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Paced Beats Following Single Nonsensed Complexes in a “Codependent” Cardioverter Defibrillator and Bradycardia Pacing System: Potential for Ventricular Tachycardia Induction
Author(s) -
CALLANS DAVID J.,
HOOK BRUCE G.,
MARCHLINSKI FRANCIS E.
Publication year - 1991
Publication title -
pacing and clinical electrophysiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.686
H-Index - 101
eISSN - 1540-8159
pISSN - 0147-8389
DOI - 10.1111/j.1540-8159.1991.tb02868.x
Subject(s) - bradycardia , medicine , cardiology , ventricular tachycardia , cardioversion , tachycardia , sinus bradycardia , anesthesia , sinus rhythm , ventricular fibrillation , implantable cardioverter defibrillator , electrocardiography , heart rate , atrial fibrillation , blood pressure
Patients with implantable defibrillotors often require bradycardia pacemakers. Adverse interactions between separate defibrillator and bradycardia pacing units hove occurred. Including failure in detect ventricular fibrillation due to persistent bradycardia pacing during the arrhythmia. A device with combined bradycardia pacing and antitachycardia therapy capability may obviate adverse device interactions. We describe a previously unrecognized phenomenon that may occur in a combined device when the algorithms for sensing bradycardia and tachycardia are “codependent”; that is, the circuitry for brady and tachyarrhythmia detection relies on the same automatic gain sense amplifier. Three of 37 patients in whom the device was implanted had ventricular tachycardia initiated when bradycardia pacing stimuli were delivered by the device after probable nonsensed sinus beats. In each case, nonsensed beats appeared to have a markedly diminished amplitude, occurred after ventricular premature depolarizations that produced large amplitude electrograms, and had an electrogram morphology that matched that of sinus rhythm. In each case, the bradycardia pacing interval was at least 1,200 msec (range 1.200 to 1,714 msec). In two of the three patients, large amplitude ventricular premature depolarizations or nonsustained ventricular tachycardia caused an adjustment of the gain control that potentiated the failure to sense the subsequent lower amplitude signal. In all three patients, the induced arrhythmia was rapidly terminated by pacing or cardioversion. Decreasing the bradycardia pacing interval by 110–514 msec has prevented recurrence during short‐term follow‐up. Our findings suggest that codependent bradycardia and antitachycardia devices may have their own unique potential difficulties in adapting to rapid changes in rate and signal amplitude.