25/6 Weekend SAQ LOs Flashcards

1
Q

Describe inter ventricular dependence in IPPV

A

IPPV -> increased intrathoracic pressure on inspiration

Increased pulmonary pressure and right heart after load. Bulging of septum to left compressing LV -> reduce LV preload.

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2
Q

Write out law of LaPlace

A

Wall tension = transmural pressure x radius / (2x wall thickness)

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3
Q

How does IPPV improve the cardiac function of someone in heart failure?

A

Heart failure -> venous congestion -> person operates at the top end of the Frank-Stalin curve.

  • IPPV preload reduction puts the person back to optimal position on FS curve
  • Reduction in after load is good.
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4
Q

Why would ageing cause LV concentric hypertrophy?

A

Stiff aorta from calcification -> LV after load

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5
Q

What is the consequence of connective tissue replacing LV myocytes?

A

decrease compliance
concentric hypertrophy
reliance on atrial kick
Tachycardia poorly tolerated

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6
Q

What is the effect of baroreceptor reflex attenuation in aging?

A

orthostatic hypotension, syncope

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7
Q

What is the relative increase in risk of difficult intubation for pregnant women?

A

7-10 folds

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8
Q

What is the effect of relaxin in rib cage in pregnancy?

A

increase AP / transverse diameter of thoracic cage to partially compensate for cephalad diaphragm displacement

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9
Q

Describe the changes in lung volumes in pregnancy

A

Reduced FRC and RV.
TLC minimal reduction
Vital capacity unchanged.

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10
Q

What is the effect of respiratory alkalosis in pregnancy

A

Increase foetal CO2 gradient of transfer.

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11
Q

What is the Monroe-Kellie doctrine

A

Cranium is a closed space with one major outlet

Any increase in one intracranial substance must come at the expense of another or else pressure rises drastically .

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12
Q

Graph of the ICP and ischaemia, what are the axis and units

A

Y-axis intracranial pressure in mmHg (20-50 focal, >50 global)

X-axis volume of intracranial substance in mL

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13
Q

Describe the hydrostatic change of head down position

A

~10mmHg for 13cm head down from heart

  • Increase arterial pressure slightly, small increase in arterial volume
  • Increase venous pressure from to +10, large increase in venous volume
  • Compensate by CSF displacement
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14
Q

Describe urea recycling

A

Urea is freely filtered, 50% reabsorbed, same 50% secreted in LOH and same 50% reabsorbed at medullary collecting duct.

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15
Q

What are the issues of using urea as a marker of renal function?

A

Not an ideal marker as it is both reabsorbed and secreted

Variation with degree of protein metabolism

[Urea] is inversely proportional to hydration

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16
Q

Describe the graph of GFR vs. Creatinine, units and implications

A

Y axis - creatinine in micromol/L, range 45-100
X axis - GFR ml/min, range 0-120

Sharp increase in creatinine when GFR < 40

Greater than 50% decrease in GFR before significant increase in creatinine or urea

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17
Q

What is the formula for estimating GFR and what is its problem?

A

Cockcroft-Gault equation, incorporating lean body weight and serum creatinine

Estimation only, multiple variables
Renal failure -> increased secreted fraction -> overestimation of GFR

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18
Q

In hypovolaemic shock, what other factors can exacerbate lactic acidosis (aside from anaerobic glycolysis)

A

Increased cardiac work -> increased lactic acid production
decreased liver lactic acid clearance
Increased respiratory work

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19
Q

What is the effect of hypovolaemic shock on the respiratory system

A

Metabolic acidosis

  • Right shift Hb-O2 curve
  • Pulmonary vasoconstriction

Increased dead space

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20
Q

Describe the MOA and effect of local anaesthetic and cardiac toxicity

A

Inhibition of cardiac VDNaC with very high affinity
First phase increased HR and MAP
Second phase myocardial depression
Third phase peripheral vasodilation -> arrhythmia and arrest

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21
Q

What is the effect of tissue-blood partition coefficient on volatile wash in?

