# Real life senerio for you! Its a fairly easy one....



## HappyParamedicRN (Mar 27, 2011)

Called to a house for the fall.  Upon arriving you found a 69 year old female who is normally alert and oriented and able to ambulate laying supine on the floor with moaning and incomprehensible words when you ask her questions. Her son reports she fell out of bed while he was out for a walk, but she is confused.  He reports she has been generally weak over the past few days and today was just in bed all day long.  

what additional information would you assess for?


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## Anjel (Mar 27, 2011)

Vitals?

Focusing on BP, Pulse, bgl, and skin conditions and does she have a fever.

(I am reading this from the basic perspective)

When is the last time she ate?


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## HappyParamedicRN (Mar 27, 2011)

Anjel1030 said:


> Vitals?
> 
> Focusing on BP, Pulse, bgl, and skin conditions and does she have a fever.
> 
> ...




Son doesn't know when she last ate, hasn't really had much of an appetite for several days.


Carotid Pulse is 32 , no radial pulse is palpable

BP 78/40

RR 42

Oxygen saturation unable to obtain at initial evaluation becuase of hypotension

Patient is pale, COLD, and dry.

CBS normal ( I forget the exact number)


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## Anjel (Mar 27, 2011)

Dehydration maybe.

decompensating Hypovolemic Shock.

I'm not to sure. Breathing way to fast though. So I am not sure what would cause that.


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## exodus (Mar 27, 2011)

Gimme a quick EKG. If her pulse really is 32 i'm going to load her up with versed and probably pace her back up. 

Expose the chest, do I see any scars? I got a feeling this patient is a cardiac patient who's pacemaker failed and now they're just bradying down because of it. Manual pacing should bring the BP back up and would probably bring orientation back up but I'm not going to let her feel the pacing.


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## Smash (Mar 27, 2011)

exodus said:


> Gimme a quick EKG. If her pulse really is 32 i'm going to load her up with versed and probably pace her back up.
> 
> Expose the chest, do I see any scars? I got a feeling this patient is a cardiac patient who's pacemaker failed and now they're just bradying down because of it. Manual pacing should bring the BP back up and would probably bring orientation back up but I'm not going to let her feel the pacing.



That's a long bow to draw from the minimal information given so far.  The causes of bradycardia are many and varied, and pacing may not be the best option for some of them.


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## HappyParamedicRN (Mar 28, 2011)

exodus said:


> Gimme a quick EKG. If her pulse really is 32 i'm going to load her up with versed and probably pace her back up.
> 
> Expose the chest, do I see any scars? I got a feeling this patient is a cardiac patient who's pacemaker failed and now they're just bradying down because of it. Manual pacing should bring the BP back up and would probably bring orientation back up but I'm not going to let her feel the pacing.




EKG shows a ventricular escape rhythm with occasional non conducted pwaves, but they are not consistent.  No scars present and the son verifies no hx of a pacemaker.  

Pacing pads were applied and patient was paced at rate of 80 with mechanical and electircal capture.  Radial pulses remained absent. No IV was in place as of yet becuase pacing seemed to be the higher priorty; however an IV was established shortly thereafter.   

Pulse with pacing 80

BP 84/48

Patient remained cold with no change in her mental status or RR 


What next?


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## Handsome Robb (Mar 28, 2011)

With the pacing in place with good capture, and an IV established, would it be appropriate to give a fluid bolus to try and bump the pressure up a bit and see if we get a change in mentation?


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## HappyParamedicRN (Mar 28, 2011)

NVRob said:


> With the pacing in place with good capture, and an IV established, would it be appropriate to give a fluid bolus to try and bump the pressure up a bit and see if we get a change in mentation?



Well that would depend on lung sounds which no one, suprisingly has aked for give her tachypnea and lack of o2 sat informatin..


Lung sounds are clearer then clear and she is given fluid wide open.

BP goes up to 89/49 after 1200 mL

Oxygen saturation is 100 percent on supplimental and her end tidal reading is in the low 20s

RR remains in the 30s to low 40s 

Patient is now  responsive to painful stimuli only

Mechanical and electrical capture of pacing remaines intact

Skin is pale, cold, and dry


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## exodus (Mar 28, 2011)

Where was the patient found? What history DOES she have? Has she seen the doctor recently? Is she on dialysis?  Meds she's on? Anything new? What type of social history is there? How does the house look?

