Physiology · Year 1 · from Physiology
Case 2: Hyperkalemia - Membrane Potential Disturbance
Clinical Image
Source: Wikimedia Commons - ECG in hyperkalemia - CC BY-SA 3.0
Patient Presentation
A 68-year-old male with a history of chronic kidney disease (CKD stage 4), type 2 diabetes mellitus, and hypertension presents to the emergency department with generalized weakness, fatigue, and palpitations that began this morning. He ran out of his prescribed medications, including furosemide and sodium polystyrene sulfonate, one week ago and has been eating his usual diet including bananas and orange juice daily.
Demographics
- Age: 68 years
- Sex: Male
- Past Medical History: CKD stage 4, Type 2 DM, HTN
Chief Complaint
Generalized weakness, fatigue, and palpitations
Physical Examination
- Blood pressure: 158/94 mmHg
- Heart rate: 52 bpm (bradycardic)
- Temperature: 36.8C
- Respiratory rate: 16/min
- General: Alert but appears fatigued
- Cardiovascular: Bradycardic, irregular rhythm, no murmurs
- Neurological: Decreased deep tendon reflexes, mild proximal muscle weakness
- Extremities: 1+ bilateral lower extremity edema
Workup
- Serum potassium: 7.2 mEq/L (severely elevated; normal 3.5-5.0)
- Serum creatinine: 4.8 mg/dL (elevated from baseline of 3.5)
- BUN: 68 mg/dL
- Glucose: 186 mg/dL
- ECG: Peaked T waves, prolonged PR interval (0.24s), widened QRS (0.14s)
Diagnosis
Severe hyperkalemia with ECG changes in the setting of acute-on-chronic kidney disease
Treatment
- Immediate cardiac monitoring
- IV calcium gluconate 1g for cardiac membrane stabilization (immediate effect)
- IV regular insulin 10 units with D50W to shift potassium intracellularly
- Nebulized albuterol to promote intracellular potassium shift
- Sodium bicarbonate if acidemic
- Sodium polystyrene sulfonate (Kayexalate) or patiromer for potassium elimination
- Consider emergent hemodialysis if refractory
- Dietary potassium restriction education
- Medication reconciliation and adherence counseling
Physiological Principles Demonstrated
- Resting membrane potential: The resting membrane potential (-70 to -90 mV) depends on the potassium gradient across the cell membrane. Normal intracellular K+ is ~140 mEq/L while extracellular is ~4 mEq/L.
- Nernst equation: The equilibrium potential for potassium (E_K = -94 mV) approaches zero as extracellular potassium rises, depolarizing the resting membrane potential.
- Effect on excitability: Elevated extracellular K+ reduces the K+ gradient, partially depolarizing cardiac myocytes. This inactivates sodium channels, reducing excitability and slowing conduction.
- ECG manifestations: Progressive hyperkalemia causes peaked T waves (rapid K+ repolarization), prolonged PR interval (slowed atrial conduction), widened QRS (slowed ventricular conduction), and eventually sine wave pattern leading to ventricular fibrillation or asystole.
- Na+/K+-ATPase: Insulin stimulates the Na+/K+-ATPase, actively pumping potassium into cells and temporarily lowering serum levels. Beta-2 agonists like albuterol have a similar effect.
- Calcium and membrane stabilization: Calcium gluconate increases the threshold potential, widening the gap between resting and threshold potentials, protecting against arrhythmias without changing serum potassium.