A

N2O < des < sevo

Lower TBPC -> reduce tissue uptake -> increase rate of rise

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22
Q

curve of flow-metabolism uncoupling for sevo.

What are the axis?

A

Cerebral blood flow vs. CMRO2

23
Q

What is anaesthetic preconditioning of coronary circulation with sevoflurane

A

Mimics ischaemic preconditioning.
Activation of vascular K+ ATP channel
Onset in minutes, offset 3-4 days.

24
Q

Describe the proportion of CO2 buffering in blood

A

90% HCO3
Carbamino compound 5%
Dissolved 5%

25
Q

Outline the HCO3 buffering effect

A

H+ binding to the imidazole groups of histidine residues

CO2 + H2O -> H+ + HCO3-

H+ bound to imidazole groups of Hb and plasma proteins

HCO3 exchanged fro Cl- at membrane via Hamburger effect.

Carbamino compound essentially the same by binding to amino groups.

26
Q

How much does Haldane effect contribute to CO2 buffering?

A

70% by carbamino formation

30% by increased imidazole group buffering.

27
Q

What is the baseline CMRO2?

A

3.5ml/min/100g

28
Q

How is the concentration of effect site derived for TCI model?

A

derived from relationship between plasma concentration and EEG data

29
Q

How does distribution of pharmacokinetic influence the time to recovery for muscle relaxants?

A

Bolus dose - recovery from distribution. Higher Vd = faster recovery
After infusion - recovery from metabolism and excretion. Lower VD = faster recovery

30
Q

How does aminoglycoside influence duration of NMB?

A

slows the rate of recovery.

Reduce presynaptic ACh release

31
Q

How is tramadol metabolised and excreted?

A

Phase 1
2D6 -> O-desmethyltramadol
3A4 -> N-desmethyltramadol

Phase 2
Glucuronidation of tramadol

90% Renal excretion (30% parent, 60% metabolite)
10% into bile

32
Q

Describe the quantal dose response curve.

A

% population vs. log [drug dose] graph
Binary endpoint, sigmoid shaped curve

Flat beginning due to high safety margin of Ach as 70% of receptors blockade required for any effect (spare receptor theory)

Final plateau portion represents >95% receptor blockade and adding more NMB does not achieve greater effect.

33
Q

What is ED95 of NMB.

What is the ED95 of rocuronium

A

ED95 - dose required to produce 95% depression of the first twitch response in 50% of population.

For Roc, this is 0.3mg/kg

Intubating dose = 2x ED95, the dose to produce 95% first twitch reduction in 95% of population.

34
Q

What is a supra maximal stimulus and why is it needed?

A

SMS = initial threshold for stimulation x 2.5

Eliminates variation in muscle response caused by partial depolarisation of nerve.

35
Q

What are the sites of NMJ monitoring?

A

Ulnar nerve - adductor pollicis adduction

Facial nerve

Tibial nerve for plantarflexsion of big toe

Common perineal nerve for foot dorsiflexion

36
Q

For NMB, compare laryngeal muscle and adductor pollicis

A

Laryngeal muscle has
- Greater blood flow, greater Ach release, greater amount of Ach receptors.

Clinical effect
- Faster onset, less depth, shorter duration.

For NMB monitoring of ulnar nerve, if TOF is >90%, then there is more certainty that laryngeal muscle is also reversed.

37
Q

what is Lambert-Eaton syndrome?

A

autoantibody against presynaptic VDCC -> reduced competition with Ach

38
Q

What is the absorption frequency of CO2 and N2O

A

CO2 - 4.7 micrometer

N2O - 4.5 micrometer

39
Q

What are the three axis for intubation?

