Showing papers on "Hypoventilation published in 2003"

Respiratory failure in chronic obstructive pulmonary disease

Abstract: Respiratory failure is still an important complication of chronic obstructive pulmonary disease (COPD) and hospitalisation with an acute episode being a poor prognostic marker. However, other comorbid conditions, especially cardiovascular disease, are equally powerful predictors of mortality. The physiological basis of acute respiratory failure in COPD is now clear. Significant ventilation/perfusion mismatching with a relative increase in the physiological dead space leads to hypercapnia and hence acidosis. This is largely the result of a shift to a rapid shallow breathing pattern and a rise in the dead space/tidal volume ratio of each breath. This breathing pattern results from adaptive physiological responses which lessen the risk of respiratory muscle fatigue and minimise breathlessness. Treatment is directed at reducing the mechanical load applied to each breath, correcting specific precipitating factors, e.g. bacterial infection, and maintaining gas exchange. Both bronchodilators and oral corticosteroids can improve spirometric results in exacerbations of COPD and should be routinely offered to patients with respiratory failure. Controlled oxygen is still not always prescribed appropriately and high inspired oxygen concentrations can lead to severe acidosis by either worsening ventilation/perfusion mismatching and/or inducing a degree of hypoventilation. Ventilatory support using noninvasive ventilation has revolutionised the approach to these patients. Acute respiratory failure due to chronic obstructive pulmonary disease remains a common medical emergency that can be effectively managed. More attention should be focused on the prevention of these episodes and identifying the factors which cause early relapse.

Long-term noninvasive mechanical ventilation for children at home: A national survey†

Abstract: Experience with domiciliary noninvasive mechanical ventilation (NIMV) in children is limited. The aim of this study was to determine the number of patients and categorize the use of domiciliary NIMV in children in France. An anonymous cross-sectional national study was performed, using a postal questionnaire sent to all specialist centers utilizing domiciliary NIMV for chronic respiratory failure. Patients aged <18 years and receiving home NIMV were included in the study. Detailed information was obtained from 102 patients from 15 centers: 4/15 centers cared for 84% of patients; 7% of patients were under 3 years old; 35% were between 4-11 years old; and 58% were older than 12 years. Underlying diagnoses included neuromuscular disease (34%), obstructive sleep apnea (OSA) and/or cranio-facial abnormalities (30%), cystic fibrosis (17%), congenital hypoventilation (9%), scoliosis (8%), and other disorders (2%). NIMV was started because of nocturnal hypoventilation (67%), acute exacerbation (28%), and/or failure to thrive (21%). Volume-targeted ventilation was preferred in restrictive disorders (56%) and central hypoventilation (56%), while pressure support ventilation (PSV) was preferred in cystic fibrosis (71%). Patients with OSA and/or cranio-facial abnormalities were ventilated with continuous positive airway pressure (45%) or bilevel PSV (52%). In conclusion, NIMV is currently used in France for the domiciliary management of children with a variety of conditions causing chronic respiratory failure. However, NIMV in children is still performed on a small scale, and combined with the heterogeneity of the patient population, its application would best be served by centers specializing in the initiation and long-term follow-up of these patients.

Benefit-risk assessment of transdermal fentanyl for the treatment of chronic pain

