Wednesday, November 7, 2018

A young man with back spasms

Written by Pendell Meyers with edits by Steve Smith

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 highly suspicious for hypokalemia. There is diffuse minimal STD, with prolonged QT interval and characteristic "down-up" 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!

Because of the prominent U-wave merging with the end of the T-wave, it is almost impossible to measure the QT interval, so let's measure the QU interval:

It is difficult, or even impossible, to determine the end of the T-wave because of a prominent U-wave. You can see here that there is a huge U-wave visible in V2. If we draw the line down to lead II across the bottom, you can see that what appeared to be the end of the T-wave in lead II is really the end of the U-wave. 


Because the T-wave is not discernible, we cannot calculate a QT or QTc interval. We could calculate a QU and QUc interval (QU = 560 ms; using Bazett's formula with HR=71 bpm, then QUc = 609 ms), however this is not really necessary or particularly helpful.

The important lesson here is that a large U-wave, especially as it is often due to critical hypokalemia, may be just as dangerous or more as a long QT without prominent U-waves. Here are some key points of logic and evidence that should leave you with the assumption (until proven otherwise) that prominent U-waves and long QUc should portend risk of arrhythmias:

1) The more cells repolarizing later, then the larger the U-wave, the more it fuses with the T-wave, the greater the amplitude of the T-U wave, and the higher the risk of arrhythmia. This assertion is indirectly supported by data from Kirchof et al, who compared ECG findings of 35 patients with LQTS (15 congenital, 20 acquired) with 40 patients with PVCs and normal QTc (1). Kirchof et al found that blinded analyzers often could not differentiate between the T- and U-waves in the recordings of patients who had imminent TdP, and that the amplitude of the largest T-U wave immediately preceding TdP was more than 3 times larger in LQTS patients with TdP compared with the LQTS patients without TdP. In fact, they found that "a marked increase in T–U-wave amplitude (3-fold higher amplitude compared with ECGs without TdP, 80% increase compared with the largest repolarizing wave in the entire ECG recording) was specific for imminent TdP."

From Kirchof et al: Graph A: The T–U-wave amplitude before TdP in LQTS patients, before PVC in patients with other heart disease (control subjects), and before PVCs that did not initiate TdP in LQTS patients. You can clearly see that those with TdP had higher TU amplitude than those without.



2) Early afterdepolarizations (EADs) are widely considered to trigger Torsade de Pointes (TdP). It has also been shown that low extracellular potassium augments EADs. (2) Low extracellular potassium is frequently associated with prominent U-waves, as we have shown countless times on this blog.

3) Kirchof et al (1) also found that the U-wave in long QTc syndrome closely correlated with EADs at the cellular level, and also that most episodes of TdP occur from EADs occurring on giant T-U waves and many occur on U-waves when there is a normal QT interval.



Back to the case:

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.



References:

1) Kirchhof P, Franz MR, Bardai A, Wilde AM. Giant T-U waves precede torsades de pointes in long QT syndrome: a systematic electrocardiographic analysis in patients with acquired and congenital QT prolongation. J Am Coll Cardiol. 2009;54(2):143-149.

2) Rautaharju PM, Surawicz B, Gettes LS, et al; American Heart Association Electrocardiography and Arrhythmias Committee, Council on Clinical Cardiology; American College of Cardiology Foundation; Heart Rhythm Society; Endorsed by the International Society for Computerized Electrocardiology. AHA/ACCF/HRS recommendations for the standardization and interpretation of the electrocardiogram: part IV: the ST segment, T and U waves, and the QT interval: a scientific statement from the American Heart Association Electrocardiography and Arrhythmias Committee, Council on Clinical Cardiology; the American College of Cardiology Foundation; and the Heart Rhythm Society.J Am Coll Cardiol. 2009; 53(11):982-991.


