents by binding allosterically to GABA-A receptors, leading to CNS depression via enhancing neurotransmitters at inhibitory synapses.

37
Q

Which IV GA is extensively used in day surgeries?

A

Propofol

- Most common IV

38
Q

Why is propofol extensively used as IV GA in day surgeries?

A

1) Ready-made in injectable form, no need to reconstitute
- Most common IV anaesthetic used in Singapore

2) Induction rate similar to thiopentone, recovery is more rapid
- Used for both induction and maintenance

3) Rapid onset of action: unconsciousness within 60 seconds
- Short duration of action: 3 – 5mins following single injection
- Rapid redistribution from brain to other tissues
- However, need continuous, low-dose infusion for extended effects.

39
Q

What are some possible side effects of propofol?

A

1) Reduced postoperative vomiting
- May be related to antiemetic action

2) Significant CVS effect during induction:
- Hypotension (decreased BP) & negative inotropic (i.e. force) cardiac effect

40
Q

What are some possible side effects of thiopental?

A

1) Greater tolerance & dependency than BZDs
2) More severe withdrawal effects than BZDs
- i.e. disturbed sleep, rebound anxiety, tremors & convulsions
3) Medullary depression & coma
- Impt. autonomic responses are heavily depressed at very high doses
- Absent in increasing dose of BZD due to plateau of dose-response curve, unlike positive correlation for barbiturates

41
Q

Which selected populations should propofol be used with caution when administering as IV GA?

A

Elderly
Compromised cardiac function
Hypovolemia

42
Q

Describe the mechanism of action of ketamine.

A

Depress neurotransmission at excitatory synapses via blocking glutamate neurotransmitters from acting on NMDA receptors thus preventing NMDA receptor activating.

43
Q

What state is ketamine known to produce as part of its intended effect as an IV GA?

A

Dissociative anaesthesia

  • Pt feel dissociated from environment, but still has awareness
  • Altered state of consciousness
44
Q

What are some possible side effects of ketamine?

A

CNS: Hallucination, disturbing dreams, delirium during recovery
- Reduced w/ premedication of diazepam or midazolam

45
Q

Explain why ketamine is very popular in its use as IV GA in developing countries?

A

Only IV anaesthetic w/ analgesic property w/o need of INH GA

  • Causes sedation, immobility, analgesia & amnesia as one drug
  • Available as IM, PO & rectal formulations as well
  • Suitable for continuous infusion w/o lengthening duration of action due to large Vd & rapid clearance
46
Q

Which stereoisomer of ketamine is more potent as an INH GA?

A

S- > R+

- However, only available as a racemic mixture

47
Q

What is the main intention behind the use of anaesthetic adjuncts?
List all available drug classes used as anaesthetic adjuncts.

A

Allow lower dose of GA.

1) BZDs
- Anxiolytics, amnesia, sedation prior to induction of anaesthesia
2) Alpha-2 adrenergic agonists (i.e. dexmedetomidine)
- Sedation prior to and/or during procedures in non-intubated patients
3) Analgesics (i.e. NSAIDs & opioids)
- Typically administered w/ GA to reduce anaesthetic requirements
4) Neuromuscular blocking agents (NMBA)
- Induction of anaesthesia to relax muscles (jaw, neck, airway) to facilitate laryngoscopy & endotracheal intubation
- Aids many surgical procedures & provide additional insurance of immobility
- Depolarising: Succinylcholine
- Non-depolarising: Vecuronium

48
Q

What are the clinical indications of using midazolam IV as an anaesthetic adjunct?

A

1) Anxiolysis, amnesia and sedation prior to induction (perioperative period)
OR
2) Sedation during procedures NOT requiring GA (e.g. endoscopy)

49
Q

How are the side effects of midazolam IV minimised?

A

Low-dose midazolam IV results in less CVS & respiratory depressing effect.

  • Minimised by avoiding concurrent usage of other anaesthetic agents
  • Inject midazolam slowly (over 2 or more min) & waiting another 2 or more min for full effects to develop before dosing again.
50
Q

What are some important clinically significant properties of dexmedetomidine as an anaesthetic adjunct?

A

Highly selective alpha-2 adrenergic agonist

  • Short term sedation (< 24h)
  • ONLY produces sedation & analgesic effects; unreliable GA even at max dose
  • Little respiratory depression
  • Tolerable decrease in BP & heart rate
51
Q

What are some possible side effects of dexmedetomidine?

A

Little respiratory depression
Tolerable decrease in BP & heart rate
Antiadrenergic SE: Hypotension, nausea, dry mouth, bradycardia
- Alpha-2 agonism results in antiadrenergic SE

52
Q

Which drug class is contraindicated when a patient is administered with either succinylcholine or vecuronium as an anaesthetic adjunct?

A

Barbiturates (i.e. thiopental)

  • Precipitates when mixed w/ NMBA
  • Should be allowed to clear for IV line prior to injection of NMBA
53
Q

Which opioid, when used as an anaesthetic adjunct, is not eliminated via hepatic metabolism?

A

Remifentanil

54
Q

How is remifentanil eliminated from the body?

A

Hydrolysed by tissue & plasma esterases

Subsequently excreted by urine or as bile.

PR3136 PT4 (14 decks)

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