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'B33CNS - Pharmacology & Therapeutics > Anaesthetics, hypnotics and sleep management > Flashcards

Anaesthetics, hypnotics and sleep management Flashcards

1
Q

Define: anaesthesia. (20:41)

A
  • Provision of insensibility to pain during surgical, obstetric (childbirth), therapeutic and diagnostic procedures
  • Involves monitoring and restoration of homeostasis during postoperative period
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2
Q

How do local anaesthetics work? Examples?

A
  • Blocks generation and conduction (propagation) of nerve impulses at local contact site
  • Consciousness is maintained (e.g. dental work)

Examples: lignocaine, bupivacaine, ropivacaine(___caine suffix; cocaine was discovered as OG anaesthetic)

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3
Q

What are some clinical examples of local anaesthetic use?

A

Topical
- Nasal mucosa and wound margins

Infiltration
- Vicinity of peripheral nerve endings and major nerve trunks in dental practice

Regional
- IV injection leading to numbing of larger area of body in labour/childbirth (e.g. caesarean section)

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4
Q

What is the mechanism of action of local anaesthetics?

A
  • Affects depolarisation
  • Charged and uncharged LAs at equilibrium in the ECF
  • Uncharged LAs pass through lipid bilayer, becoming charged in the ICF and bind to NaV ion channel on the inside
  • Charged thus ‘trapped’ in the ICF (like base trapping), Na+ channels closed thus no influx = no depolarisation
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5
Q

How do general anaesthetics?

A
  • Alters central neural processing
  • Readily reversible loss of consciousness, with decreased response to painful stimuli and muscle tone
  • Two types: inhalation and IV aneasthetics
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6
Q

What historical techniques for general anaesthetics were performed?

A
  • ‘Knock-out’ blows
  • Carotid artery compression (in the neck)
  • Ingestion of ethanol and herbal mixtures
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7
Q

What are the three main stages of anaesthesia, and what do they entail?

A

A; Induction
- Inhalation or IV agents used

B; Maintenance
- Mainly w/volatile agents (good for even distribution of anaesthesia)

C; Recovery
- Monitoring to assure recovery (vitals in order)

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8
Q

What are the four main stages of analgesia WRT the depth of analgesia given?

A

I - Analgesic stage (onset)
II - Excitement stage (erratic)
III - Surgical anaesthesia stage (ideal)
IV - Medullary paralysis stage (danger)

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9
Q

Describe the Analgesic stage WRT the depth of anaesthesia.

A

• First stage WRT depth of anaesthesia; induction

  • Less higher cortical function
  • Consciousness not lost; but thoughts blurred (people tripping out before unconsciousness)
  • Reflexes present
  • Small and PAIN lost at this stage
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10
Q

Describe the Excitement stage WRT the depth of anaesthesia.

A

• II stage; more complex, unpredictable

  • Cortical inhibitory centres depressed
  • Increased muscle tone
  • Potential vomiting; anti-emetic given before
  • Temperature control lost; suppressing hypothalamus; give blanket
  • A-rhythm of EEG desynchronised (brain activity)
  • Respiration increased/irregular (suppressed respiratory centres in the brain)
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11
Q

Describe the Surgical anaesthesia stage WRT the depth of anaesthesia.

A

• III stage; predictable/ideal stage

  • Slow synchronised EEG rhythms (brain)
  • Regular slow breathing
  • Medullary centres depressed; patient attached to artificial ventilator for respiration
  • Reflexes lost
  • Pupils dilated
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12
Q

Described the medullary paralysis stage WRT the depth of anaesthesia.

A

• IV stage; DANGER

  • Loss of respiration (medullary centre v. depressed)
  • EEG waves; small; lost
  • Death
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13
Q

Describe the signs of the Analgesic (induction) stage WRT the depth of anaesthesia.

A
  • Pupils; normal size, responsive to light (constrict)
  • Respiration; regular
  • Pulse; irregular
  • BP; normal
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14
Q

Describe the signs of the Excitement stage WRT the depth of anaesthesia.

A
  • Pupils; normal size, responsive to light (constrict)
  • Respiration; slightly increased/irregular
  • Pulse; irregular and fast
  • BP; high (erratic)
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15
Q

Describe the signs of the Surgical anaesthesia stage WRT the depth of anaesthesia

A
  • Pupils; normal size; UNRESPONSIVE to light (reflexes lost)
  • Respiration; slow and regular
  • Pulse; steady and slow
  • BP; normal
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16
Q

Describe the signs of the Medullary paralysis stage WRT the depth of anaesthesia

A
  • Pupils; dilated (medullary centre depressed?); remain dilated w/light
  • Respiration; loss of
  • Pulse; weak & thready
  • BP; low
    »> DANGER OF DEATH
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17
Q

What are the types of inhaled general anaesthetics? Give examples.

