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Author Topic: CO2 NARCOSIS  (Read 18433 times)

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yogenbhatt1

  • Yogen Bhatt, Mumbai, India
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CO2 NARCOSIS
« on: November 20, 2007, 11:57:50 AM »
Recently I was called by an anaethesiologist as the patient was not coming out. A case of TKR where Epidural did not work and GA was given. Intubation was not possible and LMA was used. Patient did not come out of GA after reversal.  LMA was removed and mask ventilltion was going on.
     On reaching there I realised that ETCO2 was 90plus( we have a portable Capnogram of our own).These monitors are still not used as a routine over here. We intubated over a guide wire. ABG showed PCO2 of 86. We noticed convulsions on facial muscles. We just kept on ventillating with a venti for an hour and a half and she came out completely. Tube was removed and was shifted to ICU for observation.
     Many things were wrong in management.
     I want members to throw light on what all happens in CO2 narcosis, if they have seen one. and also the pathophysiology.
« Last Edit: November 20, 2007, 12:00:38 PM by yogenbhatt1 »
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jafo1964

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Re: CO2 NARCOSIS
« Reply #1 on: November 21, 2007, 12:41:49 AM »
I will post the details later, but surprisingly the first gas used experimentally to produce anaesthesia was CO2 by Henry Hill Hickman
Well managed
Just goes to prove how and why ETCO2 monitoring is so important during anaesthesia
regs
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yogenbhatt1

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Re: CO2 NARCOSIS
« Reply #2 on: November 21, 2007, 12:53:15 PM »
     Thanks for a quick reply. Actually I missed you all for almost a month. No body had posted any thing in a month. So I posted this case.
     ETCO2 monitor has a very important role to play, but the anaesthetist had a better role to play. The reversal was given purely on assumption that it is an hour since Pancuronium was given ( few ppl still use pancuronium here.) TOF-Watch is also never used. After this, I am wondering why LMA was removed and mask ventillation was going on? The pt was hardly attempting breathing. I think some ppl really need to be more watchfull while reversing.
Eagerly waiting for your reply on sequele of events in CO2 Narcosis.
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jafo1964

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Re: CO2 NARCOSIS
« Reply #3 on: November 25, 2007, 08:17:05 PM »
Hypercapnia and the CNS
1. Increased CBF causes cerebral edema
2. Increased ICP due to increased CBF
3. CNS acidosis - CO2 easily crosses BBB and forms carbonic acid and finally H+ ion. This H+ ion cannot be easily moved across the BBB. Similar effect when soda bicarb is given

These may be the factors that lead to delayed recovery in CO2 narcosis

regs
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yogenbhatt1

  • Yogen Bhatt, Mumbai, India
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Re: CO2 NARCOSIS
« Reply #4 on: November 26, 2007, 01:50:34 AM »
    My observation in past few cases show, that when CO2 Narcosis takes place, the patient takes quite some time to sattle down, because the cerebral edema also takes its own time to go down. It takes nearly 6 to 8 hours to become normal even after the PCO2 has come back to normal.
  I am sure, other effects like Acidotic cardio myopathy also must be coming in picture to reduce cardiac function.
Thanks for the reply,
Regards, Yogen Bhatt
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Pascal

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Re: CO2 NARCOSIS
« Reply #5 on: January 04, 2008, 03:51:53 PM »
    My observation in past few cases show, that when CO2 Narcosis takes place, the patient takes quite some time to sattle down ...

