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Showing papers on "Hypoventilation published in 1999"


Journal ArticleDOI
TL;DR: The results suggest that leptin can prevent respiratory depression in obesity, but a deficiency in central nervous system leptin levels or activity may induce hypoventilation and the Pickwickian syndrome in some obese subjects.
Abstract: Human obesity leads to an increase in respiratory demands. As obesity becomes more pronounced some individuals are unable to compensate, leading to elevated arterial carbon dioxide levels (PaCO2), alveolar hypoventilation, and increased cardiorespiratory morbidity and mortality (Pickwickian syndrome). The mechanisms that link obesity and hypoventilation are unknown, but thought to involve depression of central respiratory control mechanisms. Here we report that obese C57BL/6J-Lepob mice, which lack circulating leptin, also exhibit respiratory depression and elevated PaCO2 (> 10 mm Hg; p < 0. 0001). A role for leptin in restoring ventilation in these obese, mutant mice was investigated. Three days of leptin infusion (30 microg/d) markedly increased minute ventilation (V E) across all sleep/wake states, but particularly during rapid eye movement (REM) sleep when respiration was otherwise profoundly depressed. The effect of leptin was independent of food intake, weight, and CO2 production, indicating a reversal of hypoventilation by stimulation of central respiratory control centers. Furthermore, leptin replacement in mutant mice increased CO2 chemosensitivity during non-rapid eye movement (NREM) (4.0 +/- 0.5 to 5.6 +/- 0.4 ml/min/%CO2; p < 0.01) and REM (-0.1 +/- 0.5 to 3.0 +/- 0.8 ml/min/%CO2; p < 0.01) sleep. We also demonstrate in wild-type mice that ventilation is appropriately compensated when obesity is diet-induced and endogenous leptin levels are raised more than tenfold. These results suggest that leptin can prevent respiratory depression in obesity, but a deficiency in central nervous system (CNS) leptin levels or activity may induce hypoventilation and the Pickwickian syndrome in some obese subjects. O'Donnell CP, Schaub CD, Haines AS, Berkowitz DE, Tankersley CG, Schwartz AR, Smith PL. Leptin prevents respiratory depression in obesity.

375 citations


Journal ArticleDOI
TL;DR: The data indicate that hypoventilation may be the major factor leading to hypoxia during sleep, and that reversal of hypovENTilation during sleep should be a major therapeutic strategy for these patients with respiratory failure.
Abstract: The mechanisms leading to hypoxemia during sleep in patients with respiratory failure remain poorly understood, with few studies providing a measure of minute ventilation (V I) during sleep The aim of this study was to measure ventilation during sleep in patients with nocturnal desaturation secondary to different respiratory diseases The 26 patients studied had diagnoses of chronic obstructive pulmonary disease (COPD) (n = 9), cystic fibrosis (CF) (n = 2), neuromusculoskeletal disease (n = 4), and obesity hypoventilation syndrome (OHS) (n = 11) Also reported are the results for seven normal subjects and seven patients with effectively treated obstructive sleep apnea (OSA) without desaturation during sleep Ventilation was measured with a pneumotachograph attached to a nasal mask In the treated patients with OSA and in the normal subjects, only minor alterations in V I were observed during sleep In contrast, mean V I for the group with nocturnal desaturation decreased by 21% during non-rapid-eye-movement (NREM) sleep and by 39% during rapid-eye-movement (REM) sleep as compared with wakefulness This reduction was due mainly to a decrease in tidal volume (V T) Hypoventilation was most pronounced during REM sleep, irrespective of the underlying disease These data indicate that hypoventilation may be the major factor leading to hypoxia during sleep, and that reversal of hypoventilation during sleep should be a major therapeutic strategy for these patients

