# Scenario posed to me by ICU nurse



## tom.watkins (Jun 29, 2009)

So I was in the ICU today doing some rounds for class and an RN hit me up for my opinion on a call she heard about....
"A 50 y/o male patient was driving along the highway between Toppenish and Goldendale, (pretty desolate stretch of HWY 97 in Washington state) when he lost control of his vehicle for unknown reasons and drove off the road, rolling at least one time.  Time to dispatch was apprx. 10 mins, and first medic unit on scene arrived about 20 mins later.  Pt was upside down, secured by seatbelt and was unable to free himself.  Reporting party was unsure about moving him so he left him in place untill medics arrived.  EMT and medic "cleared" c-spine and noted that pt was A&O to person, place, time and event; also denies loss of conciousness, denies chest pain, denies SOB, CMS normal in upper extremeties.  Apprx. 1 minute after cutting the pt loose and safely removing him from the vehicle he becomes apneic and pulseless.  Fast patches placed on pt, monitor shows assystole in 3 leads; CPR and ACLS on scene and continued for 40 mins to the nearest hospital.  Pt pronounced DOA by ER physician."  So that's a brief synopsis of the call, and the RN wanted to know my ideas behind the pt's sudden downturn.  She brought up the idea of a massive lactic acid release, which I guess is feesible, but I don't know what the pt's labs showed in regards to LA.  I do know that he was negative for troponin, negative for thrombi and had a clean echo except for some minor mitral valve regurg. (although I'm not sure how the echo was done correctly since the pt never had a ROSC).  I'm leaning towards a massive increase in preload following removal from the vehicle, possibly causing trauma to baroreceptors and subsequent drop in BP, although I don't know all the particulars about the pt, i.e. numbness in legs, pedal pulses, etc.  Or maybe a transient thrombus?  I'd appreciate any ideas you have.


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## daedalus (Jun 29, 2009)

Lactic acid release? Was there a trapped extremity or something to cause her suspicion of such? I honestly do not have a clue as to how this might have happened. You say sudden cardiac arrest, with monitor applied immediately showing asystole? 

I will defer conjecture, would like to hear what others think.


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## tom.watkins (Jun 29, 2009)

I asked her if there was compression to an extremity and she said no, and as for the immediate asystole, I would assume that the pt was in either v-fib/tach prior to the patches being applied and that it might have been a "documentation error" but I would not begin to imply that the medic did anything unlawful/illegal.  The crews that respond out there do a wonderful job, but as we are all well aware, things happen that are completely inexplicable.


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## Flight-LP (Jun 29, 2009)

Unless a lactic acid level was drawn when alive or a shock index established, you may never know outside of an autopsy.

I'm curious as to how the spine was "cleared" (I hate that term, you aren't clearing anything, selective immobilization is a better term) with a dangerous mechanism present? A rollover per established criteria is an automatic for a collar and board.

Perhaps a transverse fracture or complete cord transection in the superior cervical spine when he was moved??


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## tom.watkins (Jun 29, 2009)

Autopsy was conducted, however I have no idea the outcome.  I asked about trauma and she said that there was absolutely none present anywhere.


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## VentMedic (Jun 29, 2009)

The most common fxs we see from rollovers, either in Trauma or SCI Rehab, are C1 -C2. The deficit may not be immediately apparent due to the ligaments holding the bones stable...until moved. Then, it may be death or the remainder of their life on a ventilator. However, if treated carefully, these two fxs can be the most stable and with a few months in a halo or C-collar, they may be just fine with minimal complications.

These fxs may also be hard to detect due to location which is why a CT Scan is used to clear rollover MVCs. 

Neuro deficits are also not always obvious until the cord is damaged by bones fragments or swelling. I also don't always trust the patient to say "No, I don't remember losing consciousness".   When you are dealing with C1-C2 damage, one would also have to consider the brainstem.


