Can anyone explain this call?

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laurenee123

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Went on a call yesterday for a guy with difficulty breathing. Get there, he has audible rales and sweating profusely. It looked like someone just poured a bottle of water on him. So we get him in the truck: hook up the monitor it read sinus tach 130, pulse ox read 60, put him on CPAP, ran a 12 lead. Everything was fine. Then his SpO2 dropped to 55. He was breathing regularly at about 30 per minute. His rales cleared up almost instantly after putting cpap on. His breath sounds were clear in all fields but the pulse ox was still reading 55. So we took him off of cpap and put a NRB on 15L and his sats went up to about 64/65. So we kept him on that.
His only hx was that he went to the doctor last week because he was having some DB. The doctor gave him some type of antibiotic and an inhaler but he didn't know the diagnosis or why they gave him that. Not to mention he was only 36yo. He stopped sweating once his lung sounds cleared up. But I can't understand why cpap would lower his sats. He told us at the hospital that he was on Coumadin because he gets blood clots. So I was leaning more towards a PE. But the whole situation doesn't make sense to me. Any thoughts?
 
Sounds like a saddle PE to me. You could give him all the oxygen and his sats wouldn't improve.
 
If he was on a NRB before you put him in CPAP his SpO2 probably went down because you reduced the FiO2 he was getting. Most disposable CPAP setups do 35-45% FiO2 vs 85-100% with a NRB.

Like DE said, probably a PE with what you describe.
 
Would maintaining CPAP therapy instead of switching to a NRB been the way to go in this case?
I would be inclined to think of staying with CPAP as his lung sounds improved, but the primary problem is circulation/perfusion after all.

Then again I am a bit biased, as NJ BLS systems have just started adopting CPAP and we may be getting the FlowSafe II soon.
 
Just a side note to address Rob's point of FiO2 on CPAP: If you think your patient requires the higher FiO2 or his sats drop when you put him on CPAP, you can put a NC under the CPAP mask attached to a separate oxygen source. That will give your pt a bump in FiO2 while maintaining PEEP.
 
This person doesn't necessarily need a ton of PEEP. They need an embolectomy. The pulmonary edema is more than likely secondary to the pulmonary HTN caused by the PE.

Another option is bag assisting with a PEEP valve. That way you can get near 100% FiO2 as well as PEEP. What STX said is a great option as well. You could probably turn the NC up past 6lpm as well with little discomfort to the patient due to the PPV they're already getting from the CPAP mask.

It would be interesting to run a sidestream EtCO2 cannula on this guy to not only add to the FiO2 but also see how bad the V/Q mismatch really is.
 
STXmedic said:
Just a side note to address Rob's point of FiO2 on CPAP: If you think your patient requires the higher FiO2 or his sats drop when you put him on CPAP, you can put a NC under the CPAP mask attached to a separate oxygen source. That will give your pt a bump in FiO2 while maintaining PEEP.
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Mix that with an ETCO2 on the NC and you are set haha
 
It was SOC to use a ETCO2 NC on all CPAP patients at the last job. They're... uh... less focused on that kind of stuff here.
 
Oh! Sorry forgot to add that part. His ETCO2 was 13? And the initial thing we did was cpap. From there we moved to NRB.
 
I'd go with PE as well. Here once we place CPAP we don't D/C unless we move to BVM or ET.

Thanks for that tip STX, I'll add that to my bag o' tricks.

Was that ETC02 taken before CPAP or during? was it by NC or inline as in the flowsafe? If it was NC under the CPAP the washout will be ~10mm or so.
 
A low EtCO2 definitely points towards a PE as well. The embolism reduces or completely denies perfusion to part of the lung which increases alveolar dead space and reduces surface area for gas exchange thus causing a drop in or initial low value of EtCO2. Without other factors which could affect the value the lower the reading the more alveolar dead space which can give you an idea of the size of the PE (ie saddle embolus vs one which is more distal in the pulmonary arterial system).

Assuming it was placed as a sidestream cannula under the CPAP mask and assuming a 5-10mmHg washout due to increased FiO2 provided by the CPAP system you're looking at an EtCO2 of 18-23mmHg.

I may be mistaken but if I remember correctly PaCO2 and PEtCO2 closely correlate in patients with good perfusion, oxygenation and ventilation however in the presence of a V/Q mismatch the values are not as closely correlated. I may be wrong but I believe with a PE the EtCO2 will be low however the PaCO2 will be high due to inadequate gas exchange however that's not a comparison we can make unless your system has iSTATs or you're doing an IFT with a set of ABGs in the labs.