224 citations


Journal ArticleDOI
01 May 1999-Thorax
TL;DR: This paper reviews surgery that impairs the function of the respiratory muscles—namely cardiac, thoracic, and upper abdominal surgery, and possible pathophysiological mechanisms are reviewed.
Abstract: Respiratory muscles are the only skeletal muscles vital to life. Surgical procedures can affect the respiratory muscles by a number of pathophysiological mechanisms including thoracoabdominal mechanics, reflexes, neuromechanical coupling, and loss of muscular integrity. Impairment of respiratory muscle function after surgery may lead to postoperative complications such as hypoventilation, hypoxia, atelectasis, and infections, some of which may be life threatening. In this paper we review surgery that impairs the function of the respiratory muscles—namely cardiac, thoracic, and upper abdominal surgery. Therapeutic interventions or protective measures for respiratory muscles during or after each type of surgery are also briefly addressed. Lung transplantation and lung volume reduction surgery are discussed, since both have been shown to improve the function of respiratory muscles, and possible pathophysiological mechanisms are reviewed. The preoperative assessment of respiratory muscle function is also considered. Furthermore, when postoperative pulmonary complications occur it is worth considering whether the cause could be dysfunction of the respiratory muscles and thus a proper assessment of their function is needed. The most important function of the respiratory muscles is breathing since they are the motor arm of the respiratory system. Breathing, a lifelong task, is borne mainly by the inspiratory muscles, especially the diaphragm. The other inspiratory muscles contribute little to quiet breathing but are recruited when higher levels of ventilation are required, such as in exercise and obstructive or restrictive lung disease. The expiratory muscles are not usually used during breathing except at high levels of ventilatory effort. A second function of the respiratory muscles is to perform explosive manoeuvres such as coughing and vomiting. The respiratory muscles also have a role as stabilisers of the thorax and abdomen since they take part in the formation of the thoracic and abdominal walls. Respiratory muscle function depends on the function of the respiratory centres, …

162 citations


Journal ArticleDOI
TL;DR: The ventilatory effects of ketamine, in combination with alfentanil, are determined using infusions to different pseudo steady‐state concentrations, usinginfusions toDifferent pseudo steady-state concentrations.
Abstract: Background: The effects of ketamine on respiration, alone, or in combination with opioids, have not been completely clarified. Both stimulant and depressant effects have been reported, as well as attenuation of opioid-induced hypoventilation at the expense of increased oxygen consumption. These conflicting results might partly be due to dose-dependent mechanisms. We have, therefore, determined the ventilatory effects of ketamine, in combination with alfentanil, using infusions to different pseudo steady-state concentrations. Methods: On two separate days, eight healthy male volunteers were given alfentanil as a continuous computer-controlled infusion, aiming at a plasma concentration of 50 ng · mL−1. After reaching apparent steady-state for alfentanil, racemic ketamine or placebo was administered in a protocol randomised for the two days. On the ketamine days a computer-controlled infusion, aiming for escalating ketamine plasma concentrations of 50, 100 and 200 ng · mL−1, was added to the alfentanil infusion. On the placebo days saline was added. Using a face-mask with an occlusion valve, respiratory parameters were measured during air-breathing and after 6 repetitive 30-s CO2 challenges. Results: The alfentanil infusion induced hypoventilation by decreasing respiratory rate, while tidal volume and respiratory drive were unaffected. This hypoventilation was antagonised by ketamine in a concentration-dependent manner mainly through an increase in respiratory rate. The CO2 response was not affected by alfentanil or ketamine. Conclusion: In the dose range of interest for postoperative, intensive-care and pain-clinic settings, ketamine antagonises the resting hypoventilation induced by alfentanil.

41 citations


Journal Article
TL;DR: To stimulate pulmonary and thoracic growth, intermittent ventilatory assistance by pressure preset ventilator should be performed as soon as possible and pursued up to 8 years of age, at least, more if necessity, to prevent respiratory insufficiency.
Abstract: In kyphoscoliosis restrictive ventilatory defect occurs. In idiopathic scoliosis vital capacity failure is significantly correlated with Cobb angle, vertebral rotation, and thoracic lordosis. Maximum voluntary ventilation is the most affected measurement. Forced expiratory volume in 1 second is reduced. Residual volume remains longtime normal. Hypoxemia due to decrease of diffusing capacity occurs, with initially reflex hyperventilation hypocapnia, and secondary hypercapnia. Pulmonary hypertension and cor pulmonale is related to hypoventilation and hypoxia. The lung situated on the concave side of the scoliosis curve shows a more functional derangement. Ventilatory pattern consists of low tidal volume and high respiratory rate with increase of ventilatory work. Scoliosis that appears in the earlier stage of the life has the worst respiratory prognosis (before 5 years of age) with impairement of lung and thoracic growth. To stimulate pulmonary and thoracic growth, intermittent ventilatory assistance by pressure preset ventilator should be performed as soon as possible and pursued up to 8 years of age, at least, more if necessity. In over 60 degrees angle idiopathic scoliosis, respiratory failure appears after 40 to 50 years of age. Non invasive ventilatory assistance with preset pressure ventilator by oral way in moderate cases and nocturnal nasal ventilation by volume ventilator or inspiratory assistance ventilator, in the most severe cases are efficient. In very severe and acute respiratory insufficiency (scoliosis over 90 degrees) ventilation by intubation then tractheostomy may be required. Earlier orthopedic management and surgical procedure to correct and stabilize spinal deformities is the best to prevent respiratory insufficiency. For scoliosis below 60 degrees, post operative pulmonary complications are very low, with no requirement of post operative ventilatory support. In very severe respiratory insufficiency treatment of respiratory failure precedes, and follows, orthotic treatment and surgical procedures; it shouldle pursued afterwards.

