How will you save this critically ill patient? A fundamental and lifesaving ECG interpretation that everyone must recognize instantly.

Written by Pendell Meyers

A woman in her 30s called EMS for acute symptoms including near-syncope, nausea, diaphoresis, and abdominal pain. EMS arrived and found her to appear altered, critically ill, and hypotensive. 

An ECG was performed:

What do you think?

Extremely wide complex monomorphic rhythm just over 100 bpm. The QRS is so wide and sinusoidal that the only real possibilities left are hyperkalemia or Na channel blockade. Hyperkalemia is by far more common.

Indeed, further history revealed two missed dialysis sessions. And of course on exam she has a dialysis fistula.

EMS reportedly gave 4 grams of calcium (unknown whether CaCl or gluconate) and 50 mEq of sodium bicarbonate. There was concern that the rhythm might represent ventricular tachycardia, so lidocaine was given and one attempt at cardioversion was performed. It is unclear what changes happened to the rhythm based on the EMS interventions, but the patient arrived to the ED remaining critically ill and with a very wide complex reported (no ECGs from ED available sadly).

Hyperkalemia was diagnosed and more treatment was given including more calcium, bicarb, insulin/dextrose, and albuterol.

The potassium level returned at 9.7 mEq/L.

Emergent dialysis was prioritized after stabilization. 

She did well and stabilized after dialysis. 

Here is her ECG the next day with normal potassium level:

She did well.

See our other countless hyperkalemia cases below:

General hyperkalemia cases:

A 50s year old man with lightheadedness and bradycardia

Patient with Dyspnea. You are handed a triage ECG interpreted as "normal" by the computer. (Physician also reads it as normal)

Severe shock, obtunded, and a diagnostic prehospital ECG. Also: How did this happen?

A woman with near-syncope, bradycardia, and hypotension

What happens if you do not recognize this ECG instantly?

A woman in her 50s with dyspnea and bradycardia

A patient with cardiac arrest, ROSC, and right bundle branch block (RBBB).

Is this just right bundle branch block?

Is This a Simple Right Bundle Branch Block?

A 60-something who has non-specific generalized malaise and is ill appearing.

HyperKalemia with Cardiac Arrest. 

Peaked T waves: Hyperacute (STEMI) vs. Early Repolarizaton vs. Hyperkalemia

What will you do for this altered and bradycardic patient?

I saw this computer "normal" ECG in a stack of ECGs I was reading

What is the diagnosis?

Found comatose with prehospital ECG showing "bigeminal PVCs" and "Tachycardia at a rate of 156"

An elderly woman found down with bradycardia and hypotension

A middle aged man with unwitnessed cardiac arrest

Test almost all of your most important ECG rhythm interpretation skills with this case.

Sinus rhythm with a new wide complex QRS

This ECG is pathognomonic and you must recognize it.

A Very Wide Complex Tachycardia. What is the Rhythm? Use Lewis Leads!!

A Very Wide Complex

Are these peaked T-waves the patient's baseline T-waves?

Bradycardia, SOB, in a Dialysis Patient

Cases of hyperkalemia mimicking OMI:

Acute respiratory distress: Correct interpretation of the initial and serial ECG findings, with aggressive management, might have saved his life.

"Steve, what do you think of this ECG in this Cardiac Arrest Patient?"

Hyperkalemia and ST Segment Elevation, Post 1

A Tragic Case, related to the last post

A patient with chest pain and ST Elevation in V1 and V2

You MUST recognize this pattern, even if it is not common

ST Elevation. What is it?

This ECG Pattern Told the Story When the Patient Could Not

What are these ST elevations, ST depressions, and tall T waves diagnostic of?

Another Shark Fin. With a twist.

Do you recognize this ECG yet?

Right Bundle Branch Block with ST Elevation in V1?

ST elevation in aVL with reciprocal ST depression in the inferior leads

Shock, bradycardia, ST Elevation in V1 and V2. Activate the Cath Lab?

Another deadly and confusing ECG. Are you still one of the many people who will be fooled by this ECG, or do you recognize it instantly?

Bradycardia with a Wide Complex. Sometimes 2 pathologies are present. Which?

An elderly woman was found to be bradycardic.  She was awake with a BP of 120/70.

Here is her prehospital ECG:

What do you think?

I thought this was likely due to hyperkalemia.  I do not see P-waves.  It appears to be sinus arrest with ventricular escape.  The ST deviations could be ischemia, but are very often the result of hyperkalemia.

First ED ECG:

Pretty much the same

She was given multiple doses of Calcium gluconate.  6 grams as I recall.  

And another ECG was recorded 9 min later:

3rd 2.5 hours later

There are some possible P-waves here, but if they are, there is complete AV block as well, with continued ventricular escape.

We continued giving calcium.  We also gave insulin, D50, IM terbutaline 0.25 mg (beta-2 agonist), 80 mg of furosemide.

