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

[HappyParamedicRN]

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?

 

[Anjel]

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?

 

[HappyParamedicRN]

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?

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)

 

[Anjel]

Dehydration maybe.

decompensating Hypovolemic Shock.

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

 

[exodus]

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.

 

[Smash]

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.

 

[HappyParamedicRN]

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?

 

[Handsome Robb]

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?

 

[HappyParamedicRN]

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

 

[exodus]

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!!

 

[HappyParamedicRN]

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

 

[MrBrown]

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.

 

[usafmedic45]

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

 

[HappyParamedicRN]

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

 

[HappyParamedicRN]

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

 

[usafmedic45]

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.

 

[HappyParamedicRN]

"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!


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 not on calcium channel blockers or a beta blocker she was on lisinopril for her BP. The son assists her with her medications, he lives with her, and states she has not needed the pain meds in a couple of days. She is also tachypnic so that was not a conern on my assessment.

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

Happy

 

[usafmedic45]

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.

 

[Farmer2DO]

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

 

[Aidey]

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.