Abstract: Transdermal fentanyl is effective and well tolerated for the treatment of chronic pain caused by malignancy and non-malignant conditions when administered according to the manufacturer’s recommendations. Compared with oral opioids, the advantages of transdermal fentanyl include a lower incidence and impact of adverse effects (constipation, nausea and vomiting, and daytime drowsiness), a higher degree of patient satisfaction, improved quality of life, improved convenience and compliance resulting from administration every 72 hours, and decreased use of rescue medication. Transdermal fentanyl is a useful analgesic for cancer patients who are unable to swallow or have gastrointestinal problems. Transdermal fentanyl forms a depot within the upper skin layers before entering the microcirculation. Therapeutic blood levels are attained 12–16 hours after patch application and decrease slowly with a half-life of 16–22 hours following removal. Patients with chronic pain should be titrated to adequate relief with short-acting oral or parenteral opioids prior to the initiation of transdermal fentanyl in order to prevent exacerbations of pain or opioid-related adverse effects. Transdermal fentanyl can then be initiated based on the 24-hour opioid requirement once adequate analgesia has been achieved. The prolonged elimination of transdermal fentanyl can become problematic if patients develop opioid-related adverse effects, especially hypoventilation. Adverse effects do not improve immediately after patch removal and may take many hours to resolve. Patients who experience opioid-related toxicity associated with respiratory depression should be treated immediately with an opioid antagonist such as naloxone and closely monitored for at least 24 hours. Because of the short half-life of naloxone, sequential doses or a continuous infusion of the opioid antagonist may be necessary. Transdermal fentanyl should be administered cautiously to patients with pre-existing conditions such as emphysema that may predispose them to the development of hypoventilation. Transdermal fentanyl is indicated only for patients who require continuous opioid administration for the treatment of chronic pain that cannot be managed with other medications. It is contraindicated in the management of acute and postoperative pain, as pain may decrease more rapidly in these circumstances than fentanyl blood levels can be adjusted, leading to the development of life-threatening hypoventilation. Cognitive and physical impairments such as confusion and abnormal co-ordination can occur with transdermal fentanyl. Therefore, patients should be instructed to refrain from driving or operating machinery immediately following the initiation of transdermal fentanyl, or after any dosage increase. Patients may resume such activities once the absence of these potential adverse effects is documented.

Sleep hypoventilation in hypercapnic chronic obstructive pulmonary disease: prevalence and associated factors

Abstract: Sleep hypoventilation (SH) may be important in the development of hypercapnic respiratory failure in chronic obstructive pulmonary disease (COPD). The prevalence of SH, associated factors, and overnight changes in waking arterial blood gases (ABG), were assessed in 54 stable hypercapnic COPD patients without concomitant sleep apnoea or morbid obesity. Lung function assessment, anthropomorphic measurements, and polysomnography with ABG measurement before and after sleep were conducted in all patients. Transcutaneous carbon dioxide tension (Pt,CO2) was measured in sleep, using simultaneous arterial carbon dioxide tension (Pa,CO2) for in vivo calibration and to correct for drift in the sensor. Of the patients, 43% spent > or = 20% of sleep time with Pt,CO2 > 1.33 kPa (10 mmHg) above waking baseline. Severity of SH was best predicted by a combination of baseline Pa,CO2, body mass index and per cent rapid-eye movement (REM) sleep. REM-related hypoventilation correlated significantly with severity of inspiratory flow limitation in REM, and with apnoea/hypopnoea index. Pa,CO2 increased mean+/-SD 0.70+/-0.65 kPa (5.29+/-4.92 mmHg) from night to morning, and this change was highly significant. The change in Pa,CO2 was strongly correlated with severity of SH. Sleep hypoventilation is common in hypercapnic chronic obstructive pulmonary disease, and related to baseline arterial carbon dioxide tension, body mass index and indices of upper airway obstruction. Sleep hypoventilation is associated with significant increases in arterial carbon dioxide tension night-to-morning, and may contribute to long-term elevations in arterial carbon dioxide tension.

Ventilatory response to brief arousal from non-rapid eye movement sleep is greater in men than in women.

Abstract: Sleep apnea syndromes are more common in men than in women. The ventilatory response to arousal from sleep may be an important determinant of respiratory stability/instability and could contribute to this sex difference. We therefore compared changes in ventilation, end-tidal carbon dioxide (CO2), upper airway resistance, heart rate, and finger photoplethysmogram pulse wave amplitude after both spontaneous and tone-induced arousal from non–rapid eye movement sleep in 13 men and 13 women. At sleep onset, ventilation fell and both upper airway resistance and end-tidal CO2 rose, but these changes were not different between sexes. Spontaneous arousal (duration, 6.6 ± 0.2 seconds) resulted in a biphasic ventilatory response consisting of brief hyperventilation (5 seconds) followed by prolonged hypoventilation (30–40 seconds) on resumption of sleep. The biphasic ventilatory response was greater in men than in women and did not appear to be explained by different wake-to-sleep increments in end-tidal CO2 or uppe...