Here lactate returned at 8.5, K 7.4, Cr 2.9

Later, after 21 g of calcium and more shifting, the K was down to 5.8.  

This ECG was recorded:

There is now an atrial rate of about 100 with complete AV block and a probable ventricular (vs. junctional) escape that is much narrower.

So in spite of massive management of hyperK, the complete AV block persisted.

The patient was made comfort care only, and there was no further management.

Learning Points

1. Bradycardia and AV block can be caused by Hyperkalemia.

2.  There can be simultaneous AV node disease and hyperkalemia. 

3. If the AV block does not resolve with management of hyperkalemia, then there is underlying intrinsic AV node disease.

Severe shock, obtunded, and a diagnostic prehospital ECG. Also: How did this happen?

A middle-aged woman was found down in her apartment unconscious. She was in shock with thready pulses.

A prehospital ECG was recorded:

Limb leads:

Precordial Leads

What is the therapy?

This is pathognomonic of hyperkalemia (I suppose it could be due to a massive overdose of a sodium channel blocking drug, maybe).

Is it ventricular tachycardia (VT) due to hyperK or is it a supraventricular rhythm with hyperK? 
---I don't think that it is possible to say for certain, and it does not matter.  The rate is not fast enough to be causing shock, so if it is VT, the priority is still to treat hyperK and secondarily to cardiovert.

The patient should receive immediate IV calcium (and also treatment to shift the potassium into the cells).

The medics did not recognize hyperkalemia. They thought it was VT, but did not shock.  They later told me that even if they had diagnosed hyperK, the only calcium they have is Calcium chloride, not gluconate.   ....However, it is perfectly fine to give Calcium chloride!!  Just have a reliable IV so that it will not extravasate.  The morbidity of extravasated CaCl is minimal compared to the mortality of life threatening hyperkalemia.  Important: It takes 3 grams of calcium gluconate to equal the amount of calcium in 1 gram of Ca Cl. 

They transported to the ED.  On arrival, the patient was in shock, was intubated, and had an immediate cardiac ultrasound.

What does a heart look like on ultrasound when the EKG looks like that?

Here you go:

It's not the world's greatest cardiac ultrasound video, but it does appear to show poor function and low volume.

She was treated with:

5 g Ca gluconate, 100 mEq bicarb, 7.5 mg nebulized albuterol, 160 mg furosemide, 10 units insulin,
50 mL 50% dextrose.

The K returned at 7.4 mEq/L.

The followup ECG is here:

Now the QRS is only slightly prolonged. There is some ST depression and peaked T-waves.

The history, obtained subsequently, is interesting:

The patient had been seen at an outside ED 2 days prior and the K was 2.5 mEq/L and a creatinine 1.5 mg/dL.  Hospital admission had been recommended, but she left that ED against medical advice.

At that discharge, she was prescribed KCl 40 mEq tabs to take 3 times daily.  She had home health nurse visits, and a BMP was sent the next day (the day prior to admission, presumably after 120 mEq of KCl replacement -- if she was taking as directed).  At that time, her potassium had risen to 4.7 mEq/L. 

Apparently, her prescription was for yet more doses, so by the next day she was dangerously hyperkalemic.

This patient weighed only 51 kg.

Comment on this K replacement

A 70 kg patient with a K of 2.5 is probably in a deficit of at least 200 mEq, but one at a weight of 50 kg is in a significantly lower deficit.

This brings up the topic of how much K to give someone who is dangerously hypokalemic.

I address K replenishment is a couple posts and repost that commentary below.


Here are other posts on hyperK, large calcium doses for hyperK, and ventricular tachycardia in hyperK

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:

Sinus rhythm with a new wide complex QRS

This shows on serial ECGs the effect of Calcium:

The Effect of Calcium on Severe Hyperkalemia

Terbutaline and Albuterol for Lowering of Plasma Postassium

Replenishing K in hypokalemia

This comes from this post:

STEMI with Life-Threatening Hypokalemia and Incessant Torsades de Pointes

Could the dysrhythmias have been prevented?

I could find very little literature on the treatment of severe life-threatening hypokalemia.  There is particularly little on how to treat when the K is less than 2, and/or in the presence of acute MI.  Here are the American Heart Association Guidelines: 

• 2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care

Part 10.1: Life-Threatening Electrolyte Abnormalities

Treatment of Hypokalemia

"The treatment of hypokalemia consists of minimizing further potassium loss and providing potassium replacement.  IV administration of potassium is indicated when arrhythmias are present or hypokalemia is severe (potassium level of less than 2.5 mEq/L).  Gradual correction of hypokalemia is preferable to rapid correction unless the patient is clinically unstable.

"Administration of potassium may be empirical in emergent conditions.  When indicated, the maximum amount of IV potassium replacement should be 10 to 20 mEq/h with continuous ECG monitoring during infustion  A more concentrated solution of potassium may be infused if a central line is used, but the tip of the catheter used for the infusion should not extend into the right atrium.

