Research Mentor Name

M Safwan Badr

Research Mentor Email Address

sbadr@med.wayne.edu

Institution / Department

Internal Medicine

Document Type

Research Abstract

Research Type

clinicalresearch

Level of Research

no

Abstract

Central sleep apnea (CSA) is characterized by recurrent cycles of apnea/hypopnea alternating with hyperpnea. Brief arousals following apnea/hypopnea are postulated to perpetuate CSA via hypocapnia below the apneic threshold.

We hypothesized that apnea or hypopnea would follow hyperventilation due to induced-respiratory arousals. Participants diagnosed with mild to severe sleep-disordered breathing (AHI: 10-64 events per hour) were enrolled. We studied 5 patients with CSA who were otherwise healthy (4 male, 1 female, age: 62-72 years, BMI: 25.6-37.2 kg/m2) During overnight polysomnography (PSG), participants were initially stabilized with PAP therapy set to the pressure level required to maintain airway patency (holding pressure). We used PAP withdrawal for three breaths to induce upper airway obstruction in patients receiving optimal PAP therapy- with stable sleep, respiration, and oxygenation.

Induced respiratory arousal was associated with increased minute ventilation (VE) from 8.1 L/min +/- 5.0 L/min/- to 19.5 L/min +/- 5.9 L/min (p<0.05). Post-arousal ventilation also showed an increase in VE at 13.9 L/min +/- 4.6 L/min (p<0.05). Nadir ventilation was 94.6% of baseline.

Induced respiratory arousal resulted in a brief hyperpnea and a return to baseline respiration, but no apnea or hypopnea occurred.

Possible explanations include: a) short duration of hyperventilation is insufficient to induce sufficient medullary hypocapnia, b) recurrent events following CSA may be due to an additive effect of hypoxia and arousals, and c) the lack of post-arousal hypopnea may explain the lack effect of suppressing arousals on CSA severity.

Disciplines

Medicine and Health Sciences

Download

Share

COinS