The patient was an obese 31-year-old woman (body mass index: 43.7 kg/m2). She was examined at our hospital laboratory 1-year before severe SAS, with 132 episodes of apnea/hour and significant hypoxia in polysomnography. A 24-h electrocardiogram (ECG) detected an inverted T wave, but no arrhythmias. She denied a history of hypertension, diabetes mellitus, or dyslipidemia. She had no habit of smoking or a family history of SAH or intracranial aneurysm. She presented with a worsening headache, but was alert and oriented, with no neurological deficit (World Federation of Neurosurgical Societies [WFNS] Grade 1). Head computed tomography revealed SAH, and computed tomography arteriogram showed a carotid-posterior communicating artery aneurysm with a bleb [Figure 1]. Continuous ECG monitoring on admission showed sinus tachycardia (mean: 120 beats/min) with frequent ventricular premature complexes [Figure 2]. However, a transient bradycardia (mean: 30 beats/min) was occasionally observed, especially during sleep apnea.
The patient agreed to endovascular treatment to prevent rebleeding, and coil embolization for the ruptured aneurysm was performed under general anesthesia on postbleed day (PBD 1) [Figure 3]. Worsening bradycardia and repetitive transient asystole lasting 3-12 s with hypotension occurred during postoperative care in the intensive care unit [Figure 4]. To treat the recurrent severe bradycardia, our cardiologists performed temporary pacemaker insertion (back-up VVI pacing at 40 beats/min) the day after surgery. The patient, who was postoperatively receiving mechanical ventilation under sedation to control her unstable circulatory status, was able to be weaned from ventilation and extubated on the same day. Temporary pacing was induced once per hour to prevent severe asystole until 2 days after insertion, regardless of the presence of sleep apnea. At PBD 5, the back-up pacing was decreased to once per 4 h, and bradycardia only occurred during sleep apnea. The following day, there were only three requirements for back-up pacing, and the bradycardia and ventricular premature complexes were rarely detected, even during sleep apnea. Thereafter, temporary pacing was not required. All types of arrhythmia decreased, and a final 3 s episode of sinus arrest was observed 7 days later. The 24-h ECG monitoring was continued until 21 days after admission. She did not experience any other complications such as cerebral vasospasm or hydrocephalus caused by SAH and was discharged home with no neurological deficit at 30 days after admission.