Breathing disorder detection and therapy delivery device and method

Abstract: A device and method are provided for managing the treatment of a patient with respiratory disorders or symptoms. Respiratory parameters are sensed and recorded and communicated to an external device to provide information to a patient and/or provider for further treatment or diagnosis. Also respiratory disorders such as apnea or hypoventilation may be treated by electrically stimulating the diaphragm muscle or phrenic nerve in response to a sensed respiratory parameter or characteristic.

A model of the ventilatory depressant potency of remifentanil in the non-steady state.

Abstract: Background: The C 50 of remifentanil for ventilatory depression has been previously determined using inspired carbon dioxide and stimulated ventilation, which may not describe the clinically relevant situation in which ventilatory depression occurs in the absence of inspired carbon dioxide. The authors applied indirect effect modeling to non-steady state PaCO 2 data in the absence of inspired carbon dioxide during and after administration of remifentanil. Metbods: Ten volunteers underwent determination of carbon dioxide responsiveness using a rebreathing design, and a model was fit to the end-expiratory carbon dioxide and minute ventilation. Afterwards, the volunteers received remifentanil in a stepwise ascending pattern using a computer-controlled infusion pump until significant ventilatory depression occurred (end-tidal carbon dioxide [PeCO 2 ] > 65 mmHg and/or imminent apnea). Thereafter, the concentration was reduced to 1 ng/ml. Remifentanil pharmacokinetics and PaCO 2 were determined from frequent arterial blood samples. An indirect response model was used to describe the PaCO 2 time course as a function of remifentanil concentration. Results: The time course of hypercarbia after administration of remifentanil was well described by the following pharmacodynamic parameters: F (gain of the carbon dioxide response), 4.30; k e0 carbon dioxide, 0.92 min -1 ; baseline PaCO 2 , 42.4 mmHg; baseline minute ventilation, 7.06 1/min; k e1,CO2, 0.08 min -1 ; C 50 for ventilatory depression, 0.92 ng/ml; Hill coefficient, 1.25. Conclusion: Remifentanil is a potent ventilatory depressant. Simulations demonstrated that remifentanil concentrations well tolerated in the steady state will cause a clinically significant hypoventilation following bolus administration, confirming the acute risk of bolus administration of fast-acting opioids in spontaneously breathing patients.

Nasal Continuous Positive Airway Pressure Improves Quality of Life in Obesity Hypoventilation Syndrome

Abstract: We studied the quality of life of obesity hypoventilation syndrome (OHS) by comparing it with age- and body mass index-matched patients without hypoventilation and age-matched obstructive sleep apnea (OSA) patients with body mass index (BMI) under 30, and the efficacy of nasal continuous positive airway pressure (CPAP) therapy for 3 to 6 months on the quality of life in these patients. Prospectively recruited patients from six sleep laboratories in Japan were administered assessments of the general health status by the Short-Form 36 Health Survey (SF-36) and subjective sleepiness by the Epworth Sleepiness Scale (ESS). Compared with matched healthy subjects, OHS and OSA patients not yet treated had worse results on the ESS scores and the SF-36 subscales for physical functioning, role limitations due to physical problems, general health perception, energy/vitality, role limitations due to emotional problems, and social functioning. The ESS scores of OHS patients were worse than those of the OSA groups including the age- and BMI-matched OSA patients. In the SF-36 subscales of OHS patients, only the subscale of social functioning showed worse results compared with that of BMI-matched OSA patients. After 3 to 6 months of treatment, ESS scores and these SF-36 subscales in all three patient groups improved to the normal level. These results suggested that the quality of life of OHS before nasal CPAP was significantly impaired and that nasal CPAP for OHS improved the quality of life associated with the improvement of daytime sleepiness to the level of the other OSA patients.

