Tutorials – Week of 6 Sept 2012

Wow. I am being prolific tonight.

Next week is a long weekend so there will be one tutorial only – this will be on Wednesday following the meeting.

Dr Sheldon will cover Muscle relaxants which should nicely round out the section on muscular function. Feel free to badger him wil any questions you have relating to Phase II block. ūüôā

Mike

 

Neuromuscular Junction – Phase II block

I wanted to clarify the phase II block that we discussed today at the tutorial (ok, the one that the 8 people who were at the tut discussed)

Some facts about Phase II block

  • It occurs exclusively with exposure to depolarising muscle relaxants
  • Prolonged exposure of the neuromuscular¬†junction to scoline causes one of two events to occur – desensitisation block or phase II block
  • What I described to you today was desensitisation block – remember that the receptors fluctuate constantly between open, closed and desensitised states. Agonists (scoline) predispose to desensitisation as they have a higher affinity for the desensitised receptors and they promote transition to the desensitised state. It follows that prolonged exposure will result in an increase in the average number of receptors which are desensitised. Normally ACh is so rapidly inactivated that desensitisation does not occur. This may be a safety mechanism.
  • Phase II block differs from desensitisation block. It is characterised by fade, tetanic fade and post-tetanic facilitation. After initial depolarisation, the membrane potential gradually returns to normal even though the nAChRs are still exposed to drug and neurotransmission is blocked.
    • There is still debate about the actual process
    • It may be a presynaptic phenomenon (at another AchR where scoline can bind (not the alpha3Beta2))
    • It may result from some postjunctional receptor desensitisation
    • It may be due to activation of the NA/K ATPase pump by initial depolarisation of the postsynaptic membrane which repolarises it.

 

This probably doesn’t clarify this much, but to be honest, i’ve done a (very brief) literature review and most papers are pretty vague as to what causes phase II block.

What they are clear about is that treatment is controversial. If the pt is known to have NORMAL AChE then the recommendation is to give neostigmine. If the patient has ABNORMAL AChE then neostigmine will at best have no effect and at worst worsen the block.

I hope this helps somewhat.

Mike

 

Venturi Question – possible answer (edited 1 Aug)

Hi all.

I have been approached to give an opinion on the answer to question 3C of the Mar 2010 physics paper.

The question is as shown

The key (as I see it) is this. If you are given information, you need to use it!

So, this is how I approached it

Given Information

500ml tidal volume

40% venturi at 8lpm – blocked venturis (so assume 100% coming out of venturi?)

rr 30/min

IE 1:2  

What is average inspired oxygen?

 Minute volume = 6000ml = 100ml/sec BUT only inspiring 33% of the time therefore inspiratory flow = 300ml/sec

mask flow 8000ml/min  = 133ml/sec

insp time 20secs

exp time 40secs

 ?how much is rebreathed?

assuming zero volume in mask? 

Initial calculation from last night not accurate. The final calculation as I see it is as follows.

We require 300ml/sec but only 133ml/sec is being supplied. So the inspired volume/second is made up as follows Р267ml entrained air at Fi of 0.21 and 133ml supplied at FiO2 of 1. 

Thus, 56ml of the entrained air is oxygen added to the 133ml of supplied oxygen giving you 189ml/sec of oxygen inspired out of the 300ml/sec total which calculates out to a percentage of 63%.

That is how I see it.

Comments welcome. I guess the take home point is that, if your respiratory rate increases significantly, your true inspired oxygen concentration may well drop. I have made a number of assumptions here. Firstly, the mask doesn’t fit so tightly that expired gas can’t escape. Secondly, the volume of the mask is negligible for purposes of calculation.

Have fun!

Mike

Next week, 30 August

Hi guys

Next weeks tuts are as follows:

Tuesday: NMJ junction with Dr. Blackburn at gen at 17h00
Wednesday: muscle physiology with Dr. De Wet after combined meeting at DGMC

Questions for this week:

Physiology:
discuss the immune system under te following headings:
1 humoral immunity
2 cell mediated immunity
3 complement

Pharm:
Describe the mechanism of action of the following antibiotics:
1 Penicillins
2 Quinilones
3 Metronidazole
4 linezolid

Physics:
Discuss all devices and their mechanisms for measurement of body temperature.

Enjoy:)

Regards

Dave

Tutorial 25 July

A quick note. Tomorrows tutorial will be at CMJAH at 16:30 following the CMJAH m and m.

Tutorials next week ( 23-27 July 2012)

Hi all.

A quick heads up for the tutorials next week. Ie the week after the refresher course.

There will be three tutorials (sorry)
Tuesday 17:00 CMJAH – Dr G Morgan – Renal Function testing
Wednesday after combined meeting – Dr J Starkowitz – crystalloids and colloids
Thursday 17:00 CMJAH – Dr B Madlener – diuretics

Will try and do some Questions for you chaps in the next day or so (once the August roster is done)

Mike

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Week of 16 July 2012

Hi all

 

I think it probably goes without saying that there will be no tutorials this week due to the refresher course.

Attendance at wednesday afternoon’s RC sessions is compulsory.

 

Mike

 

Pacemaker/icd review articles

Ok. These are pretty good for function and malfunction
Parts 1 and 2
Anesthesiology vol 95, no 5, nov 2001 1265-1280
Anesthesiology vol 95 no 6 dec 2001 1492-1506

Tutorials – week starting 9 July 2012

I’m more or less on the ball this week!
Tutorials next week are as follows

On Wednesday Dr Wagner will do renal anatomy (I have confirmed this tutorial with her) following the combined meeting

On Thursday, Dr Nam will cover the ABG electrodes. 17:00 CMJAH.

Mock questions on Monday.
Have a great weekend.
Mike

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Venue for tuts 4 July 2012

Quick note for today’s tut. The venue is 18 Eton, not the CMSA.