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## Hockey (Jun 29, 2009)

VentMedic said:


> The most common fxs we see from rollovers, either in Trauma or SCI Rehab, are C1 -C2. The deficit may not be immediately apparent due to the ligaments holding the bones stable...until moved. Then, it may be death or the remainder of their life on a ventilator. However, if treated carefully, these two fxs can be the most stable and with a few months in a halo or C-collar, they may be just fine with minimal complications.
> 
> These fxs may also be hard to detect due to location which is why a CT Scan is used to clear rollover MVCs.
> 
> Neuro deficits are also not always obvious until the cord is damaged by bones fragments or swelling. I also don't always trust the patient to say "No, I don't remember losing consciousness".   When you are dealing with C1-C2 damage, one would also have to consider the brainstem.




So basically, his neck was broke, they or patient moved his neck, "pushing the injury over the hill" resulting in his death right?


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## VentMedic (Jun 29, 2009)

Hockey9019 said:


> So basically, his neck was broke, they or patient moved his neck, "pushing the injury over the hill" resulting in his death right?


 
I made this statement:


> Originally Posted by *VentMedic*
> 
> 
> _The *most common fxs we see from rollovers*, either in Trauma or SCI Rehab, are C1 -C2. _


 
I did not say the paramedics killed the patient.


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## Flight-LP (Jun 29, 2009)

No, however the poor decision of the crew to not restrict spinal motion in this "hypothetical" scenerio probably did not help.


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## br16 (Jun 30, 2009)

Sounds interesting.  I have been working on a Class for Fall Arrest Systems Trauma (Anotherwards suspension trauma) and how to deal with it.  This sounds almost like that, becasue like suspension trauma where a person is stuck in a harness hanging.  In this case the person was "hanging" upside down while being trapped. 

What I have found is that they begin to have venous pooling, and orthostatic intolerance.  With the pooling, this causes shock to the heart because of the sudden rush of blood back to the heart.

All OSHA training on Suspension Trauma states that they should not be laid down immediatley, like we are taught with other trauma patients.

Just my 2 cents.


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## ffemt8978 (Jun 30, 2009)

Actually, I work under the protocols for the county in question, and I've posted our C-spine procedures on here before.  We are not to use MOI as an indicator to initiate C-spine precautions...there's a list of criteria to be met first.

I'm wondering if the seat belt cause some Compartmentalization Syndrome.


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## tom.watkins (Jun 30, 2009)

That's the road I was going down.  It seemed sorta unlikely that the pt would succumb to it in only 30 mins, but then again this was a watered-down version of the story from an ICU nurse so who knows.  Oh ya, and I forgot to say earlier that Yakima county doesn't go on mechanism alone....


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## Flight-LP (Jun 30, 2009)

MOI alone, no, however not taking into consideration the kinematics is neglegent. I realize the NEXUS criteria does not take into account MOI, but this in particular is why the Canadian C-Spine Rule has been documented superior to the NEXUS criteria. Personally, knowing the physics involved, I would have restricted them. To each their own based off their medical director's beliefs.

https://content.nejm.org/cgi/reprint/349/26/2510.pdf


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## VentMedic (Jun 30, 2009)

This is where more emphasis is placed on a "recipe" rather than commonsense.

Yes, it is good to follow the checklist for charting but sometimes there must also be some logic used.  If a small car with limited head room and flimpsy roof rolls many times, I may be a little more cautious than with a sturdy sport SUV that gently rolled to its side.  But, some will just read the recipe and not understand there are exceptions to every rule.  Unfortunately critical thinking takes a back seat for some. 

I also would like to know how these EMT(P)s cleared a spine with a patient hanging upside down still in the seat belt.  There is this little thing of stretching the spine in a different position. If anyone has even don't inverter exercises they can feel a different spinal alignment.


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## daedalus (Jun 30, 2009)

I thought C Spine protection didn't work...


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## Shishkabob (Jun 30, 2009)

Abd aorta laceration?


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## Melclin (Jun 30, 2009)

Here in Australia petrol (gas) sniffing is a big problem amongst certain elements of the poor, indigenous population. I've read that that hey are often seen to die from sudden cardiac arrest a short while after the inhalation. Could you're pt have copped a load of fuel fumes from his smashed up ride? h34r:

There are probably a million more likely things, these are definitely zebra hoof beats, but thought I'd mention it.