Clinical Applications of Breathing Regulation: Beyond Anxiety Management

Abstract: Breathing training is widely used as an aid in reducing anxiety states, but several other applications also show promise. This article reviews evidence that normalizing breathing patterns may offer help in some cases of essential hypertension, angina, functional chest disorder, chronic obstructive pulmonary disease (COPD), and cardiac rehabilitation. Hyperventilation and hypoventilation, inhibited breathing, and breath suspension are all deviations from an optimal breathing pattern in which breathing volume is closely matched to metabolic needs. Such disordered breathing has varying effects on acid/base balance, arterial diameter, and sodium retention by the kidneys. Therefore, a chronic breathing imbalance can contribute to pathophysiology, which may be remediable to an extent by altering habitual breathing patterns.

Cross-talk between two organs: how the kidney responds to disruption of acid-base balance by the lung.

Abstract: Hypoventilation increases PaCO2 (hypercapnia) and initiates the acid-base disorder known as respiratory acidosis. Hyperventilation decreases PaCO2 (hypocapnia) and initiates the

Chronic respiratory failure.

Abstract: The recent case report by Smyth and Riley1 describes an extremely uncommon chronic respiratory failure due to hypoventilation secondary to brainstem stroke, and documents a new treatment option with medroxyprogesterone acetate. We recently saw two patients also with central hypoventilation resulting in chronic type II respiratory failure and treated both with, among other things, medroxyprogesterone acetate (30 mg twice daily) with good results. The first patient, a 69 year old man with a medical history of glomus caroticum resection due to malignancy with postoperative radiotherapy in 1979, presented to our outpatient clinic with polyglobulia. Arterial blood gas …

Quality of life in obesity hypoventilation syndrome.

Abstract: The first paper of this issue of Sleep and Breathing reports that the quality of life (QOL) assessed by the SF-36 and the Epworth Sleepiness Scale (ESS) in obesity hypoventilation syndrome (OHS) was compared with age- and body mass index-matched patients without hypoventilation (obese OSA), nonobese OSA patients, and healthy subjects. The QOL in OHS was worst among these four groups. After 3 to 6 months of nasal continuous positive airway pressure (CPAP) treatment, the QOL in OHS improved to the normal level similar to the two other OSA groups. We have observed severe nonobese OSA patients with hypoventilation. One of the risk factors, which related to a severe general condition, seems to be a small craniomandibular structure, which could induce an increase in upper airway resistance during sleep. Characteristics of Japanese OSA patients may be different from those in other countries. Although belatedly, the clinical study and management of sleep disordered breathing have just begun.

Diaphragm pacing with the spinal cord stimulator.

Abstract: Chronic hypoventilation because of dysfunction of the brainstem or the high cervical spinal cord poses a serious medicosocial problem. Patients with such hypoventilation are usually managed with the use of artificial ventilators. However, chronic use of positive pressure ventilation is not physiological, easily causes infections, and restricts the patient’s activities. It has been known for a long time that diaphragm pacing with an implanted electric device to stimulate the phrenic nerve is a reasonable solution for such patients [1–5]. Almost all the patients with diaphragm pacing so far have been using a device specifically made for this purpose by Avery Laboratories Inc. (Commack, NY). Because this device is not readily available in our country, we applied a stimulator for spinal cord stimulation or deep brain stimulation for pain control to electrical stimulation of the phrenic nerves to pace the diaphragm. The aim of this study is to prove the feasibility of diaphragm pacing with electrical stimulators originally made for pain relief. Patients and Methods From March 2000 to September 2004, we performed diaphragm pacing using a stimulator for spinal cord stimulation in 6 patients with chronic hypoventilation because of brainstem dysfunction who were on a ventilator. After detailed discussion with the patient’s family and the patient, if possible, we obtained written informed consent. There were one man and three women ranging in age from 34 to 63 years (mean age, 51.6 years). These patients were reviewed, retrospectively. Table 1 summarizes the profile of these patients with regard to age, gender, and the cause, and duration of hypoventilation.

