Electrocardiogram
Hypokalemia leads to characteristic ECG changes (PR prolongation, ST-segment and T-wave depression, U-wave formation).The earliest electrocardiographic (ECG) findings, associated with hypokalemia, are decreased T wave height. Then, ST depressions and T inversions appear as serum potassium levels reduce further. Due to prolonged repolarization of ventricular Purkinje fibers, prominent U waves occur (usually seen at V2 and V3 leads), frequently superimposed upon T waves, therefore producing the appearance of prolonged QT intervals, when serum potassium levels fall below 3 mEq/L. Amount
The amount of potassium deficit can be calculated using the following formula:Kdeficit (in mmol) = (Knormal lower limit − Kmeasured) × body weight (kg) × 0.4
Meanwhile, the daily body requirement of potassium is calculated by multiplying 1 mmol to body weight in kilograms. Adding potassium deficit and daily potassium requirement would give the total amount of potassium need to be corrected in mmol. Dividing mmol by 13.4 will give the potassium in grams. Treatment
Treatment includes addressing the cause, such as improving the diet, treating diarrhea, or stopping an offending medication. People without a significant source of potassium loss and who show no symptoms of hypokalemia may not require treatment. Acutely, repletion with 10 mEq of potassium is typically expected to raise serum potassium by 0.1 mEq/L immediately after administration. However, for those with chronic hypokalemia, repletion takes time due to tissue redistribution. For example, correction by 1 mEq/L can take more than 1000 mEq of potassium over many days.
This deficiency—known as apparent mineralocorticoid excess syndrome—can either be congenital or caused by consumption of glycyrrhizin, which is contained in extract of licorice, sometimes found in herbal supplements, candies, and chewing tobacco. Rare hereditary defects of renal salt transporters, such as Bartter syndrome or Gitelman syndrome, can cause hypokalemia, in a manner similar to that of diuretics. As opposed to disease states of primary excesses of aldosterone, blood pressure is either normal or low in Bartters or Gitelmans. Distribution away from extracellular fluid
In addition to alkalosis, other factors can cause transient shifting of potassium into cells, presumably by stimulation of the Na+/K+ pump. These hormones and medications include insulin, epinephrine, and other beta agonists (e.g. salbutamol or salmeterol), and xanthines (e.g. theophylline). Stimulants (amphetamines, methylphenidate, cocaine) can also cause hypokalemia by stimulating beta-2 receptors. Rare hereditary defects of muscular ion channels and transporters that cause hypokalemic periodic paralysis can precipitate occasional attacks of severe hypokalemia and muscle weakness. These defects cause a heightened sensitivity to the normal changes in potassium produced by catecholamines and/or insulin and/or thyroid hormone, which lead to movement of potassium from the extracellular fluid into the muscle cells. Other
A handful of published reports describe individuals with severe hypokalemia related to chronic extreme consumption (4–10 L/day) of colas. The hypokalemia is thought to be from the combination of the diuretic effect of caffeine and copious fluid intake, although it may also be related to diarrhea caused by heavy fructose ingestion.