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## Second (Jun 30, 2009)

I know I'm behind on this one. but I would of C-collard him and used a KED to safely and slowly move him out since A&Ox4. to me if you know he rolled at least once on a decolet streach of hiway he was probly speeding 65-70mph (I would be thinking about all this on the way to the sceen). but this is just me I'm sure I'm wrong, so correct me on anything.


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## ResTech (Jul 4, 2009)

That's an interesting case to say the least. My thoughts are what other's have already said which is a spinal cord injury possibly and the manipulation from removing from the seatbelt was the final insult. With being suspended upside down in a vehicle by a seatbelt.... it is impossible to not have any manipulation of the c-spine no matter what technique you use.... KED board or not. Im not saying dont immobilize in that situation but thats an extremely hard position to immobilize someone... especially if its a heavier person.  

Also, a first thought I had was an internal abd rupture or hemorrhage of some sorts that perhaps the lap belt was tamponading and upon release the pt. bled out. I know that's getting pretty creative but ne thing's possible, right? Or just from the blunt force the pt. had an aneurysm. 

And the lactic acid possibility... I would have to say highly doubt it.... there would have to be a complete occlusion of blood flow to a particular region for an extended period of time (2-3hrs) before the anaerobic metabolism creates a level of lactic acid and potassium to cause death. 

I would love to hear what the autopsy showed.


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## usafmedic45 (Jul 4, 2009)

> I would love to hear what the autopsy showed.



Good luck trying to get a Washington coroner to release the results.  I am still trying to get them to release redacted records for my research.   Stupid privacy laws....


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## maxwell (Jul 7, 2009)

Lactic Acid?  That's a new one for me.

Asystole that promptly was probably a vascular catastrophe of some sort.  Let us not forget why he crashed the car (a PE?  MI?  CVA?  Lost a bet?) as a source for his demise.


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## VentMedic (Jul 7, 2009)

maxwell said:


> Lactic Acid? That's a new one for me.


 
That was a big issue with MAST.  It is still a concern for compression or entrapment.


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## maxwell (Jul 7, 2009)

VentMedic said:


> That was a big issue with MAST.  It is still a concern for compression or entrapment.



Right, but a high lactate doesn't tank the pH to the point that you arrest THAT quickly (if at all).  Hell, usually it doesn't tank your pH for a good while after the initial insult.  They'd get dyspneic, altered...and *maybe* arrest a few hours later from a pH less than 7.  Seems sketchy.


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## CAOX3 (Jul 7, 2009)

I would also state some type of aortic injury.  Tear maybe, the fact that he was asymptomatic to asystole im guessing against lactic acid cause and more towards traumatic aortic injury of some sort.


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## VentMedic (Jul 7, 2009)

maxwell said:


> Right, but a high lactate doesn't tank the pH to the point that you arrest THAT quickly (if at all). Hell, usually it doesn't tank your pH for a good while after the initial insult. They'd get dyspneic, altered...and *maybe* arrest a few hours later from a pH less than 7. Seems sketchy.


 
Lactic acid is the result of tissue hypoxia and hypoperfusion which force cells to breakdown glucose anaerobically. When a large part of the body is compressed by the MAST or in some crush injury, anaerobic metabolism occurs. Considering the area of the lower extremities, that sudden change in pH when the blood with lactic acid is mixed into the central circulation can have profound results to the body quickly. As well, when the MAST was deflated, that was the equivalient to losing a significant volume of blood in a few seconds dramically affecting after load.


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## Bloom-IUEMT (Aug 7, 2009)

These are more questions than suggestions:
Rhabdomylosis? Is it possible to have that without any outward signs of trauma or c/o pain?  I have read that ODing on certain meds causes rhabdo.

Could it have been something similar to orthostatic intolerance/suspension trauma even though the patient was conscious?

