Harvey's Garden

Electrolyte imbalance

3 min read

ConditionClinical PresentationEKG Findings
HypokalemiaNeuromuscular: Muscle weakness, cramping, fasciculations, paralysis, respiratory failure, ileus, rhabdomyolysis. Other: Polyuria, polydipsia, metabolic alkalosis.- Flattened or inverted T waves
- U waves (prominent)
- ST depression
- Apparent prolonged QT interval (actually QU interval)
- Can lead to Torsades de Pointes, VT/VF
HyperkalemiaNeuromuscular: Muscle weakness, paralysis, paresthesias. Often asymptomatic until severe. GI: Nausea, vomiting, abdominal pain.- Tall, peaked T waves (earliest sign)
- PR interval prolongation
- P wave flattening or loss
- QRS widening
- “Sine wave” pattern in severe cases, preceding cardiac arrest.
HypocalcemiaNeuromuscular: Tetany (perioral numbness, tingling in fingers/toes), muscle cramps, carpopedal spasm. Signs: Chvostek’s sign (facial muscle twitch), Trousseau’s sign (carpal spasm). Other: Seizures, laryngospasm.- Prolonged QT interval (due to ST segment lengthening)
- T wave may be normal or inverted.
- Can lead to Torsades de Pointes (less common than with hypokalemia).
Hypercalcemia”Stones, bones, groans, thrones, and psychiatric overtones”:
- Stones: Renal stones, polyuria, polydipsia.
- Bones: Bone pain (from PTH or malignancy).
- Groans: Abdominal pain, constipation, nausea, pancreatitis.
- Thrones: Polyuria leading to dehydration.
- Psychiatric: Confusion, depression, lethargy, coma.
Other: Muscle weakness.		- Shortened QT interval
- PR interval prolongation
- T wave flattening or inversion.
- Bradycardia, heart block in severe cases.

ECG changes

Hypokalemia

Low extracellular potassium (K+) primarily affects repolarization (Phase 3 of the action potential).

  • Pathophysiology:
    • Low extracellular K+ hyperpolarizes the resting membrane potential (making it more negative).
    • It also paradoxically inhibits the outward-rectifier K+ channels (I_Kr), which are responsible for repolarization. This slows down Phase 3, prolonging the action potential duration.
  • Resulting EKG Changes:
    • T-wave flattening/inversion & ST depression: These reflect the delayed and less efficient ventricular repolarization.
    • Prominent U waves: The exact cause is debated, but it is thought to result from the delayed repolarization of Purkinje fibers or mid-myocardial cells, becoming visible as the T-wave diminishes.

Hyperkalemia

High extracellular potassium (K+) makes the resting membrane potential less negative (more depolarized), leading to faster repolarization but slower overall conduction.

  • Pathophysiology:
    • Accelerated Repolarization: The increased K+ gradient speeds up Phase 3 repolarization, making it occur more rapidly and synchronously.
    • Slowed Depolarization: The less negative resting potential inactivates some of the fast voltage-gated sodium (Na+) channels. This slows the initial depolarization (Phase 0) and reduces the rate of impulse conduction throughout the heart.
  • Resulting EKG Changes:
    • Peaked T waves: The earliest sign, caused by the rapid and efficient repolarization.
    • PR Prolongation & P wave flattening: Result from slowed conduction through the atria.
    • QRS Widening: Occurs as ventricular conduction slows due to Na+ channel inactivation. In severe cases, this can merge with the T wave to form a “sine wave” pattern.

Hypocalcemia

Low extracellular calcium (Ca2+) affects the plateau phase (Phase 2) of the cardiac action potential.

  • Pathophysiology:
    • Phase 2 is maintained by an influx of Ca2+. With less extracellular Ca2+, the driving force for this inward current is reduced.
    • This prolongs the duration of the plateau phase (Phase 2) of the action potential.
  • Resulting EKG Changes:
    • QT Interval Prolongation: This is a direct consequence of the lengthened plateau phase, which corresponds to the ST segment on the EKG. The T-wave itself is typically unaffected.

Hypercalcemia

High extracellular calcium (Ca2+) also affects the plateau phase (Phase 2), having the opposite effect of hypocalcemia.

  • Pathophysiology:
    • Increased extracellular Ca2+ enhances the inward Ca2+ current during Phase 2.
    • This leads to a more rapid activation of calcium-dependent K+ channels and earlier inactivation of Ca2+ channels, which shortens the plateau phase of the action potential.
  • Resulting EKG Changes:
    • Short QT Interval: This is caused by the shortened ST segment, which directly reflects the shorter plateau phase.

Graph View