"If cardiac arrest from hypokalemia is imminent (i.e., malignant ventricular arrhythmias are present), rapid replacement of potassium is required.  Give an initial infusion of 10 mEq IV over 5 minutes; repeat once if needed.  Document in the patient's chart that rapid infusion is intentional in response to life-threatening hypokalemia."

Comment:
This last section is appropriate for this case.  Everyone is appropriately worried about giving K too fast.  How much does rapid infustion increase the K?  There is, again, little empirical data on this topic that I can find (see 2 studies below, which do not really answer the question).  Perhaps there are studies in animals that I have not found?  

Total Body Potassium: a 70 kg person has about 7500 mEq of total body K, but the extracellular fluid has only about 48 mEq!   Of course the difficulty with K replenishment is that the total body stores may be depleted by far more than can possibly be quickly repleted.  The estimated deficit associated with a serum decrease from 4.0 to 3.0 mEq/L is 100-200 mEq of total body K, and from 3.0 to 2.0, the associated loss is double, at 200-400 mEq.* [Sterns RH, et al. Internal potassium balance and the control of the plasma potassium concentration. Medicine (Baltimore) 1981;60:339-54].  

But 100 mEq given all at once would raise the serum K by 30 mEq/L (and be immediately fatal)!!

*The NEJM review referenced below (and ACLS, for what that is worth), states that, on average, in a "typical" 70 kg person, the serum K falls by 0.3 mEq/L for every 100 mEq total body deficit.  However, this review references the Sterns article above, which by my reading does not state this.

Here are some calculations for a safe rapid dose:
A 70 kg person has about 5 liters of blood, and 3 liters are serum (2 liters are RBCs).  If 10 mEq is given very rapidly, leaving no time for intracellular shift, then it will raise serum K by about 3.3 mEq/L.  If the patient is at 1.8, that will raise it to 5.1 mEq/L.  One need only get the K above 3.0 to greatly decrease risk (although in STEMI, the optimal level is about 4.0-4.5 mEq/L).  5 mEq rapid bolus would raise this patient's K from by 1.6, from 1.8 to 3.4 mEq/L.   The difficulty is in estimating the ongoing shift.  As you infuse K, it will start to shift into depleted cells and the serum K will fall again rapidly.  Thus, it is critical  in patients like this to repeatedly and rapidly, after each bolus, measure the K, and supplement as needed.

In the case presented, it is not clear to me that the 10 mEq of K was given rapidly.  I suspect it was set to go over 1 hours on a pump, which is the usual practice.  It would be difficult to get a nurse to give it faster!  However, in this case, it would be appropriate to give it over 5-10 minutes, with monitoring, then immediately measure the K again and be ready to give more.

Further complicating the issue is that severe hypokalemia can result in rhabdomyolysis and subsequent K release, with resulting hyperkalemia!

Here is another post on hypoK: 

Patient with severe DKA, look at the ECG

In this post, I discussed another patient I took care of: 

Prehospital Cardiac Arrest due to Hypokalemia

I recently had a case of prehospital cardiac arrest that turned out to be due to hypokalemia.
We could not resuscitate her, but we did have excellent perfusion with LUCAS CPR, such that pulse oximetry had excellent waveform and 100% saturations, end tidal CO2 was 35, and cerebral perfusion monitoring was near normal throughout the attempted resuscitation.  This was before we started doing ECMO for refractory V Fib.

During the resuscitation, I ordered 10 mEq KCl push, but the patient received 40 mEq of KCl, push (far more than recommended)  The resident had ordered 40 mEq and that is what the nurses heard.

Is 40 mEq too much? Or the right amount?

Contrary to my expectations, after pushing 40 mEq, the K only went up to 4.2 mEq/L.

What is the right amount of K to push in life-threatening hypoK?

In a 70 kg person, there are 5 liters of blood and 3 liters of serum.  Since it takes some time (how long?) for K to shift out of the intravascular space into the interstitial space and then into the intracellular space, 3.0 mEq of K pushed fast and circulated theoretically would raise serum K immediately by 1.0 mEq/L, and 10 mEq would increase it by 3.3 mEq/L, from 1.9 to 5.2.   Thus, 40 mEq should raise it by 13 mEq/L!! 

But this is before redistribution to the interstitial space.

As I indicated above, in our cardiac arrest case, after pushing 40 mEq, the K only went up to 4.2 mEq/L.   

  

There are about 13 liters of extracellular fluid in a 70 kg person (10 liters interstitial fluid + 3 liters serum).  So if K redistributes very quickly to this extracellular space, then 40 mEq is appropriate.

The difficulty is in estimating the ongoing shift.  As you infuse K, it will start to shift into depleted cells and the serum K will fall again rapidly.  Thus, it is critical in patients like this to repeatedly and rapidly, after each bolus, measure the K, and supplement as needed.