Abstract: SA-PO0514
Severe Hypocalcemia Causing Bradycardia Following Red Blood Cell Transfusion
Session Information
- Fluid, Electrolyte, and Acid-Base Disorders: Clinical - 3
November 08, 2025 | Location: Exhibit Hall, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Fluid, Electrolytes, and Acid-Base Disorders
- 1102 Fluid, Electrolyte, and Acid-Base Disorders: Clinical
Authors
- Salvatierra, Juan, Medical University of South Carolina, Charleston, South Carolina, United States
- Carpin, Daniel, Medical University of South Carolina, Charleston, South Carolina, United States
- Rao, Rohini, Medical University of South Carolina, Charleston, South Carolina, United States
- McMahon, Blaithin A., Medical University of South Carolina, Charleston, South Carolina, United States
Introduction
Cardiovascular manifestations of acute hypocalcemia include hypotension and reversible myocardial dysfunction. There is limited literature on bradycardia as a feature of hypocalcemia. Citrate-phosphate-dextrose (CPD) is used as an anticoagulant-preservative of red cell units and has been associated with hypocalcemia.
Case Description
A 48-year-old man with hypertension and end-stage renal disease due to focal segmental glomerulosclerosis who received a kidney transplant 21 years before was admitted to the hospital due to elevated creatinine. He had not seen a nephrologist in the last 2 years. He stated he felt well and was compliant with cyclosporine, prednisone and amlodipine.
Serum creatinine was 9.7, increased from baseline 4.3 mg/dL. Physical exam was benign except for 2+ edema below the knees, heart rate (HR) was 60. Other laboratory analyses were significant for calcium 6.2 mg/dL with albumin 3 g/dL and hemoglobin 6.6 g/dL. In anticipation of transplant kidney biopsy, transfusion of 1 red cell unit was initiated. He became progressively bradycardic with nadir HR 38, though normotensive and asymptomatic. Point-of-care ionized calcium was 0.89 mEq/L. Calcium gluconate 2 g IV was given with improvement in HR. Amlodipine was discontinued. A second unit was transfused without issue; however, bradycardia recurred during a third RBC unit the next day.
Discussion
We report a case with a clear and repeated temporal relation between blood transfusion, worsening hypocalcemia (due to citrate in CPD) and bradycardia. Dihydropyridine calcium channel blockers such as amlodipine may cause reflex tachycardia rather than bradycardia. This is not a case of BRASH syndrome as our patient was not on AV blocking agents nor had hypotension or hyperkalemia. Renal failure was due to graft loss from severe interstitial fibrosis noted on the aglomerular biopsy sample. Animal models suggest high extracellular potassium in old (40-50 days) red cells may induce bradycardia. All units given to our patient were before 30 days from donation. Thus, we conclude that bradycardia may be a manifestation of hypocalcemia.