A

Gas:
- Nitrous oxide (NO; laughing gas)

Volatile liquids:
- Halothane
- Enflurane
- Isoflurane
- Sevoflurane
- Desflurane
(\_\_\_ane suffix; vaporised through anaesthetic gas machine through face mask)
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18
Q

What are the types of IV general anaesthetics?

A

Inducing agents (first stage of anaesthesia):

  • Thiopental
  • Methohexitone/methohexital
  • Propofol
  • Etomidate

Benzodiazepines (multiple function; muscle relaxant + calm/sedates patient):

  • Diazepam
  • Lorazepam
  • Midazolam

Dissociative anaesthesia:
- Ketamine

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19
Q

What are the characteristics of an ‘ideal’ inhalation anaesthetic?

A
  • Stable over range of temperatures
  • Not degraded by light (storage)
  • Odourless (don’t want it to be an irritant)
  • Analgesic, anti-emetic, muscle relaxant properties
  • Minimal respiratory depression
  • Minimal CV effects
  • Excreted completely by respiratory system
  • Not metabolised/no active metabolites; don’t want clearance by kidney/liver (aid recovery stage)
20
Q

How is the potency of inhaled analgesics measured?

A
  • Defined as minimum alveolar concentration (MAC)
  • Inhaled dose that prevents movement to a standard surgical stimulus (skin incision) in 50% of patients
  • < MAC no. = more potent (less required)
  • > MAC no. = less potent
21
Q

What are the most/least potent inhalation anaesthetics according to MAC?

A
  • Halothane = 0.75 (% in 100% O2; most potent)
  • Isoflurane, Enflurane, Sevoflurane = 1.15 - 2.05%
  • Nitrous Oxide (N2O) = 104% (least potent; can’t work on its own)
22
Q

What characteristics of inhaled anaesthetics allow it to pass through the BBB? What variables need considering?

A
  • Lipid soluble (target is brain)
    Lungs > Blood > Brain
  • Partial pressure gradient; driving anaesthetic from respiratory pathway to the brain
  • Steady state; for maintenance of anaesthesia; dependent on partial pressures of alveoli, blood and brain
23
Q

What are the different phases that an inhalation anesthetic goes through from Lungs to Brain?

A
  • Phase I; anaesthetic ‘wash-in’
  • Phase II; uptake and distribution (blood-gas partition coefficient, cardiac output, alveolar-to-venous partial pressure gradient)
  • Phase III; uptake and distribution to the brain
  • Phase IV; elimination/recovery
24
Q

What does Phase I of the inhalation anaesthetic journey (anaesthetic wash-in) entail?

A

Equilibrium between gas present in functional residual capacity (air lefts in lungs already) and anaesthetic achieved

25
Q

What does a high blood-gas partition coefficient mean re. Phase II of an inhaled anaesthetic’s journey? Give an example

A
  • Greater amount of anaesthetic must be dissolved in arterial blood in order to equilibrate with the alveoli
    »> Slower rate of induction and recovery (need more)
    E.g. halothane
26
Q

What does a low blood-gas partition coefficient mean re. Phase II of an inhaled anaesthetic’s journey? Give an example

A
  • Minimal amount of anaesthetic must be dissolved in arterial blood in order to equilibrate w/alveoli
    »> Quick induction; blood is not target site, brain is&raquo_space;> inducing anaesthetic faster means better recovery
    E.g. nitrous oxide
27
Q

What relevance is the blood-gas partition coefficient with inhaled anaesthetics?

A
  • Relevant in Phase II of its journey

- Influences speed of anaesthetic induction e.g. nitrous oxide quickly saturates blood

28
Q

What does a high cardiac output mean for inhaled anaesthetics?

A
  • Phase II of its journey (uptake and distribution)
  • High cardiac output means faster removal of the anaesthetic from alveoli to the peripheral tissues
  • Slower to gain access to the brain
    »> Peripheral tissue is NOT target
29
Q

What does a low cardiac output mean for inhaled anaesthetics?

A
  • Phase II of its journey (uptake and distribution)
  • Low cardiac output results in slower removal of anaesthetic from alveoli to peripheral tissues
  • Thus faster to gain access to the brain
30
Q

What is the relevance of the rate of cardiac out WRT inhaled analgesics?

A

Influences speed of anaesthetic induction (low cardiac output good; faster gaining access to the brain)

31
Q

What relevance is the alveolar-to-venous partial pressure gradient of anaesthetic?

A
  • Anaesthetic transferred to peripheral tissues from arterial blood due to pressure gradient
  • Venous circulation depleted of anaesthetic returns to lungs with more gas moving into the blood due to a partial pressure gradient
    »> Anaesthetic concentration difference between alveolar (arterial) blood and venous; the higher the uptake, the slower the induction (BAD)
  • Will take longer to get to the brain
32
Q

What does Phase III of inhaled anaesthetic intake entail?

