SAQs 2017 Flashcards

1
Q

a) Describe the generation and features of a normal awake EEG (15 marks).
b) Briefly discuss the processing performed by quantitative EEG monitors (such as BIS or Entropy) to produce a single number from the EEG (10 marks).

A

EEG is a surface recording of summed excitatory and inhibitory electrical potentials that arise from neurones in the cerebral cortex.
Normal awake EEG is usually comprised of alpha rhythm with beta activity. It is asynchronous, low amplitude and high frequency as compared to asleep (or anaesthetised) EEG.
Normal awake EEG has the following features:
Alpha rhythm
- normal wakefulness, more prominent (↑amplitude) when eyes closed
- location = usu. posterior dominance
- frequency = 8 ~ 12 Hz (younger children = lower freq)
- amplitude = 20 ~ 100 V
- morphology = rhythmic, regular, waxing and waning amplitude
Beta activity
- relaxed wakefulness or early drowsiness, more prominent during early stages of
sleep, attenuated by voluntary movement
- location = usu. frontocentral (more variable)
- frequency=usu.18~25Hz(defn is>13Hz)
- amplitude = 5 – 20 milliV
- morphology = rhythmic, waxing and waning amplitude
Raw EEG is complex and requires expertise to interpret, which currently makes it impractical for use during clinical anaesthesia.

BIS- Method for monitoring depth of anaesthesia - 2 monitors available: BIS, entropy
Both display and analyse a processed EEG
- Gives an indication of the changes commonly associated with use of
majority of agents
o Not ketamine, opioid based anaesthetic
Analyses: combined to calculate a BIS number. The relative contributions of each component vary with the depth of anaesthesia
1. Timedomainanalysis:(tisonthexaxis)
- looks at burst suppression v time
o ↑depth of anaesthesia → ↑burst suppression
- β wave activity
o ↑depth of anaesthesia → ↑β wave frequency
2. Frequencydomainanalysis:(frequencyisonthexaxis)
- utilises Fourier analysis: each complex waveform can be broken down
into a series of sine waves that have different frequencies, amplitudes,
and phases.
- Epoch (time interval packet) looks at the frequency / amplitude of the
waves within that packet
o As ↑depth of anaesthesia → move from low frequency high amp →
high freq low amp
o Need to average multiple epochs
- Spectral edge frequency
o If a vertical line was drawn where 95% of the curve lay to the LEFT
of it…this is the spectral edge frequency 3. BispectralAnalysis
- looks at the phase relationships b/n difference frequencies

combination of time and frequency domain analysis
- Fourier transformation of raw frontal EEG into its component sine waves and
then power spectrum is obtained
- Shannon function is applied to obtain the spectral entropy (a measure of
“disorder” within the power spectrum)
- interference (e.g. diathermy) is filtered out
- spectral entropy obtain over the entire range of frequencies (0.8 Hz to 47 Hz) =
response entropy  contains both EEG and EMG components
- spectral entropy obtained over narrower frequency range (0.8 Hz to 32 Hz) =
state entropy  contain predominantly EEG component
- both SE and RE are dimensionless numbers between 0 and 100, with 0
representing completely synchronous cortical activity (i.e. silence) and 100
represent completely irregular cortical activity (i.e. wakefulness)
- if RE = SE  EMG contribution is zero
- if RE&raquo_space; SE  significant EMG contribution (suggest muscle relaxant worn off or
inadequate analgesia)

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2
Q

Describe the visceral and somatic pain of labour with particular reference to the anatomy of the pain pathways

A

3 phases of labour:

1: start = onset of uterine contractions leading to cervical effacement. end = full cervical dilatation
2: Fully dilated until baby delivered
3: ends with delivery of the placenta

Phase 1 pain:
Pain Mechanism
- pain caused by visceral stretch (uterus and cervix)
- uterine contraction -> distension of lower uterine segment (LUS) + cervix –>
visceral pain
- escalating poorly localised pain
Pain pathway
- nociceptors in LUS and cervix -> visceral afferent (Adelta and C fibres) travels via sympathetic efferent fibres -> uterine plexus -> inferior hypogastric plexus -> sympathetic chain -> T10 – L1 dorsal horn