What about an internal defibrillator that was dislodged during the crash?  (Maybe I watch too much tv)

Is it possible to have some sort of pontine/midbrain injury that doesn't present with altered LOC or pain?

Doesn't your heart adjust its pump volume and/or rate when you are inverted? Could that sudden change cause an arrest?


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## medic_texas (Aug 22, 2009)

I wonder if it's a combination of problems.  

Possibly an aortic tear that pooled blood around the heart; all of the shunting from his lower extremities and abdomen provided enough blood for the 20 minutes he was upside down.  Once he was right side up, the heart had nothing to pump, hypoexmia, maybe a few seconds of V-tach and then asystole.  

Also, a cervical fracture that didn't severe the spinal cord until he was extricated.  This possibly causing the apnea.

Crazier things have happened.


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## Akulahawk (Aug 22, 2009)

VentMedic said:


> The most common fxs we see from rollovers, either in Trauma or SCI Rehab, are C1 -C2. The deficit may not be immediately apparent due to the ligaments holding the bones stable...until moved. Then, it may be death or the remainder of their life on a ventilator. However, if treated carefully, these two fxs can be the most stable and with a few months in a halo or C-collar, they may be just fine with minimal complications.
> 
> These fxs may also be hard to detect due to location which is why a CT Scan is used to clear rollover MVCs.
> 
> Neuro deficits are also not always obvious until the cord is damaged by bones fragments or swelling. I also don't always trust the patient to say "No, I don't remember losing consciousness".   When you are dealing with C1-C2 damage, one would also have to consider the brainstem.


Yep. You can also find C1 decapitation injuries as well. 


ffemt8978 said:


> Actually, I work under the protocols for the county in question, and I've posted our C-spine procedures on here before.  *We are not to use MOI as an indicator* to initiate C-spine precautions...there's a list of criteria to be met first.
> 
> I'm wondering if the seat belt cause some Compartmentalization Syndrome.


MOI is a very poor indicator of actual injury. It can suggest places to look for injury, but that's about it. As to the seatbelt causing a compartment syndrome... I highly doubt it. It takes a while for sufficient pressure to build within a closed compartment to shut down the vasculature. 


ResTech said:


> That's an interesting case to say the least. My thoughts are what other's have already said which is a spinal cord injury possibly and the manipulation from removing from the seatbelt was the final insult. With being suspended upside down in a vehicle by a seatbelt.... it is impossible to not have any manipulation of the c-spine no matter what technique you use.... KED board or not. Im not saying dont immobilize in that situation but thats an extremely hard position to immobilize someone... especially if its a heavier person.
> 
> Also, a first thought I had was an internal abd rupture or hemorrhage of some sorts that perhaps the lap belt was tamponading and upon release the pt. bled out. I know that's getting pretty creative but ne thing's possible, right? Or just from the blunt force the pt. had an aneurysm.
> 
> ...





CAOX3 said:


> I would also state some type of aortic injury.  Tear maybe, the fact that he was asymptomatic to asystole im guessing against lactic acid cause and more towards traumatic aortic injury of some sort.


I'd think perhaps an aortic injury and perhaps a decap or C1-C2 injury that manifested itself upon extrication. 


VentMedic said:


> Lactic acid is the result of tissue hypoxia and hypoperfusion which force cells to breakdown glucose anaerobically. When a large part of the body is compressed by the MAST or in some crush injury, anaerobic metabolism occurs. Considering the area of the lower extremities, that sudden change in pH when the blood with lactic acid is mixed into the central circulation can have profound results to the body quickly. As well, when the MAST was deflated, that was the equivalient to losing a significant volume of blood in a few seconds dramically affecting after load.


Lactic Acid production occurs any time the body has to break down glucose anaerobically. This can occur in compartment syndromes, crush injury, tourniquet application, and even during high output athletic activity. You won't normally see Lactic Acid levels during athletics that approaches anywhere near the levels you can see when blood flow stops in an area. LA buildup can be extremely uncomfortable...

IIRC, not can you get a pretty significant volume of low pH blood returning to central circulation, you also get a significant amount of potassium, myoglobin, and phosphorus (from rhabdomyolysis) from the injured area also returning to the central circulation. 

