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27/6 Week Learning Points > SAQ LOs > Flashcards

SAQ LOs Flashcards

1
Q

What is the range of PCO2 value that CBF responds to?

A

20-80mmHg

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2
Q

What is the PR interval. What is the usual duration?

A

Time between excitation of the atrium to excitation of ventricle. Allows adequate ventricular filling.

From start of P wave to start of Q wave

Normally less than 200ms

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3
Q

What is the usual duration and height of P wave

A

<120ms

<2.5mm

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4
Q

What is the scale of a standard ECG?

A

25mm/sec, 10second strip

1 mv / 10mm

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5
Q

What is the QT interval?

A

from start of Q wave to end of T wave

Corrected using Bazett formula

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6
Q

List some causes of short PR

A

Increased SNS
Increased temp and metabolic rate
WPW syndrome

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7
Q

List the drugs that can cause long PR

A

Beta blocker
Verapamil, diltiazem
Digoxin

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8
Q

Describe the lipid hypothesis

A

Accumulation of volatile agent in CNS bilayer causes distortion of membrane function (critical volume hypothesis)

Rationale - Myer-Overton correlation

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9
Q

What are the reasons for discrediting lipid hypothesis

A

Steroisomers have similar O:G coefficient but varied anaesthetic potency

Increasing molecular chain length increases lipid solubility, but there is a ceiling effect. No further increase in potency when n >13

Raising body temp has no anaesthetic effect when it affects lipid membranes

At similar hypnotic dose, some agents are better than others at inducing immobility

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10
Q

What is protein hypothesis?

A

VA interaction with the hydrophobic areas of key membrane proteins

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11
Q

What are some other theories (aside from protein / lipid hypothesis) to explain action of volatile agents?

A

NMDA receptor inhibition, particularly by gaseous agents like N2O and xenon.

Physically swelling neuronal membrane

Interference of release of neurotransmitters from presynaptic membrane.

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12
Q

Describe the Bowditch effect.

A

Increased heart rate independently increases contractility

HR -> increased Ca -> increase contractility

Part of the homeometric auto regulation

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13
Q

Describe the Amrep effect

A

Myocardial contractility increases with increased afterload.

Increased after load -> increased end-diastolic LV pressure -> increased stretch of sarcomeres -> increase force of contraction

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14
Q

How quickly will 2L of CSL distribute into different fluid compartments?

A

T1/2a 5 mins

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15
Q

Describe the metabolic pathway of paracetamol

A

Both phase 1 (CYP2E1) and phase 2 (glucuronidation / sulfation)

  • Saturable phase 2 in high dose -> shunts to phase 1
  • Phase 1 metabolite NAPQI -> build up = toxic

NAPQI conjugated with glutathione to form cysteine conjugate or mecaptopuric acid conjugate -> inactive.

Build up of NAPQI -> centrilobar necrosis / acute liver failure

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16
Q

How many genes / alleles are there to code for plasma pseudo-cholinesterase?

A

2 copies of the gene on chromosome 3, 4 different alleles, 10 different phenotypes

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17
Q

What happens to plasma cholinesterase content for 1) neonates 2) pregnancy

A

1) reduced

2) larger ECF / Vd -> same amount of PCHE but reduced concentration

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18
Q

What drugs inhibit plasma pseudocholinesterase?

A 
neostigmine
ketamine 
metoclopramide 
Lithium 
Ester LA 
Oral contraceptive
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19
Q

What happened to the ion channels in phase 3 of SAN action potential?

A

Activation of K+ channels for repolarisation / hyper polarisation

Inactivation of HCN and Calcium channels

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20
Q

What factors affect the automaticity of the SAN?

A

Autonomic nervous system - major
age - fibrosis of nodal cells -> bradycardia
Temperature - increased temperature = increased action of ion channels -> increase slope of phase 0 - tachycardia

Hypoxia -> unable to reset ionic gradient via Na/K ATPase

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21
Q

What is the Bohr-Enghoff equation for?

How does inaccuracy arise?

A

Calculation of physiological dead space

VD/VT = (FACO2 - FCO2 at mouth level) / FACo2

Alveolar CO2 is hard to measure due to variables.

Apical PACO2 = 28mmHg vs. basal PACO2 of 42

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22
Q

What is the Enghoff modification of the Bohr equation?

A

Use arterial CO2 instead of alveolar CO2, easier to measure, but still influenced by dead space and shunt, diffusion abnormality, V/Q mismatch

Enghoff dead space is generally larger than Bohr dead space.

23
Q

What is the Fowler’s method and what does it measure?

A

Single breath 100% vital capacity breath, then measure nitrogen wash out

At end inspiration, anatomical dead space is completely filled with oxygen

Phase 1 - O2 only, no N2
Phase 2 - exhaled nitrogen concentration rises rapidly
Phase 3 - pure alveolar gas

Split phase 2 in the middle + phase 1 = anatomical dead space

24
Q

What is the reason for the 3-5 difference between PaCO2 and ETCO2

A

Inherent V/Q mismatch within the lung due to gravity resulting in alveolar dead space

25
Q

What colour is nitrous oxide cylinder?