38 citations


Journal ArticleDOI
TL;DR: Investigation of the effects of hyper- and hypoventilation on gastric and sublingual tissue PCO(2) before, during, and after reversal of hemorrhagic shock found statistically similar decreases and increases in Pg(CO)2 and Psl(CO(2).
Abstract: We investigated the effects of hyper- and hypoventilation on gastric ( Pg CO 2 ) and sublingual (P sl CO 2 ) tissue P CO 2 before, during, and after reversal of hemorrhagic shock. Pg CO 2 was measu...

38 citations


Journal ArticleDOI
TL;DR: The most important consequence of chronic alveolar hypoventilation is pulmonary hypertension which is only observed in patients with daytime arterial blood gases disturbances, and which can lead to right heart failure.

35 citations


Journal ArticleDOI
TL;DR: For the chronic progressive forms of alveolar hypoventilation, there is currently a need for quality randomized controlled clinical trials to define physiologic indicators and appropriate timing for mechanical support of minute ventilation.
Abstract: Alveolar hypoventilation associated with neuromuscular disease can occur in acute and chronic forms. In the acute form, progressive weakness of respiratory muscles leads to rapid reduction in vital capacity followed by respiratory failure with hypoxemia and hypercarbia. Symptoms are those of acute respiratory failure, including dyspnea, tachypnea, and tachycardia. In the chronic form, impairment of the respiratory muscles affects mechanical properties of the lungs and chest wall, decreases the ability to clear secretions, and eventually may alter the function of the central respiratory centers. Symptoms include orthopnea, fatigue, disturbed sleep, and hypersomnolence. Treatment and outcome of the disease's chronic form are dependent on the underlying clinical cause of the alveolar hypoventilation. For chronic but stable diseases such as old polio, quadriplegia, or kyposcoliosis, mechanical support of minute ventilation can reverse symptoms. For chronic and progressive disease such as muscular dystrophy and amyotrophic lateral sclerosis, mechanical support of minute ventilation provides only symptomatic relief and is usually associated with deterioration to the point of complete ventilator dependency for survival. For the chronic progressive forms of alveolar hypoventilation, there is currently a need for quality randomized controlled clinical trials to define physiologic indicators and appropriate timing for mechanical support of minute ventilation.

34 citations


Journal ArticleDOI
TL;DR: Three principal issues have become apparent: 1) the autonomic nervous system is involved universally in CCHS cases, albeit to a varying extent; 2) the use of novel functional imaging approaches incorporating refined stimulus paradigms may provide essential research and clinical insights into localization and assessment of neural sites underlying the phenotypic expression of this syndrome.
Abstract: Congenital central hypoventilation syndrome (CCHS) is a rare and unique condition that may prompt unparalleled approaches to the discovery of genes involved in development of cardiorespiratory control and gas exchange homeostasis. Its higher risk of recurrence in families and its association with Hi

33 citations


Journal ArticleDOI
TL;DR: The rationale and explanation for a management protocol for obesity-hypoventilation that is currently being assessed in the VA Medical Center and Case Western Reserve University training program in Pulmonary and Critical Care Medicine are presented.
Abstract: A survey of our pulmonary service revealed little consensus as to the definition, work-up, and management of hypoventilation, more often encountered in the presence of obesity. If hypoventilation is defined by an arterial carbon dioxide level above 45mmHg, 22% of artrial blood gas samples over a 5-month period met this criterium, suggesting a high “any-cause” prevalence. This article presents the rationale and explanation for a management protocol for obesity-hypoventilation that is currently being assessed in the VA Medical Center and Case Western Reserve University training program in Pulmonary and Critical Care Medicine.

