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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
What does a high blood-gas partition coefficient mean re. Phase II of an inhaled anaesthetic's journey? Give an example
- 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
What does a low blood-gas partition coefficient mean re. Phase II of an inhaled anaesthetic's journey? Give an example
- 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 >>> inducing anaesthetic faster means better recovery E.g. nitrous oxide
27
What relevance is the blood-gas partition coefficient with inhaled anaesthetics?
- Relevant in Phase II of its journey | - Influences speed of anaesthetic induction e.g. nitrous oxide quickly saturates blood
28
What does a high cardiac output mean for inhaled anaesthetics?
- 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
What does a low cardiac output mean for inhaled anaesthetics?
- 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
What is the relevance of the rate of cardiac out WRT inhaled analgesics?
Influences speed of anaesthetic induction (low cardiac output good; faster gaining access to the brain)
31
What relevance is the alveolar-to-venous partial pressure gradient of anaesthetic?
- 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
What does Phase III of inhaled anaesthetic intake entail?
- 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
What does Phase IV of inhaled anesthetic intake entail?
- Similar to uptake and distribution w/nitrous oxide, exiting the body faster than halothane (with low blood/gas coefficient)
34
How does the oil-gas partition coefficient influence inhaled anaesthetic uptake?
- 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
What is the typical journey like through the body for an intravenous anaesthetic?
- 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
What are the preferred qualities of an intravenous anaesthetic?
- Unbound - Lipid soluble - Unionised >>> Cross the BBB the quickest
37
What IV anaesthetics are availible?
- Propofol - Thiopental - Etomidate - Ketamine
38
Describe Propofol's efficacy as an IV anaesthetic. | Which stage is it used in?
• 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
Describe Thiopental's efficacy as an IV anaesthetic. | What is it similar to?
- 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
Describe Etomidate's efficacy as an IV anaesthetic. | When is it used?
- 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
Describe Ketamine's efficacy as an IV anaesthetic. | When is it used?
- 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
What is the proposed mechanism of action of general anaesthetics?
- 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
What occurs when uncharged anaesthetic molecules concentrate in lipid membranes?
- Membrane expansion; conformational change | - Induces anaesthesia
44
What is the target site for general anaesthetics?
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
What is the typical practical anaesthesia regime for general anaesthetic goal, given no single agent is ideal?
• 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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