A patient suffering from congestive heart failure is at increased risk of cardiac arrhythmogenesis during sleep, particularly if experiencing central sleep apnea as a co-morbidity. Low intensity peripheral neurostimulation therapies that target imbalance of the autonomic nervous system have been shown to improve clinical outcomes. Thus, bi-directional autonomic regulation therapy is delivered to the cervical vagus nerve at an intensity that is insufficient to elicit pathological or acute physiological side effects and without the requirement of an enabling physiological feature or triggering physiological marker. The patient's physiology is monitored to identify periods of sleep. In one embodiment, upon sensing a condition indicative of tachyarrhythmia following a period of bradycardia, as naturally occurs during sleep, an enhanced “boost” dose of bi-directional neural stimulation intended to “break” the tachyarrhythmic condition is delivered. In a further embodiment, the boost dose is delivered upon sensing a physiological pattern indicative of Cheyne-Stokes respiration.