25 citations


01 Jan 1999
TL;DR: In this paper, a 49-year-old man with intermittent bradycardia, cranial nerves dysfunctions and a slight right-sided hemiparesis was diagnosed and treated immediately with high-dose heparin.
Abstract: Ischemic lesions of the brainstem can lead to complex neurologic deficits. Failure of the automatic control of ventilation (Ondine’s curse syndrome) is a possible but rare syndrome following localized brainstem dysfunction. We report on a 49-year-old man with intermittent bradycardia, cranial nerves’ dysfunctions and a slight right-sided hemiparesis. An acute brainstem ischemia was diagnosed and treated immediately with high-dose heparin. Cerebral angiography revealed a proximal occlusion of the left vertebral artery but a normal right vertebral artery and a hyperplastic right posterior inferior cerebellar artery. Cranial Computed Tomography and MRI scan demonstrated multiple ischemic lesions in the posterior circulation. During a 4-week treatment course the patient underwent six episodes of acute severe hypoxia and hypercapnia requiring orotracheal intubation twice and manual ventilation by air mask over a few minutes for four times after a tracheostomy had been performed. Twice a short-term episode of hypothalamic Diabetes insipidus was observed following hypoventilation. We conclude that both Ondine’s curse syndrome and diabetes insipidus were due to transient vertebrobasilar ischemia. © 1999 Elsevier Science B.V. All rights reserved.

Journal ArticleDOI
TL;DR: The Ondine's curse is a rare neuropathologic syndrome characterized by an inadequate respiratory drive with hypoventilation and periods of prolonged apnea resulting in hypercarbia and hypoxemia.

Journal ArticleDOI
TL;DR: Both Ondine's curse syndrome and diabetes insipidus were due to transient vertebrobasilar ischemia, a 49-year-old man with intermittent bradycardia, cranial nerves' dysfunctions and a slight right-sided hemiparesis.

Journal ArticleDOI
TL;DR: An 11‐year‐old boy with severe asthma requiring mechanical ventilation was given high doses of parenteral steroids and neuromuscular blockade with non‐depolarizing agents in order to achieve controlled hypoventilation with an ensuing hypercapnoea, and developed rhabdomyolysis and renal impairment secondary to myoglobinuria.
Abstract: Acute myopathy complicating treatment of status asthmaticus has been increasingly recognized since its original description in 1977. We report a case of an 11-year-old boy with severe asthma requiring mechanical ventilation. He was given high doses of parenteral steroids and neuromuscular blockade with non-depolarizing agents in order to achieve controlled hypoventilation with an ensuing hypercapnoea. He developed rhabdomyolysis with elevated creatinine kinase and renal impairment secondary to myoglobinuria. Electrophysiological studies revealed myopathic abnormalities. The aetiology for this myopathy appears to be related to therapy with parenteral steroids, muscle-relaxant agents and respiratory acidosis. Patients treated with steroids and neuromuscular blocking agents should be regularly monitored for development of myopathy.

Journal ArticleDOI
TL;DR: It is concluded that heart rate control, but not ventilatory control, is sensitive to relatively small increases in hydrostatic pressure.
Abstract: We sought to determine whether hydrostatic pressure contributed to bradycardia and hypoventilation in hyperbaria. Eight men were studied during exercise at 50, 150, and 250 W while breathing 1) air...

Journal Article
TL;DR: Nocturnal NIPPV improves awake gas exchange in patients with chronic respiratory failure and a considerable reduction in the need for subsequent hospital admission was noted in the group as a whole following institution of NIPPVs.
Abstract: The development of positive pressure ventilation delivered through a nasal or face mask has greatly expanded the use of non-invasive ventilation in patients with chronic respiratory insufficiency, particularly during sleep. Disorders ranging from neurologic and neuromuscular, such as polio and muscular dystrophy, central alveolar hypoventilation, thoracic cage disorders such as kyphoscoliosis, and pulmonary disorders such as COPD, particularly of the blue-bloater type. The relative hypoventilation that is common to each condition is due to varying combinations of an inadequate respiratory drive and an increase in the work of breathing. Previous studies have shown sustained reversal of awake hypercapnia in patients with alveolar hypoventilation syndrome using nocturnal NIPPV. We analysed 10 consecutive patients with chronic respiratory insufficiency due to diverse aetiologies over a period of time using long-term domiciliary nocturnal NIPPV. Awake hypercapnia and hypoxaemia improved in nine patients over time and deteriorated in one patient. There was no significant change in pulmonary function apart from one patient with progressive muscular dystrophy who deteriorated. A considerable reduction in the need for subsequent hospital admission was noted in the group as a whole following institution of NIPPV. We conclude that nocturnal NIPPV improves awake gas exchange in patients with chronic respiratory failure.

