Hypoventilation

About: Hypoventilation is a research topic. Over the lifetime, 1772 publications have been published within this topic receiving 40799 citations. The topic is also known as: respiratory depression.

Neural Respiratory Drive and Ventilation in Patients with Chronic Obstructive Pulmonary Disease during Sleep

Abstract: To the Editor: Patients with chronic obstructive pulmonary disease (COPD) experience sleep-related hypoventilation (1, 2) However, there is controversy as to whether this occurs due to an increase in upper airway resistance or a reduction in neural respiratory drive Elevated neural respiratory drive in wakefulness is well documented in COPD (3) O’Donoghue and coworkers (4) reported in patients with COPD that a sleep-related hypoventilation was due to increased upper airway resistance, and Ballard and coworkers (5) reported an increase in upper airway resistance moving from wakefulness to sleep, although upper airway resistance was not consistently greater during sleep (see Figure 3 of their article [5]) Moreover, in healthy young adults, a poor correlation was observed between changes in ventilation and upper airway resistance (6) Morrell and coworkers (7) addressed the question directly in tracheotomized subjects, confirming hypoventilation during sleep, thus excluding an obligate contribution from upper airway resistance To further address the question, we performed diaphragm electromyography (EMGdi) using a multipair esophageal electrode as an index of neural respiratory drive (8–11) Some of the data have been previously reported in abstract form (12) A total of 17 stable patients with moderate to very severe COPD and 14 age-matched normal subjects participated All subjects were free from obstructive sleep apnea (OSA; apnea–hypopnea index < 50 events/h) and snoring confirmed by prior overnight polysomnography, and were free from clinically significant coexisting diseases, including neuromuscular disorders The study was approved by the Ethics Committee of the Chinese State Key Laboratory of Respiratory Disease, and all patients gave their informed consent to participate A multipair esophageal electrode catheter (Yinghui Medical Technology Co, Ltd, Guangzhou, China) was used as previously described (8) to record the EMGdi during overnight polysomnography (9–11) Airflow was recorded with a pneumotachograph connected to a full facemask Maximal EMGdi was recorded from maximal voluntary inspiratory maneuvers Polysomnography was manually analyzed based on standard criteria (13) The root mean square (RMS) of the EMGdi (RMSEMGdi) was calculated by computer with a time constant of 100 milliseconds Efficacy of neural respiratory drive was defined as the ratio of minute ventilation to peak RMSEMGdi of each breath Data were selected during stable breathing without respiratory events Data collected for 10 minutes before sleep and for at least 15 minutes during non–rapid eye movement (NREM) and REM in the supine position were selected for analysis Two-way ANOVA was used to test differences between wakefulness, NREM, and REM sleep; data are presented as means (±SD), and statistical significance was determined as a P value of less than 005 Some subjects could not tolerate the full facemask, and satisfactory measurements were therefore obtained in 10 male patients with COPD (age, 593 ± 115 yr; body mass index, 208 ± 31 kg/m2; FEV1, 342 ± 158% predicted; FEV1/FVC, 378 ± 116%; oxygen saturation <90%, 20 ± 40% of total sleep time) and 10 control subjects (nine males and one female, age, 581 ± 90 yr; body mass index, 228 ± 28 kg/m2; FEV1 978 ± 95% predicted) The maximal RMSEMGdi measured from patients with COPD was similar to control subjects (1807 ± 920 μV vs 1617 ± 536 μV) RMSEMGdi, as a percent maximal, in patients with COPD was significantly higher than that in normal subjects during