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Neuroscience > Anaesthetics > Flashcards

Anaesthetics Flashcards

1
Q

What is the goal of anaesthetics?

A

Unconsciousness, amnesia, analgesia, loss of reflexes of the autonomic nervous system, and in some cases paralysis of skeletal muscles.

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2
Q

Potential pharmacologic targets of general anaesthetics are…

A

GABA, glutamate receptors, voltage-gated ion channels, and glycine and serotonin receptors.

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3
Q

How does halothane act?

A

Halothane has been found to be a GABA agonist

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4
Q

How does ketamine act?

A

Ketamine is an NMDA receptor antagonist.

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5
Q

What three changes happen to the CO/PRESSURE graph when an anaesthetic is added?

A

Starling curve shifted downwards to represent the fall in cardiac output

Gradient of Cv is increased due to venodilatory effect

Arterial vasodilation results in an increase in gradient of the arterial part of the graph.

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6
Q

What happens to CO when given anaesthetic?

A

Cardiac depressant effect - CO falls and starling curve is shifted downwards

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7
Q

What happens to venous system and compliance after given anaesthetic?

A

Venodilation and thus increases venous compliance

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8
Q

What happens to the arterial system under anaesthetic?

A

Arterial vasodilation

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9
Q

How do Pv and Pa lines meet and why?

A

Arterial curve meets the venous curve (as at zero cardiac output the pressures in arterial and venous system are the same).

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10
Q

What is shown by the intersection between Pv/Pa and starling curve?

A

Pv/Pa at specific cardiac output

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11
Q

When anaesthetic is added and we extrapolate the new starling curve to the new Pv/Pa lines, how are values different to without anaesthetic?

A

Much lower value for both Pv and Pa (especially for Pa) at the new lower CO.

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12
Q

Potential sites of action for cardiovascular depression of Anaesthetics

A

Myocardium itself

Vessels themselves

Sympathetic control of myocardium and vessels (indirect)

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13
Q

How does halothane affect the myocardium?

A

Elongation of R-R interval and P-R interval

Hypothesise that R-R interval elongation caused by depression of SA node and P-R due to the affected conductance of A-V node.

When give a higher dose, heart block is shown, total block due to loss of A-V conductance.

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14
Q

How do anaesthetics affect vessels directly?

A

DAG activates non-selective cation channel leading to depolarisation - activating a voltage gated Ca2+ channel.

These channels are blocked by nifedipine/ calcium channel blocker

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15
Q

How may halothane reduce intracellular Ca2+ and thus contractility?

A

Reduce Ca2+ flux through cell membrane L-type channels via inhibition.

Effect on Ca release/uptake by sarcoplasmic reticulum

SR releases its full load but there is just LESS calcium.

Some agents (sevoflurane) act to reduce release from SR (but there is still the same amount of Ca2+).

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16
Q

How can a modest decrease in Ca2+ flux via L-type channels lead to large reductions in intracellular Ca2+

A

CICR

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17
Q

How is perfusion maintained in anaesthesia when there is cardiac depression? Describe the relative effects on the graph.

A

IV fluids are given, shifting the venous compliance line to the right, increasing venous filling pressure.

As these arterial line has to meet venous line at zero, this also moves to the right

Give a cardiac inotrope to increase contractility. Starling curve moves upwards.

Give arterial vasoconstrictor - this moves the gradient of the arterial line lower.

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18
Q

What happens to ventilation as anaesthetic is given?

A

Depression of alveolar ventilation, if left unchallenged, the CO2 level will rapidly increase.

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19
Q

What acts to counteract CO2 rise after ventilatory depression?

A

As pCO2 rises the chemoreceptor drive (mainly central chemoreceptor) leads to stimulation of ventilation.

Interaction between sensitivity of our chemoreflex loop and ventilatory/CO2 state.

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20
Q

What is the effect of reducing sensitivity of chemoreflex loop?

A

Greater pCO2 levels required for increasing the ventilatory drive

This effect is the lowering of ventilatory drive and the rising of pCO2 - this is the effect of anaesthetics.

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21
Q

How do anaesthetics affect the chemoreceptors?

A

Reduce sensitivity

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22
Q

Do volatile anaesthetics affect the central or peripheral chemoreflex loop?

A

Peripheral NOT central

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23
Q

Do IV anaesthetics affect the chemoreflex loop?

A

No, chemoreflex is intact

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24
Q

How do IV anaesthetics affect breathing?

A

Central rhythm generation depression (not chemoreceptors)

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25
Q

How does anaesthesia affect chemoreceptor response to hypoxia?

A

Complete abolition of hypoxia response

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26
Q

How is O2 sensing silenced by anaesthesia?

A

Halothane and other volatile anaesthetics also generate other ROS by their metabolism - this silences the glomus cells by mimicking the environment of O2, thus TASK channels open and cells hyperpolarized.

Chemoreceptors do not fire even in hypoxic environment.

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27
Q

Describe relative airway patency, when may certain regions become compromised (and close)?

A

Bony nasopharynx and trachea is well supported, but oropharynx inbetween is less so.

Pressure at mouth, is atmospheric, but it soon falls to sub atmospheric as it enters the negative pressure of the lungs.

This can cause collapse of the oropharynx

28
Q

What normally keeps the oropharynx open?

A

Glossopharyngeal nerve stiffens the pharyngeal muscles (from respiratory center) which precedes the stimulus to the diaphragm by a few seconds, this prepares this region from collapse upon initiation of breathing.

29
Q

What happens to oropharynx under anaesthesia and why?

A

Oropharynx may shut due to negative pressure

Under anaesthetics, the output to the glossopharyngeal nerve is impaired, this is more sensitive than the output to the diaphragm.

30
Q

Why can drive to breathe be present but ability to breathe impaired?

