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.

Ophthalmologic Impairment during Adulthood in Central Congenital Hypoventilation Syndrome: A Longitudinal Cohort Analysis of Nine Patients

Abstract: Background: Congenital central hypoventilation syndrome (CCHS) is a rare dysgenetic form of neurocristopathy associated with dysfunction of the autonomic nervous system. Ophthalmologic abnormalities are reported in CCHS children, and range from pupillary and iris abnormalities to ptosis, strabismus and convergence deficiency. Since earlier CCHS diagnosis and multidisciplinary management, combined with improved ventilatory support techniques, the lifespan of children with CCHS has been considerably lengthened. The oldest of them have now reached adult age and we report in this study the results of their ophthalmologic examination.Materials and methods: Nine CCHS adult patients were prospectively included during a 14-month period. Each patient underwent complete ophthalmologic examination, static pupillometry with scotopic and photopic pupillary diameter (PD) measures, Humphrey 24-2 visual field analysis, macular OCT and complete orthoptic assessment including a Hess-Lancaster test.Results: Ophthalm...

Die überbewertete Hypoxämie

Abstract: Extreme mountain climbers and patients with stable but severe ventilatory insufficiency (e.g. obesitas hypoventilation-syndrome, scoliosis) sometimes experience a state of severe hypoxemia without any or only mild subjective disturbances. Organ failure is never observed in these periods. On the other hand there are two well documented studies concerning long term oxygen therapy (LTOT) that have shown in hypoxemic COPD-patients (pO 2 lower then 55 mm Hg) a doubling the life expectancy under oxygen. This contradiction can be elucidated if the influence of oxygen on the ventilation is taken into account. These study patients treated with LTOT all had more or less hypercapnia (hypoventilation) due to an overload of their respiratory pump. Oxygen reduces the ventilation (seen as hypercapnia) which leads to an unloading of the respiratory muscles. Later studies to LTOT found a positive correlation between the extent of stable hypercapnia and life expectancy. In this article the physiopathologic background of this findings are discussed. The main parameter of the regulator for the oxygen transport is not pO 2 but the oxygen content. The oxygen content multiplied by cardiac output determines the extent of oxygen delivery. Many regulatory systems (e.g. polyglobuly or expression of oxygen resistant isoenzymes of the respiratory chain) are involved to compensate the hypoxemia associated with hypoventilation which prevents an organ threatening hypoxia. This pathophysiologic finding has important impact on intensive care medicine, which usually takes only pO 2 into account for therapeutic decisions (e. g. high FiO 2 and high pressure support). This sometimes leads to "overtreatment", with possible harm to the patient.

Monitoring Long Term Noninvasive Ventilation: Benefits, Caveats and Perspectives

Abstract: Long term noninvasive ventilation (LTNIV) is a recognized treatment for chronic hypercapnic respiratory failure (CHRF). COPD, obesity-hypoventilation syndrome, neuromuscular disorders, various restrictive disorders, and patients with sleep-disordered breathing are the major groups concerned. The purpose of this narrative review is to summarize current knowledge in the field of monitoring during home ventilation. LTNIV improves symptoms related to CHRF, diurnal and nocturnal blood gases, survival, and health-related quality of life. Initially, patients with LTNIV were most often followed through elective short in-hospital stays to ensure patient comfort, correction of daytime blood gases and nocturnal oxygenation, and control of nocturnal respiratory events. Because of the widespread use of LTNIV, elective in-hospital monitoring has become logistically problematic, time consuming, and costly. LTNIV devices presently have a built-in software which records compliance, leaks, tidal volume, minute ventilation, cycles triggered and cycled by the patient and provides detailed pressure and flow curves. Although the engineering behind this information is remarkable, the quality and reliability of certain signals may vary. Interpretation of the curves provided requires a certain level of training. Coupling ventilator software with nocturnal pulse oximetry or transcutaneous capnography performed at the patient's home can however provide important information and allow adjustments of ventilator settings thus potentially avoiding hospital admissions. Strategies have been described to combine different tools for optimal detection of an inefficient ventilation. Recent devices also allow adapting certain parameters at a distance (pressure support, expiratory positive airway pressure, back-up respiratory rate), thus allowing progressive changes in these settings for increased patient comfort and tolerance, and reducing the requirement for in-hospital titration. Because we live in a connected world, analyzing large groups of patients through treatment of “big data” will probably improve our knowledge of clinical pathways of our patients, and factors associated with treatment success or failure, adherence and efficacy. This approach provides a useful add-on to randomized controlled studies and allows generating hypotheses for better management of HMV.

[O2 chemoreflex drive of ventilation in the awake rat (author's transl)].

Abstract: Resting ventilation, arterial pH and gas tensions in the arterial blood and ventilatory responses to transient O2 inhalation were studied by plethysmography, under normoxic and hypoxic (FIO2 = 0.12) conditions, in the awake rat before and after chronic bilateral denervation of the carotid bodies. 1. In the intact rat, the O2-chemoreflex drive of ventilation controlled about 50% of the normoxic minute volume, and 85% in hypoxia. 2. Chronic bilateral carotid body denervation reduced the chemoreflex drive to half, and was accompanied by a hypoventilation with arterial hypercapnia. 3. In acute hypoxia hyperventilation was reduced in carotid-body denervated animals, and was accompanied by a light respiratory insufficiency. These results suggest that the rat has a powerful arterial chemoreflex drive of breathing which is essential in determining the eupneic level of ventilation in acute hypoxia.

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.