Probable Hypocalcemia Induced Ventricular Fibrillation and Torsades de Pointes following Blood Product Administration

Abstract

A 35-year-old male underwent open-heart surgery and required multiple blood product transfusions. Citrate, a preservative in blood products, caused serum ionized calcium chelation leading to hypocalcemia, a prolonged corrected QT (QTc) interval, and separate episodes of ventricular fibrillation and torsades de pointes (TdP). This case highlights an uncommon complication of blood product transfusion-induced hypocalcemia with precipitant arrhythmia.

Keywords: arrhythmia; blood transfusion; citrate; hypocalcemia; torsades de pointes; ventricular arrhythmias.

Figure 1. Admission electrocardiogram

Electrocardiogram (ECG) showing the prolonged corrected QT (QTc) interval of 516 ms, which was further corrected to 469 ms to account for his left bundle branch block [4]. The ventricular (vent.) rate was 70 beats per minute (BPM).

Figure 2. Telemetry strip showing torsades de pointes

The red arrow in the figure above shows the onset of torsades de pointes. Note the telemetry interpretation is ventricular fibrillation/ventricular tachycardia (VFIB/VTAC).

Figure 3. Electrocardiogram obtained directly after the episode of torsades de pointes

Electrocardiogram (ECG) showing QTc of 562 ms when accounting for his wide QRS rhythm [4]. Bifid T-waves in leads II, III, V3-V5 are present (blue arrows), which is a characteristic of an acquired prolonged corrected QT (QTc) interval. The ventricular (vent.) rate was 72 beats per minute (BPM) and the blood pressure (BP) was 110/70.

Figure 4. Electrocardiogram prior to discharge

Electrocardiogram (ECG) with a left bundle branch block and corrected QT (QTc) interval of 401 ms when accounting for the wide QRS rhythm [4]. The bifid T-waves have now resolved with improvement in the patient's serum ionized calcium and normalization of the QTc interval. The ventricular (vent.) rate was 71 beats per minute (BPM).

Figure 5. Normal ventricular action potential

This image shows a normal ventricular action potential with phase 2 consisting of the calcium influx and potassium efflux. The balance of potassium and calcium flow during phase 2 gives the classic plateau shape to the ventricular action potential. Below the ventricular action potential is the relative flow of calcium (Ca2+) and potassium (K+) corresponding to their flow rate throughout phase 2 and 3.

Figure 6. Abnormal ventricular action potential due to hypocalcemia induced QTc prolongation

This figure shows the prolonged phase 2 and 3 of the ventricular action potential due to hypocalcemia. The lower half of this figure details the relative flow rates of calcium (Ca2+) and potassium (K+) through the cardiac membrane. When there is less free ionized calcium in systemic circulation, the rate of influx of calcium through the cardiac membrane and into the cardiac myocytes occurs at a slower rate. The closure of the cardiac myocyte calcium channels is thought to be regulated by total intracellular calcium concentration. The slower rate of calcium influx causes the calcium channels to be open for a longer period of time causing a prolongation of ventricular repolarization and subsequently a prolongation of the QTc interval. The red bump in the figure above indicates an early afterdepolarization occurring towards the end of phase 2. The propagation of an early afterdepolarization prior to the ventricular action potential reaching its baseline resting membrane potential is thought to be one of the ways in which an individual with a prolonged QTc could trigger an episode of torsades de pointes [7-8].