Electrolyte imbalances are more than lab abnormalities — they can be life-threatening and are often first suspected through an ECG. Electrocardiography (ECG or EKG) is not only essential for diagnosing cardiac disorders but also a powerful tool to detect biochemical derangements. Among the most critical are potassium and calcium imbalances, which alter cardiac conduction patterns significantly. Recognizing these changes on ECG can be a game-changer in timely diagnosis and intervention.
This comprehensive guide explores how electrolyte disturbances—hypokalemia, hyperkalemia, hypocalcemia, and hypercalcemia—manifest on ECG, what each wave shift means, and how to interpret them correctly in clinical scenarios.
Normal ECG: Understanding the Baseline
Before diving into electrolyte-induced abnormalities, let’s anchor our understanding with the normal ECG:
- P wave – Atrial depolarization
- PR interval – AV node conduction (120–200 ms)
- QRS complex – Ventricular depolarization (≤120 ms)
- ST segment – Ventricular repolarization begins
- T wave – Ventricular repolarization
- QT interval – Total time for ventricular depolarization and repolarization
In a healthy individual, all these components appear rhythmic and well-structured.
Hypokalemia: Low Potassium and Its ECG Signatures
When potassium levels fall below normal (typically <3.5 mEq/L), the heart’s electrical stability becomes vulnerable.
Key ECG Findings in Hypokalemia:
- Prolonged QT interval: Caused by delayed ventricular repolarization.
- Prominent U waves: Small waves following the T wave, best seen in leads V2-V3.
- Flattened or inverted T waves
- ST segment depression
Clinical Relevance: Hypokalemia can lead to ventricular arrhythmias such as torsades de pointes or ventricular tachycardia, especially in patients on diuretics or with diarrhea or vomiting.
Mnemonic: “Low K prolongs everything except the T wave.”
Hyperkalemia: High Potassium and the Peaked T Wave
Hyperkalemia (>5.5 mEq/L) affects the myocardium profoundly due to its role in resting membrane potential.
Classic ECG Findings in Hyperkalemia:
- Peaked T waves: Narrow-based, tall and symmetrical—“tented” T waves.
- Shortened QT interval
- Widened QRS complex
- P wave flattening or disappearance
- Sine wave pattern in severe cases (>7.5 mEq/L) indicating impending cardiac arrest
Clinical Implication: Hyperkalemia is a medical emergency. It often occurs in patients with chronic kidney disease, Addison’s disease, or those taking ACE inhibitors or potassium-sparing diuretics.
Mnemonic: “Hyper-K = High T, Wide QRS, no P.”
Hypocalcemia: When Calcium Falls, QT Stretches
Calcium plays a vital role in phase 2 of the cardiac action potential. Low calcium levels (<8.5 mg/dL) prolong ventricular depolarization.
ECG Characteristics of Hypocalcemia:
- QT interval prolongation
- T waves remain normal or mildly altered
- No significant change in QRS or P waves
Clinical Danger: Prolonged QT from hypocalcemia predisposes to torsades de pointes, though less commonly than hypokalemia or drugs.
Mnemonic: “Hypo-Ca = QT long = Cardiac wait.”
Hypercalcemia: The Short QT Story
Opposite to hypocalcemia, high calcium levels (>10.5 mg/dL) shorten the action potential duration.
ECG Findings in Hypercalcemia:
- Shortened QT interval
- Abbreviated ST segment
- T wave remains upright but may appear closer to the QRS
Clinical Concern: Often seen in parathyroid disorders, malignancy, or vitamin D intoxication. Short QT is a hallmark clue on ECG.
Mnemonic: “Hyper-Ca = Quick QT = Quick contract.”
Why ECG Changes Matter: Clinical Scenarios and Red Flags
Electrolyte disturbances can masquerade as ischemia, arrhythmias, or drug toxicity. Correctly interpreting ECG changes helps prevent misdiagnosis and directs the clinician toward the correct metabolic culprit.
For example:
- A patient on thiazide diuretics with fatigue and muscle cramps shows U waves and a long QT → Think hypokalemia
- A renal failure patient with muscle weakness and tall T waves → Hyperkalemia
- An elderly patient on calcium supplements and showing a very short QT → Hypercalcemia
ECG Changes in Electrolyte Imbalance: Comparison Table
| Electrolyte Imbalance | Key ECG Features | Clinical Risk |
|---|---|---|
| Hypokalemia | Prolonged QT, U waves, flat T wave | VT, Torsades de Pointes |
| Hyperkalemia | Peaked T wave, wide QRS, no P wave | Asystole, VFib, cardiac arrest |
| Hypocalcemia | Prolonged QT interval | Torsades de Pointes |
| Hypercalcemia | Shortened QT, short ST segment | Bradyarrhythmias, digoxin sensitivity |
Real-Life Case Examples
Case 1:
A 70-year-old CKD patient presents with weakness. ECG shows tall, peaked T waves. Labs confirm potassium 6.8.
Diagnosis: Hyperkalemia
Action: IV calcium gluconate, insulin with dextrose, and dialysis.
Case 2:
A young woman on a crash diet presents with palpitations. ECG reveals prominent U waves and long QT.
Diagnosis: Hypokalemia
Action: Potassium replacement and dietary correction.
People Also Ask (PAA) - FAQ Schema
What is the normal ECG pattern?
A normal ECG includes a P wave, QRS complex, and T wave, with a regular rhythm and standard intervals (PR: 120–200ms, QRS: ≤120ms, QT: 350–450ms).
How does hypokalemia affect ECG?
Hypokalemia causes prolonged QT, prominent U waves, and flat or inverted T waves, increasing the risk of ventricular arrhythmias.
What does hyperkalemia do to an ECG?
Hyperkalemia results in tall, peaked T waves, wide QRS complexes, and the loss of P waves in severe cases, indicating risk of cardiac arrest.
What ECG change is seen in hypocalcemia?
Hypocalcemia leads to prolonged QT interval due to delayed ventricular repolarization.
What is the main ECG finding in hypercalcemia?
Shortened QT interval and abbreviated ST segment are the hallmark findings in hypercalcemia.