Combine that with a C1-C2 injury and you've got a recipe for what happened...


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## Dominion (Aug 22, 2009)

I wanted to lean towards aortic injury (descending aorta tear?).


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## rescue99 (Aug 22, 2009)

Orhtostatic Shock. There were no signs of trauma found, correct?


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## firefly2581 (Aug 22, 2009)

tom.watkins said:


> So I was in the ICU today doing some rounds for class and an RN hit me up for my opinion on a call she heard about....
> "A 50 y/o male patient was driving along the highway between Toppenish and Goldendale, (pretty desolate stretch of HWY 97 in Washington state) when he lost control of his vehicle for unknown reasons and drove off the road, rolling at least one time.  Time to dispatch was apprx. 10 mins, and first medic unit on scene arrived about 20 mins later.  Pt was upside down, secured by seatbelt and was unable to free himself.  Reporting party was unsure about moving him so he left him in place untill medics arrived.  EMT and medic "cleared" c-spine and noted that pt was A&O to person, place, time and event; also denies loss of conciousness, denies chest pain, denies SOB, CMS normal in upper extremeties.  Apprx. 1 minute after cutting the pt loose and safely removing him from the vehicle he becomes apneic and pulseless.  Fast patches placed on pt, monitor shows assystole in 3 leads; CPR and ACLS on scene and continued for 40 mins to the nearest hospital.  Pt pronounced DOA by ER physician."  So that's a brief synopsis of the call, and the RN wanted to know my ideas behind the pt's sudden downturn.  She brought up the idea of a massive lactic acid release, which I guess is feesible, but I don't know what the pt's labs showed in regards to LA.  I do know that he was negative for troponin, negative for thrombi and had a clean echo except for some minor mitral valve regurg. (although I'm not sure how the echo was done correctly since the pt never had a ROSC).  I'm leaning towards a massive increase in preload following removal from the vehicle, possibly causing trauma to baroreceptors and subsequent drop in BP, although I don't know all the particulars about the pt, i.e. numbness in legs, pedal pulses, etc.  Or maybe a transient thrombus?  I'd appreciate any ideas you have.


I would figure their could have been some internal bleeding. The man drove off the rd, flipped, and put yourself in this situation: Although their was a seatbelt worn, it doesn't prevent movement of the body entirely. The pt also could have been struck by random crap in his car (tossed around). On top of it all, the pt has arenaline running through his body from the mva. Therefore, not feeling pain (or much of) while beeing observed by onlookers at the scene. So you got internal bleeding, being tamponaded by the seatbelt for about 30 minutes......seatbelt is removed, and so the blood sitting still accumilated toxins.....how's that sound?


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## rescue99 (Aug 22, 2009)

rescue99 said:


> Orhtostatic Shock. There were no signs of trauma found, correct?



umm...OrthO-static shock  C'mon all you Firefighters and mountain climbers! Suspension injury is the most plausible when no other cause could be determined.


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## ResTech (Aug 26, 2009)

This months issue of JEMS has a good article discussing this exact cause... Suspension Trauma.


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## knxemt1983 (Aug 29, 2009)

would it be possible that while he was upside down 2 things could have happened, or one of these

1. he had a c-spine fx that, while upside down with no weight on his neck, didnt show since his torso was supported by his seatbelt

2. bleeding in his abd cavity that was partially controlled by his lapbelt until released, then allowing for a rapid deterioration

I would have boarded him regardless, any rollover has a high index of suspicion because of the various and unpredictable forces involved. (example: things flying around car, unknown number of flips, unknown angle of flip etc).

my policy, at least for those of less than 60 or so is that its better to board and them be ok, than to not and them hav a fx that i missed when clearing.


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## tom.watkins (Sep 2, 2009)

Lots of good dx's here! I'm gonna try and find out a little more about the case, and I'm definitely gonna check out that JEMS article on suspension injuries....side-note: i only need 2 tubes left to be done with medic school! Somebody do the EMS code dance for me and drum me up a couple of calls requiring my extensive intubation skills! Lol. But seriously, i need them....now. Tired of school....so very tired.


