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StCEMT

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Dispatched for a 93 y/o F who had fallen and was found by her son on the floor. He had been gone for 2 hours.

Find her assisted to an upright sitting position. Pt is altered (GCS of 12ish, she isn't cooperating) and usually A&O, no obvious injuries noted. No unilateral weakness, she is resisting us pretty good for 93.

Vx: 112 pulse, BGL HI, RR 25-30, SpO2 94ish, BP was hypertensive, EtCO2 10ish, temp 98.8.

Hx: CHF, DM, HTN

Tx: x-collar, 12 lead.

Pt remained semi combative for most of transport and would not remain still when attempting any assessment or intervention. She quite rapidly went from moving about--> seizure --> unresponsive and very hypotensive--> pulseless and apneic. The sudden change was less than a mile from the ED.

And go.
 

mgr22

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Based on the ETCO2, tachypnea, BGL and PMH, I'd say she was trying to compensate for metabolic acidosis. The resulting hypocapnia could have caused the seizure and the hypotension.

Or not.
 

Gurby

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This almost certainly has to either be a primary neurologic or a metabolic problem, I think... Most likely either an ischemic or hemorrhagic stroke I would guess, given such acute onset?

Any more info from the son about how she is normally? Was she 100% stone cold normal when he left 2 hours ago? How well does she control her blood sugar / take her meds, has she had any problems like this in the past, has she been to the hospital for any reason in the past few days/weeks/months? Is she type 1 or type 2 diabetes (could this be DKA?)? What meds does she take / any blood thinners?

I would guess you couldn't get a good 12-lead if the patient was moving around, but did you see anything egregious through the artifact? IE, I would think you might be able to pick up really significant hyperkalemia even with a lot of movement.

You mentioned she is altered and not cooperative... What did her speech sound like, was it garbled, word salady, slurred?

What was her heart rate / rhythm after the seizure? When she went pulseless, was it PEA or asystole?
 

StCEMT

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The son was not a great historian. He says she is perfectly healthy as I am looking at a handful of meds. According to him, she was normal. Unknown on med compliance or recent hospitalizations. Considering the house was not the greatest of living conditions, I didn't expect good compliance with her meds.

Actos, hydrochlorothiazide, and a HTN med are all I remember.

I actually did get a decent 12, the file was too large to upload here. I'll try to find an alternative. Looked like sinus tach, nothing blatantly wrong with it. No signs of Hyperkalemia.

The rapid decomp 12 I believe was right around the transition to PEA, it was taken as soon as I saw it changing. She did have a period of asystole after going into PEA.

Son said her speech was normal and she had no notable facial drooping. Verified because I couldn't tell if there was a change or it was just the effects of 93 years of age.
 

Akulahawk

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Sounds like DKA/Metabolic Acidosis that decompensated very quickly on you.
 

Tigger

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What sort of PEA are we talking about: narrow, wide, or kind of garbage? Widening of the QRS or prolonged QT prior to arrest?
 

Aprz

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Like others said, this is almost certainly a metabolic issue because of the patient's hyperglycemia. Hyperglycemia isn't usually a sugar only problem, but messes up all of their other electrolytes. They are at risk of hyperkalemia (high potassium) and hyponautremia (low sodium). Hyperkalemia does not always present with classic ECG changes like widening of the QRS, loss of P-waves, or tall symmetrical T-waves that you wouldn't want to sit on. Amal Mattu calls hyperkalemia the syphilis of ECGs. In my opinion, most clinicians are not good at recognizing signs of hyperkalemia on the ECG even when it is present. I would love to see the 12-lead if you feel comfortable sharing it. If the patient had a pulse after the seizure, I would've strongly considered hyponautremia, and I would've stopped normal saline administration if the patient was still receiving it. In cardiac arrest, I would've strongly considered administering calcium chloride or gluconate.
 

Gurby

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It just seems strange to me that she could go from being (presumably) normal, to cardiac arrest from DKA 2 hours later...