Edit: And you said fairly easy so I figured Oh! Pacemaker, that's an obvious one!!


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## HappyParamedicRN (Mar 28, 2011)

exodus said:


> Where was the patient found? What history DOES she have? Has she seen the doctor recently? Is she on dialysis?  Meds she's on? Anything new? What type of social history is there? How does the house look?
> 
> Edit: And you said fairly easy so I figured Oh! Pacemaker, that's an obvious one!!



Haha not that easy Exodus  


Son states he found her on the floor after he got home from a walk.  We found her on the bed which was about 2 ft high.  No outward signs of trquma prsent from the fall.

She has hx of NIDDM,  HTN, high cholesterol, and gait disturbance per the son. she has also been having on going hip pain and was recievi g narcotic pain medication, but she has not had that in at least a day or two.   Over the past few days patients has been weak, not able to ambulatr as well as normal and in bed for the day when we found her.  Has not had much of anything to eat or drink per tje son who was a bit slow.  He reports no urine output for at least 12 hours with no hx of renal isaues that he is aware of.

House is clean and she has only been to the dr recently for that nagging hip pain.

I forgot what meds she was on, but you can kinda guess given the hx. No new meds.

Happy


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## MrBrown (Mar 28, 2011)

Browns differential would include hypoglycaemia, DKA, sepsis, hypovolaemic shock (from say a burst AAA) or stroke

Brown would put a drip into this lady, if lung sounds clear, infuse a litre of fluid and give her some atropine.  If the atropine didn't work mix up an adrenaline drip, if that didn't work, knock her out with midaz/low dose ketamine and pace.


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## usafmedic45 (Mar 28, 2011)

PE?  That could explain the low CO2 reading.  What does her heart sound like?


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## HappyParamedicRN (Mar 28, 2011)

MrBrown said:


> Browns differential would include hypoglycaemia, DKA, sepsis, hypovolaemic shock (from say a burst AAA) or stroke
> 
> Brown would put a drip into this lady, if lung sounds clear, infuse a litre of fluid and give her some atropine.  If the atropine didn't work mix up an adrenaline drip, if that didn't work, knock her out with midaz/low dose ketamine and pace.



Mr. Brown her cbs was within a normal range.  She was NIDDM so no DKA, abdomen was flat, bur firm on palpatiin with no evidence of AAA rupture.  Patient moving all extremities equally.

Atropine was not given because the escape mechanism was venticular and she only had occational P waves that were not being conducted.

Over here our first lines are atropine and pacing, no pressors unless they are still hypotensive despiite pacing.

Could not sedate her because of her lack of BP.  She was so altered not sure she knew what was going on anyway.

Happy


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## HappyParamedicRN (Mar 28, 2011)

usafmedic45 said:


> PE?  That could explain the low CO2 reading.  What does her heart sound like?



She was oxygenating really well and you would expect cyanosis, tachycardia or dead with a PE. she was pale with no cyanosis.

I am no good at heart sounds so did not listen to them..I would assume given the oitcome they would have been normal


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## usafmedic45 (Mar 28, 2011)

> She was oxygenating really well and you would expect cyanosis, tachycardia or dead with a PE. she was pale with no cyanosis.



"Expect" and "definitely see" are two very separate things.   You do realize that the lungs catch clots all the time and people don't die right?  It's one of the secondary functions of the pulmonary vasculature.  Just because in EMS training they teach us that PE = massive PE = :censored::censored::censored::censored:ed up patient, does not make it so.


My other questions would be do we really know if she has not been getting her pain meds and what is she on for her HTN.  This sounds a lot like a calcium channel antagonist toxicity.  



> She was NIDDM so no DKA



You don't have to be insulin dependent to have DKA.  It's more common in IDDM but it's not unheard of.