A
  • Uptake and distribution to the brain
  • Partial pressure of alveolar blood is in equilibrium to the arterial blood and that in turn is in equilibrium with brain partial pressure
    »> Desired (steady state); inhalation favourable as a result

Cerebral blood flow:
- Brian is highly perfused; rapidly achieves steady with partial pressure of anaesthetic in the blood

33
Q

What does Phase IV of inhaled anesthetic intake entail?

A
  • Similar to uptake and distribution w/nitrous oxide, exiting the body faster than halothane
    (with low blood/gas coefficient)
34
Q

How does the oil-gas partition coefficient influence inhaled anaesthetic uptake?

A
  • The greater the lipid solubility, the better the drug gain entry to the brain via the BBB
    E.g. N2O (nitrous oxide) has a low blood-gas coefficient, but has a high oil-gas partition coefficient; difficult to access the brain (halothane converse)
35
Q

What is the typical journey like through the body for an intravenous anaesthetic?

A
  • Once in bloodstream, some of the drug binds to plasma proteins (e.g. albumin); rest remains unbound and ‘free’
  • Drug is transported through venous blood then systemic circulation, eventually gaining access to cerebral circulation
  • Partial pressure gradient permits entry of the anaesthetic to the brain, where it takes effect
36
Q

What are the preferred qualities of an intravenous anaesthetic?

A
  • Unbound
  • Lipid soluble
  • Unionised
    »> Cross the BBB the quickest
37
Q

What IV anaesthetics are availible?

A
  • Propofol
  • Thiopental
  • Etomidate
  • Ketamine
38
Q

Describe Propofol’s efficacy as an IV anaesthetic.

Which stage is it used in?

A

• Induction

  • Short acting w/onset of 30 seconds, rapid recovery
  • Decreases BP and intracranial pressure
  • Does NOT provide analgesia (thus analgesic required)
  • Accompanied by excitatory phenomena; muscle twitching, yawning, hiccups etc.
  • Some antiemetic effects post-recovering
39
Q

Describe Thiopental’s efficacy as an IV anaesthetic.

What is it similar to?

A
  • Similar to propofol; fast acting within 1 minute (induction good)
  • S/Es; may cause apnoea (cessation of breathing), coughing, chest wall spasm, laryngospasm
  • Not commonly used; better agents availible
40
Q

Describe Etomidate’s efficacy as an IV anaesthetic.

When is it used?

A
  • Hypnotic agent; induces anaesthesia BUT lacks analgesia
  • Benefit; little to no effects on CV system (favoured for CVD surgery)
  • Used in sufferers of cardiac dysfunction
41
Q

Describe Ketamine’s efficacy as an IV anaesthetic.

When is it used?

A
  • Patient unconscious but appears awake; induces amnesia, hence dissociative anaesthesia (person has no recollection)
  • Increases blood pressure and cardiac output (resulting in faster removal of drug from alveolar to periphery; bad)
  • Potent bronchodilator; useful for asthmatics
    »> Favoured in children or elderly
  • NOT favoured in young adults due to induction of hallucinations
42
Q

What is the proposed mechanism of action of general anaesthetics?

A
  • Increases GABAa/strychnine-sensitive glycine levels, resulting in increased Cl- influx (hyperpolarisation) and thus leading to greater INHIBITORY processes (most anaesthetics)
  • Also; role in decreasing EXCITATORY transmission (inhibiting receptor subtypes?) e.g. lesser 5-HT3, neuronal nicotinic, Glu at NMDA/AMPA (ketamine, NOS)
43
Q

What occurs when uncharged anaesthetic molecules concentrate in lipid membranes?

A
  • Membrane expansion; conformational change

- Induces anaesthesia

44
Q

What is the target site for general anaesthetics?

A

Reticular activating system:
- Arousal, sleep, wakefulness
> Results in transmission (radiation across cerebral cortex e.g. increased GABAa/strychnine-sensitive glycine) = CNS suppression/depression

Effects on:

  • Visual impulses
  • Reticular formation
  • Ascending general sensory tracts; touch, pain, temperature
  • Descending motor projections to spinal cord
  • Auditory impulses
45
Q

What is the typical practical anaesthesia regime for general anaesthetic goal, given no single agent is ideal?

A

• Premedication:

  • Atropine; decrease secretions (muscarinic blocker)
  • Benzodiazepine; sedation (if anxious)

• Fast induction:
- Thiopental (IV; within a minute)

• Maintenance:
- Isoflurane (inhaled)

• Muscle relaxation:
- Neuromuscular blocking drug e.g. BDZ dual effect

• Reduce pain:
- Analgesic (opiate; also used post-operatively)

'B33CNS - Pharmacology & Therapeutics (13 decks)

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