Severe respiratory compromise secondary to cervical disk herniation in two dogs.

Abstract: Two dogs presented with acute tetraparesis, hypoventilation, and bradycardia with a second-degree atrioventricular heart block. Neurological examination localized both lesions to the cervical spine. Diagnostic imaging revealed a ventral extradural compression at the second to third cervical (C(2)-C(3)) region in one dog and at the third to fourth cervical (C(3)-C(4)) region in the other. Following surgical correction of the extruded disk, the hypoventilation and bradycardia resolved. Cervical disk extrusions are a common cause of acute tetraparesis in the dog. This report shows that respiratory and cardiac complications may occur concurrently. The authors recommend screening dogs with cervical myelopathies for respiratory and cardiac dysfunctions and treating appropriately. Prompt surgical intervention and supportive care can improve the prognosis.

Respiratory Pattern in a Rat Model of Epilepsy

Abstract: Summary: Purpose: Apnea is known to occur during seizures, but systematic studies of ictal respiratory changes in adults are few. Data regarding respiratory pattern defects during interictal periods also are scarce. Here we sought to generate information with regard to the interictal period in animals with pilocarpine-induced epilepsy. Methods: Twelve rats (six chronically epileptic animals and six controls) were anesthetized, given tracheotomies, and subjected to hyperventilation or hypoventilation conditions. Breathing movements caused changes in thoracic volume and forced air to flow tidally through a pneumotachograph. This flow was measured by using a differential pressure transducer, passed through a polygraph, and from this to a computer with custom software that derived ventilation (VE), tidal volume (VT), inspiratory time (TI), expiratory time (TE), breathing frequency (f), and mean inspiratory flow (VT/TI) on a breath-by-breath basis. Results: The hyperventilation maneuver caused a decrease in spontaneous ventilation in pilocarpine-treated and control rats. Although VE had a similar decrease in both groups, in the epileptic group, the decrease in VE was due to a significant (p < 0.05) increase in TE peak in relation to that of the control animals. The hypoventilation maneuver led to an increase in the arterial Paco2, followed by an increase in VE. In the epileptic group, the increase in VE was mediated by a significant (p < 0.05) decrease in TE peak compared with the control group. Systemic application of KCN, to evaluate the effects of peripheral chemoreception activation on ventilation, led to a similar increase in VE for both groups. Conclusions: The data indicate that pilocarpine-treated animals have an altered ability to react to (or compensate for) blood gas changes with changes in ventilation and suggest that it is centrally determined. We speculate on the possible relation of the current findings on treating different epilepsy-associated conditions.

Impact of sleep on ventilation and gas exchange in chronic lung disease.

Abstract: Sleep has many effects on breathing, all potentially adverse, ranging from the respiratory centre to the lower airways and chest wall. The overall effect is to diminish ventilation with consequent hypoxaemia and hypercapnia. These physiological changes can have major adverse effects on patients with chronic lung disease, particularly if already hypoxaemic. Patients with obstructive airway disease are particularly adversely affected during sleep with hypoventilation and reduced tidal volume, whereas patients with interstitial disease maintain overall ventilation although respiratory frequency falls. Sleep-related effects are most pronounced in rapid-eye-movement (REM) sleep and can have significant cardiovascular consequences including sleep-related cardiac arrhythmias and pulmonary hypertension and can also predispose to nocturnal death, particularly during acute exacerbations.