Journal Article
Lewis Da1
TL;DR: The salient features, underlying pathophysiologic mechanisms, and treatment of abnormalities of sleep in patients who have respiratory disease are discussed.
Abstract: Recent studies have emphasized the high prevalence and significant consequences of sleep abnormalities in patients who have underlying respiratory disease. Such abnormalities include the nocturnal increase in airway resistance in patients who have asthma, the impaired sleep quality and nocturnal desaturation (particularly during REM sleep) in patients who have chronic obstructive pulmonary disease, and the sleep-related hypoventilation and hypoxemia in patients who have various restrictive respiratory disorders. This article discusses the salient features, underlying pathophysiologic mechanisms, and treatment of these abnormalities of sleep in patients who have respiratory disease.

Journal ArticleDOI
TL;DR: The findings suggest that the respiratory modulation of preganglionic sympathetic activity in the CST consists of expiration-related activity in normal acid-base status, which probably constitute a subgroup of sympathetic neurons which is activated under increased respiratory drive.
Abstract: Activity in preganglionic sympathetic neurons projecting in the cervical sympathetic trunk (CST) of rats was analysed with respect to changes in the pattern of the respiratory modulation during a long lasting hypoventilation. Under normal acid-base status (pH: 7.36+/-0.04, pCO2: 42.1+/-6.1 mm Hg, pO2: 135.8+/-43 mm Hg) a maximum of activity during expiration (expiration-related activity) was observed in all nerve recordings (n = 27). No other pattern of respiratory modulation was observed under this condition. Under a hypoventilation a dissociation between the duration of phrenic nerve activity and that of the inspiratory inhibition in neurons with expiration-related activity was observed as the inhibition was significantly prolonged by 49+/-24.9% and outlasted inspiration in 5/7 multifibers. When acid-base status was systematically changed (pH: 7.15+/-0.05, pCO2: 80.4+/-11.8 mm Hg, pO2: 62.8+/-17.5 mm Hg [n = 7]) by a hypoventilation lasting for several hours activity with a maximum peak during central inspiration (inspiration-related activity) emerged and disappeared when control conditions were reestablished. Neurons with expiration-related activity showed a cardiac rhythmicity (CR) of 62.5+/-14.6% (n = 27) and were inhibited to baroreceptor stimulation whereas neurons with inspiration-related activity showed no discernible CR (23.1+/-5.1%; n = 7) and were not inhibited to baroreceptor stimulation. Furthermore, expiration-related neurons were inhibited by 32.5+/-18.3% (n = 27) during noxious cutaneous stimulation while neurons with inspiration-related activity were activated by 21.5+/-12.1% (n = 7). These findings suggest that the respiratory modulation of preganglionic sympathetic activity in the CST consists of expiration-related activity in normal acid-base status. During hypoventilation neurons with inspiration-related activity are recruited. These neurons show reflex patterns distinct from expiration-related neurons and probably constitute a subgroup of sympathetic neurons which is activated under increased respiratory drive.

Journal ArticleDOI
TL;DR: The authors suggest that for infants or children who exhibit vocal cord paralysis, mitochondrial disorders, such as Leigh disease, should be considered.

Journal Article
TL;DR: Ten adult patients with this disorder (average age 46 y), who were treated from 1990 to 1996, were hypercapnic while awake and during sleep, and the CO2-rebreathing response was negative.
Abstract: The term "Ondine's curse" is normally used for congenital central hypoventilation in children. We report on 10 adult patients with this disorder (average age 46 y), who were treated from 1990 to 1996. They were hypercapnic while awake (mean 57 Torr) and during sleep (mean 87 Torr). The CO2-rebreathing response was negative. During exercise test minute ventilation volume did not rise adequately (mean pCO2 : 63 Torr, mean pH: 7.21). Five of these patients underwent emergency intubation before diagnosis, 2 presented with hypoventilation syndrome and 2 with decompensated cor pulmonale, 1 was diagnosed without complaints. 8 patients needed intermittent positive pressure ventilation therapy, 7 of them noninvasive, 1 via tracheal canula. One female patient has already died, the others are under stable clinical condition with the underlying central disorder remaining unchanged. Only 2 patients showed central defects visible in magnetic resonance tomography.

