Arrhythmogenic potential develops rapidly at graft reperfusion before the start of hypotension during living-donor liver transplantation

Detailed profiles of acute hypothermia and electrocardiographic (ECG) manifestations of arrhythmogenicity were examined to analyze acute hypothermia and ventricular arrhythmogenic potential immediately after portal vein unclamping (PVU) in living-donor liver transplantation (LT). We retrospectively analyzed electronically archived medical records (n = 148) of beat-to-beat ECG, arterial pressure waveforms, and blood temperature (BT) from Swan-Ganz catheters in patients undergoing living-donor LT. The ECG data analyzed were selected from the start of BT drop to the initiation of systolic hypotension after PVU. On reperfusion, acute hypothermia of < 34℃, < 33℃ and < 32℃ developed in 75.0%, 37.2% and 11.5% of patients, respectively. BT decreased from 35.0℃ ± 0.8℃ to 33.3℃ ± 1.0℃ (range 35.8℃-30.5℃). The median time to nadir of BT was 10 s after PVU. Difference in BT (ΔBT) was weakly correlated with graft-recipient weight ratio (GRWR; r = 0.22, P = 0.008). Compared to baseline, arrhythmogenicity indices such as corrected QT (QTc), Tp-e (T wave peak to end) interval, and Tp-e/QTc ratio were prolonged (P < 0.001 each). ST height decreased and T amplitude increased (P < 0.001 each). However, no correlation was found between ΔBT and arrhythmogenic indices. In living-donor LT, regardless of extent of BT drop, ventricular arrhythmogenic potential developed immediately after PVU prior to occurrence of systolic hypotension.