Mu S, Howard ME, Hannan L. Autocycling during noninvasive positive pressure ventilation producing a prolonged severe apnea and syncope, further insights. J Clin Sleep Med. 2019;15(9):1379.
We thank Dr Karim and Professor Esquinas for their interest in our case report and we acknowledge that the alternative hypotheses they have proposed have face validity.1 It is certainly suspected clinically, although not confirmed objectively, that the patient described in this report has pulmonary hypertension and it is possible that this contributed to the prolongation of the oxygen desaturation observed during this event.2 We also agree that both response times and, potentially, accuracy (with reference to SaO2) may be better with ear probe pulse oximetry than finger probe. We believe that both the oximetry trace and transcutaneous carbon dioxide trace in combination with the reduction in spontaneous respiratory effort observed during the episode support our conclusion of a prolonged central apnea with associated hypoxaemia being the primary cause of syncope rather than this episode being explained by peripheral vasoconstriction in response to reduced cardiac output. In addition, the sequence of events that occurred on the night would also not support the alternative hypothesis. While we acknowledge that excessive ventilation from autocycling could have increased intrathoracic pressure thus compromising venous return and cardiac output,3,4 syncope occurred only on removal of ventilation rather than while it was applied, making it unlikely that this was the primary cause of syncope although it may have been a contributor to impaired oxygen delivery. This in combination with spontaneous improvement postevent and lack of postevent confusion or disorientation make the likelihood of primary cardiac or neurological explanations for this episode less likely.
All authors listed have seen and approved the manuscript. The authors report no conflicts of interest.