The lab findings don't fit too well, so the question is which you are going to ignore.

> Initial ABG is Ph: 6.77, PCO2: 15.4, PO2 47.8, Base Xs: 
> -19.3, HCO3: 10.6, 
> Lactate: 12, Blood Sugar: 19.2

Normal post cardiorespiratory arrest values. Or during and soon after an epileptic fit. If her clinical condition improves rapidly you would expect these to improve rapidly as well.
Taking it a bit further, initial arrest was likely respiratory as these gases suggest a period of aerobic metabolism after the gas stopped shifting in and out.

> On arrival at ED she is GCS 5/15 tolerating an OPA with 
> agonal resps.

What took her above 3 (eyes, motor or verbal)? (Also, "agonal respirations" is not all that descriptive: paradox, Kussmal, Cheyne Stokes or Biot?)

> I wonder can anyone reconcile the massively elevated d-dimers with a 
> negative CTPA and the original ABG which improved rapidly following 
> ventilation? 

Yes. D- dimers have a lot of false positives (they can be increased by the trauma of CPR but if the cause was chest trauma I'd expect the TNI to be raised as well presumably). CTPA has a fair number of false negatives (a large clot causing arrest, then split up into a lot of little bits would do it). ABGs explained above.

My guess is that the likely causes of this are PTE with false negative CTPA; some sort of primary airway blockage that has resolved and primary tonic seizure with secondary cardiac arrest. The NSTEMI one is not likely in the absence of a raised TNI and the lack of changes in wall movement on the echo makes it a little bit more unlikely (and as noted, the primary arrest was respiratory, so you're talking about a cardiac event causing cerebral hypoperfusion before cardiac arrest and then the heart recovering quickly despite sufficient respiratory problems to cause metabolic acidosis. Not impossible but a bit complicated when there are other simpler explanations). That said, cardiac ischaemia next to a previously damaged area might be enough to precipitate an arrythmia.

> Indeed the original collapse could have been an arrhythmia but unusual to become so acidotic and have a respiratory 
> arrest without a cardiac arrest if so?

Relatively unusual. The mechanism I'd be thinking of would be arrythmia in a structurally fairly sound heart causing decreased cerebral circulation causing respiratory arrest. It is a bit odd that an ischaemic heart would then recover despite additional general hypoxia. 

> Pesticide? Has she been cooking up some chemical weapons in 
> her kitchen?
> Fits the case nicely - any Japanese cults next door?

Not sure I agree that toxins do fit the case. Organophosphates/ sarin would have much more obvious signs. The cyanide sort give a good going metabolic acidosis but rapid recovery is unlikely. Same goes for phosgene and the like.


Matt Dunn


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