A 68-year-old man with stage 4 CKD (eGFR 22 mL/min) on lisinopril and spironolactone presents to the emergency department with palpitations and weakness. His serum potassium is 6.8 mEq/L. An ECG is performed and shows the characteristic findings marked in the diagram. The structure marked **A** — tall peaked (tented) T waves with narrow base, most prominent in the precordial leads — represents the earliest and most characteristic ECG manifestation of his condition. Which of the following best describes the underlying cardiac electrophysiological mechanism responsible for this ECG finding?

Explanation

## Why "Depolarization of the resting membrane potential by elevated extracellular K+, leading to inactivation of fast sodium channels and accelerated repolarization" is right The peaked T waves marked **A** in the diagram are the hallmark of hyperkalemia (K+ 5.5–6.5 mEq/L). The pathophysiological mechanism is: elevated extracellular K+ depolarizes the resting membrane potential (makes it less negative) → inactivates fast sodium channels → reduces phase 0 depolarization velocity → shortens repolarization time (accelerated repolarization) → produces the characteristic tall, narrow-based, symmetric ("tented" or "Eiffel Tower") T waves. This is the EARLIEST and MOST CHARACTERISTIC ECG change in hyperkalemia, appearing before P-wave flattening, PR prolongation, or QRS widening. The accelerated repolarization shortens the QT interval. (Harrison 21e Ch 51; KDIGO Hyperkalemia Guidelines) ## Why each distractor is wrong - **Hyperpolarization of the resting membrane potential, causing prolonged phase 0 depolarization and delayed repolarization**: Hyperkalemia causes *depolarization*, not hyperpolarization. Hyperpolarization would delay repolarization and widen the T wave, not create peaked T waves. This describes hypokalemia, not hyperkalemia. - **Increased intracellular calcium influx through L-type channels, resulting in prolonged action potential duration and widened QRS complex**: While calcium is used therapeutically in hyperkalemia to stabilize the myocardium, it does not cause the peaked T waves. Increased calcium influx would prolong, not shorten, repolarization. QRS widening is a *later* sign (K+ >6.5), not the earliest finding. - **Blockade of potassium channels in the ventricular myocardium, leading to prolonged repolarization and QT interval lengthening**: Hyperkalemia does not block K+ channels; rather, the high extracellular K+ gradient is reduced, which *accelerates* repolarization and *shortens* the QT interval. Prolonged repolarization would produce broad, flattened T waves, not peaked T waves. **High-Yield:** Peaked T waves = accelerated repolarization from depolarized resting potential in hyperkalemia; earliest ECG sign; requires immediate calcium gluconate to stabilize myocardium. [cite: Harrison Principles of Internal Medicine 21e Ch 51; KDIGO Hyperkalemia Guidelines]