End-tidal versus arterial CO2 causes

Time for round 2 with Pat are very generous trainee who's offered to be quizzed on our podcast.

Here are the questions from this round:

Stem 5

1.     How does heparin work?

2.     How about low molecular weight heparin?

3.     Why do we monitor unfractionated heparin but not low molecular weight heparin?
 Due to lower binding to plasma proteins and to cell surfaces, the plasma anti Xa activity generated by a given dose of LMWH is more predictable than for UH. 

4.     How do we monitor unfractionated heparin’s effect?

5.     How is the clearance of unfractionated heparin different to that of low molecular weight heparin?

Stem 6

1.     What are the main differences between intracellular and extracellular ion concentrations?

2.     What is the function of potassium?

3.     What is the NERST potential?

4.     What are the ECG changes in hyperkalaemia?

5.     What is the treatment for hyperkalaemia?

Stem 7

1.     What are the functions of the placenta?

2.     How is the placenta different to the lung?

3.     How are substances transferred across the placenta?

4.     What are the factors that affect transfer of O2 across the placenta?

5.     What are the factors that affect placental blood flow?

Stem 8

1.     During anaesthesia, you notice a difference between the End Tidal CO2 and Arterial CO2. What can you do to minimise this difference?

2.     How do you measure physiological dead space?

3.     How do you measure anatomical dead space?

4.     What increases anatomical dead space?

5.     What is closing capacity? 

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If you have any questions, please email Lahiruandstan@gmail.com 

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