A

Glossopharyngeal nerve impulse to oropharynx more sensitive than output to diaphragm - normally IX keeps oropharynx open

31
Q

What happens to V/Q under anaesthesia?

A

Distribution of V/Q shifts to the left (there is more lower V/Q units) (more hypoxic than usual)

32
Q

How do volatile agents affect hypoxic pulmonary vasoconstriction?

A

Normally - when not much ROS, the vessel vasoconstrict to improve V/Q matching.

Anaesthesia attenuates it as it stimulates vasoconstriction at all regions regardless of hypoxia.

33
Q

4 effects of volatile anaesthetics

A
  1. Depress myocardium directly
  2. Vasodilate directly
  3. Depress peripheral chemoreception
  4. Attenuate HPV causing V/Q heterogeneity
34
Q

2 effects of IV anaesthetics

A
  1. Depress sympathetic efferent discharge (indirect effect on heart and circulation)
  2. Depress respiratory rhythm generation in central respiratory centre
35
Q

Stage I anaesthesia?

A

Analgesia (drowsiness and reduced nociceptive input)

36
Q

Stage II anaesthesia?

A

Loss consciousness and most pain perception, reflex action to painful stimuli. Involuntary movement and talking, fluctuations in breathing

37
Q

Stage III anaesthesia?

A

Surgical (Planes 1 - 4)

38
Q

What are planes 1-4 of anaesthesia?

A

Plane 1 - Light anaesthesia. Most reflexes (Animals: pedal, corneal, palpebral) are still present.

Plane 2 - Medium anaesthesia. Most surgeries are conducted at this level. Muscles are relaxed. Most reflexes (pedal, palpebral, corneal) are absent. Looks like non-REM slow-wave sleep.

Plane 3 - Deep anaesthesia. Intercostal muscles are relaxed; ability to maintain respiration is endangered. Pupillary light reflex may be slow or absent.

Plane 4 - Too Deep. All muscles, including diaphragm and intercostal muscles, are paralysed.

39
Q

What level of anaesthesia looks like non-REM slow wave sleep?

A

Plane 2

40
Q

Stage IV anaesthesia?

A

Paralysis of respiration and motor control ceases, death

41
Q

What is the triad of changes in behaviour and perception?

A

immobilisation (muscle relaxation), unconsciousness (hypnosis) and analgesia

42
Q

What is a anaesthetic which gives hypnosis but remains consciousness and analgesia?

A

Thiopental

43
Q

What gives muscle relaxation?

A

Neuromuscular blocking agent

44
Q

What gives analgesia?

A

Opioid

45
Q

Gaseous anaesthetics

A 
Nitrous oxide 
Chloroform 
Ether 
Halothane 
Isoflurane 
Enflurane
Desflurane
Sevoflurane
46
Q

Injectable anaesthetics

A 
Thiopental 
Propofol
Ketamine
Remifentanil 
Midazolam
Succinylcholine
47
Q

Efficacy of GA action is related to…

A

Oil to water partition coefficient

48
Q

What is MAC

A

Minimum alveolar concentration: concentration of the vapour in the lungs that is needed to prevent movement (motor response) in 50% of subjects in response to surgical (pain) stimulus.

49
Q

What is the usual MAC?

A

More than 90% of all patients become anaesthetised following the administration of 1.3 MAC and 1.5 to 2.0 MAC is required to ensure anaesthesia in all patients.

50
Q

Onset of GA action is related to?

A

Blood to gas partition coefficient.

51
Q

What is the oil to water partition coefficient?

A

The ratio of concentrations of a compound in a mixture of two immiscible solvents at equilibrium - show drug distribution

52
Q

What is the blood-gas partition coefficient?

A

The blood-gas partition coefficient is the principal determinant of the rate at which the alveolar concentration (FA) increases toward a constant inspired concentration (FI).

53
Q

How does solubility in blood relate to onset of action?

A

Low solubility in blood equates to a rapid onset of action.

Nitrous faster - but used at a much higher concentration

54
Q

How do GA work?

A

Effects on Ion channels and membranes

Promote inhibitory GABA/glycine channels
Inhibit excitatory 5-HT, Nicotinic and NMDA glutamate channels

55
Q

How does NO work?

A

Nitrous oxide blocks NMDARs by 50% at a concentration of 30%, making this one of its most potent effects

Low potency, may promotes opioid release. 30% nitrous having analgesic actions equivalent to 10–15 mg morphine

56
Q

What is given with modern era inhalable anaesthetics?

A

Neuromuscular blocking drugs (e.g. vecuronium) are applied to induce paralysis a more reliable paralysis (used in 46% of all GA patients).

57
Q

Propofol action

A

Acts by potentiating GABAA (γ-aminobutyric acid type A) receptors

58
Q

Suxamethonium use

A

Nicotinic acetylcholine receptor agonist used to induce muscle relaxation and short-term paralysis (phase 1 and phase 2 block).

Facilitate tracheal intubation.

Adverse effects include life-threatening malignant hyperthermia, hyperkalaemia, and anaphylaxis.

59
Q

What may be used to calm patient with high pre-operative anxiety?

A

Anxiolytics i.e temazepam

60
Q

What is a common anti-emetic?

A

Ondansetron

61
Q

The actions of some types of neuromuscular blocking drug may be reversed by administration of

A

Cholinesterase inhibitor

62
Q

Active warming is applied in order to manage

A

Hypothermia

63
Q

Effects of vecuronium reversed by

A

Cholinesterase inhibitor (neostigmine)

64
Q

Side effects of cholinesterase inhibitor reversed by

A

Muscarinic antagonist

65
Q

Short duration local anaesthetics used in general anaesthesia for

A

Reducing postoperative pain

Neuroscience (19 decks)

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