Transmission of Oral Pressure Compromises Oronasal CPAP Efficacy in the Treatment of OSA.

BACKGROUND: An oronasal mask is frequently used to treat OSA. In contrast to nasal CPAP, the effectiveness of oronasal CPAP varies by unknown mechanisms. We hypothesized that oral breathing and pressure transmission through the mouth compromises oronasal CPAP efficacy. METHODS: Thirteen patients with OSA, well adapted to oronasal CPAP, were monitored by full polysomnography, pharyngeal pressure catheter, and nasoendoscope. Patients slept with low doses of midazolam, using an oronasal mask with sealed nasal and oral compartments. CPAP was titrated during administration by the oronasal and nasal routes, and was then reduced to induce stable flow limitation and abruptly switched to the alternate route. In addition, tape sealing the mouth was used to block pressure transmission to the oral cavity. RESULTS: Best titrated CPAP was significantly higher by the oronasal route rather than the nasal route (P = .005), and patients with > 25% oral breathing (n = 5) failed to achieve stable breathing during oronasal CPAP. During stable flow limitation, inspiratory peak flow was lower, driving pressure was higher, upper airway inspiratory resistance was higher, and retropalatal and retroglossal area were smaller by the oronasal rather than nasal route (P < .05 for all comparisons). Differences were observed even among patients with no oral flow and were abolished when tape sealing the mouth was used (n = 6). CONCLUSIONS: Oral breathing and transmission of positive pressure through the mouth compromise oronasal CPAP.

Impact of Acute Changes in CPAP Flow Route in Sleep Apnea Treatment.

BACKGROUND: CPAP is the gold standard treatment for OSA and was conceived to be applied through a nasal interface. This study was designed to determine the acute effects of changing the nasal CPAP route to oronasal and oral in upper airway patency during sleep in patients with OSA. We hypothesized that the oronasal route may compromise CPAP's effectiveness in treating OSA. METHODS: Eighteen patients (mean ± SD age, 44 ± 9 years; BMI, 33.8 ± 4.7 kg/m2; apnea-hypopnea index, 49.0 ± 39.1 events/hour) slept with a customized oronasal mask with nasal and oral sealed compartments connected to a multidirectional valve. Sleep was monitored by using full polysomnography and induced by low doses of midazolam. Nasal CPAP was titrated up to holding pressure. Flow route was acutely changed to the oronasal (n = 18) and oral route (n = 16) during sleep. Retroglossal area was continuously observed by using nasoendoscopy. RESULTS: Nasal CPAP (14.8 ± 4.1 cm H2O) was able to stabilize breathing in all patients. In contrast, CPAP delivered by the oronasal and oral routes promoted obstructive events in 12 (66.7%) and 14 (87.5%) patients, respectively. Compared with stable breathing during the nasal route, there was a significant and progressive reduction in the distance between the epiglottis and tongue base and the retroglossal area when CPAP was delivered by the oronasal and oral routes. CONCLUSIONS: CPAP delivered through the oronasal route may compromise CPAP's effectiveness in treating OSA.

Effects of different mechanical ventilation strategies on the mucociliary system.

OBJECTIVE: To evaluate the effects of different mechanical ventilation (MV) strategies on the mucociliary system. DESIGN AND SETTING: Experimental study. SUBJECTS: Twenty-seven male New Zealand rabbits. INTERVENTIONS: After anesthesia, animals were tracheotomized and ventilated with standard ventilation [tidal volume (Vt) 8 ml/kg, positive end expiratory pressure (PEEP) 5 cmH(2)O, flow 3 L/min, FiO(2) 0.4] for 30 min. Next, animals were randomized into three groups and ventilated for 3 h with low volume (LV): Vt 8 ml/kg, PEEP 5 cmH(2)O, flow 3 L/min (n = 6); high volume (HV): Vt 16 ml/kg, PEEP 5 cmH(2)O, flow 5 L/min (n = 7); or high pressure (HP): Ppeak 30 cmH(2)O, PEEP 12 cmH(2)O (n = 8). Six animals (controls) were ventilated for 10 min with standard ventilation. Vital signals, blood lactate, and respiratory system mechanics were verified. Tracheal tissue was collected before and after MV. MEASUREMENTS: Lung and tracheal tissue sections were stained to analyze inflammation and mucosubstances by the point-counting method. Electron microscopy verified tracheal cell ultrastructure. In situ tracheal ciliary beating frequency (CBF), determined using a videoscopic technique, and tracheal mucociliary transport (TMCT), assessed by stereoscopic microscope, were evaluated before and after MV. RESULTS: Respiratory compliance decreased in the HP group. The HV and HP groups showed higher lactate levels after MV. Macroscopy showed areas of atelectasis and congestion on HV and HP lungs. Lung inflammatory infiltrate increased in all ventilated groups. Compared to the control, ventilated animals also showed a reduction of total and acid mucus on tracheal epithelium. Under electron microscopy, injury was observed in the ciliated cells of the HP group. CBF decreased significantly after MV only in the HP group. TMCT did not change significantly in the ventilated groups. CONCLUSIONS: Different MV strategies induce not only distal lung alterations but also morphological and physiological tracheal alterations leading to mucociliary system dysfunction.