A 20-year-old woman with fatigue and palpitations
A 20-year-old woman presents to the emergency department with fatigue and the sudden onset of palpitations. She reports no history of significant illness or surgery. She says she is not currently taking prescription or over-the-counter medications. She does not smoke, drink alcohol, or use illicit drugs.
Her weight is 52 kg (115 lb), her height is 170 cm (67 in), and her body mass index (BMI) is 18 kg/m2. Vital signs: temperature 35.7°C (96.4°F), blood pressure 92/48 mm Hg, heart rate 73 bpm, respiratory rate 5 breaths per minute, and oxygen saturation 98% on room air.
She appears tired but is alert, conversant, and cooperative. Her skin is normal, and dentition is fair. Her pulse is regular, and respirations are slow. The abdomen is soft, non-tender, and flat. Strength is 4 on a scale of 5 in all extremities. Deep-tendon reflexes are 2+ and symmetric.
Electrocardiography (Figure 1) in the emergency department shows ST-segment depression, a prolonged corrected QT interval of 665 msec, T-wave inversion, PR prolongation, increased P-wave amplitude, and U waves.
1. Which electrolyte abnormality is associated with this electrocardiographic picture?
- Hypercalcemia
- Hyperkalemia
- Hypocalcemia
- Hypokalemia
Hypokalemia is the likely cause of these findings. The finding of U waves is considered significant when they are inverted, merged with the T wave, or have an amplitude greater than the T wave.1 U waves are best seen in the precordial leads. When severe, hypokalemia can lead to potentially fatal arrhythmias such as high-grade atrioventricular block, ventricular tachycardia, and ventricular fibrillation.2
Hyperkalemia is associated with peaked T waves, a prolonged PR interval, decreased P wave amplitude, and a widened QRS complex.2 When acute and severe, hyperkalemia is associated with ventricular arrhythmia.
Hypocalcemia is associated with a prolonged QT interval and ventricular dysrhythmia, but not U waves.2
Hypercalcemia is associated with bradydysrhythmia, as well as with a shortened QT interval.2
LABORATORY TESTING
Laboratory testing shows the following:
- Sodium 126 mmol/L (reference range 135–145)
- Potassium 1.5 mmol/L (3.5–5.1)
- Chloride 58 mmol/L (100–110)
- Bicarbonate 62 mmol/L (20–30)
- Blood urea nitrogen 16 mg/dL (7–18)
- Creatinine 0.8 mg/dL (0.5–1.0)
- Glucose 106 mg/dL (70–110)
- Ionized calcium 4.4 mg/dL (4.5–5.3)
- Magnesium 1.8 mg/dL (1.7–2.3)
- Phosphorus 4.1 mg/dL (2.5–4.5)
- Venous blood gases pH 7.56 (7.35–7.45), Pco2 69 mm Hg (35–45).
POTASSIUM HOMEOSTASIS
Ninety-eight percent of potassium is intracellular and only 2% is extracellular.3 The main cellular stores are myocytes and hepatocytes. Patients with decreased muscle mass may be at a higher risk of hypokalemia as a result of decreased skeletal muscle stores.4
The acute development of hypokalemia occurs from transcellular shifts. Alkalosis, insulin secretion, and beta-adrenergic stimulation promote the intracellular uptake of potassium. The major hormonal regulator of potassium excretion is aldosterone, which is stimulated by renal hypoperfusion and promotes potassium-ion secretion in the distal convoluted tubule.
Chronic hypokalemia develops in patients with ongoing renal or gastrointestinal potassium loss. If the cause of potassium loss is not elucidated by the history, the physical, and a review of medications, then one of two things is possible: either the patient has renal tubular disease affecting acid-base and potassium regulation, causing excessive mineralocorticoid secretion, which is associated with an abnormal response to aldosterone; or the patient is not being forthcoming in the history.
