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Hypokalemia refers to abnormally low levels of potassium in the blood.
In normal circumstances, more than 90% of the total body potassium is INTRA-cellular; the remaining is in the EXTRA-cellular fluid and blood plasma. The ratio of intracellular to extracellular potassium is important for generation of action potentials and is essential for normal functions of neurons, skeletal muscles and cardiac muscles. This is why potassium levels in the blood are strictly regulated within a narrow range between 3.5 and 5mmol/L. As the normal daily dietary intake of potassium varies widely and can be as much as 100mmol a day, the body must quickly and precisely react to keep blood potassium levels within the normal limits. This is achieved by 2 mechanisms:
– Excretion of potassium through the kidneys and intestines; with the kidneys playing a predominant role.
– Shifting of potassium from the extracellular fluid into the cells by the sodium/potassium pump. The pump is mainly regulated by hormones such as insulin and catecholamines.
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 HYPER-polarization. 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, HYPER-excitability 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 RE-polarization 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 afterdepolarization 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.