Again I may be mistaken but with a PE as PaO2 falls and PaCO2 rises the chemoreceptors trigger the bodies compensatory mechanisms attempting to correct the acidosis, which in this case would be respiratory in nature.

I'm far from the smartest person here so I'm hoping those who know this stuff better than me will chime in and correct anything I'm mistaken on.
 
Handsome Robb said:
A low EtCO2 definitely points towards a PE as well. The embolism reduces or completely denies perfusion to part of the lung which increases alveolar dead space and reduces surface area for gas exchange thus causing a drop in or initial low value of EtCO2. Without other factors which could affect the value the lower the reading the more alveolar dead space which can give you an idea of the size of the PE (ie saddle embolus vs one which is more distal in the pulmonary arterial system).

Assuming it was placed as a sidestream cannula under the CPAP mask and assuming a 5-10mmHg washout due to increased FiO2 provided by the CPAP system you're looking at an EtCO2 of 18-23mmHg.

I may be mistaken but if I remember correctly PaCO2 and PEtCO2 closely correlate in patients with good perfusion, oxygenation and ventilation however in the presence of a V/Q mismatch the values are not as closely correlated. I may be wrong but I believe with a PE the EtCO2 will be low however the PaCO2 will be high due to inadequate gas exchange however that's not a comparison we can make unless your system has iSTATs or you're doing an IFT with a set of ABGs in the labs.

Again I may be mistaken but with a PE as PaO2 falls and PaCO2 rises the chemoreceptors trigger the bodies compensatory mechanisms attempting to correct the acidosis, which in this case would be respiratory in nature.

I'm far from the smartest person here so I'm hoping those who know this stuff better than me will chime in and correct anything I'm mistaken on.
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I am still in paramedic school so I promise I'm by far not the smartest on here. That's why I was looking for an explanation. We did have the ETCO2 as a cannula. And we discontinued the CPAP because his sats lowered when we put it on. His lung sounds cleared up but his SpO2 was higher when he wasn't on anything, that's why we took him off.
 
Sounds pretty good to me, @Handsome Robb.

@laurenee123: to be honest, it sounds like that oximetry reading may have been spurious. Which is not to say that the patient wasn't hypoxic, but very low readings that don't seem to correlate with the patient's condition are often just following the quantum ether.

As Sarah Koenig would say, it's like trying to map out the coordinates of a dream and wondering why it doesn't add up.
 
Sp02 below about 75 is generally very inaccurate, so any change from 55-65 is probably meaningless. Vasoconstriction is probably a factor here, too.
 
Well, SpO2 below 75 MAY be inaccurate, at least. (The idea is that it simply hasn't been validated in that range, because no device company is going to drop someone's oxygenation that low just to see if the numbers line up.)

But I basically agree.
 
Brandon O said:
Sounds pretty good to me, @Handsome Robb.
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I'm glad I got it correct. I don't want to be explaining concepts wrong. While I feel like my CCEMTP class was poorly done with basically 99%powerpoint with s few small discussion/Q and A sessions scattered thrifty the time I was in the calls before I was dropped for attendance (that's a whole story in itself. Basically if you take UMBC's course don't miss any hours whatsoever. I missed 4 of the 100ish, for a good reason I might add, and was dropped) I also feel like I did learn a few things and reinforce concepts that I felt I understood decently.
 
If you understand pulmonary physiology, you understand most of the key mechanics in the human body. Great model for diffusion, circulation, etc.
 
Brandon O said:
Well, SpO2 below 75 MAY be inaccurate, at least. (The idea is that it simply hasn't been validated in that range, because no device company is going to drop someone's oxygenation that low just to see if the numbers line up.)

But I basically agree.
Click to expand...

Actually there is more to it than lack of validation. There are both physiologic and technical (algorithmic) reasons why the lower the Spo2, the less reliable they are. Lots of studies show less accuracy at 92% than 99%, for instance. I was taught that about 75% is the point where statistically, the margin of error is just too great to rely on it at all. Whether that's entirely true I don't know, and of course clinically it doesn't much matter at that point. I've seen wide variations first hand in neonates with cyanotic heart lesions who live with sats in the 80's.
 
Would love to see those studies if you have them.
 
I imagine the processing used to correct the absorbance signal is optimized towards the high end because the absurdly low readings are as Remi said, clinically insignificant.
 
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