Handed this ECG from triage. What will you do?

 Written by Sean Trostel MD

I returned to my desk after seeing a patient and saw this screening ECG sitting on my desk to be read. The patient was a man in his 80s with chief complaint listed as: "hyperglycemia, weakness, ground level fall."


ECG #1 @ 15:30

What do you think?

Slow, irregular rhythm - likely slow atrial fibrillation

Very wide QRS measuring ~180 ms in some leads, not fitting LBBB morphology and wider than vast majority of LBBB

No signs of OMI, no modified Sgarbossa criteria

Peaked T-waves in the lateral precordial leads


Together, these findings are highly concerning for severe hyperkalemia, but could easily be mistaken for slow a-fib with LBBB or intraventricular conduction delay (without life threatening findings).


An old ECG was available, confirming this wide QRS is new and appears to be a dramatically widened version of his normal, narrow QRS:

I stood up from my desk and asked our nurses to draw a VBG and place the patient on a monitor. As I did this, another nurse said, “room 19 is in V-tach!”


On examination, the patient was awake and conversational but confused, and did have a pulse. I placed pads on the patient and immediately gave 1g calcium chloride but his rhythm deteriorated to polymorphic VT. He was shocked and converted to a severely bradycardic rhythm requiring pacing. I gave an additional 1g calcium chloride and 1 amp of sodium bicarbonate. His intrinsic rate improved, and pacing was stopped. He was moved to a resuscitation room and ultimately received additional calcium (total of 3 g CaCl and 3 g CaGlc) and adjunctive treatments for hyperkalemia.


Repeat ECGs over the following 30 minutes, after receiving additional calcium and other medications:

ECG #2 @ 15:46, following 2g CaCl + 1 amp NaHCO3

ECG #3 @ 16:08, following additional calcium and adjunctive treatments.

QRS is becoming still narrower

Note with each ECG there is progressive narrowing of the QRS and dampening of the peaked T-waves.

Labs resulted, showing a potassium of 8.0 mEq/L, glucose of  greater than 900 mg/dL, and anion gap metabolic acidosis consistent with DKA. The patient stabilized and was transferred for ICU admission. He was discharged home several days later.



Learning points:

Your differential for wide QRS (by itself) and bradycardia (by itself) must include hyperkalemia.  Both together are VERY likely to be due to hyperkalemia.

When QRS duration approaches or exceeds 200 msec, the differential includes emergencies such as hyperkalemia and sodium channel blockade.  

Do not be afraid to push multiple standard doses of calcium chloride or gluconate in an unstable hyperkalemic patient. Titrate calcium to improvement in ECG morphology.   You can do this BEFORE confirming hyperkalemia, as calcium therapy is safe.

Smith comment: 

Left Bundle Branch Block (LBBB) has a QRS duration over 170 ms in only 13% of cases.

Hyperkalemia in the setting of Left Bundle Branch Block

Right Bundle Branch Block (RBBB) has a QRS duration over 160 ms in only 10% of cases.

Is This a Simple Right Bundle Branch Block?

Don't forget beta agonists in the treatment of hyperkalemia:

Terbutaline and Albuterol for Lowering of Plasma Postassium (includes many abstracts)

The below abstracts show that beta 2 adrenergic agonists are effective at treating hyperkalemia.  They do so by "shifting" K into the cells. 

--0.5 mg of IV albuterol reduces K by about 1.2 mEq/L. 

-- A 20 mg neb (most are 2.5 mg) lowers it by about 1.0 mEq/L.  

--A 10 mg neb lowers it by about 0.6 mEq/L.

I give 0.25 mg of IM terbutaline to an adult, but only if it is critical, and add nebulized albuterol also.  I've never given it IV, as I'm a bit reluctant to risk the cardiac irritability.