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The ECG shows T-wave inversions with prominent U-waves in leads V3-V6, and less prominent in leads II, II, aVF. The QT interval is also prolonged. All signs pointing towards hypokalemia. This patient’s potassium level of 2.3 mEq/L. With the patient’s history of weakness following exertion and his recent consumption of a large carbohydrate meal (two hints), this patient may have a condition called hypokalemic periodic paralysis (HPP).
Hypokalemia definition:
Mild: serum K+ < 3.5
Moderate: serum K+ < 3.0
Severe: serum K+ <2.5
ECG findings associated with hypokalemia:T-wave flattening is typically seen in hypokalemia. In severe cases (as in this one), you may see T-wave inversions.
U-waves can have several causes including hypokalemia, hypocalcemia, and hypomagnesemia, although hypokalemia is the most common. No one is sure where U-waves come from but one theory is that they represent delayed repolarization of the His/Purkinje system. These can be independent of the T-wave or on occasion they can merge to produce a double-hump if the T-wave is upright or a biphasic wave if the T-wave is inverted.
A prolonged QTc is also typically seen with hypokalemia. In the case of merged T- and U-waves, the QT interval should be extended to include the U-wave, so the QT interval actually becomes a QU interval. Prolonged QU intervals increase the risk of torsades de pointes or ventricular tachycardia via the ‘R on T’ phenomenon.
ST-depressions may also be seen in hypokalemia, in addition to T-wave flattening/inversion, mimicking subendocardial ischemia. None are present on this ECG.
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Diagnostics:Electrolytes, including potassium, calcium, phosphate, and magnesium, should be checked, as well as thyroid function tests. If this is indeed HPP, the problem lies within cell membrane ion channels, which cause an exaggeration of insulin and epinephrine’s effect on driving potassium intracellularly. Intracellular potassium shifting effectively hyperpolarizes skeletal muscle fibers, which prolongs the refractory period. Therefore, the problem is NOT depleted total body potassium. In fact, total body potassium is usually normal. The problem in HPP is with potassium shifting.
Management:Management should include replenishing potassium as needed (w/ magnesium if also hypomagnesemic). If known HPP or positive family history (autosomal dominant), potassium should be administered very gingerly (<10mEq/hr) with levels checked periodically over 24hrs to minimize the risk of rebound hyperkalemia. The most common pitfall in treating these patients is overzealous administration of potassium. If labs indicate that this is thyrotoxic periodic paralysis (TPP), treatment includes slow administration of potassium (as above) along with propranolol 1mg IV q10mins up to 3mg. TPP is a form of HPP. They have a common mechanism, being that both cause an exaggerated response to insulin and epinephrine, resulting in hypokalemia. However, in TPP excess thyroid hormone sensitizes the sodium-potassium ATPase of skeletal muscle to the effects of insulin and epinephrine.
References:
Lu KC, Hsu YJ, Chiu JS, et al. Effects of potassium supplementation on the recovery of thyrotoxic periodic paralysis. Am J Emerg Med 2004;22:544
Tassone H, Moulin A, Henderson SO. The pitfalls of potassium replacement in thyrotoxic periodic paralysis: a case report and review of the literature. J Emerg Med. 2004;26(2):157.
Life in the Fast Lane: Hypokalemia. http://lifeinthefastlane.com/ecg-library/basics/hypokalaemia/.
Martindale, Jennifer and Brown, David. “Chapter 8. QT Abdnormalities and Electrolyte Disturbanc”. Rapid Interpretation of ECGs in Emergency Medicine. Philadelphia, PA: Lippincott Willimas & Williams, 2012.
The views expressed on this blog are the author's own and do not reflect the views of their employer. Please read our full disclaimer
here. Any references to clinical cases refer to patients treated at a virtual hospital,
Janus General Hospital.
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