Reversal of Neuromuscular Blockade and Perioperative Arrhythmias

Influence of the Neuromuscular Blockade and Its Reversal on Perioperative Arrhythmias

Patients scheduled for elective abdominopelvic laparoscopic surgery under general anesthesia were included. Rocuronium was used for the neuromuscular blockade (NMB) and the level of NMB was monitored with train-of-four (TOF) measurements. The participants from whom informed consent had been received were allocated to two groups according to the agent used for reversal of NMB, sugammadex, or neostigmine. The ECG recordings of the subjects were followed with a rhythm Holter device throughout the procedure until the postoperative 12th hour. Additionally, preoperative and immediate postoperative 12-lead ECGs were evaluated for corrected QT calculations and QT dispersion. Proarrhythmogenicity was assessed with QT related measurements. The documented arrhythmic events on the Holter monitoring were designated as clinical end-points.

Eighty consecutive patients, to whom an elective abdominopelvic surgery under general anesthesia was planned, were included in the study. Participants were allocated to two groups considering the agent to be used for the reversal of neuromuscular blockade by closed-envelope randomization. Neostigmine was used for this purpose in Group N, while sugammadex was used in Group S. Demographic features including hypertension, diabetes mellitus, presence of coronary artery disease, heart failure, and previous arrhythmia were noted. Body mass index was calculated with the Du Bois method. In the operation room, heart rate, blood pressure, body temperature, arterial oxygen saturation, and TOF ratio were recorded. General anesthesia was induced with midazolam, fentanyl, and propofol; and maintained by remifentanil and sevoflurane. In Group N, 50 mcg/kg neostigmine and 20 mcg/kg atropine were used for NMB reversal. In Group S, reversal was achieved by the administration of sugammadex at a dose of 2 mg/kg. QT interval was measured in leads DII or V5 and adjusted to the heart rate by the Bazzett formula. QTc values at the baseline and postoperative ECGs were recorded and presented with milliseconds. An increase of over 60 ms in QTc interval or a postoperative measurement over 500 ms were assumed to be distinctly abnormal. QT dispersion was calculated by extracting the minimum QT length from the maximum QT length in 12-lead ECG. In rhythm holter monitoring, minimum and mean heart rates and specific arrhythmic events were recorded. In the heart rate variability analysis, the standard deviation of the interbeat intervals of normal sinus beats (SDNN) and the root mean square of successive differences between normal heartbeats (rMSSD) were calculated. The following events were designated as clinical end-points.

• Pause (no waves on ECG recording at least for 3 seconds)
• Significant bradycardia (sinus bradycardia persisted at least for 30 seconds with a rate below 50 beats/min)
• High-grade atrioventricular block (2nd-degree Mobitz Type II or 3rd degree)
• Supraventricular tachycardia (sudden onset tachycardia with narrow QRS complexes persisted over 30 seconds)
• Atrial flutter or fibrillation (sustained over 30 seconds)
• Frequent premature ventricular beats (≥30 beats/hour)
• Any ventricular tachycardia (wide QRS complexes)

Inclusion Criteria:

• Planned abdominopelvic surgery under general anesthesia
• ASA II-IV
• Willing to give consent

Exclusion Criteria:

• Significantly impaired left ventricular systolic function (ejection fraction < 40%)
• Significant ongoing arrhythmia (sinus bradycardia with a heart rate below 40 beats/min, Mobitz Type II or 3rd-grade atrioventricular block, persistent or permanent atrial flutter or fibrillation, bigeminal or trigeminal ventricular premature beats, documented ventricular tachycardia)
• Severely reduced renal function (glomerular filtration rate < 30 ml/min/1.73 m2)
• Severe respiratory diseases, neuromuscular disorders, and known allergy to anesthetic agents or adjuvants
• Pregnancy and breastfeeding
• Observing the typical signs of a channelopathy (short QT syndrome, long QT syndrome, Brugada syndrome, etc.) and history of recent medical therapy with agents exhibiting a high probability of QT prolongation