Journal Article
TL;DR: This study demonstrates that lung tissue PO2 registrations can be made in a suitable animal (pig) model, and that hypoventilation induced an almost reversible decrease in lung tissue oxygen pressure distributions.
Abstract: The objective of the present study was to investigate the possibility of measuring lung tissue oxygen pressure (PtO2) distributions at the microvascular level, and also if a change in the lung tissue oxygenation could be detected during hypoventilation (50% reduction in ventilatory settings). Experiments were carried out on eight mechanically ventilated ketamine-anaesthetised pigs. A thoracotomy was performed through the third right intercostal space. PtO2 measurements were made using a Clark-type multiwire microelectrode placed onto the pleural surface of the middle lobe. PtO2 was measured during normoventilation, hypoventilation (3 minutes) (reduction of respiratory volume/minute and frequency by 50%), and a second period of normoventilation. Baseline PtO2 was 5.8 (range 4.4 to 10.3) kPa and decreased to 2.9 (range 1.6 to 4.2) kPa during hypoventilation, associated with some PtO2 values close to zero. The PtO2 increased to 5.4 (range 3.6 to 8.4) kPa during the second normoventilatory period, some values still close to zero. This study demonstrates that lung tissue PO2 registrations can be made in a suitable animal (pig) model, and that hypoventilation induced an almost reversible decrease in lung tissue oxygen pressure distributions. In addition, no microscopically visible tissue damage was inflicted by the electrode on the underlying lung surface.

Journal Article
TL;DR: DV in awake patients is equally effective for the treatment of CVI, when compared to NV, and there were no significant differences between the groups in the improvement of the measured parameters.
Abstract: BACKGROUND Nocturnal hypoventilation is associated with chronic ventilatory insufficiency (CVI). Noninvasive mechanical ventilation (NIV) performed overnight relieves symptoms of hypoventilation and improves daytime blood gases in CVI. In order to test whether the efficacy of NIV depends on its being applied during sleep we conducted a prospective case controlled study comparing daytime mechanical ventilation (DV) in awake patients with nocturnal mechanical ventilation (NV) given in equal quantities. PATIENTS AND METHODS We enrolled 34 clinically stable patients (age: 56.1 +/- 12.1 years, 20 female) with CVI due to both restrictive lung and chest wall disorders and neuromuscular disease. Using a prospective case-control design, matched subjects were allocated alternately to DV and NV. RESULTS AND CONCLUSIONS There were no significant differences between the groups in the improvement of the measured parameters; (e.g. PaCO2; DV: from 57.6 +/- 4.3 to 44.0 +/- 4.6 mm Hg, NV: from 55.5 +/- 3.5 to 45.0 +/- 4.1 mm Hg, p < 0.0001). We conclude that in many respects, when compared to NV, DV in awake patients is equally effective for the treatment of CVI.

Journal ArticleDOI
TL;DR: Controlled mechanical hypoventilation with reduced tidal volumes and peak inspiratory pressures has been introduced into the treatment of ARDS in order to avoid pulmonary hyperinflation and ventilator-induced lung injury.
Abstract: Controlled mechanical hypoventilation with reduced tidal volumes and peak inspiratory pressures has been introduced into the treatment of ARDS in order to avoid pulmonary hyperinflation and ventilator-induced lung injury. The concomitant increase of arterial PCO2 has been denoted as permissive hypercapnia. Recent clinical studies suggest a potential benefit of this concept for patients with acute respiratory failure, although several organ systems can be affected by the increase of PaCO2. The impaired pulmonary gas exchange in ARDS can be effectively improved by patients with positioning acute respiratory failure prone. A redistribution of pulmonary blood flow has been suggested earlier to account for this observation. However, recent data from animal studies showed a decrease of the vertical pleura pressure gradient, which could facilitate reopening and ventilation of previously atelectatic lung segments.

Journal Article
TL;DR: In contrast to the COPD group in patients with chronic respiratory failure due to thoracic restriction nocturnal mechanical ventilation causes substantial reduction in pulmonary artery pressure after a one year application.
Abstract: Intermittent non-invasive (or nocturnal mechanical ventilation) eliminates symptoms of hypoventilation and improves gas exchange in patients with chronic respiratory failure. Performing right heart catheterisation we studied the influence of nocturnal mechanical ventilation on pulmonary hemodynamics. We investigated 20 patients with restrictive thoracic diseases (Post-TBC: n = 9, scoliosis: n = 11, PaCO2: 59.8 +/- 7.6 mmHg) and 13 patients with COPD (n = 13, PaCO2: 58.5 +/- 7.8 mmHg). All patients were mechanically ventilated in controlled mode. During the study the medication was not changed; COPD patients with long-term oxygen maintained this therapy. Right-heart catheterisation was performed immediately before and after 1 year nocturnal mechanical ventilation. In patients with thoracic restriction NMV induced a marked reduction of pulmonary artery pressure (PAP) from 33.2 +/- 10.0 mmHg before to 24.8 +/- 6.2 mmHg after 1 year nocturnal mechanical ventilation. In the COPD group PAP increased from 25.3 +/- 6.0 mmHg before to 27.5 +/- 6.0 mmHg after 1 year nocturnal mechanical ventilation. In contrast to the COPD group in patients with chronic respiratory failure due to thoracic restriction nocturnal mechanical ventilation causes substantial reduction in pulmonary artery pressure after a one year application.