A

Oral
Pharyngeal
Laryngeal

40
Q

What are the changes in neonatal upper airway

A

Large occiput - neck flexion in supine
Narrow nasal passage, obligate nasal breather, auto PEEP
Large tongue - difficult BMV (Guedel useful)
U-shaped epiglottis, floppy - tip of epiglottis can obstruct intubation view, glottis obstruction with LMA

Higher and more anterior larynx (C3 at birth) - difficult to align intubation axis

Cone shaped outlet, narrowest point at cricoid - increased risk of subglottic stenosis

Short trachea - risk of dislodging of inadvertently advance ETT

Narrow trachea - higher airflow resistance.

41
Q

What are the proposed mechanism of Ergometrine

A

Unclear but may work on dopamine, adenosine, or 5HT receptors.

42
Q

What is the adverse effect of using Nitrous oxide as a tocolytic?

A

tachyphylaxis
Cerebral VD
Met-Hb (rare)

43
Q

Amiodarone

  • Bioavailability
  • Protein binding
  • Metabolic and excretion pathway
A

60-80%
96%

N-des-ethyl-amiodarone, active metabolite
Enterohepatic circulation in bile, minimal renal excretion

44
Q

Describe the CVS effects of amiodarone

A
Class I-IV anti-arrhythmic, mainly class III 
- Increases refractory period, decreases automaticity, prolong QT 

Adverse effects

  • Mild bradycardia, mild direct negative ionotropy
  • Vasodilation via A-blocking -> reduce SVR -> reduce MAP
  • Torsades
45
Q

list the toxic effects of amiodarone

A

NQR-BITCH
Neurotoxicity - peripheral neuropathy, ataxia
QT prolongation -> torsades
Respiratory effects - high mortality interstitial fibrosis in 5-15% patients on chronic therapy.

Blue-grey skin discolouration / photosensitivity
Inhibition of CYP enzymes
Thyroid - structure similar to thyroxine, 2% incidence, hyper or hypo
Corneal deposits - reversible
Hepatitis / LFT derangement

46
Q

Describe the sensor -> control -> effector pathway for baroreceptor reflex

A
S - aortic and carotid bodies 
Afferent neurons - glossopharyngeal (carotid), vagus (aortic) 
Control - NTS -> RVLM 
Efferent - SNS efferent 
Effector - heart and vessels
47
Q

Describe the sub-tracts of spinothalamic tract

A

Anterior - neospinothalamic, sensory discriminative, mainly A-delta input from Lamina 1

Lateral - paleospinothalamic, autonomic/emotional, mainly C fibres.

48
Q

List some other tracts for pain other than spinothalamic tract

A

Spinoreticular, spinolimbic, spinoparabrachial

49
Q

Describe the cardiovascular effects of sleep

A

REM - increase heart rate

NREM - decrease HR, decrease vascular tone, decrease BP

50
Q

Describe the respiratory effects of sleep

A

REM - increase MV by increasing RR, reduce TV

  • Reduced ++ pharyngeal muscle tone
  • Reduced O2 and CO2 response for ventilation

NREM

  • Also reduce pharyngeal tone and ventilatory drive
  • Reduce MV, unchanged R, reduce RV
51
Q

Describe the metabolic effects of sleep

A

REM
- Increase BMR, increase ACTH / cortisol

NREM

  • Reduce BMR, reduce temp, reduce shivering threshold
  • Reduce ACTH
  • Increase growth hormone, prolactin, melatonin
52
Q

What is the bimetallic strip?

A

Safety feature of plnuem vaporiser
Two pieces of metal with different coefficient of thermal expansion.

Increase concentration -> increase uptake -> reduce vaporiser temperature -> divert greater flow to vaporiser chamber

53
Q

What is a plenum vaporiser and why do we use it?

A

Plenum vaporiser relies on a pressure gradient provided by fresh gas flow to allow vaporisation of liquid anaesthetic agent.

High resistance and must be outside of the circle.

Delivers controlled vaporisation of liquid anaesthetic agents into a vapour for controlled administration

54
Q

What are the different types of plenum vaporiser?

A

Variable bypass - relies on vaporising and bypass stream

Measured flow - separate flow of vapour that’s independently added to patient’s fresh gas flow to produce required concentration of VA (desflurane)