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.
These studies suggest that the dis-regulated overproduction of interleukin 5 by blood mononuclear cells is an underlying cause of the eosinophilia found in at least some families with this disorder. Diagnosis
The diagnosis of familial eosinophilia rest upon a) familial clustering of the disorder; b) exclusion of "family acquired eosinophilia" (i.e. eosinophilia due to chronic parasite or other infestations that afflict multiple members of a family); c) lack of eosinophil-induced tissue destruction such as that which occurs in the hypereosinophilic syndrome; d) absence of signs or symptoms of other hereditary eosinophilias (e.g. hyperimmunoglobulin E syndrome, Omenn syndrome), Wiskott–Aldrich syndrome, and numerous other primary immunodeficiency syndromes); and d) lack of evidence for reactive eosinophilias (e.g. allergy-related), neoplastic eosinophilias (e.g. eosinophilic leukemia, clonal eosinophilia), or eosinophila associated with various hematological and non-hematological malignancies as outlined in causes of eosinophilia. Treatment
Since longitudinal data, including eosinophil counts obtained over a 20- to 30-year periods in some family members, show remarkable stability in the absolute eosinophil count with no evidence of disease   attributable to eosinophil-related tissue injury, therapy to lower eosinophil counts such as corticosteroids, tyrosine kinase inhibitors, and antibodies directed against interleukin 5 have in general not been used to treat familial eosinophilia. One patient with severe heart damage was treated with a corticosteroid but soon thereafter died. Familial eosinophilia unassociated with possible eosinophil-related tissue injuries may not require drug treatment, those cases with such tissue injuries, it is suggested, should be considered for such interventions. In all cases, however, regular follow-up of the disorder is strongly recommended.