wakefulness, NREM, and REM (Table 1) Compared with wakefulness, the RMSEMGdi decreased by 31 (±12)% in NREM, and further decreased by 49 (±12)% in REM sleep in patients with COPD Similarly, ventilation decreased by 30 (±14)% in NREM and 44 (±11)% in REM As shown in Table 1, the reduction in ventilation was principally mediated by tidal volume The reductions in the RMSEMGdi and ventilation were of smaller magnitude in normal subjects The efficacy of neural respiratory drive in normal subjects was significantly higher than that in patients with COPD during both wakefulness and sleep However, sleep did not change the efficacy of neural respiratory drive in either patients with COPD or normal subjects (Table 1 and Figure 1) Table 1 The Root Mean Square of the Diaphragm Electromyography and Ventilation during Wakefulness and Sleep and Their Change Compared with Wakefulness Figure 1 Polysomnography including five-channel diaphragm electromyography (EMGdi; 1–5) from a multipair esophageal electrode, airflow from pneumotachograph, end-tidal CO2, electroencephalogram (EEG; C3A2 and C4A1), and left and right electrooculograms This is the first study to simultaneously accurately record ventilation with a pneumotachograph connected to a full facemask and EMGdi, during wakefulness, NREM, and REM sleep, in patients with COPD without coexisting OSA The efficacy of neural respiratory drive reflects upper airway resistance if lung mechanics and lower airway resistance remain the same Because this is considered to be the case (4, 5), we speculate that the unchanged efficacy of neural respiratory drive between wakefulness and sleep argues against a substantial increase in upper airway resistance during sleep in either nonobese patients with COPD or normal subjects This result is consistent with the work of Meurice and coworkers (14), who reported that upper airway resistance changed little in some patients with COPD during sleep Although O’Donoghue and colleagues (4) concluded that sleep-related hypoventilation in patients with COPD was because of a threefold increase in upper airway resistance, the subjects they studied may have had mild OSA, because an apnea–hypopnea index up to 10 events/h was permitted Our results are consistent with the results reported by Morrell and coworkers (7), who showed that the development of sleep-related hypoventilation is independent of upper airway resistance, because the reduction of ventilation from wakefulness to NREM sleep in subjects who were breathing through the upper airway was similar to that in laryngectomized subjects who were breathing through a tracheal stoma Our conclusions are also consistent with other data supporting the case that reduction of neural respiratory drive is important in sleep-related hypoventilation For example, when continuous positive airway pressure is applied in patients with COPD to eliminate upper airway resistance (1), or to normalize upper airway resistance to waking levels in normal subjects (15), sleep-related hypoventilation is still evident Naturally, our study has some limitations We had a relatively small sample size, and all patients were from one ethnic group and were not in respiratory failure, which could modify pharyngeal behavior (15) Our data are only representative of those who could sleep while instrumented Thus, our findings should not be extended uncritically to all patients with COPD However, in contrast to the previous hypothesis that hypoventilation is principally due to upper airway resistance, our study suggests that sleep-associated hypoventilation in patients with COPD is mainly related to reduction of neural respiratory drive This observation suggests that noninvasive positive-pressure ventilation is a more logical approach than continuous positive airway pressure to the treatment of nocturnal hypoventilation in COPD

