Just looking for some thoughts on this call the other day.

Hahaha!

Seriously, with the trend now to train every layperson to address adult loss of consciousness with (at least) hands-only CPR, we need to start seeing postmortems recording if the CPR we teach causes signifcant cardiac insult to offset benefit. Used to be starting CPR when any pulse was palpable was a "horror of horors".
 
firefite said:
Based on my limited knowledge I would say I agree with a possible PE.

My mother had a PE and all her symptoms area exactly the same as what has been described except for the stiff mass and luckily the PEA.
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What is a PE???
 
Pulmonary embolism
 
Halfway through reading this my idea was PE, then it changed to a witnessed AAA, and now I am some what torn between the two (hahah torn.. :rofl:). He was playing racket ball earlier.. might have gotten hit in the chest causing a dislodge of plaque going into his lung causing a chain reaction and death.

I would be interested to know what the FAST exam showed. If he was still in PEA at the hospital, doubtful, but I would hope that the hospital would be aggressive to try everything for him.

Did you guys mess around on the scene or was this like a 4 minute scene time? Not that it would have changed anything at all- but just wondering.
 
Do you have the 12 lead still? I'd like to see it.
 
Maine iac said:
I would be interested to know what the FAST exam showed. If he was still in PEA at the hospital, doubtful, but I would hope that the hospital would be aggressive to try everything for him.

Did you guys mess around on the scene or was this like a 4 minute scene time? Not that it would have changed anything at all- but just wondering.
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you know what, honestly, they didnt try for very long. Me and my medic where kinda hopefull... We both were kinda bummed afterwards cus it seemed like they didnt try as hard as they could have for a witnesssed arrest like this.

Scene time was prolly 10-15 minutes... 45 seconds getting to patient, patient coded about 5 min after, we worked on him for about 7 minutes, then transported. 10-15ish...
 
Never heard of blunt force dislodging plaque. Those are in the vessel wall, not like grease in the drain trap like we initially thoght.
But blunt force could cause cardiac tamponade (see above).
 
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Aidey said:
*facepalm* I bet $10 the guy had an umbilical hernia totally unrelated to anything going on. That is the only thing I can think of that would be in that spot and would show up when sitting up and disappear when lying down.


And when was the last time anyone heard of a patient with an SpO2 of 94% and non-localized cyanosis?
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Echo echo echo. I was just thinking the same thing about the hernia but you beat me to it! I agree with everyone else. Most likely a PE. Depending on the location of the clot, could be why he was so tachy and hypotensive with decreased SpO2. The clot probably dislodged and put him in full blown cardiac arrest. Not much you could do different. The "mass" probably had nothing to do with it. He probably had a hernia that he did or did not know about. Certainly fits the description you gave when you sat him up.
 
Lets say for a second it was an aneurysm and the patient did go into a PEA full arrest. Is it possible(and/or probable) that the PEA showing on the monitor and verified by a lack of palpaple pulse was in fact Wrong??? Again, Assuming for a second that it was in fact an aneurysm is it possible that the heart was still beating, but due to the aneurysm, the distant pulses were not pulsating?

Obviously, the heart bleeding out wouldn't last for long with the drop in blood volume, (resulting in a true arrest) but Does any one auscultate the heart in a full arrest just to verify this???

***Noticed, when they called him later at the hospital, he was still in "PEA". ***
 
Im thinking AAA also just because of the mass. Did you notice if it was pulsating at all?
 
Aidey said:
*facepalm* I bet $10 the guy had an umbilical hernia totally unrelated to anything going on. That is the only thing I can think of that would be in that spot and would show up when sitting up and disappear when lying down.


And when was the last time anyone heard of a patient with an SpO2 of 94% and non-localized cyanosis?
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I don't see how they got a decent SpO2 on this patient to begin with, considering the lack of peripheral pulses, unobtainable pressure, and obvious shunting away from the periphery.
 
Not an AAA, but rather a rupturing thoracic aneurysm. With a thoracic aneurysm it is not uncommon to get upper limb cyanosis, just like an AAA can cause lower limb cyanosis. The difficulty breathing sounds like referred pain and an attempt to "self splint" by decreasing chest wall movement. I had a patient a few years ago that exactly matches the description of this patient and a postmortem revealed an aneurism that began at the aortic arch and descended past the diaphragm.

And who was it earlier that questioned the use of high flow O2? Really? When a patient looks like crap, give them the extra fuel. The whole issue of using lower amounts of O2 pertains mainly to prolonged use and stable ACS or COPD patients, remember that you should never withhold O2 if they're really sick. You don't look smart when you do that, it just shows that you haven't truly read the research about what you're preaching.
 
TheLocalMedic said:
And who was it earlier that questioned the use of high flow O2? Really? When a patient looks like crap, give them the extra fuel. The whole issue of using lower amounts of O2 pertains mainly to prolonged use and stable ACS or COPD patients, remember that you should never withhold O2 if they're really sick. You don't look smart when you do that, it just shows that you haven't truly read the research about what you're preaching.
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Right, high flow O2 makes all the difference for hypemic issues because the oxygen carrying capacity of plasma is so great :rolleyes:...

If you truly have a ruptured abdominal aneurysm to the point of exangunation you'd likely only have a distended, rigid abdomen due to the amount of peritoneal irritation. A ruptured thoracic aneurysm is more likely but my money is on PE.
 
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I still want to see the 12-lead :D

As far as listening for an apical pulse you could but if you can't find a carotid pulse the guy isn't perusing his brain so I doubt it's going to matter much. Might be viable for organ donation but with the shunting I'm not sure the organs would be viable anyways...
 
NVRob said:
I still want to see the 12-lead :D.
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I looked for it when i came back to work and realized fire used their monitor, its saved on their LP15... In other words its gone, sorry.
 
I know this thread is a couple of months old so don't yell at me for reviving it but I am really interested in this scenario.

While I don't have the experience yet to really offer a guess I have noticed that no one has keyed on the fact that the patient was playing Racket ball prior to onset of symptoms.

Is it possible that the patient took a hit to the chest by the ball? That would be enough of blunt force trauma to cause a pericardial tamponade (sp?) I would think.

Having played racket ball myself I know those hard rubber balls can really get moving. I've seen players get broken bones from those balls.
 
leoemt said:
...I have noticed that no one has keyed on the fact that the patient was playing Racket ball prior to onset of symptoms.

Is it possible that the patient took a hit to the chest by the ball? That would be enough of blunt force trauma to cause a pericardial tamponade (sp?) I would think.
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Actually, someone did bring that up:

Maine iac said:
Halfway through reading this my idea was PE, then it changed to a witnessed AAA, and now I am some what torn between the two (hahah torn.. :rofl:). He was playing racket ball earlier.. might have gotten hit in the chest causing a dislodge of plaque going into his lung causing a chain reaction and death.
Click to expand...

I'm really intrigued by this scenario too, but unfortunately, I don't think we will ever know because we don't have access to any records other than the first-hand experience provided. Really, I think only an autopsy could be definitive.
 
Problems with coarctation of aorta/dissection
Saddle embolus?

Murder and a fake story
 
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Was he in chronic A fib or was this new onset? Any current medications, particularly any Anticoags? Not with this situation but with symptoms after physical activities it always keep spontaneous pnuemo --> tension pneumo in the back if my mind.


Blue from the clavicles up....Line of demarcation?
 
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