Hypokalemic periodic paralysis (hypoPP) is a disorder characterized by episodic, short-lived, and hypo-reflexive skeletal muscle weakness. Familial hypoPP is an autosomal dominant inheritance with mutations in the expression of the sodium voltage-gated channel alpha subunit 4 (SCN4A) gene or calcium ion channels (CACNA1S; Calcium voltage-gated channel subunit alpha1 S). Although the frequency of familial hypoPP is not known, the incidence of 1 per 100,000 people has been reported. In some cases, it has been identified as idiopathic or sporadic hypoPP in some cases without family history. A 28-year-old man who visited the emergency room for paralytic attack was assessed in this study. He exhibited motor weakness in four limbs. There was no previous medical history or family history. The initial electrocardiogram showed a flat T wave and QT prolongation. His blood test was delayed, and sudden hypotension and bradycardia were observed. The blood test showed severe hypokalemia (potassium 1.50 mmol/L). After correcting hypokalemia, his muscle paralysis recovered without any neurological deficits. The patient’s thyroid function and long exercise test results were normal. However, because of the history of high carbohydrate diet and exercise, hypoPP was suspected. Hence, next-generation sequencing (NGS) was performed, and a mutation of Arg669His was noted in the SCN4A gene. The patient was educated about aggravation factors that could help prevent symptoms, and potassium tablets were provided for use when muscle weakness occurred. The patient is undergoing regular follow-up and has been in a stable state without any paralysis attacks for more than 6 months. Although hypoPP is a rare disease, it can be suspected in patients with hypokalemic paralysis, and identification of this condition is important for preventing further attacks and improving patient outcomes. Diagnosing hypoPP through targeted NGS is a cost-effective and useful method.