Steven H. Mitchell1 and William J. Brady2 1 Department of Emergency Medicine, University of Washington School of Medicine, Seattle, WA, USA 2 Departments of Emergency Medicine and Medicine, University of Virginia School of Medicine, Charlottesville, VA, USA Hyperkalemia, the elevation of serum potassium, is a common electrolyte disturbance that can be seen in many clinical situations (Box 16.1). Hyperkalemia can be considered a true “silent killer” as elevated serum levels may produce few symptoms despite ECG changes that may rapidly lead to terminal events. Recognition of ECG changes from toxic potassium levels can lead to early, life‐saving interventions (Box 16.2). Potassium (K+) is the most abundant cation in the body, with most being stored intracellularly. It is this large potassium gradient across the cell’s membrane that contributes to the excitability of cardiac cells as well as other cells throughout the body. The body’s internal potassium management is primarily managed by the kidney. Most daily potassium loss (90%) is through renal excretion. Patients with renal failure, therefore, have impaired ability to regulate serum potassium and become prone to hyperkalemia. In addition, there are a number of medications and clinical conditions that may contribute to or cause hyperkalemia. In a basic sense, elevated serum potassium disrupts electrical function in the heart. This disruption not only affects the pacemaking foci of the heart but also the conduction tissues, resulting in bradycardia and conduction abnormalities. Serum potassium concentration is tightly regulated in the normal range. It is important to note that the relation between ECG changes and serum potassium will vary between people. Patients with frequent past exposures or slowly progressive elevations tend to tolerate higher serum levels before the development of significant ECG abnormality. Conversely, the sudden increase in serum potassium, such as with a toxin ingestion or rapid development of acute kidney injury (renal failure), will likely produce ECG abnormality at lower total levels of elevation. In a general sense, Table 16.1 lists the association between serum potassium level and ECG manifestation; this association should be used as a guide and is most often seen with sudden, acute elevations as opposed to chronic, recurrent hyperkalemia. The ECG changes of hyperkalemia progress in a relatively predictable manner and are outlined below. The peaked, or “tented” T wave, as a result of increased membrane repolarization, is the earliest ECG manifestation of hyperkalemia (Figure 16.2). It is also perhaps the most easily observed finding. Peaked T waves are best seen in the inferior (leads II and III) and precordial (leads V2–V4) leads (Figure 16.3). The peaked T wave is typically tall and narrow. It has the appearance of a “church steeple”; the T wave will broaden as further increases in serum potassium occur (Figure 16.3). Whether the T wave is narrow or wide, however, the morphology remains symmetric, which helps differentiate it from the asymmetric appearance of the ischemic, hyperacute T wave of early ST segment elevation myocardial infarction (STEMI). T waves that are typically inverted such as in left ventricular hypertrophy may become upright or “pseudonormalized.”
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The Electrocardiogram in Hyperkalemia
Electrocardiographic Manifestations
T Wave
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