On the question of CO2 retention I wonder if anyone can tell me or give me a reference in answer to the following question:

If an average paralysed or sedated adult with a PaCO2 of 30 - 40 mmHg and who is afebrile is left apnoeic after a period of ventilation with oxygen being supported with apnoeic oxygenation at what rate does the PaCO2 rise?  I have tried to find the answer to this question in physiology texts but so far without success.  From my training days I seem to recall the figure is 2.5 mmHg per minute.  Is this correct?
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jafo1964

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Re: CO2 NARCOSIS
« Reply #6 on: January 05, 2008, 11:29:41 PM »
Rate of increase is the same as seen in apnoec oxygenation techniques

1st minute Co2 increases by 6 mm Hg
all subsequent minutes  3 -4 mm Hg

So the max duration for which patient can remain on Apnoec insufflation technique is between 6 to 7 mins

Ref: Miller's Anaesthesia
Anaesthesia for thoracic surgery - William.C.Wilson & Jonathan.L.Benumof
Page 1901

regs
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Pascal

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Re: CO2 NARCOSIS
« Reply #7 on: January 06, 2008, 02:36:30 PM »
Thank you jafo1964 for your information and reference.  It is exactly what I was looking for and it was in relation to apnoeic oxygenation that I was seeking the information.  I find where I work that Recovery Room nurses have next to no knowledge of apnoeic oxygenation and can be quite worried about the patient being left apnoeic for as little as one or two minutes even though I am present and the SO2 is 99 the whole time.  It appears that there is an unwritten policy not to teach them about this subject. Do you have this problem?
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jafo1964

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Re: CO2 NARCOSIS
« Reply #8 on: January 08, 2008, 12:12:20 AM »
A word of caution
In the Apnoec oxygenation technique
patient is anaesthetized, paralysed and not breathing
a catheter is placed past the cords into the trachea and positioned above the carina
it is in this position that high flow oxygen is delivered to acheive the desired effect
the anaesthetist is ready to intervene if any deviation from accepted monitoring norms occurs

i wonder if post-operatively will it apply to a patient on Hudson mask and all the residual effects of anaesthesia
regs
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Pascal

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Re: CO2 NARCOSIS
« Reply #9 on: January 08, 2008, 11:58:58 AM »
i wonder if post-operatively will it apply to a patient on Hudson mask and all the residual effects of anaesthesia

It certainly does work at the end of an operation or in a Recovery Room.  There is a lot of wooley thinking on this subject.  Most anaestheists perhaps unwittingly use apnoeic oxygenation when after reversal of a muscle relaxant and a few breaths of oxygen they stop the ventialtion and await resumption of spontaneous breathing.

I have taken this practice a step further.  For some thirty years I have looked on the end of the operation as usually being the end of the need for the patient to be in theatre.  Once the dressing is complete, and the patient transferred to the trolley, provided he is haemodynamically stable I take him to Recovery Room.  There the LMA (or ETT) is attached to a 300 ml light plastic open bag and oxygen source.

These bags are very nice.  If you fill the bag, occlude the opening and turn the oxygen off you have a very good monitor of both the heart and lungs, far better than looking at or feeling the abdomen which is what nurses instictively do.

If there is no breathing you simply turn the oxygen on, give a few puffs and leave the patient apnoeic in the same way as you would in theatre.  While the oxygen is off it is quite instructive to demonstate that you can quite easily see the heart beat and even make out the heart rhythm.  Furthermore, if you can see the heart beat it tells you immediately that there is no upper airway obstruction as with laryngeal occlusion or spasm.

After a short time breathing will resume.  In the meantime the theatre orderley has been able to clean the theatre and get the next patient on the table.  There is a definite and significant saving in time.

In thirty years I have not had any major problem with this policy.  I work in smaller hospitals and the nursing staff are used to me.  I find it more comfortable than trying to establish spontaneous breathing in theatre.  There is no pressure.  There is no need to lighten the patient, perhaps prematurely.  During transport the patient is quiescent.  It always strikes me as odd to actively go from a stable quiescent state to an unstable awakening state just before transporting a patient to Recovery Room.

I routinely take the filter and mask to the Recovery Room.  If after removal ot the LMA or ETT there is any stridor or breathholding or even just as a routine I attach the 300 ml bag to the mask via the filter and have a ready means of applying positive pressure breathing and CPAP.
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