Sunday, June 9, 2024

Prehospital "Altered mental status and hypotension due to probable DKA" (everyone must know this ECG diagnosis)

A patient presented with hypotension and altered mental status and presumption of DKA.

As the medics arrived, they handed me this ECG:

What medication did I call for IMMEDIATELY when I saw this?



















This is obviously severe hyperkalemia and the patient is near cardiac arrest.  The medics had no idea.

I called for 2 grams of Calcium Chloride.

There was no IV access, so we obtained intraosseous (IO) access, but she arrested before we could give her all the calcium.

Over the next 10 minutes we resuscitated with high doses of Calcium, Epinephrine, and Bicarbonate.

We also gave insulin and furosemide (which take much longer to have their effect)\

First K returned at 7.7 mEq/L.

After episodes of asystole, VF with defibrillation, and VT, she obtained ROSC and this 12-lead was recorded:
The monitor around this time was NOT showing a very wide complex
What do you think?

Here is the transesophageal echo (TEE) which was placed during arrest (and which is great for real-time assessment of resuscitation) at the same time as this 2nd ECG:


Excellent LV Function.  
How could that be with such a 12-lead?
I have had many cases of severe Hyperkalemia with wide complex that show good cardiac function.


The ECG above is bizarrely wide.  It is nearly a sine wave.  One might think that it is all due to hyperkalemia, but the K returned at 4.0 and the monitor around this time was not showing a very wide complex.  

This is actually Accelerated Idioventricular Rhythm (AIVR).  There are no P-waves (this can also happen in hyperkalemia due to sino-ventricular rhythm), but here is it slow and even wider than


9 minutes later:



The patient eventually did well and fully recovered.


Learning Point:

You MUST learn the many morphologies of hyperkalemia.  See the cases below in order to learn them.

Hyperkalemia and Cardiac Arrest






Large calcium doses for hyperkalemia, and VT in hyperkalemia.

Weakness, prolonged PR interval, wide complex, ventricular tachycardia


Very Wide and Very Fast, What is it? How would you treat?


This patient with VT in the context of hyperK required both defibrillation and 13 g of Calcium Chloride (CaCl):

A middle aged man with unwitnessed cardiac arrest


See this amazing case in which hyperK was not initially diagnosed:

This shows on serial ECGs the effect of Calcium:

Sine wave, or nearly so, due to hyperK:







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ADDENDUM — by KEN GRAUER, MD (6/10/2024):

===================================

Did the 2nd ECG show AIVR?
I found the 2nd ECG in today's case to be especially interesting. For clarity in Figure-1 — I've reproduced and labeled this tracing.
  • As per Dr. Smith — the rhythm in ECG #2 is almost completely regular with extremely wide complexes, simulating AIVR. 
  • That said — the BLUE arrow in the long lead II rhythm strip highlights a vertical spike that confused me. RED arrows are seen throughout this long lead II, regularly occurring at the same interval after each of the wide complexes.
  • Vertical dotted BLUE lines suggest that similar spikes are seen in other simultaneously-recorded leads at the same point in time.

QUESTIONS:
  • Could these regularly-occurring, small-amplitude vertical spikes be QRS complexes?
  • If so — Does that mean that rather than the QRS complexes of AIVR — that the wide complexes are artifact?
  • If so — then this would explain why serum K+ was normal — and why the QRS on the monitor at around this time looked to be narrow.

  • BUT — still unexplained, is what would (could) produce these bizarrely wide but surprisingly regular complexes that are seen before each of the small-amplitude vertical spikes on this tracing? This patient does not have a pacemaker — and these small-amplitude vertical spikes are not P waves. These wide complexes also do not represent PTA (Pulse-Tap Artifact) — because none of the standard limb leads are normal, and these wide deflections occur before the small-amplitude vertical spikes (whereas PTA occurs after the QRS since it is a systolic phenomenon).

As I like to do in problematic cases like this — I sent ECG #2 to David Richley for his expert opinion. Dave agreed that the shape of the wide deflections looked very unusual to be QRS complexes — but he could not explain why, if the wide complexes were artifact — they would occur before (and not after) the QRS. Therefore:
  • We will never know for certain what the rhythm in ECG #2 was. The "good news" — is that clinically this turned out not to be important because the 3rd and final ECG in today's case (done just 9 minutes later) showed sinus rhythm with a normal (narrow) QRS complex — and the patient did well and fully recovered.

  • KEY Point: It is sometimes exceedingly difficult to recognize artifact. As a result — the BEST approach when you suspect that there may be a "technical misadventure" — is to go to the bedside and LOOK at the patient! Surprisingly often — looking at the patient will reveal some obvious movement or tremor that clarifies the source of artifact. 
  • If not — check out your suspicion regarding a possible technical misadventure by replacing the electrode leads, verifying their correct placement — and repeating the ECG to see if the unusual deflections have now disappeared.

Figure-1: I've labeled the 2nd ECG in today's case (See text).

  




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