In some conditions continuous positive airway pressure (CPAP) or bilevel positive airway pressure (BIPAP) therapy alone fails to provide satisfactory oxygenation. In these situations oxygen (O2) is often being added to CPAP/BIPAP mask or hose. Central sleep apnea and obstructive sleep apnea (OSA) are often present along with other chronic conditions, such as chronic obstructive pulmonary disease (COPD), congestive heart failure, pulmonary fibrosis, neuromuscular disorders, chronic narcotic use, or central hypoventilation syndrome. Any of these conditions may lead to the need for supplemental O2 administration during the titration process. Maximization of comfort, by delivering O2 directly via a nasal cannula through the mask, will provide better oxygenation and ultimately treat the patient with lower CPAP/BIPAP pressure.

To explore the effects of neural respiratory drive on ventilation in patients with chronic obstructive pulmonary disease (COPD) during sleep.Diaphragm electromyogram (EMG) from a multipair esophageal electrodes and airflow derived from pneumotachgraphy were recorded during overnight polysomnography in 13 patients with stable COPD recruited from outpatient clinic of First Affiliated Hospital of Guangzhou Medical College from May 2010 to May 2011. Changes in diaphragm EMG and ventilation during wakefulness and different sleep stages were observed.Diaphragm EMG decreased by 26% in non-rapid eye movement sleep (NREM) stage and 39% in rapid eye movement (REM) as compared with wakefulness. Coinciding with change in diaphragm EMG, ventilation (VE) (ml×min(-1)×kg(-1)) significantly decreased from wakefulness (156 ± 53) ml×min(-1)×kg(-1) to steady NREM stage (112 ± 35) ml×min(-1)×kg(-1) (P < 0.05) and further decreased from NREM stage to REM stage (95 ± 27) ml×min(-1)×kg(-1) (P < 0.05). Oxygen saturation also decreased significantly from 97.1% ± 1.8% in wakefulness to REM stage (94.0% ± 3.9%) (P < 0.01).Reduced neural respiratory drive contributes to nocturnal hypoventilation in COPD patients.

Introduction: Patients with the congenital central hypoventilation syndrome (CCHS) suffer from life-threatening hypoventilation when asleep, making them dependent on mechanical ventilation (MV) at night or during naps. State-of-art respiratory management consists of intermittent positive-pressure ventilation via a tracheotomy or mask. In some patients hypoventilation is permanent, in which case ventilatory support must be extended to the waking hours. Diaphragm pacing can prove useful in such situations. 
Methods and results: This report describes the case of a 26-year-old woman with CCHS in whom failure to achieve adequate MV led to life-threatening pulmonary hypertension (PH), with a systolic pulmonary artery pressure (PAP) of 80 mmHg and right ventricular hypertrophy, despite optimization of all possible measures and despite extensive therapeutic education efforts. Diaphragm pacing using laparoscopically implanted intradiaphragmatic phrenic nerve stimulation electrodes corrected alveolar hypoventilation and lastingly reversed PH (systolic PAP below 40 mmHg after 2 months, sustained after 2 years). Diaphragm pacing induced shoulder pain, however, involving the chronic use of analgesics. The pacing had to be stopped for tolerance reasons after two years, leading to PH worsening and the need for diurnal MV. 


Conclusions:

Diaphragm pacing appears likely effective to restore alveolar ventilation and reverse PH in adult CCHS patients.

Obstructive sleep apnea (OSA) is characterized by recurrent upper airway obstruction resulting in apneas, hypopneas, oxygen desaturation, and arousal from sleep. Obesity is one of the most significant risk factors for OSA. Although continuous positive airway pressure is considered the first choice of treatment of OSA, weight reduction is another important measure in obese OSA patients. Conversely, a couple of studies showed that OSA itself might lead to increase weight gain by the reduction in sleep and/or the daytime sleepiness. And obesity hypoventilation syndrome (OHS) is defined as chronic daytime hypercapnia in combination with obesity and OSA. OHS patients are more likely to suffer from congestive heart failure, pulmonary hypertension and have worse prognosis than obese eucapnic OSA patients.

Patients with chronic neuromuscular diseases such as spinal cord injury, amyotrophic lateral sclerosis, and muscular dystrophies experience respiratory complications that are cared for by the respiratory practitioner. An organized anatomical approach for evaluation and treatment is helpful to provide appropriate clinical care. Effective noninvasive strategies for management of hypoventilation, sleep-disordered breathing, and cough insufficiency are available for these patients.

ABSTRACT

.: Deep and slow breathing (DSB) is a central part of behavioral exercises used for acute and chronic pain management. Its mechanisms of action are incompletely understood.

OBJECTIVES

.: 1) To test the effects of breathing frequency on experimental pain perception in a dose dependent fashion. 2) To test the effects of breathing frequency on cardiorespiratory variables hypothesized to mediate DSB analgesia. 3) To determine the potential of the cardiorespiratory variables to mediate antinociceptive DSB effects by regression analysis.

DESIGN.

: Single-blind, randomized, crossover trial. SUBJECTS.: Twenty healthy participants.

INTERVENTIONS.

: Visually paced breathing at 0.14 Hz, 0.10 Hz, 0.06 Hz, and resting frequency. OUTCOME MEASURES.: Cardiorespiratory variables: RR-interval (= 60 seconds/heart rate), standard deviation of the RR-interval (SDRR), and respiratory CO2 . Experimental pain measures: heat pain thresholds, cold pain thresholds, pain intensity ratings, and pain unpleasantness ratings.

