A 52-year-old man with chronic kidney disease presents with an ECG showing peaked T waves and prolonged QT interval. Which feature best distinguishes hyperkalemia-induced peaked T waves from other causes of T wave peaking?

Explanation

## Distinguishing Hyperkalemia-Induced Peaked T Waves from Other Etiologies ### Morphological Features of Hyperkalemia T Waves **Key Point:** Hyperkalemia produces a characteristic **narrow-based, symmetrical, peaked ("tented") T wave** that is pathognomonic when present. This morphology is distinct from T wave peaking seen in other conditions. | Feature | Hyperkalemia | Myocardial Ischemia | LVH | Pulmonary Embolism | |---------|--------------|-------------------|-----|-------------------| | **T wave shape** | Symmetrical, narrow-based, peaked | Asymmetrical, inverted or biphasic | Asymmetrical, inverted | Inverted in V1–V4 | | **T wave base** | Narrow (acute angle) | Broad | Broad | Variable | | **Associated ECG changes** | Prolonged QT, ST depression, bradycardia | ST elevation/depression, Q waves | LVH voltage criteria, strain pattern | Sinus tachycardia, S1Q3T3 pattern | | **Serum K^+^ level** | Typically > 6.5 mEq/L | Normal K^+^ | Normal K^+^ | Normal K^+^ | ### Pathophysiology of Hyperkalemia T Waves **High-Yield:** Elevated extracellular K^+^ shortens the duration of ventricular repolarization by: 1. Increasing the outward K^+^ gradient (enhanced K^+^ efflux) 2. Accelerating early repolarization in the epicardium 3. Creating a **steep, narrow repolarization vector** → symmetrical, peaked T wave This is distinct from ischemic T wave inversion (which reflects regional repolarization abnormality) or LVH strain (which shows asymmetrical, broad-based T wave inversion in lateral leads). ### Clinical Pearl **Warning:** Do not confuse hyperkalemia T waves with: - ~~Ischemic T wave inversion~~ (asymmetrical, broad-based, often with ST changes) - ~~LVH strain pattern~~ (asymmetrical T wave inversion in V5–V6, I, aVL; associated with voltage criteria) - ~~Pulmonary embolism~~ (T wave inversion in precordial leads with S1Q3T3 pattern) ### ECG Evolution in Hyperkalemia ```mermaid flowchart TD A["K⁺ elevation"]:::outcome --> B["K⁺ 5.5–6.5 mEq/L"]:::outcome B --> C["Peaked T waves"]:::action C --> D["K⁺ 6.5–7.5 mEq/L"]:::outcome D --> E["Prolonged PR interval<br/>Widened QRS"]:::action E --> F["K⁺ > 7.5 mEq/L"]:::outcome F --> G["Sine wave pattern<br/>Cardiac arrest risk"]:::urgent ``` ### Diagnostic Approach **Tip:** When you see peaked T waves on ECG: 1. **Check serum K^+^** — if elevated (> 6.0 mEq/L), peaked T waves are likely hyperkalemia 2. **Assess T wave morphology** — narrow-based and symmetrical → hyperkalemia; broad-based and asymmetrical → other cause 3. **Look for associated changes** — prolonged PR, widened QRS, ST depression → supports hyperkalemia 4. **Clinical context** — renal failure, ACE inhibitor use, potassium supplementation → hyperkalemia more likely **Mnemonic:** **PEAKED T waves in HyperKalemia** = **P**eaked (narrow-based), **E**levated K^+^, **A**cute (symmetrical), **K**idney disease context, **E**CG changes (PR prolongation, QRS widening), **D** = Danger (cardiac arrhythmia risk) [cite:Harrison 21e Ch 297]