Electrolyte effects on ECG

Hyperkalemia - Tall Tented Terrors

• A progressive, life-threatening emergency. ↑ extracellular K⁺ partially depolarizes myocyte membranes, inactivating Na⁺ channels and slowing conduction.
• Mild (K⁺ > 5.5 mEq/L): Tall, narrow, peaked T-waves are the earliest sign.
• Moderate (K⁺ > 6.5 mEq/L): PR interval prolongs, P-wave flattens and eventually disappears.
• Severe (K⁺ > 7.0 mEq/L): QRS widens significantly, may merge with T-wave.
• Terminal (K⁺ > 8.0 mEq/L): Classic "sine wave" pattern precedes ventricular fibrillation or asystole.

⭐ The "sine wave" morphology represents the fusion of a wide QRS complex with the T-wave, indicating a pre-terminal, slow ventricular rhythm. It's a critical sign demanding immediate intervention to prevent imminent cardiac arrest.

Hypokalemia - Low, Slow, U-Show

📌 Mnemonic: "Low, Slow, U-Show" summarizes the key ECG changes.

• ECG Findings:
  • ↓ T-wave amplitude (flattening or inversion)
  • Prominent U-waves, especially in precordial leads (V2-V3)
  • ST-segment depression
  • ↑ PR interval and ↑ QT interval (risk of TdP)
• Clinical Context: Often seen with diuretic use, GI losses, or refeeding syndrome.

⭐ Severe hypokalemia (< 2.5 mEq/L) significantly potentiates digoxin toxicity, increasing the risk of dangerous ventricular arrhythmias.

Hypercalcemia - Short & Stoned QT

• Primary ECG Change: Shortened QT interval, resulting from an accelerated ventricular repolarization (shortened ST segment).
• Mechanism: ↑ extracellular Ca²⁺ enhances cardiac myocyte contractility and shortens the plateau phase (Phase 2) of the action potential.
• Other Findings: PR interval prolongation and QRS widening can occur in severe cases.

⭐ Severe hypercalcemia (>14 mg/dL) potentiates digoxin toxicity by competing for the same binding sites on the Na⁺/K⁺-ATPase pump, increasing the risk of arrhythmias.

📌 Systemic Features: "Stones, Bones, Groans, Thrones, Psychiatric Overtones."

Hypocalcemia - Long Live the QT

• Pathophysiology: ↓ extracellular Ca²⁺ prolongs phase 2 (plateau) of the myocyte action potential. This delays ventricular repolarization.
• ECG Findings:
  • Prolonged QT interval (QTc > 0.44s)
  • Specifically, a lengthened ST segment
  • Normal T wave duration and morphology

⭐ A prolonged QT interval is a major risk factor for developing Torsades de Pointes (TdP), a life-threatening polymorphic ventricular tachycardia.

📌 HypoCalcemia = Long QT.

Magnesium - Torsades' Twisted Tale

• Hypomagnesemia (< 1.8 mg/dL):

  • Often co-exists with ↓K⁺ & ↓Ca²⁺.
  • ECG: Prolonged QT interval → risk of Torsades de Pointes (TdP).
  • Treatment: IV Magnesium Sulfate (drug of choice for TdP).

• Hypermagnesemia (> 2.6 mg/dL):

  • Rare; iatrogenic or in renal failure.
  • ECG: ↑PR interval, ↑QRS duration, bradycardia → complete heart block, asystole.
  • Treatment: IV Calcium Gluconate.

⭐ Magnesium is a cofactor for Na⁺/K⁺-ATPase. Low Mg²⁺ impairs K⁺ correction, making hypomagnesemia a key cause of refractory hypokalemia.

High‑Yield Points - ⚡ Biggest Takeaways

• Hyperkalemia classically presents with peaked T waves, progressing to a widened QRS and a sine wave pattern in severe cases.
• Hypokalemia is marked by U waves, flattened T waves, and ST depression.
• Hypercalcemia is associated with a shortened QT interval, while hypocalcemia leads to a prolonged QT interval.
• Hypomagnesemia is a key risk factor for Torsades de Pointes.
• Digitalis effect causes ST segment scooping and a shortened QT interval.