Sleep dysfunction in neuromuscular disorders

Abstract: There is an increasing awareness of sleep dysfunction in neuromuscular disorders. Most of the sleep disturbances in neuromuscular disorders are secondary to sleep disordered breathing. Sleep-disordered breathing in neuromuscular disorders is commonly associated with a slowly developing chronic respiratory failure, particularly in the advanced stages, but the condition often remains unrecognized and untreated. The most common sleep-disordered breathing in neuromuscular disorders is sleep-related hypoventilation which initially manifests during REM sleep and later as the disease advances, it is also noted during non-REM sleep and even during daytime. In addition to the hypoventilation, central and upper airway obstructive apneas as well as hypopneas occur. Hypoventilation during sleep gives rise to hypoxemia and hypercapnea causing chronic respiratory failure. The abnormal blood gases may later persist during the daytime. Some patients may, however, have sleep onset or maintenance insomnia as a result of associated pain, muscle immobility, contractures, joint pains and muscle cramps as well as anxiety and depression.The commonest complaint in patients with neuromuscular disorders associated with sleep-disordered breathing is excessive daytime somnolence as a result of repeated arousals and sleep fragmentation due to sleep hypoventilation and transient nocturnal hypoxemia. Sleep-disordered breathing causing sleep disturbance is well known in patients with poliomyelitis, postpolio syndrome, amyotrophic lateral sclerosis, also known as motor neuron disease, primary muscle disorders including muscular dystrophies and myotonic dystrophy, congenital or acquired myopathies, neuromuscular junctional disorders and polyneuropathies. All of these conditions may cause weakness of the diaphragm, the intercostal and accessory muscles of respiration causing breathlessness and other respiratory dysrhythmias. As a result of the respiratory and upper airway muscle weakness, the normal sleep-related respiratory physiologic vulnerability becomes pathological in these patients with neuro-muscular disorders causing hypoventilation or central and upper airway obstructive apneas during sleep. Multiple factors are responsible for sleep-disordered breathing in neuromuscular disorders causing sleep hypoventilation and other respiratory dysrhythmias, and these include: impaired chest bellows, increased work of breathing, hypo-responsive respiratory chemoreceptors, increased upper airway resistance, decreased minute and alveolar ventilation, REM-related marked hypotonia or atonia of the respiratory muscles except the diaphragm, respiratory muscle fatigue and kyphoscoliosis secondary to neuromuscular disorders causing extrapulmonary restriction of the lungs. Nocturnal hypoventilation and chronic respiratory failure in neuromuscular disorders may present insidiously and initially may remain asymptomatic. A high index of clinical suspicion is needed. Clinical clues suggesting sleep-disordered breathing include daytime hypersomnolence, breathlessness, disturbed nocturnal sleep and unexplained leg edema. If the clinical clues strongly suggest sleep-disordered breathing, a physical examination must be directed to uncover bulbar and respiratory muscle weakness. Patients with neuromuscular disorders showing these clinical features must be investigated to uncover nocturnal hypoventilation to prevent serious consequences of chronic.

A Sudden Death Due to Central Hypoventilation in A 3-Year-Old Boy with Idiopathic Hypothalamic Dysfunction

Abstract: Idiopathic hypothalamic dysfunction is a rare disorder associated with adipsia, obesity and other symptoms such as central hypoventilation without any hypothalamic structural lesion. We report the case of a 3-year-old boy who died suddenly due to central hypoventilation. His obesity index increased from 0% to 75% during the 7 months prior to 3 yr 0 mo. During this clinical course, adipsia, hyperthermia, sudoresis, mild central hypoventilation, blepharoptosia, a change of character, hypernatremia, and hypothalamic hypopituitarism were observed. No treatment was given for hypoventilation. He died from sudden respiratory arrest because of central hypoventilation at 3 yr 8 mo. MRI examination was performed twice at 3 yr 3 mo and 3 yr 4 mo and revealed neither specific lesion nor invisible pituitary stalk. At autopsy, local inflammation and gliosis of the hypothalamus were present. So far at least 14 patients with idiopathic hypothalamic dysfunction have been reported. Eight cases including ours had central hypoventilation. Six out of the eight had poor respiratory prognosis, and central hypoventilation in hypothalamic dysfunction could be potentially fatal. In conclusion the patients with hypothalamic dysfunction should be treated intensively if they are suspected of having central hypoventilation.

Supplemental oxygen is not required in trauma patients treated with IV opiates.