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## HappyParamedicRN (Mar 28, 2011)

usafmedic45 said:


> "Expect" and "definitely see" are two very separate things.   You do realize that the lungs catch clots all the time and people don't die right?  It's one of the secondary functions of the pulmonary vasculature.  Just because in EMS training they teach us that PE = massive PE = :censored::censored::censored::censored:ed up patient, does not make it so.
> 
> uh yes i do, you do realize that if she had a large PE that was big enough to cause such svere symptoms that she would have signs of hypoxia like CYANOSIS!
> 
> ...


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## usafmedic45 (Mar 28, 2011)

> uh yes i do, you do realize that if she had a large PE that was big enough to cause such svere symptoms that she would have signs of hypoxia like CYANOSIS!



I hate to whip this out, but which one of us do you think has seen more diagnosed massive PEs?  I've seen a couple with a saddle thrombus who presented almost exactly like this case.  No cyanosis, but they looked as pale as an overeager goth hemophiliac who went neck first through a plate glass window.  If you want to get into a pissing for distance contest over who knows more about cardiovascular and pulmonary pathophysiology, let's dance.  



> Yes you do! NIDDM patients suffer from something called HHNK NOT DKA!


 


> DKA mainly occurs in patients with type 1 diabetes, but it is not uncommon in some patients with type 2 diabetes.


SOURCE:  http://emedicine.medscape.com/article/118361-overview 

Like I said, you want to argue pathophysiology with me, I have no problem with it but don't get snide when I point out where you are deficient in your knowledge.

Ketoacidosis, if you understand the actual physiology behind it, can exist even in the absence of diabetes.  The best example of this is the form associated with alcohol abuse.  http://emedicine.medscape.com/article/765856-overview



> She is also tachypnic so that was not a conern on my assessment.



Hypotension tends to be a much bigger problem with most narcotics than respiratory depression.


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## Farmer2DO (Mar 28, 2011)

USAFmedic45 is spot on.

I'll add another link:

http://www.uptodate.com/contents/tr...iabetic-ketoacidosis-in-children/abstract/4-8

Reference #5, second article down.  "Diabetic ketoacidosis was present in>25% of NIDDM patients."

Do a google search of NIDDM DKA.  I came up with 52,300 results.

As for PE, you are talking about textbook presentation for a large, saddle embolus.  In 21 years in EMS and 13 as a paramedic, I don't think I've seen anyone present perfectly, but have seen many, many patients with much more subtle presentations that had large or saddle PEs.  So not having the textbook presentation certainly does not rule it out.  Also, you didn't initially tell us if she was rate controlled, so placing PE on the list was not out of line at all.  

You were the one that started this thread, and then when someone makes intelligent, well thought out posts, you dial up the drama and get nasty in your replies.  If you didn't want to hear what other people had to say, why ask?

USAFmedic45, when I read your reference to the goth through the plate glass window, I laughed so hard I started snorting.  In the school library.  People are looking at me like I have a penis on my forehead.  Thanks


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## Aidey (Mar 28, 2011)

Farmer2DO said:


> As for PE, you are talking about textbook presentation for a large, saddle embolus.  In 21 years in EMS and 13 as a paramedic, I don't think I've seen anyone present perfectly, but have seen many, many patients with much more subtle presentations that had large or saddle PEs.



I had a transfer patient a few months ago with the biggest PE anyone could remember seeing in a living patient. Saddle PE with extension into the heart and all the way down to the distal vasculature in the lungs. His CC was SOB, more specifically dyspnea on exertion, with RA SpO2 in this 80s. 95-96% on 8lpm. I remember the CO2 was low, but not anything too crazy, 20s I think. 

He had no chest pain, BP was fine. Mentation was fine. He had increasing dyspnea on exertion over a month, and finally got it checked out when the SOB didn't go away with rest.


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## usafmedic45 (Mar 28, 2011)

> USAFmedic45, when I read your reference to the goth through the plate glass window, I laughed so hard I started snorting. In the school library. People are looking at me like I have a penis on my forehead. Thanks



Glad to be of service.