PHASE ONE NERVE ROOTS = T10 TO L1
INFERIOR HYPOGASTRIC PLEXUS

Phase 2:

  • Pain caused by fetus travelling through pelvis and birth canal.
  • Fetal descent causes stretching and tearting of perineum, which is SOMATIC pain
  • fetal descent causes pressure on bladder, urethra, rectum, causes VISCERAL pain (poorly localised, referred to lower back/inner thigh)

Pain pathway:
- Nociceptors in cervix and perineum –> somatic afferent (Adelta) via pudendal nerve

PUDENTAL NERVE S2-S4

Phase 3:
Pain mechanism:
- Somatac pain from passage of placenta
- Visceral pain associated with contraction of uterus, cramps can persist for days
- pain pathway the same as phase 2 but much less intense.

Final common pathways:
Nerve will synapse in dorsal horn, ascend via anteriolateral spinothalamic tract to thalamus, synapses again, becomes 3rd order neuron and travels to sensory cortex.

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3
Q

Describe the effects of morbid obesity on the respiratory system

A

Definition: BMI >35kg/m^2.

Main effects:

  • increased fatty tissue and weight
  • –> Decreased FRC (atelectasis)
  • –> cephelad displacement of diaphragm
  • –> decreased compliance
  • ——–> increased WOB
  • –> Increased VO2 and CO2 production
  • ——–> Need to compensate for this, so MV is drastically increased
  • Increased blood volume
  • —-> From obesity and polycythemia due to OSA and increased VO2

Anatomy - upper airway:

  • Decreased pharyngeal diameter
  • Fatty infiltrate of the pharynx
  • Increased tendency to collapse during sleep/sedation

Anatomy: - lower airway:

  • Decreased chest wall compliance
  • Decreased ERV (therefore decreased FRC)
  • Decreased compliance due to lower lung volume
  • Decreased TLC

Resistance:

  • Increased due to decreased lung volumes
  • Specific conductance remains unchanged

Resp muscles:

  • Increased mass
  • Increased respiratory effort (more resistance, lower lung volumes)
  • increased oxygen demand from resp muscles

Gas exchange:

  • Lower PaO2
  • Increased V/Q mismatch due to atelectasis

Obesity hypoventilation syndrome:

  • Resting PaCO2 increased even awake
  • Decreased reactivity of respiratory control centre

Demands on respiratory system:
- Increased body mass –> Increased VO2, increased CO2 production, increased MV.

Parameters:

  • RR increased
  • TV: decreased
  • MV: Increased
  • ERV: Decreased
  • FRC: decreased
  • FEV1: Decreased
  • FEV1/FVC: unchanged (restrictive picture)
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4
Q

Describe how the large daily volume of glomerular filtrate is altered by the kidney to form a relatively low volume of concentrated urine

A

Daily volume of GF is 180L in 70kg adult male.

Urine output can be titrated from 430ml to 23L.

RBF is 25% of CO, approx 1500ml/min.

This means blood filtered about 60x/day, important to filter molecules in small concentrations in the blood.

Picture of nephron

As the ultrafiltrate travels down the nephron, at various parts it is reabsorbed.

PCT:

  • Most important
  • 65% of sodium and water are reabsorbed here
  • Transcellularly and intercellular routes.
  • By osmosis

DLOH
- Permeable to water, and as osmotic gradient between interstitium and filtrate is high due to counter-current multiplier, water passes into interstitium concentrating the filtrate.

ALOH
- Impermeable to water, so water stays concentrated.

Collecting duct:

  • Where up to 20% of water is absorbed.
  • Largely dependent on presence of ADH
  • ADH is synthesised in the hypothalamus and released from the posterior pituitary gland during both hyperosmolar states and on hypovolaemia.
  • ADH acts on V2 receptors, increasing transcribing for AQ2 channels, which then increase the permeability to water for the collecting ducts, allowing water to be reabsorbed.

Role of urea:
- Provides 50% of the osmolarity of interstitium

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