
John, a 71-year-old university professor, came to the Long Beach Memorial Medical Center in November 2005. Relevant history included a long-term history of atrial fibrillation, presumably from rheumatic heart disease. He had chronic sinus symptoms with daily secretions and nasal blockage symptoms requiring nasal lavage. He also had hypertension, hyperlipidemia, benign prostate hyperplasia (BPH), and rare mild episodes of asthma. Recently he’s been found to have some mild left ventricular dysfunction and coronary artery disease. He is recently status-post percutaneous coronary angioplasty (PTCA) with stent placement.
John was referred for a split-night sleep study in January 2003. The AHI with bilevel was 61/hr, with centrals outnumbering obstructive events by 35/26. Multiple treatments failed to stabilize John’s sleep-disordered breathing John was largely unaffected by either continuous positive airway pressure (CPAP) or bilevel therapy during the second half of night, with an AHI of 62/hr and centrals outnumbering obstructive events by 54/8. We recommended repeat titration with oxygen entrainment. Total sleep AHI was 47/hr, with centrals outnumbering obstructive events by 35/12. Simple CPAP seemed to do a better job at obliterating obstructive events (which decreased substantially), while bilevel nearly obliterated central events (with a concomitant increase in obstructive events). Neither treatment sufficiently stabilized John’s sleepdisorderedbreathing.
John used CPAP at home for about six months, then abandoned it. In early 2004, he underwent extensive upper airway surgery (UPPP and sinus surgery) at another facility. In late 2005, John returned to his ENT who ordered a split-night sleep study. Post-operative study results were similar to our pre-operative studies. We decided to do a baseline study with nasal O2 (we had done O2 plus CPAP/bilevel in the past, but never O2 alone) to determine whether the central component could be reduced. Central apnea index dropped to < 1/hr. However, obstructive events persisted at about 19/hr. We were encouraged with this progress. John was initiated on nocturnal O2 at home, and although he did have some clinical benefit, we wanted to try to do better. We then combined CPAP (between pressures of 4–9 cm H2O) with O2 entrainment (flow rates between 2–6 L/min). Surprisingly, this produced an increase in the AHI from about 19 to about 40/hr. Central events returned. Moreover, there were more obstructive events (26/hr) than there had been with O2 alone (19/hr). While these numbers may not be statistically different, they are interesting.
Now, we had a compelling reason to proceed to VPAP Adapt SV, a new servo-ventilator available for the treatment of central sleep apnea, complex sleep apnea, mixed apnea and periodic breathing. During a VPAP Adapt SV titration with default pressure settings at 8/5 cm H2O, John experienced an AHI of 3/hr with 0/hr central events. After all this time, effort and expense, the positive response to VPAP Adapt SV is quite gratifying.
Stephen E. Brown, MD
Medical Director
MemorialCare Sleep Disorders Center
Long Beach Memorial Medical Center