Could it possibly have been a poisoning/ingestion, either accidental or intentional/suicide?

St, what were her breaths like, were they deep and kussmaul-ish?
 

StCEMT

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See if this link will work. Pre-12 and immediately after EKG changes seen 12. Right after we hit print on #2 we confirmed she was pulseless.
@Tigger The QRS measurement was wide after pulses were lost. I'm not sure if I believe as wide as it says, but there was a noticeable change regardless. It did not look like VTach either considering the QRS was still well within a normal axis range.The There was a prolonged QTc on the first 12 lead as well.

@Aprz the pt was Hypokalemic. I have labs from about 20 minutes after arrest, K level was 2.7 I believe. She had urinated on herself, so she fit DKA pretty well. And based on the inaccuracies of the son's medical history statements, I'm inclined to believe she had been for more than just 2 hours.

@Gurby I didn't believe that she was fully normal 2 hours prior. Maybe not severely altered, but beyond that I didn't believe what he said. I didn't see any reason to suspect a poisoning looking at meds, the room, etc. She was breathing rapidly and Kussmaul-ish for the majority of time with her. Pretty much until the last few minutes.
 

Tigger

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I recently stumbled on this, it's from LITFL and while the research isn't great, it's an interesting take on PEA arrests.
The Littman algorithm use ECG waveform and echo findings to help stratify likely causes (Littman et al, 2014):

  • Step 1: Determine if the PEA is narrow (QRS duration <0.12) or wide (QRS duration ≥0.12) on ECG monitor
  • Step 2: Narrow-complex PEA is generally due to mechanical problems caused by right ventricular inflow or outflow obstruction
  • Step 3: Wide-complex PEA is typically due to metabolic problems, or ischemia and left ventricular failure (or the above causes with co-existent conduction abnormality)
 

Aprz

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Thanks for the follow up.
 

mgr22

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Thanks for that Littman material, Tigger, I hadn't heard of it.

I'm attaching some relevant research my department did back in the early 2000s (pp 72-73). One hypothesis was that PEA sometimes involves a low-flow state with unpalpable pulses. I don't think that will be news to many of you, but the data may be useful.
 

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Tigger

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Thanks for that Littman material, Tigger, I hadn't heard of it.

I'm attaching some relevant research my department did back in the early 2000s (pp 72-73). One hypothesis was that PEA sometimes involves a low-flow state with unpalpable pulses. I don't think that will be news to many of you, but the data may be useful.
I think narrow complex PEAs are very likely to be "low-flow" arrests, often because of an obstructive cause. If nothing else, it encourages you to really consider if there is some reversible cause and not just blow through all them real quick and call it.

I recently had an arrest that was witnessed and received immediate CPR. We arrived within four minutes and had a shock onboard in about one. After that, the patient remained in a wide, but regular PEA. Eventually we got ROSC and transported and after his post-reperfusion rhythms calmed down, he was in a very wide sinus rhythm that didn't look like any BBB I'd ever seen. He was a renal patient and I ended up treating him as HyperK which narrowed the QRS. His initial K was quite high as I recall. Made me wonder if I should have been more aggressive during the actual arrest and treated the renal issues, perhaps we would have achieved ROSC sooner. This patient also apparently lived, not sure what the final outcome was.
 

mgr22

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I think narrow complex PEAs are very likely to be "low-flow" arrests, often because of an obstructive cause. If nothing else, it encourages you to really consider if there is some reversible cause and not just blow through all them real quick and call it.
I think this is a very important point. I'd just add the possibilities of profoundly symptomatic brady or tachy arrhythmias to the list of what might be force-fitted to PEA algorithms.
 

StCEMT

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@Tigger that was my concern initially. Immediately after it stopped I reassessed/adjusted all my monitoring equipment and the SpO2 and BP were both low. In regards to your thoughts, I believe the BP was in the 50's. I didn't even bother to calculate a MAP, because I knew it was absolute **** and not really helpful to the position I was in. I can't really say this want a low flow state and I don't have ultrasound to confirm one over the other.
 
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