A

French blue

26
Q

What is the critical temperature of N2O

A

36.5

27
Q

What are some proposed mechanisms of action of N2O??

A

Opioid receptors for analgesic action
Some GABA medication CNS depression
NMDA receptors

28
Q

What is the effect of N2O on the resp and cardio systems?

A

Resp - no change to MV, minimal increase RR, minimal decrease TV

  • Diffusion hypoxia
  • Increase PVR

Cardio - mild negative ionotrope,
indirect SNS stimulation
- Some increase in SVR / HR
- MAP typically maintained

29
Q

How is sevoflurane stored?

A

in polyethylene bottles to avoid source of Lewis acids which can corrode glass

30
Q

What is the cardiovascular effect of sevoflurane

A

Vascular - reduce SVR
Does not affect heart rate (or may increase due to baroreceptor reflex)
Does not blunt baroreceptor reflex
Negative ionotropy

31
Q

What is the CNS effect of N2O

A

Increases CMRO2 due to indirect SNS stimulation -> avoid in raised ICP

32
Q

What is anaesthetic preconditioning

A

When volatile agents are administered before a period of prolonged ischaemia

  • Activation of sarcolemmal and mitochondrial ATP-dependent K channels
  • Activation of protein kinase C

May protect myocardium from ischaemia and repercussion injury -> reduce myocardial infarct size

33
Q

What is the effect of pregnancy on ODC?

A

Left shift due to resp alkalosis
Right shift due to 2,3 DPG production
No net change

34
Q

What is the umbilical arterial and venous O2 partial pressure?

A

Arterial 18 mmHg

Venous 28 mmHg

35
Q

What is the O2 partial pressure of placental circulation?

A

Arterial 100mmHg

Venous 40 mmHg

36
Q

What is the CO2 partial pressure of

  • Umbilical A
  • Umbilical V
  • Placental A
  • Placental V
A
  • 55 mmHg
  • 35
  • 32
  • 45
37
Q

What is the mechanism of action of warfarin?

A

Vitamin K epoxide reductase inhibitor

- Prevents gamma-glutamyl carboxylation on coagulation factors

38
Q

What determines the onset of action and the initial procoagulant state of warfarin?

A

Onset due to half life of factors
- Factor II slowest of 60 hours

Protein C half life 8 hours -> procoagulant

39
Q

What is the PO and IV dose of vitamin K?

A

PO 2mg

IV 10 mg

40
Q

what is the IV dose of FFP to reverse warfarin?

A

15-30ml/kg

41
Q

What is the IV dose of prothrombinex for warfarin reversal?

A

IV 25-50 units /kg

42
Q

What is the mechanism of increased local blood flow from exercise?

How does this influence cardiac output?

A

production of lactic acid, CO2, H+
-> increases NO synthesis -> VD

Increase flow from arterial to venous side of circulation.
Increase preload -> increase CO

43
Q

What does localised vasodilation from exercise do to the vascular function curve and cardiac function curve?

A

Pivot upward with vascular function curve.
Intersects cardiac function curve at higher point
Hence functioning at a greater cardiac output.

44
Q

What is skeletal muscle pump?

A

Contraction of skeletal muscle -> increase venous return -> increased preload

45
Q

How does opioids cause urinary retention?

A

Action on the sacral neural plexus PNS
Contracts internal urethral sphincter.
Relaxes detrusor muscle

46
Q

What are the four points of the scavenging system

A

Collection
Transfer
Receiving
Disposal

47
Q

What kind of frequency can establish harmonics?

A

Any frequency that is a whole number multiple of the natural frequency

48
Q

Why does an arterial line catheter need to be short, large diameter, and stuff?

A

To achieve high system natural frequency 10x upper limit, around 40Hz

Significant margin of error to prevent harmonics with patient’s pulse rate

49
Q

The arterial line transducer has a Wheatstone bridge in it.

What is it and what is its function?

A

The bridge is an electrical circuit that converts the pressure signal via change in resistance into an electrical signal.

As the diaphragm deforms and bends -> change in resistance -> provides electrical signal.

50
Q

How does one zero the arterial line

A

Close to patient, open to air

51
Q

What is over-damping

A

When something in the arterial line acts as a shock absorber.

  • Air, more compressible than water, can absorb pressure wave through the line.
  • Kinks
  • Blood clots
  • Compliant tubing

Prevent the wave from being propagated.

Creates a slurred waveform, low peak SBP, high DBP, narrowed PP

52
Q

What is under- damping

A

Result of the pressure wave transmitted too quickly.

  • Stiff, non-compliant tubing
  • Artifact from cathetre
  • Tachycardia

Increase PP but increase SBP, decrease DBP

53
Q

List the components of an arterial line

A

Short, stiff arterial line catheter, luer lock to stiff tubing.

Connects to 3 way tap -> transducer with flush system.

Cable connection connected to transducer.

Pressurised saline flush also connected to transducer

54
Q

What is the optimal amount of damping?

A

Damping ratio of 0.64

27/6 Week Learning Points (5 decks)

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