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## So. IL Medic (Sep 6, 2009)

tom.watkins said:


> Lots of good dx's here! I'm gonna try and find out a little more about the case, and I'm definitely gonna check out that JEMS article on suspension injuries....side-note: i only need 2 tubes left to be done with medic school! Somebody do the EMS code dance for me and drum me up a couple of calls requiring my extensive intubation skills! Lol. But seriously, i need them....now. Tired of school....so very tired.



First - continuing good luck on school!

Second, suspension trauma is your most likely culprit. When you find the JEMS article, which is a pretty good one, you'll see the basic mechanism is the orthostatic intolerance of venous pooling in non-moving extremities leads to a significant amount of non-oxygenated blood just lying there until the patient is placed flat. Then bam! All that non-oxygenated blood hits the heart at once, the heart can't cope, and cardiac arrest is immediate. That's the theory in a nutshell.


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## rhan101277 (Sep 7, 2009)

So. IL Medic said:


> First - continuing good luck on school!
> 
> Second, suspension trauma is your most likely culprit. When you find the JEMS article, which is a pretty good one, you'll see the basic mechanism is the orthostatic intolerance of venous pooling in non-moving extremities leads to a significant amount of non-oxygenated blood just lying there until the patient is placed flat. Then bam! All that non-oxygenated blood hits the heart at once, the heart can't cope, and cardiac arrest is immediate. That's the theory in a nutshell.



This is a neat theory but even if you are suspended you still have a good blood pressure.  Shouldn't have much venous pooling with proper heart function.


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## audreyj (Sep 7, 2009)

My first thought was an abd. aortic injury that caused his death when released from the seat belt.  If there was a C1-C2 fx that very well could've caused death when released as well, maybe it was a combination of the two.  Would be very interesting to see the coroner's report.


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## dbslady (Sep 7, 2009)

Please click one of the Quick Reply icons in the posts above to activate Quick Reply.


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## ffemt8978 (Sep 8, 2009)

dbslady said:


> Please click one of the Quick Reply icons in the posts above to activate Quick Reply.



Huh?  What prompted that one?


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## So. IL Medic (Sep 27, 2009)

rhan101277 said:


> This is a neat theory but even if you are suspended you still have a good blood pressure.  Shouldn't have much venous pooling with proper heart function.



Not quite accurate. In effect, veins are passive capacity vessels unlike arteries which have an active musculature. Even a perfectly healthy person standing has a degree of venous pooling and it does reduce return to the heart. Think of the classic illustration of soldiers passing out while standing at attention for prolonged periods. The legs are not moving, the veins collect blood as they cannot passively move blood against gravity, venous return drops, the body compensates through increased heart rate, increased sympathetic arterial tone and blood pressure is maintained for a while. Eventually the compensation fails as more and more blood pools. 

The position and amount of movement in extremities is important for suspension trauma. Just the act of hanging in a harness with little movement for 20-30 mins can cause an healthy, uninjured person to experience cardiovascular compromise and be at risk for reperfusion arrhythmias.

I once saw a reference that compared suspension trauma to crush injuries. While the patient may be compensating, the release of the compression may cause that compensation to fail.


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## Dwindlin (Sep 27, 2009)

I think as other have said it's more likely this was some sort of vascular event.  A spinal cord injury shouldn't cause asystole.  Had it been a spinal cord issue could have caused the apnea, however it would been more likely to keep a pulse or see a PEA as even without the spinal cord the intrinsic conduction of the heart should have remained.  From the story it sounds as if he went from concsious to asystole.


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## VentMedic (Sep 27, 2009)

atkinsje said:


> A spinal cord injury shouldn't cause asystole.


 
Actually high cord injures can cause symptomatic bradycardia and asystole which is why you may find some who have been treated with methylxanthines such as Aminophylline for an attempt to prevent this.  For some patients this is effective and others do not respond to the treatment.


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