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Comment by KEN GRAUER, MD (11/7/2018):
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Insightful post by Drs. Meyers & Smith — regarding recognition that this ECG is highly suggestive of hypokalemia. I’d add the following thoughts to their excellent discussion.
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  • The initial ECG (ECG #1is most dramatically abnormal in lead V2 (See TOP tracing in Figure-1). However, at first glance of this tracing — I was not at all certain about what I was seeing for the ST-T(-U) wave in this V2 lead — because: iThere is marked artifact in this lead (ie, the ST-T-U wave baseline changes from beat-to-beat and shows multiple extra undulations for each of the 3 beats in this lead); andiiOther than lead V2 — it is not easy to say if the upright deflection near the middle of the R-R interval in ECG #1 represents a T wave, U wave, or some “fused” combination of the two.
Figure-1: Comparison between the 2 ECGs recorded in this case (See text). 
KEY POINT — It could be all-too-easy to overlook the long QT (QU) interval in ECG #1. To avoid such oversight: iYou might repeat the initial ECG — to clarify what we are truly seeing in lead V2; andiiBe sure you religiously incorporate a Systematic Approach in the ECG interpretation of each and every tracing you encounter! Doing so is the only realistic way to ensure that you do not omit potentially important ECG findings in your interpretation. 
  • I favor including assessment of the QT as one of the 3 ECG “Intervals” to look for (ie, the PR, QRS duration & QTc— and, being sure to look at Intervals early in my interpretation. That’s because IF the QRS complex is wide, it is important to determine WHY the QRS is wide before proceeding further with your interpretation. (For the Systematic Approach that I favor — CLICK HERE).
  • Assessment of the QT interval should be performed using measurements that you are certain of (ie, in which you can clearly see the beginning and end of the QT interval) — and, taken from that lead in which the QT interval looks to be longest! For example, we would not select lead I or V1 in ECG #1 to assess the QTc — because the QT interval does not look abnormal in these leads. The end of the T wave in lead I is also indistinct. 
  • Even if we exclude lead V2 from our assessment — the QTc in ECG #1 looks prolonged in leads such as lead II, in which the QT clearly exceeds half the R-R interval (CLICK HERE and scroll down to Figure-9 for the “eyeball” approach to rapid assessment of the QTc).
  • As per Dr. Meyers — it probably does not matter clinically on this initial ECG if we are measuring the QT or QU interval — since prolongation of either interval portends similar clinical consequences. Practically Speaking — the specific numerical value of this interval matters less than considering potential Causes of a Long QT (or QU) Interval. I favor consideration of this easy-to-remember LISTiCertain Drugs (and/or combinations of drugs)ii“Lytes” (low K+/Mg++/Ca++)and/oriiiCNS Catastrophes (ie, stroke, seizure, coma, head trauma, CNS bleed)NOTE — Several other conditions (ie, BBB, MI/ischemia) may also cause QT prolongation. However, the presence of these other conditions will usually be obvious from inspection of the ECG. PEARL — Whenever you see a prolonged QTc in the absence of ischemia, infarction or QRS widening — Think Drugs/Lytes/CNS as the possible cause(s). Then correlate clinically. (For more regarding use of this Long QTc List— Click HERE and HERE).
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FINAL THOUGHT — The BEST way to hone your skills for recognizing subtle abnormalities such as the QTc prolongation in ECG #1 — is to do Lead-to-Lead Comparison of the initial ECG (TOP tracing in Figure-1 — obtained when serum K+ = 2.6 mmol/L— with ECG #2, which was obtained after electrolyte repletion.
  • In my experience — the ECG is less sensitive and specific with milder degrees of hypokalemia. But in this case (as per Dr. Meyers) — given the clinical history of renal disease + an eating disorder with prior history of electrolyte abnormalities — a diagnosis of presumed hypokalemia should be immediately thought of on seeing ECG #1 until proven otherwise.



5 comments:

  1. An outstanding case as usual.
    K. Wang.

    ReplyDelete
  2. Thanks for an excellent discussion. I've always referred to a hypokalemic 12-lead ECG as demonstrating the "buoys on the bay" phenomenon. The QRS complexes look like buoys bobbing up and down in the undulating T-U waves of a bay.

    ReplyDelete
  3. excellent.
    buoys on the bay. quite poetic.
    excellent discussion. thank you.

    ReplyDelete

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