A young man with back spasms

Written by Pendell Meyers

First see this ECG without clinical context:

What do you see? Do you agree with the computer’s read of “nonspecific ST abnormality?”

The ECG is diagnostic of hypokalemia. There is diffuse minimal STD, with prolonged QT interval and characteristic “up-down” T-wave morphology in the precordial leads which is being caused by U-waves. V2 has an especially pronounced U-wave, but there is also a slightly wandering baseline. This morphology is very unlikely to be due to ischemia, and to an experienced electrocardiographer is nearly pathognomonic of hypokalemia +/- other concomitant factors such as hypomagnesemia, medication-induced long QT, etc.

Now here is the clinical scenario:

A young male in his 20s presented with back pain which he described as “back spasms” and weakness worsening all week and which became severe yesterday after lifting some boxes. Only upon review of his chart, I became aware that he had a history of CKD and eating disorder resulting in extreme electrolyte disturbances.

So I ordered this ECG:

We diagnosed hypokalemia based on the ECG and history. The computer read the QT and QTc intervals as 449ms and 488ms, respectively.

Do you agree?

No!

Here is the QT interval measured out:

It is actually almost impossible to measure the QT interval because of the U-wave.
So let’s measure the QU interval.
QT interval = 560 ms. Using Bazett’s formula, with HR=71 bpm, then QTc = 609 ms. Using Fridericia’s formula, 592 ms.

We gave him magnesium 2 gm IV before labs returned. We waited to give potassium as he had history of CKD and appeared to be clinically dehydrated, had not urinated at all the day of presentation, raising concern for acute kidney injury which may limit the rate we can replete potassium. Despite that concern, this ECG is diagnostic of hypokalemia.

Labs showed:

Na                 133 mmol/L
K                   2.6 mmol/L
Cl                  61 mmol/L
Bicarbonate  60 mmol/L
BUN             75 mg/dL
Creatinine     7.75 mg/dL (baseline 2.5)
Anion Gap   18 mmol/L
Calcium       10.6 mg/dL
Phos             3.0 mg/dL
Mg               2.3 mg/dL

ABG (hours later during admission) showed:
pH               7.49
pCO2          66 mm Hg
HCO3         49 mEq/L
BE              25.5 mEq/L

This shows a chronic metabolic alkalosis with respiratory compensation. These disorders are clearly not acute because the bicarb has had time to elevate and the pH is close to normal despite significant abnormalities.

In the setting of metabolic alkalosis, the expected compensatory CO2 can be calculated as follows:

0.9(HCO3) + 16 +/- 2 = expected CO2

0.9(49) + 16 +/- 2 = 60.1 +/- 2

Therefore the CO2 is nearly in the expected range based on the primary metabolic disturbance.

The primary mechanism in this case appears to be chronic vomiting resulting in large losses of HCl. While you could choose to think about this process as loss of H+ (therefore net gain of HCO3-), others argue that H+ and HCO3- are simply the dependent variables of acid-base processes, with the actual independent variables being strong ions, CO2, and weak acids. In this view, it would be the loss of Cl and free water that best explains the severe metabolic alkalosis. Hypochloremia causes metabolic alkalosis.

Loss of Cl and free water (with SID=0) in this case results in a Strong Ion Difference (SID) = Na – Cl = 133 – 61 = 72. In this case, the SID is much much greater than the normal SID of 38 (resulting from normal values of Na = 140 and Cl = 102). An elevated SID is an independent variable causing alkalosis because there is a relative excess of positive strong ions compared to the normal milieu (relatively more Na+ than Cl-). As biologic physical processes are beholden to the principle of maintaining electrical neutrality, the body fills the relative void of negative ions with the single negative ion to which it has unlimited supply (dependent variable): HCO3-. This is how a high SID causes metabolic alkalosis in the teaching of the Stewart acid-based model.

See Dr. Smith’s Acid Base Lecture and EMCrit’s Acid-Base Series for more acid-base practice.

These results were similar to prior admissions. We decided to use normal saline as our rehydration fluid based on these results. Mirtazapine was also identified as a medication which could contribute to his long QTc.

He did not have any documented arrhythmias. Troponin was ordered by the inpatient team, negative x 3.

After several days of potassium repletion and supportive care, here is his ECG:

Normalized

Learning Points:

Don’t trust the computer to measure QTc.

Hypokalemia (+/- hypomagnesemia) can be reliably diagnosed based on morphologic features on the ECG.

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