Hypokalemia refers to abnormally low levels of potassium in the blood.
Hypokalemia is defined as a serum potassium concentration lower than
3.5 mmol/L. Hypokalemia may result from increased excretion, inadequate intake or
shift of potassium from the extracellular fluid into the cells. Poor intake or intracellular
shift alone rarely causes the disease, but may be a contributing factor. Most commonly,
hypokalemia is caused by excessive loss of potassium in the urine, from the GI tract,
or skin. The cause is usually apparent by the patient’s history of predisposing diseases or
medication. Urine potassium levels are measured to differentiate between renal and non-renal
causes. Depending on the level of severity, symptoms may include muscle weakness, cramping,
tremor, intestinal obstruction, hypotension, respiratory depression and abnormal heart rhythms.
As potassium levels decrease in the extracellular space, the magnitude of the potassium gradient
across the cell membrane is increased, causing hyperpolarization. This moves the membrane
voltage further from the threshold, and a greater than normal stimulus is required to
generate an action potential. The result is a reduced excitability or responsiveness of
the neurons and muscles. In the heart, however, hyperexcitability is observed. This is because
hyperpolarization enhances the “funny” currents in cardiac pacemaker cells, resulting in a
faster phase-4 depolarization and thus a faster heart rate. The effect is greatest in Purkinje
fibers as these are more sensitive to potassium levels, as compared to the SA node. Increased
automaticity of Purkinje fibers may lead to the development of one or more ectopic pacemaker
sites in the ventricles, causing ventricular premature beats, tachycardia and fibrillation.
Reduced extracellular potassium, paradoxically, also inhibits the activity of some potassium
channels, slowing down potassium efflux during repolarization and thus delays ventricular
repolarization. As hypokalemia becomes more severe, especially in patients with other
heart conditions, the inward current may exceed the outward current, resulting in
early after-de-polarization and consequently extra heartbeats. Prolonged repolarization may
also promote re-entrant arrhythmias. Early ECG changes in hypokalemia are
mainly due to delayed ventricular repolarization. These include flattening or inversion of T wave,
increasingly prominent U wave, ST-segment depression, and prolonged QU interval.
Hypokalemia-induced arrhythmias require immediate potassium replacement. Oral administration is
safer but may not be effective in severe cases. If potassium infusion is indicated, continuous
cardiac monitoring and hourly serum potassium determinations must be performed to avoid
hyperkalemia complications. In the long-term, the underlying causes must be addressed.