RESULTS.:

1) There was no effect of DSB frequency on experimental pain perception. 2) SDRR and respiratory CO2 were significantly modulated by DSB frequency, while RR-interval was not. 3) Baseline-to-DSB and session-to-session differences in RR-interval significantly predicted pain perception within participants: Prolonged RR-intervals predicted lower pain ratings, while shortened RR-intervals predicted higher pain ratings. SDRR and respiratory CO2 were not found to predict pain perception.

CONCLUSIONS.:

The present study could not confirm hypotheses that the antinociceptive effects of DSB are related to changes in breathing frequency, heart rate variability, or hypoventilation/hyperventilation when applied as a short-term intervention. It could confirm the notion that increased cardiac parasympathetic activity is associated with reduced pain perception.

Stair climbing is associated with dynamic pulmonary hyperinflation and the development of severe dyspnea in patients with chronic obstructive pulmonary disease (COPD). This study aimed to assess whether (i) continuous positive airway pressure (CPAP) applied during stair climbing prevents dynamic hyperinflation and thereby reduces exercise-induced dyspnea in oxygen-dependent COPD-patients, and (ii) the CPAP-device and oxygen tank can be carried in a hip belt. In a randomised cross-over design, oxygen-dependent COPD patients performed two stair-climbing tests (44 steps): with supplemental oxygen only, then with the addition of CPAP (7 mbar). The oxygen tank and CPAP-device were carried in a hip belt during both trials. Eighteen COPD patients were included in the study. Although all patients could tolerate stair climbing with oxygen alone, 4 patients were unable to perform stair climbing while using CPAP. Fourteen COPD patients (mean FEV1 36 ± 14% pred.) completed the trial and were analyzed. The mean flow rate of supplemental oxygen was 3 ± 2 l/min during stair climbing. Lung hyperinflation, deoxygenation, hypoventilation, blood lactate production, dyspnea and the time needed to manage stair climbing were not improved by the application of CPAP (all p > 0.05). However, in comparison to climbing with oxygen alone, limb discomfort was reduced when oxygen was supplemented with CPAP (p = 0.008). In conclusion, very severe COPD patients are able to carry supporting devices such as oxygen tanks or CPAP-devices in a hip belt during stair climbing. However, the application of CPAP in addition to supplemental oxygen during stair climbing prevents neither exercise-induced dynamic hyperinflation, nor dyspnea.

Obstructive sleep apnea (OSA) may occur in association with obesity-hypoventilation (Pickwickian) syndrome, a disorder of ventilatory control affecting individuals with morbid obesity. Through the pressor effects of chronic hypercapnia and hypoxemia, this syndrome may result in pulmonary hypertension, right heart failure, and massive peripheral edema. We present a case of severe scrotal edema in a 36-year-old male with OSA and obesity-hypoventilation syndrome. A tracheostomy was performed to relieve hypoxemia and led to dramatic improvement of scrotal edema. No scrotal surgery was necessary. Followup at two months showed complete resolution of scrotal edema, improvement in mental status, and normalization of arterial blood gas measurements. This case demonstrates that OSA and obesity-hypoventilation syndrome may present with massive scrotal edema. Furthermore, if OSA is recognized as the cause of right heart failure, and if the apnea is corrected, the resultant improvement in cardiac function may allow reversal of massive peripheral, including scrotal, edema.

A wide range of clinical consequences may be associated with obstructive sleep apnea (OSA) including systemic hypertension, cardiovascular disease, pulmonary hypertension, congestive heart failure, cerebrovascular disease, glucose intolerance, impotence, gastroesophageal reflux, and obesity, to name a few. Despite this, 82 % of men and 93 % of women with OSA remain undiagnosed. OSA affects many body systems, and induces major alterations in metabolic, autonomic, and cerebral functions. Typically, OSA is characterized by recurrent chronic intermittent hypoxia (CIH), hypercapnia, hypoventilation, sleep fragmentation, peripheral and central inflammation, cerebral hypoperfusion, and cerebral glucose hypometabolism. Upregulation of oxidative stress in OSA plays an important pathogenic role in the milieu of hypoxia-induced cerebral and cardiovascular dysfunctions. Strong evidence underscores that cerebral amyloidogenesis and tau phosphorylation-two cardinal features of Alzheimer's disease (AD), are triggered by hypoxia. Mice subjected to hypoxic conditions unambiguously demonstrated upregulation in cerebral amyloid plaque formation and tau phosphorylation, as well as memory deficit. Hypoxia triggers neuronal degeneration and axonal dysfunction in both cortex and brainstem. Consequently, neurocognitive impairment in apneic/hypoxic patients is attributable to a complex interplay between CIH and stimulation of several pathological trajectories. The framework presented here helps delineate the emergence and progression of cognitive decline, and may yield insight into AD neuropathogenesis. The global impact of CIH should provide a strong rationale for treating OSA and snoring clinically, in order to ameliorate neurocognitive impairment in aged/AD patients.

Currently, more than 2200 patients in the Netherlands receive chronic ventilatory support. In the majority of patients this leads to increased survival without any complications. Nevertheless, in case of ventilatory support via a mask, problems such as skin irritation, leakage and claustrophobia can occur. In case of tracheostomy, it can lead to increased pulmonary secretion. Diaphragm pacing with an external pacemaker might be an attractive alternative to prevent these symptoms as it can replace ventilatory support by mask or tracheostomy. Current indications are patients with spinal cord injury or with congenital central hypoventilation syndrome who are chronically respiratory insufficient. In our experience, patients can be completely or partially weaned from mechanical ventilation when using the diaphragm pacer. In the Netherlands, the technique is only performed at the University Medical Center Groningen.