Could you have prevented this young man's cardiac arrest?

Written by Pendell Meyers


We received a call from an outside hospital asking to transfer a "traumatic post arrest" patient. We were told that a young patient was brought in with altered mental status but complaining of right hip and/or leg pain after being found by his mother at the bottom of the stairs into the basement. His history was significant only for IV heroin abuse, but he denied any recent use. Apparently he had been confused about why he was at the bottom of the stairs, unsure if he had fallen, unsure whether there was any specific traumatic mechanism.

The practitioner on the phone stated that he suddenly developed a wide complex PEA arrest just after he came back from CT scan (pan scan performed looking for traumatic injury). The official read was not back yet, but initial view of CT scans did not show any clear injuries in the head, chest, or abdomen per report. They stated that the patient was coded for 20 minutes, including multiple doses of epinephrine, and they also gave glucose, calcium, and bicarb. They achieved ROSC and wanted to transfer to our institution for post-arrest care.

We asked for the ECGs to be faxed over while they prepared to transfer him.

We received 4 ECGs, including his baseline on file, and three from today, including triage, peri-arrest, and post-ROSC (sorry for the poor quality due to scanning).

Prior ECG on file:

Sinus tachycardia, imperfect baseline, otherwise unremarkable.

Triage ECG, with patient awake and complaining of right lower extremity pain:

What do you see? 

Sinus tachycardia with unequivocal evidence of hyperkalemia, including widened QRS with "pulled apart" morphology (widened QRS) compared to baseline, as well as clearly peaked T-waves. This patient must receive calcium as soon as possible. Unfortunately, this was not recognized at this time.


One hour later (labs not yet returned), here is the ECG recorded just after the team noticed a sudden wide complex with precipitous decompensation, just before cardiac arrest:

Bizarre, Brady, and Broad (wide QRS). This ECG is too bizarre to be anything other than end-stage hyperkalemia.

I believe it was this point when hyperkalemia was first suspected. As stated above, resuscitation included epinephrine, calcium, and bicarb.

After ROSC achieved:

Sinus rhythm. QRS much more narrow. T-waves are still peaked but improved.

We advised them to give more calcium as well as other hyperkalemia treatment during transport. While we were on the phone we received word that the serum K level drawn at initial presentation was 8.4 mEq/L.

While awaiting his arrival, we thought out the differential for hyperkalemia in a young patient with no preexisting renal disease who is complaining of extremity pain. Rhabdomyolysis seemed to be the only rational explanation, with compartment syndrome being one of the more likely etiologies of rhabdo.

He arrived intubated but awake and following commands on only minimal sedation. His neurologic exam was excellent given reported 20-30 minutes of intra-arrest resuscitation. Exam of the right lower extremity revealed tense compartments of the right lower extremity and possibly also the posterior right thigh and gluteal areas. The right foot was mottled and pulse was not palpable but was sensed on doppler.

ECG on arrival (see below) showed only slight peaked T-waves. He had been given 3 grams Ca gluconate by EMS.

Ortho and nephrology were consulted. We placed a right IJ dialysis catheter.

Point of care labs revealed K = 6.5 mEq/L, with creatine 3.0 mg/dL (presumably normal at baseline).

A urinary catheter had been placed almost an hour before arrival, with less than 10 mL of brown urine.

Compartment pressures in the right calf were all 40-50 mmHg. At that time his diastolic blood pressure was also hovering between 45 and 55 mmHg. He required a low dose norepinephrine drip to maintain BP.

Ortho took the patient emergently for 4 compartment fasciotomy of the right lower leg.

Upon arrival in the ICU, before getting Continuous Veno-Venous Hemodialysis (CVVHD), his potassium had risen again to 7.8 mEq/L. Records state that his heart rate suddenly dropped to 30 bpm. There is no ECG available from this time. Notes state he was put on a norepinephrine drip and was given calcium with improvement, then CVVHD was started and he did not have any further decompensation.