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## HappyParamedicRN (Mar 28, 2011)

Aidey said:


> I had a transfer patient a few months ago with the biggest PE anyone could remember seeing in a living patient. Saddle PE with extension into the heart and all the way down to the distal vasculature in the lungs. His CC was SOB, more specifically dyspnea on exertion, with RA SpO2 in this 80s. 95-96% on 8lpm. I remember the CO2 was low, but not anything too crazy, 20s I think.
> 
> He had no chest pain, BP was fine. Mentation was fine. He had increasing dyspnea on exertion over a month, and finally got it checked out when the SOB didn't go away with rest.




Oh hey immagine that a low o2 sat...hmm go figure.. oh wait patirnts with PEs dont get low o2 sats just ask the expert respiratory therapis that knows it all!


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## usafmedic45 (Mar 28, 2011)

> oh wait patirnts with PEs dont get low o2 sats just ask the expert respiratory therapis that knows it all!


Two things:  1.  I don't know it all.  What I do know is where the limits of my knowledge lay and that is far more important.  It's better to know some of the questions to ask than to try to have all of the answers.
2.  I never said that they don't have low sats.  I said they don't _always_ present with cyanosis.  You do understand the difference between O2 saturation and O2 content right?  You also understand that hypoxemia and cyanosis are not the same thing, correct?  The latter is a symptom of the former, a symptom that is not always present and is not present in most patients until you get significant amounts of deoxygenated hemoglobin present (usually about 20-30% of the circulating hemoglobin level; it can be much, much higher in certain genetic conditions and in persons with dark or ruddy complexions).  Also the case you presented didn't have a reading prior to being placed on high flow O2 so we are unlikely to know if there was hypoxia or not.

It's a moot point to argue since we don't know that information. I'm also guessing that this scenario is pretty much done with since every time we question you or point out a misconception you are attempting to further, you get defensive and hateful.   Have a nice night.


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## Aidey (Mar 28, 2011)

My patient was not cyanotic, but he was significantly anemic, and to quote "pale as an overeager goth hemophiliac who went neck first through a plate glass window". 

She had cold septic shock. Can we be done with this "scenario" now? Congrats to you for figuring it out on scene. Maybe one of us could have if this had actually been presented as a scenario.


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## Handsome Robb (Mar 29, 2011)

Why is it that educational threads always turn to arguments on this forum? There are people around who have less education who are interested in learning...

I would never have even considered septic shock from what was presented... Would someone like to explain what lead to this dx for me? I'd love to know.


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## Anjel (Mar 29, 2011)

NVRob said:


> Why is it that educational threads always turn to arguments on this forum? There are people around who have less education who are interested in learning...
> 
> I would never have even considered septic shock from what was presented... Would someone like to explain what lead to this dx for me? I'd love to know.



Can we just find out what was actually wrong. Then continue on with whatever you guys wanna argue.


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## Aidey (Mar 29, 2011)

I know it was sepsis because I read a post that has since been deleted. 

Just based on the information presented here, you couldn't determine it was septic shock for sure, as there are several other possibilities. Given what we do know, it is most likely she is in some sort of shock, it is just a matter of figuring out which one based on history and assessment. 

Knowing now that it is septic shock, I can look at my quick and easy sepsis check list and see what she meets. We don't really know if she has a known or suspected infection without more history from the son. We don't know a temp, but her her respirations are over 20, Co2 under 32, and she has an AMS. That means she meets the required 2 criteria for suspected sepsis/SIRS.


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## Aidey (Mar 29, 2011)

Anjel1030 said:


> Can we just find out what was actually wrong. Then continue on with whatever you guys wanna argue.



Cold septic shock per the OP.


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## Anjel (Mar 29, 2011)

Aidey said:


> Cold septic shock per the OP.



oh sorry must have missed that.


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## usalsfyre (Mar 29, 2011)

Aidey said:


> That means she meets the required 2 criteria for suspected sepsis/SIRS.



Agreed, but pretty much any patient with any sort of mid-to-high level pathology meets SIRS criteria, so that's only of limited diagnostic value.


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## Aidey (Mar 29, 2011)

I know, but if we had more details she would likely meet more making it slightly more helpful.


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## usalsfyre (Mar 29, 2011)

Aidey said:


> I know, but if we had more details she would likely meet more making it slightly more helpful.



Gotcha


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