Abstracts

Rationale: Ictal asystole occurs in a small percentage of epilepsy patients and is thought to possibly play a role in SUDEP. Pacemaker implantation has been performed to prevent the occurrence of malignant bradyarrhythmia in those cases diagnosed with ictal asystole. Prolonged EKG monitoring has been recommended in cases of unexplained epilepsy to determine if a cardiac cause may be found. The reverse case for using EEG monitoring to diagnose idiopathic cardiac arrhythmias seems limited to neonatal cases where epilepsy is highly suspected. We report a case of recurrent asystole in an intensive care patient treated with pacemaker prior to seizures being diagnosed. Methods: A 59 year old female with peritoneal carcinomatosis with no history of seizures was admitted for intraabdominal chemotherapy. Hospital course was complicated by critical illness of sepsis, renal failure, respiratory failure, and asystolic pauses of 5 to 10 seconds duration occurring several times per day. Neurology was consulted for intermittent left sided hemiplegia, spells of altered mental status and asymmetric pupils. Her spells were characterized by bilateral arm raising and tachypnea, followed by bradycardia. Due to lack of definitive diagnosis,VEEG monitoring was instituted. Results: VEEG was performed for 2 days. During this time period, 15 electrographic seizures were identified. Clinically, the events were preceded by tachypnea followed by low amplitude head and neck clonic activity. Prior to the seizure the patient averaged a heart rate of 85 beats per minute. Within 10 seconds of EEG seizure onset, the EKG showed a slowing of the heart rate to 60 beats per minute prior to programmed pacemaker activation to control heart rate. After electrographic seizure cessation, the intrinsic heart rate returns to normal sinus rhythm and a rate of 85-100. EEG demonstrated left temporal spikes and focal slow activity as ictal pattern. Pacemaker activation did not appear to affect the slowing on EEG of which hypoperfusion may be a component in addition to ictal activity. Treatment of seizures with antiepileptic medication resulted in no further episodes of asystole, bradycardia or pacemaker activation. Conclusions: Unexplained asystole may be due to undiagnosed seizures and treated inadvertently or empirically with pacemakers. Treatment with antiepileptic drugs may be sufficient in these cases. This case further highlights the important cerebral influences on cardiac rhythm. We observed the occurrence of seizure induced aystole in critically ill patients which has usually been reported in epilepsy patients during VEEG. Prospective studies in ICU patients may help to better explain the pathophysiology of unexplained cardiac dysfunction.