Abstract: The risk of respiratory depression can prevent the proper use of opioids in trauma patients and lead to use of supplemental oxygen. However, high FiO 2 might contribute to atelectasis formation and consequently to relative hypoxia. Supplemental oxygen also can cause a risk of fire. In a randomized, controlled study we evaluated the need and effects of supplemental oxygen in 13 patients with extremity trauma who were treated pain-free with an intravenous opioid, oxycodone (dose range 6.75-13.6 mg). After opioid injection, 7 patients received 40% supplemental oxygen and 6 were breathing room air. Pulse oxygen saturation (SpO 2 ), arterial blood gases, and hemodynamic parameters were monitored for 30 minutes. Atelectasis formation was evaluated with a computed tomography scan. No hypoxia, hypoventilation, or significant atelectasis formation was detected in any of the patients. Accordingly, routinely given supplemental oxygen was not considered necessary in these patients because no complications were seen. (Am J Emerg Med 2003;21:35-38. Copyright 2003, Elsevier Science (USA). All rights reserved.)

Preconditioning by hypoventilation increases ventricular arrhythmia threshold in Wistar rats.

Abstract: Summary Hypoventilation, as one of ventilatory disorders, decreases the electrical stability of the heart similarly as ischemia. If preconditioning by short cycles of ischemia has a cardioprotective effect against harmful influences of a prolonged ischemic period, then preconditioning by hypoventilation (HPC) can also have a similar effect. Anesthetized rats (ketamine 100 mg/kg + xylasine 15 mg/kg i.m., open chest experiments) were subjected to 20 min of hypoventilation followed by 20 min of reoxygenation (control group). The preconditioning (PC) was induced by one (1PC), two (2PC) or three (3PC) cycles of 5-min hypoventilation followed by 5-min reoxygenation. The electrical stability of the heart was measured by a ventricular arrhythmia threshold (VAT) tested by electrical stimulation of the right ventricle. Twenty-minute hypoventilation significantly decreased the VAT in the control and 1PC groups (p<0.05) and nonsignificantly in 2PC vs. the initial values. Reoxygenation reversed the VAT values to the initial level only in the control group. In 3PC, the VAT was increased from 2.32±0.69 mA to 4.25±1.31 mA. during hypoventilation (p<0.001) and to 4.37±1.99 mA during reoxygenation (p<0.001). It is concluded that cardioprotection against the hypoventilation/ reoxygenation-induced decrease of VAT proved to be effective only after three cycles of HPC.

Pulmonary function screening.

Abstract: Patients who suffer from neuromuscular diseases often have complications from respiratory insufficiencies. Some neuromuscular diseases, for example Landry Guillain-Barre syndrome, may only require temporary tracheal intubation; patients with other neuromuscular diseases, such as amyotrophic lateral sclerosis, may decide with the assistance of their doctor and family to opt for lifelong noninvasive ventilatory support. Other patients may only opt for noninvasive positive pressure ventilation. Respiratory dysfunction is caused by weakness of the upper airway muscles, which can lead to sleep apnea, abnormal swallow, and decreased respiratory muscle strength, as well as a decrease in total lung volume. Early respiratory changes in patients with neuromuscular disease are often best detected during sleep. During rapid eye movement sleep, there is a reduction in respiratory drive predisposing to hypopneas and apneas. The majority of neuromuscular patients with respiratory insufficiency may be monitored and treated in the outpatient setting, thus allowing them to remain in their homes.

Central alveolar hypoventilation syndrome

Abstract: Alveolar hypoventilation of central origin and primary in appearance was described over 30 years ago: it is characterised by considerable daytime hypoxemia-hypercapnia, but which is often well-tolerated, and by the abolition of the ventilatory response to a hypercapnic stimulus. Central chemoreceptor dysfunctioning, demonstrated by an abnormal response to the CO2 stimulus, is the most characteristic trait of this syndrome [2], but peripheral chemoreceptor deficiency, responsible for the ventilatory response to hypoxia, has also been observed in some cases. The syndromes of central alveolar hypoventilation and central apnoeas are not absolutely synonymous, even if the former can elicit the latter: central apnoeas have been observed in the absence of any daytime hypoventilation, and central hypoventilation syndrome is not necessarily accompanied by central apnoeas during sleep. Nor is central alveolar hypoventilation synonymous with obesity-hypoventilation syndrome (the current term for Pickwick’s syndrome) even though these conditions have several points in common. Central apnoea syndrome and obesity-hypoventilation syndrome are described in other chapters of the present volume.