The malignant obesity hypoventilation syndrome (MOHS).

Abstract: We have coined the term 'malignant obesity hypoventilation syndrome' (MOHS) to describe a severe multisystem disease due to the systemic effects of obesity. Patients with this syndrome have severe obesity-related hypoventilation together with systemic hypertension, diabetes and the metabolic syndrome, left ventricular hypertrophy with diastolic dysfunction, pulmonary hypertension and hepatic dysfunction. This syndrome is largely unrecognized as physicians do not make the association between the patients' multiple medical problems and obesity. Because of the delayed diagnosis and progressive morbidities of this condition, all patients with a body mass index of more than 40 kg m(-2) should be screened for MOHS. The management of patients with MOHS includes short-term measures to improve the patients' medical condition and long-term measures to achieve enduring weight loss. Bariatric surgery reverses or improves the multiple metabolic and organ dysfunctions associated with MOHS and should be strongly considered in these patients.

Respiratory Care Received by Individuals With Duchenne Muscular Dystrophy From 2000 to 2011.

Abstract: BACKGROUND: Duchenne muscular dystrophy (DMD) causes progressive respiratory muscle weakness and decline in function, which can go undetected without monitoring. DMD respiratory care guidelines recommend scheduled respiratory assessments and use of respiratory assist devices. To determine the extent of adherence to these guidelines, we evaluated respiratory assessments and interventions among males with DMD in the Muscular Dystrophy Surveillance, Tracking, and Research Network (MD STARnet) from 2000 to 2011. METHODS: MD STARnet is a population-based surveillance system that identifies all individuals born during or after 1982 residing in Arizona, Colorado, Georgia, Hawaii, Iowa, and western New York with Duchenne or Becker muscular dystrophy. We analyzed MD STARnet respiratory care data for non-ambulatory adolescent males (12–17 y old) and men (≥18 y old) with DMD, assessing whether: (1) pulmonary function was measured twice yearly; (2) awake and asleep hypoventilation testing was performed at least yearly; (3) home mechanical insufflation-exsufflation, noninvasive ventilation, and tracheostomy/ventilators were prescribed; and (4) pulmonologists provided evaluations. RESULTS: During 2000–2010, no more than 50% of both adolescents and men had their pulmonary function monitored twice yearly in any of the years; 67% or fewer were assessed for awake and sleep hypoventilation yearly. Although the use of mechanical insufflation-exsufflation and noninvasive ventilation is probably increasing, prior use of these devices did not prevent all tracheostomies, and at least 18 of 29 tracheostomies were performed due to acute respiratory illnesses. Fewer than 32% of adolescents and men had pulmonologist evaluations in 2010–2011. CONCLUSIONS: Since the 2004 publication of American Thoracic Society guidelines, there have been few changes in pulmonary clinical practice. Frequencies of respiratory assessments and assist device use among males with DMD were lower than recommended in clinical guidelines. Collaboration of respiratory therapists and pulmonologists with clinicians caring for individuals with DMD should be encouraged to ensure access to the full spectrum of in-patient and out-patient pulmonary interventions.

Acid-Base Abnormalities Associated with Cocaine Toxicity in Emergency Department Patients

Abstract: There is little information on the prevalence and clinical presentation of acid-base abnormalities associated with cocaine toxicity. To address these issues, arterial blood gas results were evaluated in 156 cocaine-associated emergency department patient visits. Arterial blood gas results were obtained as part of the patient's clinical assessment. The majority of patients (52%) had a normal pH (7.35 to 7.45). Thirty-three percent of patients were acidotic, with a pH between 6.4 and 7.35. In 33 patients the acidosis was metabolic, with a HCO3- of 14 +/- 6 mmol/L. The acidosis was primarily respiratory in 18 patients, with evidence of hypoventilation. Hypoventilation was generally secondary to chest trauma or decreased mental status. Alkalosis (pH > 7.45) was observed in 15% of patients, and was usually respiratory, as evidenced by tachypnea and a low PCO2. These results indicate that metabolic and respiratory acid-base abnormalities are common during cocaine toxicity. Acidosis and alkalosis were associated with numerous patient presentations, including chest pain, shortness of breath, decreased mental status, trauma, and seizures. Acid-base abnormalities do not appear to be associated with a specific route of cocaine self-administration. Patients with a history of potential cocaine toxicity should be evaluated for acid-base abnormalities.

Hypocretin-1 deficiency in a girl with ROHHAD syndrome.

Abstract: Rapid-onset obesity with hypothalamic dysfunction, hypoventilation, and autonomic dysregulation (ROHHAD) is a rare and complex pediatric syndrome, essentially caused by dysfunction of 3 vital systems regulating endocrine, respiratory, and autonomic nervous system functioning. The clinical spectrum of ROHHAD is broad, but sleep/wake disorders have received relatively little attention so far, although the central hypothalamic dysfunction would make the occurrence of sleep symptoms likely. In this case report, we expand the phenotype of ROHHAD with a number of striking sleep symptoms that together can be classified as a secondary form of narcolepsy. We present a 7-year-old girl with ROHHAD who displayed the classic features of narcolepsy with cataplexy: excessive daytime sleepiness with daytime naps, visual hallucinations, and partial cataplexy reflected in intermittent loss of facial muscle tone. Nocturnal polysomnography revealed sleep fragmentation and a sleep-onset REM period characteristic for narcolepsy. The diagnosis was confirmed by showing an absence of hypocretin-1 in the cerebrospinal fluid. We discuss potential pathophysiological implications as well as symptomatic treatment options.