7298 Hyperventilation Associated Hypophosphatemia, Hypocalcemia, Hypokalemia And Paralysis

Abstract Disclosure: S. Afreen: Research Investigator; Self; Tandem Diabetes Care, Yes. N. Afreen: None. Introduction: Hyperventilation is over-breathing in excess of the metabolic needs of the body, which can result in respiratory alkalosis and a wide range of electrolyte abnormalities. Case: A 38 year old male with a past history of hypertension, OSA and cholecystectomy reported having episodes of palpitations, tachypnea with respiratory rate as high as 80 breaths/ minute, associated with facial numbness and tingling, tetany, progressing to paralysis of his extremities. These episodes started 7 years ago but gradually became more frequent. He denied anxiety or stressors prior to these episodes. The episodes almost always result in emergency room visits. During one of these episodes he was found to have the following labs: ionized calcium-1 mmol/l, serum phosphorus- 0.8 mg/dl, serum potassium- 2.7 mmol/l, 1.25(OH)2D- 44pg/ml, alkaline phosphatase- 60 IU/l, glucose- 94 mg/dl and GFR- 90 ml/min/1.73m2. VBG during this episode: pH - 7.59, PCO2- 23 mm Hg, and bicarbonate - 22 mmol/l. Of note, the electrolytes are normal in between the episodes. Thyroid labs are normal. Off of phosphate supplementation for 3 days, in between episodes, his serum phos- 4.2mg/dl, cr - 0.84 mg/dl. Second morning urine phos - 84 mg/dl and urine cr - 206.81 mg/dl. Tubular phosphate reabsorption was 91.9%. He had negative Holter, nuclear stress testing and MRI of the brain. No mutations were identified on genetic analysis of CACNA15, KCNJ2, RYR1, SCN4A. During his recent endocrine clinic visit, on physical exam: height- 5 feet 11 inches, weight- 366 lbs weight, BMI- 51.1 kg/m2, BP- 129/89 mm Hg, heart rate- 81 bpm and respiratory rate- 18 breaths/minute. He did have one palpable 1.5 cm left thyroid nodule. Otherwise, the exam was unremarkable. The patient was referred to pulmonology to be evaluated for potential diaphragmatic and lung causes of his tachypnea. He was also referred to psychiatry for evaluation of underlying anxiety. Since these episodes of hyperventilation associated electrolyte abnormalities lead to paralysis, he was started on calcitriol 0.25mcg daily along with 1250 mg potassium phosphate daily. Discussion: Hyperventilation can lead to a respiratory alkalosis and corresponding increase in intracellular pH. High intracellular pH can lead to increased phosphofructokinase activity and glycolysis, resulting in increased intracellular phosphate shift. Acute respiratory alkalosis can also result in ionized calcium binding to albumin. Moreover, acute respiratory alkalosis results in reduction in hydrogen ion in the intracellular fluid with extracellular potassium ion shift into cells leading to hypokalemia.These electrolyte abnormalities can cause myopathies, cardiac arrhythmias, respiratory failure, paralysis, seizures, coma and death. Physicians should be aware of the possibility of electrolyte imbalance due to hyperventilation to prevent the development of life threatening complications. Presentation: 6/1/2024

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Journal of the Endocrine Society
Published
2024-10-01
DOI
https://doi.org/10.1210/jendso/bvae163.434
Primary Topic
Electrolyte and hormonal disorders
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article
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article

7298 Hyperventilation Associated Hypophosphatemia, Hypocalcemia, Hypokalemia And Paralysis

Sadia Afreen, Nasreen Afreen
Journal of the Endocrine Society
Electrolyte and hormonal disorders
article

7298 Hyperventilation Associated Hypophosphatemia, Hypocalcemia, Hypokalemia And Paralysis

Sadia Afreen, Nasreen Afreen
article en

Abstract

Abstract Disclosure: S. Afreen: Research Investigator; Self; Tandem Diabetes Care, Yes. N. Afreen: None. Introduction: Hyperventilation is over-breathing in excess of the metabolic needs of the body, which can result in respiratory alkalosis and a wide range of electrolyte abnormalities. Case: A 38 year old male with a past history of hypertension, OSA and cholecystectomy reported having episodes of palpitations, tachypnea with respiratory rate as high as 80 breaths/ minute, associated with facial numbness and tingling, tetany, progressing to paralysis of his extremities. These episodes started 7 years ago but gradually became more frequent. He denied anxiety or stressors prior to these episodes. The episodes almost always result in emergency room visits. During one of these episodes he was found to have the following labs: ionized calcium-1 mmol/l, serum phosphorus- 0.8 mg/dl, serum potassium- 2.7 mmol/l, 1.25(OH)2D- 44pg/ml, alkaline phosphatase- 60 IU/l, glucose- 94 mg/dl and GFR- 90 ml/min/1.73m2. VBG during this episode: pH - 7.59, PCO2- 23 mm Hg, and bicarbonate - 22 mmol/l. Of note, the electrolytes are normal in between the episodes. Thyroid labs are normal. Off of phosphate supplementation for 3 days, in between episodes, his serum phos- 4.2mg/dl, cr - 0.84 mg/dl. Second morning urine phos - 84 mg/dl and urine cr - 206.81 mg/dl. Tubular phosphate reabsorption was 91.9%. He had negative Holter, nuclear stress testing and MRI of the brain. No mutations were identified on genetic analysis of CACNA15, KCNJ2, RYR1, SCN4A. During his recent endocrine clinic visit, on physical exam: height- 5 feet 11 inches, weight- 366 lbs weight, BMI- 51.1 kg/m2, BP- 129/89 mm Hg, heart rate- 81 bpm and respiratory rate- 18 breaths/minute. He did have one palpable 1.5 cm left thyroid nodule. Otherwise, the exam was unremarkable. The patient was referred to pulmonology to be evaluated for potential diaphragmatic and lung causes of his tachypnea. He was also referred to psychiatry for evaluation of underlying anxiety. Since these episodes of hyperventilation associated electrolyte abnormalities lead to paralysis, he was started on calcitriol 0.25mcg daily along with 1250 mg potassium phosphate daily. Discussion: Hyperventilation can lead to a respiratory alkalosis and corresponding increase in intracellular pH. High intracellular pH can lead to increased phosphofructokinase activity and glycolysis, resulting in increased intracellular phosphate shift. Acute respiratory alkalosis can also result in ionized calcium binding to albumin. Moreover, acute respiratory alkalosis results in reduction in hydrogen ion in the intracellular fluid with extracellular potassium ion shift into cells leading to hypokalemia.These electrolyte abnormalities can cause myopathies, cardiac arrhythmias, respiratory failure, paralysis, seizures, coma and death. Physicians should be aware of the possibility of electrolyte imbalance due to hyperventilation to prevent the development of life threatening complications. Presentation: 6/1/2024

Journal of the Endocrine SocietyVol. 8(Supplement_1)
University of Virginia (US), All India Institute of Medical Sciences (IN)
Good health and well-being
Openalex Percentile: Top 68%
Electrolyte and hormonal disorders
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