Journal Article
TL;DR: Patients with severe brain syndromes should not be selected for home-ventilation, due to the fact that home ventilation has marked consequences for the patient and his carer organic disorders of brain function.
Abstract: BACKGROUND A growing number of patients with neuromuscular diseases has been treated with mechanical ventilatory support during the last years. In some of these patients acute or chronic organic brain syndromes complicate the situation. PATIENTS AND METHODS We present case reports of 5 patients who have been ventilated at home with neuromuscular diseases but who also suffered from brain syndromes of different etiology. CASE REPORTS (1) Multifactorial acute organic brain syndrome after intensive care therapy. (2) Recurrent paranoid psychosis correlating with hypercapnia. (3) Oneiroids (awake dreamings). (4) Refusal of the rejection of mechanical ventilation facing dyspnea. (5) Persistent vegetative state after polyradiculomyeloencephalitis. DISCUSSION Patients with hypoventilation or mechanical ventilation often present with various types of brain syndromes. Careful history taking and the use of laboratory and imaging techniques allow the differentiation in primary and secondary (metabolic) brain syndromes. With respect to the fact that home ventilation has marked consequences for the patient and his carer organic disorders of brain function raise two questions: (1) Is the patient able to understand and critically reflect the consequences of long-term mechanical ventilation? (2) Is the patient able to understand and manage the practical aspects and skills of home-ventilation. e.g., does he have the mental capacity for a sufficient compliance? From our point of view patients with severe brain syndromes should not be selected for home-ventilation.

Journal ArticleDOI
08 Dec 1999-JAMA
TL;DR: Home ventilation for neuromuscular hypoventilation is typically progressive, and it is important to explain to patients that their disease can be expected to worsen; achievement of ideal ventilator settings is a trial-and-error process.
Abstract: CHICAGO—If asked to describe a respirator-dependent patient, most physicians will probably imagine a debilitated, immobilized, and sedated person, monitored in an intensive care setting with the usual array of probes, alarms, telemetry, and skilled nursing staff. During the past 10 years, however, tens of thousands of adults and children with neuromuscular diseases, and a small number with emphysema, have pursued productive lives while receiving mechanical ventilation at home. At the Chest 1999 conference here last month, Allen Goldberg, MD, president of the American College of Chest Physicians, said he remembered a time when children with muscular dystrophy or nocturnal hypoventilation syndrome would spend most of their childhood in the hospital, tethered to a ventilator. With rapidly expanding home ventilator use, these children are now free to lead a nearly normal life; Goldberg said that one of his patients, a respirator-dependent child, recently fell out of a tree and broke his arm, a normal childhood experience that otherwise would have been denied him. Dominique Robert, MD, of the Hopital de la Croix-Russe in Lyon, France, described his 20 years of pioneering work in home ventilation. His initial 6-year study, begun in 1981, found that adults with neuromuscular hypoventilation had a markedly improved life if they received home ventilation. Many of these adult patients are survivors of polio, which left them with a residual and progressive weakness of their respiratory muscles, while others have progressive neurological diseases such as amyotrophic lateral sclerosis. Robert said that such patients typically do not experience shortness of breathbut, rather, vague complaints such as loss of energy, poor concentration, and daytime hypersomnolence. Earlymorning headache, which is caused by nocturnal hypercapnia, is common. Such patients often experience profound episodes of hypoventilation, particularly during rapid eye movement sleep, as well as chronic hypoxemia and compensated respiratory acidosis. Still, the true etiology of their symptoms may go unsuspected for years. Home ventilation is accomplished by nasal intermittent positive-pressure ventilation (NIPPV), with a catheter inserted in the nostrils, or with a nasal mask. Patients are instructed to use the ventilator for as many hours per day as they require to return to an acceptable level of function. Achievement of ideal ventilator settings is a trial-and-error process. Because the system is open, with an air leak through the mouth, nasal ventilation may not always be adequate. Robert said that a mouthpiece, to which the ventilator tubes attach, can be added if necessary. He emphasized that neuromuscular hypoventilation is typically progressive, and it is important to explain to patients that their disease can be expected to worsen. Ventilation via tracheostomy should be considered for patients requiring more than 18 hours of NIPPV per day to maintain their level Rights were not granted to include this image in the online journal. Please refer to the print journal to view. Kathleen Navarre, PhD, an assistant professor of psychology at Delta College in Midland, Mich, is a polio survivor who uses noninvasive nocturnal ventilation. She uses the ventilator during a break in the day. The “rest” enhances the volume of her speech for classes later in the day. In te rn at io na lV en til at or U se rs N et w or k, St Lo ui s, M o. Margaret Pfrommer, a ventilator-dependent, quadriplegic, polio survivor lived alone independently for over 40 years. She served as a consultant and advocate for the development of technology aids and public policies that now permit persons with severe disability to work and live a life of their choice with dignity. A lle n G ol db er g, M D MEDICAL NEWS & PERSPECTIVES

