Patient-ventilator synchrony has been the focus of attention in the field of mechanical ventilation for quite some time now. Toward that end, the modern ventilators are equipped with very sensitive pneumatic triggering mechanisms, which allow for minimal wasting of patient effort. The increasingly sensitive pneumatic triggers have the potential to cause autotriggering, where stimuli other than neural signals (eg, cardiac oscillations) can trigger the mechanical breath. Although autotriggering has been well documented in brain-dead patients, its existence is difficult to prove in patients who have the ability to trigger breath through neural diaphragmatic activity. The only way to be sure that the triggered breath is indeed from the neural diaphragmatic activity rather than a spurious change in pressure or flow is to monitor neural signals during triggered mechanical breaths. Autotriggering can have deleterious effects including diaphragmatic atrophy, increased duration on the mechanical ventilator, and increased stay in the intensive care unit. Esophageal catheters, with the ability to measure phrenic nerve and diaphragmatic activity, allow for the detection of the extent of autotriggering. This article demonstrates the hitherto unknown but potentially common occurrence of autotriggering through nonneural stimuli and their amelioration by making the pneumatic autotriggering less sensitive. The full extent of the phenomenon and its deleterious effects remain to be explored in larger patient populations.