This patient is a 64 year-old cachectic white male, admitted to ICU with a five day history of nausea, vomiting, and upper abdominal discomfort. The following EKGs were collected in the ED before and after treatment. His history includes HTN, alcoholism, and IDDM.
Classic electrocardiographic indications of hyperkalemia include sharply peaked, symmetrical T-waves, suppression of atrial activity, bradycardia, a markedly widened QRS and a short QT interval. Note how the rhythm in this case approaches the appearance of a sign wave as the QT narrows and the ventricular complexes widen; this is representative of the course in worsening hyperkalemia and is sometimes responsible for the idoventricular or agonal appearance of some hyperkalemic EKGs. This should not be considered a mere “agonal appearance,” however, as typically broad and flattened P-waves with an elongated PR interval will progress toward complete atrial paralysis, frank idoventricular activity below 40bpm, and subsequent hemodynamic collapse.
Distinguishing between the T-wave morphologies of hyperkaemia, early-repolarization, and hyperacuity in early MI can become problematic for pt. outcomes in the acute setting, particularly in the latter case, and a good discussion of this issue can be found at Dr. Smith’s EKG blog. It has been said that hyperkalemic T-waves are “tented” and should be pointed enough to prick your finger. Also note Lipman and Massie’s observation that, “The uniformly wide complex in hyperkalemia differs from the wide QRS in bundle branch block (terminal QRS sluring) or pre-excitation (initial sluring) in that the uniform widening of the QRS in hyperpotassemia affects both the initial and terminal QRS portions.” Lab values are as follows:
Despite resuscitation in the ED this patient arrived in the ICU with a BP of 70/40, HR 60bpm, RR of 30, and a room air SpO2 of 88%. The patient was ultimately stabilized over a matter of days but required extensive pressor support for evolving bacteremia and HHNKC. An ultrasound of the upper abdomen revealed fatty infiltration of the liver but no cholecystitis or cholangitis. It should be noted that although a history of recent complaints could be obtained from the patient’s family members, he initially presented in a comatose state.
Of additional relevance in this case may be Lipman-Massie’s further contention that, “Low sodium levels tend to exaggerate and high sodium levels tend to neutralize the ECG effects of hyperpotassemia.”
Dramatic recordings of progressing or resolving hyperkalemia are not difficult to find about the internet. Dr. M. Rosengarten has a fine series here.
Quotations from Lipman-Massie Clinical Electrocardiography, 8th Ed. Marvin I. Dunn MD, Bernard S. Lipman MD. Yearbook Medical Publisher Inc. ©1989. See pp. 240-243.