Ketamine Sedation in Children Does Not Cause Hypoventilation

Abstract: Ketamine is often chosen as a dissociative sedative for children undergoing procedures in the emergency department, because ventilation and airway protection are maintained during its use. However, occasional reports of respiratory compromise raise …

Sleep-related breathing disorders

Abstract: Sleep-related breathing disorders cause significant morbidity through excessive hypersomnolence, cognitive impairment, unrefreshing sleep and other symptoms. Potential consequences include accidents related to sleepiness and cardiovascular diseases. In the most common obstructive sleep apnoea syndrome, apnoeas and hypopnoeas are related to intermittent upper airways collapse. In central sleep apnoea and Cheyne-Stokes respiration associated with congestive heart failure, the waxing and waning of ventilation is caused by an unstable respiratory motor output. Chronic sleep-related hypoventilation may occur in extreme obesity, in neuro-muscular disorders that affect respiratory muscles and in patients with chest-wall deformities and lung diseases. The diagnosis of sleep-related breathing disorders is suggested by typical symptoms and confirmed by a sleep study. Treatment options include various forms of positive pressure ventilation applied by a nasal or face mask, removable oral appliances that increase the upper airway lumen by advancing the mandible, and surgery in selected cases.

Gedeihstörung bei Hypoventilation im Schlaf

Abstract: Das Mädchen wurde nach 35wöchiger Schwangerschaft als erster Zwilling durch Sectio geboren. Es wog 2090 g, und der APGARScore wurde mit 9/10/10 bewertet. In den ersten Lebenstagen wurden Bradykardien und Apnoen beobachtet. Der Gewichtsverlauf entwickelte sich zunächst normal und bewegte sich um die 3. Perzentile. Ab dem 17. Lebensmonat wurde eine ungenügende Gewichtszunahme beobachtet (Gedeihstörung, Abb. 1). Ab dem 44. Lebensmonat wurde zusätzlich Nahrung mit einer PEGSonde zugeführt, was zu einer vorübergehenden Gewichtszunahme führte. Wegen einer schlafgebundenen Hypoventilation wurde ab dem 52. Lebensmonat nachts Sauerstoff verabreicht. Mehrere bronchiale Infekte und zwei Pneumonien folgten. Die Abklärung bestätigte das vermutete zentrale Apnoesyndrom. Die Polysomnographie dokumentierte eine Atemfrequenz von 5 Atemzügen/Minute und eine Sauerstoffsättigung, die zwischen 71% und 96% pendelte, mit einem Durchschnittswert von 91%. Die Schlafarchitektur war abnorm. Die Schlafeffizienz betrug 61% (Norm >90%); der Schlaf war durchbrochen von zahlreichen Weckreaktionen und im Schlaf auftretenden laryngospastischen Anfällen, die das Kind weckten und wegen Erstickungsangst nach der Mutter riefen liessen. REM-Schlaf fehlte vollständig (Norm >20%). Im Alter von 5 Jahren und 10 Monaten wurden das Mädchen und die Mutter während einer 10tägigen Hospitalisation mit einer Bi-LevelBeatmung vertraut gemacht, und das Mädchen wurde eingeschult. Bei guter Compliance (immer beatmet, wenn schlafend) trat eine Beruhigung der Nacht ein, das aggressive Verhalten bildete sich zurück und die Gewichtskurve zeigte ohne weitere Massnahme einen Wechsel in höhere Perzentilenbereiche (Abb. 1). Die Bronchitisneigung verschwand und es traten keine Pneumonien mehr auf.