Journal Article
TL;DR: The experiences of a patient suffering from chronic hypoventilation caused by a ventilatory pump failure following tetraparesis due to congenital toxoplasmosis are reported.
Abstract: BACKGROUND: Diaphragm pacing in patients with intact phrenic nerve and diaphragm can be used as an alternative to mechanical ventilation. Indications cover diseases caused by central hypoventilation like C2-quadriplegia and Ondine's syndrome. Advantages are physiological ventilation with negative pressure and an improvement in articulation. CASE REPORT: We report our experiences with a patient suffering from chronic hypoventilation caused by a ventilatory pump failure following tetraparesis due to congenital toxoplasmosis.

Journal Article
TL;DR: The GABAergic working mechanism of moxidectin does explain the development of profound central nervous depression and its sequels hypothermia, bradycardia, hypoventilation and paralytic ileus.
Abstract: A 2 day old foal was presented with central nervous depression (coma) after moxidectin overdose. Moxidectin belongs to the milbemycin anthelmintics which elicit their working mechanism through a GABA (gamma-aminobutyric acid)-stimulatory mode of action. The foal developed profound hypothermia, bradycardia and hypoventilation. Absence of urine voiding and mild abdominal distension suggested a ruptured bladder, which was confirmed by transabdominal ultrasound and clinical-pathologic parameters. Repeat auscultation of the ventral lung parts and the occurrence of gastric reflux were suggestive of an aspiration pneumonia. The foal underwent surgical bladder repair, however, did succumb due to mixed acidosis and early signs of sepsis postoperatively. The findings in this foal are suggestive for moxidectin overdosing. The GABAergic working mechanism of moxidectin does explain the development of profound central nervous depression and its sequels hypothermia, bradycardia, hypoventilation and paralytic ileus. Dyssynergia was unexpected, however, has to be related to a central nervous problem, rather than a peripheral nervous problem.

Journal Article
TL;DR: In the majority of patients hypercapnia was not only removed during ventilation but also at daytime as an indicator of improvement of ventilatory insufficiency accomplished by a clearly better quality of life and daytime activity.
Abstract: PATIENTS AND METHODS In our centre, 111 patients with chronic ventilatory insufficiency (33 females, 78 males, age 48 +/- 18 years, range 3 to 76 years) were treated by intermittent positive pressure ventilation between 1982 and 1996. Underlying diseases were neuromuscular diseases in 29%, sleep-related hypoventilation in 26%, kyphoscoliosis in 15%, chronic obstructive airway disease in 15%, and post-tuberculosis syndromes in 12%. Singular indications were 1 bronchiectasis, 1 lung fibrosis and 1 cystic fibrosis. RESULTS Until 1991, most patients were ventilated via tracheostoma (10 of 16), in the following years 87 of 95 patients could be ventilated via a nasal or facial mask. Ventilation mode was a controlled one in 80 patients and an assisted one in 31 patients, average ventilation time during night was 6 to 8 hours. In the majority of patients hypercapnia was not only removed during ventilation but also at daytime as an indicator of improvement of ventilatory insufficiency accomplished by a clearly better quality of life and daytime activity. Ten patients (9%) died due to their underlying diseases, 5 of them in the first year of intermittent ventilation.