His most recent serum CPK value was 184,510 IU/L and still rising.



Learning Points:

You must be able to recognize the early stages of hyperkalemia which precede decompensation.

Hyperkalemia findings include the classic peaked T-waves, as well as the deadly B's of hyperkalemia: Broad (wide QRS), Brady (bradycardia), Blocks (AV blocks), and Bizarre.

Calcium is immediately life-saving in the setting of critical hyperkalemia, and likely would have been able to avoid cardiac arrest in this patient. Of course this must be followed immediately with definitive therapies and potassium source control if possible.

Compartment syndrome with rhabdomyolysis is a cause of hyperkalemia and renal failure that must not be missed on history and physical exam. These patients are critically ill both surgically and medically, and we must be able to juggle both simultaneously while remembering that hyperkalemia will kill most rapidly.

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Comment by KEN GRAUER, MD (7/24/2018):

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Often the best way to present cases in order to optimally learn from mistakes made — is in the sequence that the case evolved, with no more than the information that was known at that time. This forces us to imagine “We are there” — having to make decisions in “real time” as the case evolves. Dr. Meyers skillfully walks us through the events in this case, with important lessons to be learned.

• Interpreting the initial ( = Triage) ECG that was done at 08:56 — is challenging! Having worked during much of my career at a time when “transmitting a tracing” meant sending a fax — I’ve seen more than my share of poor resolution, what’s-going-on?Tracings. The 08:56 Triage ECG is a perfect example of this (Figure-1). The 1st point to emphasize, is that there are a limited number of clinical entities about which an initial ECG is likely to be helpful — when the patient in question is a previously healthy young adult, who is now awake and talking after a fall. Acute coronary syndrome is unlikely to be one of those entities. Given the absence of chest pain — cardiac contusion is also unlikely. Awareness of WHAT you are looking for on a test — is the 1st step in finding what there is to be found.
• There are a limited number of conditions that predispose a patient to developing hyperkalemia. The most common to consider include renal failure, dehydration, acidosis, use of potassium-retaining medication, and trauma (which may result in rhabdomyolysis). By history, this patient HAD at least one of these conditions. One should therefore be looking for signs of hyperkalemia when you look at the ECG.
• Among the characteristics of the tall, peaked T waves of hyperkalemia — is that in addition to being pointed — the T waves of mild-to-moderate hyperkalemia tend to have a narrow base. Think of the Eiffel Tower. This is precisely the image of what we see in Figure-1 (despite the difficulty imposed by this being an extremely poor resolution scanned tracing). One simply does not see prominent, pointed T waves that look like this in 9 of 12 leads on a normal ECG ... (NOTE: The T waves with repolarization variants are generally not pointed at their peak — and the base of  normal variant T waves is not nearly as narrow as it is with hyperkalemia).
• Even when T waves are inverted (as they are in leads aVR and V1 of this tracing) — the inverted T waves of hyperkalemia are often also pointed!
• The QRS complex appears to be slightly widened in Figure-1. This is admittedly subtle, and difficult to assess, given that we are unable to visualize the ECG grid lines due to the poor resolution. Instead, recognition of QRS widening here is a judgment call that the “experienced eye” appreciates on sight. If you overlooked this finding — it will be worthwhile to go back and compare the 08:56 Triage ECG with the Prior ECG on file, to see clearly that there has been some QRS widening. Together with the above-described T wave changes — this suggests a more severe degree of hyperkalemia.

Bottom Line: Hyperkalemia is an increasingly common ED diagnosis that must not be missed. Looking for early signs of this disorder on ECG, especially in patients who are predisposed to developing this disorder — is the best way to detect hyperkalemia at an earlier stage. Our thanks to Dr. Meyers for this insightful presentation!

Figure-1: Taking another look at the 08:56 Triage ECG. Don’t the T waves resemble the appearance of the Eiffel Tower? (See text).