The title of this week’s blog was obviously a play on words.  Aside from the reference to the electrolyte imbalance, I was also referring to a couple of other relative highs and lows that typically go hand and hand with chronic renal failure. 

Three “highs”:  1.) T-wave voltage, 2.) blood pressure, and 3.) serum potassium level.
Three “lows”:  1.) Sinus rate, 2.) P-wave voltage, and 3.) serum calcium level.

The computer originally interpreted this ECG as:

The overreading cardiology fellow, who reviewed and confirmed this ECG, replaced the top statement of junctional bradycardia with his own.  To the computer’s original statement, he added his freehand text in all uppercase letters. 

The computer didn’t make the right call nor did the fellow get it entirely correct.  Inexplicably, the fellow included the statement of occasional PACs yet I’m not really sure where he thought he was seeing them since the rhythm is absolutely and precisely regular without even so much as a hint of early beats.  Perhaps he glanced at the sinus beats in the precordial leads and mistook the monumental height of the T-waves to be some sort of an extrasystole.  More human mistakes are made that way when attention to detail is not heeded.  Along those same lines, sometimes the computer will do what is called a “double-count” where it calculates the ventricular rate to be exactly twice what it actually is by factoring in the T-waves as separate beats.  Other times it will consider the prominent T-waves to be PVCs and generate false-positive statements by calling this ventricular bigeminy.  

The computer failed to recognize this as a markedly slow sinus bradycardia probably due to the fact that the sinus P-waves are of such low voltage.  Typically, the higher the potassium level, the flatter the sinus P-wave becomes while simultaneously the duration of the QRS interval becomes wider.  Here, the height of the P-waves in monitoring lead II is no more than 1mm at best and the QRS complex is 0.13s.  It’s unknown what the patient’s blood pressure reading was as the time this ECG was performed.

The T waves associated with hyperkalemia are often referred to by a multitude of descriptors such as:  tall, symmetrical, narrow-based, “thorn-like”, peaked, sharp, pointed, tented, and prominent.  Some even refer to them as tombstone or hyperacute but you run the risk of confusing others because both of these are also used by certain authors to describe T-waves in the presence of acute myocardial infarction.  Of various descriptors, I probably like the 2nd of “Taigman’s T-wave Rules” the most.
Rule 2:  “If the T-waves look like they would hurt your butt if you sat on them, the patient is probably hyperkalemic.” (1)  Most of those precordial T-waves do indeed look like they would be very painful to perch your hindquarters upon.

Whenever you encounter a prolonged QT interval, one of the first potential culprits you should suspect is hypocalcemia barring any antiarrhythmic drug toxicity of course.  Prolongation of the QT interval as a result of ST segment prolongation suggests hypocalcemia.  

The blood lab results of these two electrolytes came back in the patient’s computer record as so-called “panic values” and were flagged with an asterisk (*).

Serum potassium level (here K+ = 7.4* mmol/L).  Normal range = 3.5 - 5.1
serum calcium level (here Ca++ = 6.4* mm/dL).  Normal range = 8.5 - 10.1

This patient is in need of emergent dialysis to decrease their potassium while simultaneously repleting their calcium.

Incidentally, around the time this diabetic patient’s ECG was recorded their glucose level came back as 1836*.  Normal range = 74 - 106.

INTERPRETATION.
1.  Sinus bradycardia (rate = 41/min) with combined effects of both . . .
2.  . . . hyperkalemia and . . .
3.  . . . hypocalcemia in a patient with renal failure.
4.  Right axis deviation (RAD) at 98-degrees.

While I wouldn’t necessarily say that the overall QT interval is disproportionately long for this bradycardic rate, I would say that the duration of the ST segment is contributing a disproportionate amount to the QT interval when compared to the T-wave’s contribution.   In other words, the bulk of the long QT is comprised of a much prolonged ST segment.

I would not attribute the right axis deviation (RAD) to left posterior hemiblock (LPHB). LPHB is rarely observed in isolation and is almost always seen in association with RBBB which is not the case seen here.

This patient went on to live for a few more years but subsequently died from complications associated with their end-stage renal failure.

References / Sources:
1.)  Taigman, M., Canan, S., Miller, C. Taigman’s Advanced Cardiology (In Plain English). Englewood Cliffs: Brady, 1995, p. 27
2.)  Marriott HJL. Challenging ECGs. Philadelphia: Hanley & Belfus, 2002, p. 430 - 431
3.)  http://ekgumem.tumblr.com/post/21210434232/is-that-just-artifact-in-this-bradycardic-rhythm
4.)  http://img.medscape.com/article/763/564/763564-figure-1.jpg 
5.)  http://ecg.bidmc.harvard.edu/mavendata/images/case26/800x400.gif
6.)  http://img.medscape.com/fullsize/migrated/481/497/ecg_mc481497.fig.gif
7.)  http://www.metealpaslan.com/ecg/000076-03.htm 
8.)  http://www.theheart.org/documents/sitestructure/en/content/survey/1493409/images/slide1.jpg